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Endovascular Repair Can Treat Mesenteric Insufficiency
PALM BEACH, FLA. - Many patients with chronic mesenteric vascular insufficiency can be treated with an endovascular approach - either angioplasty or stenting with bare metal or covered devices.
Unlike open procedures, the endovascular approach carries a low risk of postoperative morbidity and mortality, Dr. Phillip Burns said at the annual meeting of the Southern Surgical Association. However, he noted, the recurrence rate for stenosis or occlusion was high in his retrospective series, with about one-third of patients requiring a second, or even third, intervention within the first 2 years after surgery.
Thus, an intensive follow-up is necessary for patients who undergo endovascular reconstruction. Under his protocol, patients return every 6 months for a clinical exam and duplex ultrasound, said Dr. Burns of the University of Tennessee, Chattanooga.
"Secondary procedures are often indicated for recurrent stenosis, and you have to look for this carefully," he said. Signs and symptoms might not be observed initially, "but if you continue to search for them, you will find them and be able to perform the reinterventions."
Dr. Burns and his colleagues presented a retrospective study of 107 patients with 127 vessels treated from 2004 to June 2010. All of the procedures were performed by a vascular specialist in an endovascular operating suite.
Patients were usually referred for gastrointestinal symptoms and already had undergone a GI workup. Most (88%) complained of abdominal pain; 55% had experienced weight loss and 29% reported nausea. All underwent an abdominal ultrasound that showed mesenteric vascular abnormalities.
The patients' average age was 59 years (range 18-90 years). Most (70%) were women. As a group, they displayed several important comorbidities, including hypertension, diabetes, coronary artery disease, and smoking.
Of the 127 vessels treated, 68 were superior mesenteric arteries, 52 were celiac arteries, and 7 were inferior mesenteric arteries. A balloon-expandable bare metal stent was most commonly used (66%; 87 patients) followed by balloon angioplasty (22%; 29), covered stent (10%; 14), and one self-expanding stent (1%; 1). All patients were put on either aspirin or clopidogrel therapy for at least 30 days after surgery. Patients also received continuing treatment for the hyperlipidemia that caused their atherosclerotic disease.
At 1 year, primary patency was seen in 67% of those with angioplasty, 54% of those with bare metal stents, and 100% of those with covered stents. The patency rates for the two stent types were significantly different.
More than half of the patients (57%; 55) experienced complete resolution of their symptoms, but 38% of these (21) required a second intervention. Of the 43% (41) who reported partial symptom relief, more than half (59%; 24) required a reintervention.
"That led to 45 patients going back for at least one other intervention," Dr. Burns said. "Five were not deemed treatable endovascularly and were done as open procedures. All others were done endovascularly, with 25 requiring a second reintervention and 8, a third reintervention."
In the reinterventions, 1-year patency was 86% with angioplasty, 97% with bare metal stents, and 100% with covered stents. There were 11 deaths in the cohort, 2 of which were due to chronic mesenteric vascular disease.
"In our opinion, both of those were in patients who did not follow up appropriately," said Dr. Christopher J. LeSar, also of the University of Tennessee, who closed the paper. "It's our belief that in treating this disease, the endovascular approach is reasonable if it's married to a very stringent follow-up protocol. Patients were counseled to be very wary of any recurrent symptoms and to act on them immediately if they occurred."
During the discussion, Dr. Eugene M. Langan III "facs" of the Greenville (S.C.) Hospital System University Medical Center, asked if the good outcomes associated with the covered stent are enough to recommend its use as the primary reconstruction method.
It's too early to make the assumption, said Dr. LeSar. The covered stents were only used in only 25 patients with an average follow-up of just 6 months. "This was related to the fact that we discovered [the covered stent success] later in our clinical experience," said Dr. LeSar. "In this population, one of the main problems was recurrent disease, and we found that only four patients with a covered stent required additional reinterventions, which led us to consider placing this type of stent as the primary answer for prevention of stenosis."
The crux of the issue is how to predict who can reap the biggest benefit from endovascular repair, leaving open surgery only to those who really require it, said Dr. Marc Mitchell of the University of Mississippi, Jackson. That seems to remain an unknown, said Dr. LeSar.
"We don't know why many develop hyperplasia, but some tend to and it seems to be random," he said.
Neither Dr. Burns nor Dr. LeSar reported any financial conflicts.
PALM BEACH, FLA. - Many patients with chronic mesenteric vascular insufficiency can be treated with an endovascular approach - either angioplasty or stenting with bare metal or covered devices.
Unlike open procedures, the endovascular approach carries a low risk of postoperative morbidity and mortality, Dr. Phillip Burns said at the annual meeting of the Southern Surgical Association. However, he noted, the recurrence rate for stenosis or occlusion was high in his retrospective series, with about one-third of patients requiring a second, or even third, intervention within the first 2 years after surgery.
Thus, an intensive follow-up is necessary for patients who undergo endovascular reconstruction. Under his protocol, patients return every 6 months for a clinical exam and duplex ultrasound, said Dr. Burns of the University of Tennessee, Chattanooga.
"Secondary procedures are often indicated for recurrent stenosis, and you have to look for this carefully," he said. Signs and symptoms might not be observed initially, "but if you continue to search for them, you will find them and be able to perform the reinterventions."
Dr. Burns and his colleagues presented a retrospective study of 107 patients with 127 vessels treated from 2004 to June 2010. All of the procedures were performed by a vascular specialist in an endovascular operating suite.
Patients were usually referred for gastrointestinal symptoms and already had undergone a GI workup. Most (88%) complained of abdominal pain; 55% had experienced weight loss and 29% reported nausea. All underwent an abdominal ultrasound that showed mesenteric vascular abnormalities.
The patients' average age was 59 years (range 18-90 years). Most (70%) were women. As a group, they displayed several important comorbidities, including hypertension, diabetes, coronary artery disease, and smoking.
Of the 127 vessels treated, 68 were superior mesenteric arteries, 52 were celiac arteries, and 7 were inferior mesenteric arteries. A balloon-expandable bare metal stent was most commonly used (66%; 87 patients) followed by balloon angioplasty (22%; 29), covered stent (10%; 14), and one self-expanding stent (1%; 1). All patients were put on either aspirin or clopidogrel therapy for at least 30 days after surgery. Patients also received continuing treatment for the hyperlipidemia that caused their atherosclerotic disease.
At 1 year, primary patency was seen in 67% of those with angioplasty, 54% of those with bare metal stents, and 100% of those with covered stents. The patency rates for the two stent types were significantly different.
More than half of the patients (57%; 55) experienced complete resolution of their symptoms, but 38% of these (21) required a second intervention. Of the 43% (41) who reported partial symptom relief, more than half (59%; 24) required a reintervention.
"That led to 45 patients going back for at least one other intervention," Dr. Burns said. "Five were not deemed treatable endovascularly and were done as open procedures. All others were done endovascularly, with 25 requiring a second reintervention and 8, a third reintervention."
In the reinterventions, 1-year patency was 86% with angioplasty, 97% with bare metal stents, and 100% with covered stents. There were 11 deaths in the cohort, 2 of which were due to chronic mesenteric vascular disease.
"In our opinion, both of those were in patients who did not follow up appropriately," said Dr. Christopher J. LeSar, also of the University of Tennessee, who closed the paper. "It's our belief that in treating this disease, the endovascular approach is reasonable if it's married to a very stringent follow-up protocol. Patients were counseled to be very wary of any recurrent symptoms and to act on them immediately if they occurred."
During the discussion, Dr. Eugene M. Langan III "facs" of the Greenville (S.C.) Hospital System University Medical Center, asked if the good outcomes associated with the covered stent are enough to recommend its use as the primary reconstruction method.
It's too early to make the assumption, said Dr. LeSar. The covered stents were only used in only 25 patients with an average follow-up of just 6 months. "This was related to the fact that we discovered [the covered stent success] later in our clinical experience," said Dr. LeSar. "In this population, one of the main problems was recurrent disease, and we found that only four patients with a covered stent required additional reinterventions, which led us to consider placing this type of stent as the primary answer for prevention of stenosis."
The crux of the issue is how to predict who can reap the biggest benefit from endovascular repair, leaving open surgery only to those who really require it, said Dr. Marc Mitchell of the University of Mississippi, Jackson. That seems to remain an unknown, said Dr. LeSar.
"We don't know why many develop hyperplasia, but some tend to and it seems to be random," he said.
Neither Dr. Burns nor Dr. LeSar reported any financial conflicts.
PALM BEACH, FLA. - Many patients with chronic mesenteric vascular insufficiency can be treated with an endovascular approach - either angioplasty or stenting with bare metal or covered devices.
Unlike open procedures, the endovascular approach carries a low risk of postoperative morbidity and mortality, Dr. Phillip Burns said at the annual meeting of the Southern Surgical Association. However, he noted, the recurrence rate for stenosis or occlusion was high in his retrospective series, with about one-third of patients requiring a second, or even third, intervention within the first 2 years after surgery.
Thus, an intensive follow-up is necessary for patients who undergo endovascular reconstruction. Under his protocol, patients return every 6 months for a clinical exam and duplex ultrasound, said Dr. Burns of the University of Tennessee, Chattanooga.
"Secondary procedures are often indicated for recurrent stenosis, and you have to look for this carefully," he said. Signs and symptoms might not be observed initially, "but if you continue to search for them, you will find them and be able to perform the reinterventions."
Dr. Burns and his colleagues presented a retrospective study of 107 patients with 127 vessels treated from 2004 to June 2010. All of the procedures were performed by a vascular specialist in an endovascular operating suite.
Patients were usually referred for gastrointestinal symptoms and already had undergone a GI workup. Most (88%) complained of abdominal pain; 55% had experienced weight loss and 29% reported nausea. All underwent an abdominal ultrasound that showed mesenteric vascular abnormalities.
The patients' average age was 59 years (range 18-90 years). Most (70%) were women. As a group, they displayed several important comorbidities, including hypertension, diabetes, coronary artery disease, and smoking.
Of the 127 vessels treated, 68 were superior mesenteric arteries, 52 were celiac arteries, and 7 were inferior mesenteric arteries. A balloon-expandable bare metal stent was most commonly used (66%; 87 patients) followed by balloon angioplasty (22%; 29), covered stent (10%; 14), and one self-expanding stent (1%; 1). All patients were put on either aspirin or clopidogrel therapy for at least 30 days after surgery. Patients also received continuing treatment for the hyperlipidemia that caused their atherosclerotic disease.
At 1 year, primary patency was seen in 67% of those with angioplasty, 54% of those with bare metal stents, and 100% of those with covered stents. The patency rates for the two stent types were significantly different.
More than half of the patients (57%; 55) experienced complete resolution of their symptoms, but 38% of these (21) required a second intervention. Of the 43% (41) who reported partial symptom relief, more than half (59%; 24) required a reintervention.
"That led to 45 patients going back for at least one other intervention," Dr. Burns said. "Five were not deemed treatable endovascularly and were done as open procedures. All others were done endovascularly, with 25 requiring a second reintervention and 8, a third reintervention."
In the reinterventions, 1-year patency was 86% with angioplasty, 97% with bare metal stents, and 100% with covered stents. There were 11 deaths in the cohort, 2 of which were due to chronic mesenteric vascular disease.
"In our opinion, both of those were in patients who did not follow up appropriately," said Dr. Christopher J. LeSar, also of the University of Tennessee, who closed the paper. "It's our belief that in treating this disease, the endovascular approach is reasonable if it's married to a very stringent follow-up protocol. Patients were counseled to be very wary of any recurrent symptoms and to act on them immediately if they occurred."
During the discussion, Dr. Eugene M. Langan III "facs" of the Greenville (S.C.) Hospital System University Medical Center, asked if the good outcomes associated with the covered stent are enough to recommend its use as the primary reconstruction method.
It's too early to make the assumption, said Dr. LeSar. The covered stents were only used in only 25 patients with an average follow-up of just 6 months. "This was related to the fact that we discovered [the covered stent success] later in our clinical experience," said Dr. LeSar. "In this population, one of the main problems was recurrent disease, and we found that only four patients with a covered stent required additional reinterventions, which led us to consider placing this type of stent as the primary answer for prevention of stenosis."
The crux of the issue is how to predict who can reap the biggest benefit from endovascular repair, leaving open surgery only to those who really require it, said Dr. Marc Mitchell of the University of Mississippi, Jackson. That seems to remain an unknown, said Dr. LeSar.
"We don't know why many develop hyperplasia, but some tend to and it seems to be random," he said.
Neither Dr. Burns nor Dr. LeSar reported any financial conflicts.
Man, 54, With Delusions and Seizures
A 54-year-old African-American man was brought by police officers to the emergency department (ED) after he called 911 several times to report seeing a Rottweiler looking into his second-story window. At the scene, the police were unable to confirm his story, thought the man seemed intoxicated, and brought him to the ED for evaluation.
The patient reported that he had been drinking the previous evening but denied current intoxication or illicit drug use. He denied experiencing symptoms of alcohol withdrawal.
Regarding his medical history, the patient admitted to having had seizures, including two episodes that he said required hospitalization. He described these episodes as right-hand “tingling” (paresthesias), accompanied by right-facial numbness and aphasia. The patient said his physician had instructed him to take “a few phenytoin pills” whenever these episodes occurred. He reported that the medication usually helped resolve his symptoms. He said he had taken phenytoin shortly before his current presentation.
According to friends of the patient who were questioned, he had had noticeable memory problems during the previous six to eight months. They said that he often told the same joke, day after day. His speech had become increasingly slurred, even when he was not drinking.
Once the patient’s medical records were retrieved, it was revealed that he had been hospitalized twice for witnessed grand mal seizures about six months before his current admission; he had been drinking alcohol prior to both episodes. He underwent electroencephalography (EEG) during one of these hospitalizations, with results reported as normal. On both occasions, the patient was discharged with phenytoin and was instructed to follow up with his primary care provider and neurologist.
The patient, who reported working in customer service, had no known allergies. He claimed to drink one or two 40-ounce beers twice per week and admitted to occasional cocaine use. Of significance in his family history was a fatal MI in his mother. Although the patient denied any history of rashes or lesions, his current delirium made it impossible to obtain a reliable sexual history; a friend who was questioned, however, described the patient as promiscuous.
On initial physical examination, the man was afebrile, tachycardic, and somewhat combative with the ED staff. He was fully oriented to self but only partially to place and time.
His right pupil was 3+ and his left pupil was 2+, with neither reactive to light. He spoke with tangential speech and his gait was unsteady, but no other significant abnormalities were noted. A full assessment revealed no rashes or other lesions.
Significant laboratory findings included a low level of phenytoin, a negative blood alcohol level, presence of cocaine on urine drug screening, and normal levels of thyroid-stimulating hormone (TSH), vitamin B12, and folate. The patient’s serum VDRL (venereal disease research laboratory) titer was positive at 1:256.
Electroencephalography showed diffuse slowing, and brain CT performed in the ED showed atrophy that was mild but appropriate for a person of the patient’s age, with no evidence of a cerebrovascular accident (CVA). Aneurysm was ruled out by CT angiography of the brain. MRI revealed persistent increased signal in the subarachnoid space.
The patient was admitted with an initial diagnosis of paranoid delusional psychosis and monitored for alcohol withdrawal. He was given lorazepam as needed for agitation. Consultations were arranged with the psychiatry service regarding his delusions, and with neurology to determine whether to continue phenytoin.
The patient showed little response during the next several days. Based on positive results on serum VDRL with high titer, the presence of Argyll-Robertson pupils on exam, and his history of dementia-like symptoms, a lumbar puncture was performed to rule out neurosyphilis. In the patient’s cerebral spinal fluid (CSF) analysis, the first tube was clear and colorless, with 72 cells (28% neutrophils, 59% lymphocytes); glucose, 64 mg/dL; and total protein, 117 mg/dL. The fourth tube had 34 cells (17% neutrophils, 65% lymphocytes) and a positive VDRL titer at 1:128. Results from a serum syphilis immunoglobulin G (IgG) test were positive, and HIV antibody testing was nonreactive, confirming the diagnosis of neurosyphilis.
The hospital’s infectious disease (ID) team recommended treatment with IV penicillin for 14 days. Once this was completed, the patient was discharged with instructions to follow up at the ID clinic in three months for a repeat CSF VDRL titer to monitor for resolution of the disease. His prescription for phenytoin was discontinued.
At the time of discharge, it was noted that the patient showed no evidence of having regained cognitive function. He was deemed by the psychiatry service to lack decision-making capacity—a likely sequelae of untreated neurosyphilis of unknown duration.
He did return to the ID clinic six months after his discharge. At that visit, a VDRL serum titer was drawn with a result of 1:64, a decrease from 1:128. His syphilis IgG remained positive, however.
Discussion
Definition and Epidemiology
Syphilis is commonly known as a sexually transmitted disease with primary, secondary, and tertiary (early and late latent) stages.1 Neurosyphilis is defined as a manifestation of the inflammatory response to invasion over decades by the Treponema pallidum spirochete in the CSF as a result of untreated primary and/or secondary syphilis.2 About one in 10 patients with untreated syphilis will experience neurologic involvement.3,4 Before 2005, neurosyphilis was required to be reported as a specific stage of syphilis (ie, a manifestation of tertiary syphilis4), but now should be reported as syphilis with neurologic manifestations.5
A reportable infectious disease, syphilis was widespread until the advent of penicillin. According to CDC statistics,6 the number of reported cases of primary and secondary syphilis has declined steadily since 1943. In the late 1970s and early 1980s, the number of tertiary cases also began to plateau, likely as a result of earlier diagnosis and more widespread use of penicillin. Recent case reports suggest greater prevalence of syphilis among men than women and increased incidence among men who have sex with men.7
Pathogenesis
Syphilis is most commonly spread by sexual contact or contact with an infected primary lesion (chancre). Less likely routes of transmission are placental passage or blood transfusion. Infectivity is greatest in the early disease stages.8
Primary syphilis is marked by transmission of the spirochete, ending with development of secondary syphilis (usually two to 12 weeks after transmission). A chancre commonly develops but is often missed by patients because it is painless and can heal spontaneously.7 The chancre is also often confused with two other sources of genital lesions, herpes simplex (genital herpes) and Haemophilus ducreyi (chancroid). In two-thirds of cases of untreated primary syphilis, the infection clears spontaneously, but in the remaining one-third, the disease progresses.8
Secondary syphilis, with or without presence of a chancre, manifests with constitutional symptoms, including lymphadenopathy, fever, headache, and malaise. Patients in this disease phase may also present with a generalized, nonpruritic, macular to maculopapular or pustular rash. The rash can affect the skin of the trunk, the proximal extremities, and the palms and soles. Ocular involvement may occur, especially in patients who are coinfected with HIV.8 In either primary or secondary syphilis, infection can invade the central nervous system.1
During latent syphilis, patients show serologic conversion without overt symptoms. Early latent syphilis is defined as infection within the previous year, as demonstrated by conversion from negative to positive testing, or an increase in titers within the previous year. Any case occurring after one year is defined as late or unknown latent syphilis.8
Tertiary syphilis is marked by complications resulting from untreated syphilis; affected patients commonly experience central nervous system and cardiovascular involvement. Gummatous disease is seen in 15% of patients.1
The early stages of neurosyphilis may be asymptomatic, acute meningeal, and meningovascular.1,4,8,9 Only 5% of patients with early neurosyphilis are symptomatic, with the added potential for cranial neuritis or ocular involvement.1 The late stages of neurosyphilis are detailed in the table.1,4,8
Diagnosis
A diagnosis of syphilis is made by testing blood samples or scrapings from a lesion. In patients with suspected syphilis, rapid plasma reagin (RPR) testing or a VDRL titer is commonly ordered. When results are positive, a serum treponemal test is recommended to confirm a diagnosis of syphilis. Options include the fluorescent treponemal antibody absorption test (FTA-ABS) and the microhemagglutinin assay for antibody to T pallidum (MHA-TP).5
If neurologic symptoms are present, a CSF sample should be obtained, followed by the same testing. A confirmed diagnosis of neurosyphilis is defined by the CDC as syphilis at any stage that meets laboratory criteria for neurosyphilis5; these include increased CSF protein or an elevated CSF leukocyte count with no other known cause, and clinical signs or symptoms without other known causes.7
Treatment
Treatment of syphilis generally consists of penicillin, administered intramuscularly (IM) or IV, depending on the stage. According to 2006 guidelines from the CDC,10,11 treatment for adults with primary and secondary syphilis is a single dose of IM penicillin G, 2.4 million units. If neurosyphilis is suspected, recommended treatment is IV penicillin G, 18 to 24 million units per day divided into six doses (ie, 3 to 4 million units every four hours) or continuous pump infusion for 10 to 14 days.10-12 Follow-up is recommended by monitoring CSF titers to ensure clearance of infection; retreatment may be required if CSF abnormalities persist after two years.11
Patients with a penicillin allergy should undergo desensitization, as penicillin is the preferred agent; the potential exists for cross-reactivity with ceftriaxone, a possible alternative for patients with neurosyphilis.11 All patients diagnosed with syphilis should also be tested for HIV and other sexually transmitted diseases.10-12
The prognosis of patients treated for neurosyphilis is generally good if the condition is diagnosed and treated early. In patients with cerebral atrophy, frontal lesions, dementia, or tabes dorsalis, the potential for recovery decreases.2,13,14
Teaching Points
There are several teaching points to take away from this case:
• Remember to rule out a CVA in any patient who presents with numbness, paresthesias, or slurred speech. In this case, a brain CT and CT angiography of the brain were both obtained in the ED before the patient was admitted. They both yielded negative results; because the patient’s history was consistent with alcohol and drug use and he had a history of seizures, he was monitored closely for signs of withdrawal or further seizure.
• Phenytoin is an antiepileptic agent whose use requires proper patient education and drug level monitoring. Appropriate follow-up must be ensured before phenytoin therapy is begun, as toxicity can result in nystagmus, ataxia, slurred speech, decreased coordination, mental confusion, and possibly death.15,16
• For patients with a suspected acute change in mental status, a workup is required and should be tailored appropriately, based on findings. This should include, but not be limited to, a thorough history and physical exam, CT of the brain (to rule out an acute brain injury17), and, if warranted, MRI of the brain. Also, a urine drug screen and alcohol level, a complete blood count, a TSH level (to evaluate for altered thyroid function that may explain mental status changes), comprehensive panel, RPR testing and/or a VDRL titer should be obtained, depending on the facility’s protocol18,19; at some facilities, a treponemal test, rather than VDRL, is being obtained at the outset.20 Levels of vitamin B12 (as part of the dementia workup), folate, thiamine, and ammonia (in patients with suspected liver disease) can also be obtained in patients with change in mental status.18,19 Urinalysis should not be overlooked to check for a urinary tract infection, especially in elderly patients.21
• If primary syphilis is suspected, treatment must be undertaken.20
Conclusion
Despite the decline seen since the 1940s in cases of primary and secondary syphilis, and the effectiveness of penicillin in treating the infection early, patients with late-stage syphilis, including those with neurosyphilis, may still present to the emergency care, urgent care, or primary care setting. Immediate treatment with penicillin is recommended to achieve an optimal prognosis for the affected patient.
1. Golden MR, Marra CM, Holmes KK. Update on syphilis: resurgence of an old problem. JAMA. 2003;290(11):1510-1514.
2. Simon RP. Chapter 20. Neurosyphilis. In: Klausner JD, Hook EW III, eds. Current Diagnosis & Treatment of Sexually Transmitted Diseases. USA: The McGraw-Hill Companies; 2007:130-137.
3. Sanchez FM, Zisselman MH. Treatment of psychiatric symptoms associated with neurosyphilis. Psychosomatics. 2007;48:440-445.
4. Marra CM. Neurosyphilis. Curr Neurol Neurosci Rep. 2004;4(6):435-440.
5. CDC. Sexually transmitted diseases surveillance, 2007: STD surveillance case definitions. www.cdc.gov/std/stats07/app-casedef.htm. Accessed March 23, 2011.
6. CDC. 2008 Sexually Transmitted Diseases Surveillance: Table 1. Cases of sexually transmitted diseases reported by state health departments and rates per 100,000 population: United States, 1941-2008. www.cdc.gov/std/stats08/tables/1.htm. Accessed March 23, 2011.
7. CDC. Sexually transmitted diseases (STDs): Syphilis: CDC fact sheet. www.cdc.gov/std/syphilis/STDfact-syphilis.htm. Accessed March 23, 2011.
8. Tramont EC. Chapter 238. Treponema pallidum (syphilis). In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 7th ed. Philadelphia: Elsevier Churchill Livingstone; 2009.
9. Ghanem KG. Neurosyphilis: a historical perspective and review. CNS Neurosci Ther. 2010; 16(5):e157-e168.
10. Workowski KA, Berman SM; CDC. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep. 2006;55(RR-11):1-94.
11. CDC. Sexually transmitted diseases: treatment guidelines 2006. www.cdc.gov/std/treatment/2006/genital-ulcers.htm#genulc6. Accessed March 29, 2011.
12. Drugs for sexually transmitted infections. Treatment Guidelines from the Medical Letter. 2010;95:95a. http://secure.medicalletter.org. Accessed March 23, 2011.
13. Russouw HG, Roberts MC, Emsley RA, et al. Psychiatric manifestations and magnetic resonance imaging in HIV-negative neurosyphilis. Biol Psychiatry. 1997;41(4):467-473.
14. Hooshmand H, Escobar MR, Kopf SW. Neurosyphylis: a study of 241 patients. JAMA. 1972;219 (6):726-729.
15. Miller CA, Joyce DM. Toxicity, phenytoin. http://emedicine.medscape.com/article/816447-overview. Accessed March 23, 2011.
16. Earnest MP, Marx JA, Drury LR. Complications of intravenous phenytoin for acute treatment of seizures: recommendations for usage. JAMA. 1983; 246(6):762-765.
17. Geschwind MD, Shu H, Haman A, et al. Rapidly progressive dementia. Ann Neurol. 2008;64(1): 97-108.
18. Mechem CC. Chapter 143. Altered mental status and coma. In: Ma J, Cline DM, Tintinalli JE, et al, eds. Emergency Medicine Manual, 6e. www.access emergencymedicine.com/content.aspx?aID=2020. Accessed March 23, 2011.
19. Knopman DS, DeKosky ST, Cummings JL, et al; Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: diagnosis of dementia (an evidence-based review). Neurology. 2001;56(9):1143-1153.
20. CDC. Syphilis testing algorithms using treponemal tests for initial screening—four laboratories, New York City, 2005-2006. MMWR Morb Mortal Wkly Rep. 2008;57(32):872-875.
21. Anderson CA, Filley CM. Chapter 33. Behavioral presentations of medical and neurologic disorders. In: Jacobson JL, Jacobson AM, eds. Psychiatric Secrets. 2nd ed. St. Louis, MO: Hanley & Belfus; 2001.
A 54-year-old African-American man was brought by police officers to the emergency department (ED) after he called 911 several times to report seeing a Rottweiler looking into his second-story window. At the scene, the police were unable to confirm his story, thought the man seemed intoxicated, and brought him to the ED for evaluation.
The patient reported that he had been drinking the previous evening but denied current intoxication or illicit drug use. He denied experiencing symptoms of alcohol withdrawal.
Regarding his medical history, the patient admitted to having had seizures, including two episodes that he said required hospitalization. He described these episodes as right-hand “tingling” (paresthesias), accompanied by right-facial numbness and aphasia. The patient said his physician had instructed him to take “a few phenytoin pills” whenever these episodes occurred. He reported that the medication usually helped resolve his symptoms. He said he had taken phenytoin shortly before his current presentation.
According to friends of the patient who were questioned, he had had noticeable memory problems during the previous six to eight months. They said that he often told the same joke, day after day. His speech had become increasingly slurred, even when he was not drinking.
Once the patient’s medical records were retrieved, it was revealed that he had been hospitalized twice for witnessed grand mal seizures about six months before his current admission; he had been drinking alcohol prior to both episodes. He underwent electroencephalography (EEG) during one of these hospitalizations, with results reported as normal. On both occasions, the patient was discharged with phenytoin and was instructed to follow up with his primary care provider and neurologist.
The patient, who reported working in customer service, had no known allergies. He claimed to drink one or two 40-ounce beers twice per week and admitted to occasional cocaine use. Of significance in his family history was a fatal MI in his mother. Although the patient denied any history of rashes or lesions, his current delirium made it impossible to obtain a reliable sexual history; a friend who was questioned, however, described the patient as promiscuous.
On initial physical examination, the man was afebrile, tachycardic, and somewhat combative with the ED staff. He was fully oriented to self but only partially to place and time.
His right pupil was 3+ and his left pupil was 2+, with neither reactive to light. He spoke with tangential speech and his gait was unsteady, but no other significant abnormalities were noted. A full assessment revealed no rashes or other lesions.
Significant laboratory findings included a low level of phenytoin, a negative blood alcohol level, presence of cocaine on urine drug screening, and normal levels of thyroid-stimulating hormone (TSH), vitamin B12, and folate. The patient’s serum VDRL (venereal disease research laboratory) titer was positive at 1:256.
Electroencephalography showed diffuse slowing, and brain CT performed in the ED showed atrophy that was mild but appropriate for a person of the patient’s age, with no evidence of a cerebrovascular accident (CVA). Aneurysm was ruled out by CT angiography of the brain. MRI revealed persistent increased signal in the subarachnoid space.
The patient was admitted with an initial diagnosis of paranoid delusional psychosis and monitored for alcohol withdrawal. He was given lorazepam as needed for agitation. Consultations were arranged with the psychiatry service regarding his delusions, and with neurology to determine whether to continue phenytoin.
The patient showed little response during the next several days. Based on positive results on serum VDRL with high titer, the presence of Argyll-Robertson pupils on exam, and his history of dementia-like symptoms, a lumbar puncture was performed to rule out neurosyphilis. In the patient’s cerebral spinal fluid (CSF) analysis, the first tube was clear and colorless, with 72 cells (28% neutrophils, 59% lymphocytes); glucose, 64 mg/dL; and total protein, 117 mg/dL. The fourth tube had 34 cells (17% neutrophils, 65% lymphocytes) and a positive VDRL titer at 1:128. Results from a serum syphilis immunoglobulin G (IgG) test were positive, and HIV antibody testing was nonreactive, confirming the diagnosis of neurosyphilis.
The hospital’s infectious disease (ID) team recommended treatment with IV penicillin for 14 days. Once this was completed, the patient was discharged with instructions to follow up at the ID clinic in three months for a repeat CSF VDRL titer to monitor for resolution of the disease. His prescription for phenytoin was discontinued.
At the time of discharge, it was noted that the patient showed no evidence of having regained cognitive function. He was deemed by the psychiatry service to lack decision-making capacity—a likely sequelae of untreated neurosyphilis of unknown duration.
He did return to the ID clinic six months after his discharge. At that visit, a VDRL serum titer was drawn with a result of 1:64, a decrease from 1:128. His syphilis IgG remained positive, however.
Discussion
Definition and Epidemiology
Syphilis is commonly known as a sexually transmitted disease with primary, secondary, and tertiary (early and late latent) stages.1 Neurosyphilis is defined as a manifestation of the inflammatory response to invasion over decades by the Treponema pallidum spirochete in the CSF as a result of untreated primary and/or secondary syphilis.2 About one in 10 patients with untreated syphilis will experience neurologic involvement.3,4 Before 2005, neurosyphilis was required to be reported as a specific stage of syphilis (ie, a manifestation of tertiary syphilis4), but now should be reported as syphilis with neurologic manifestations.5
A reportable infectious disease, syphilis was widespread until the advent of penicillin. According to CDC statistics,6 the number of reported cases of primary and secondary syphilis has declined steadily since 1943. In the late 1970s and early 1980s, the number of tertiary cases also began to plateau, likely as a result of earlier diagnosis and more widespread use of penicillin. Recent case reports suggest greater prevalence of syphilis among men than women and increased incidence among men who have sex with men.7
Pathogenesis
Syphilis is most commonly spread by sexual contact or contact with an infected primary lesion (chancre). Less likely routes of transmission are placental passage or blood transfusion. Infectivity is greatest in the early disease stages.8
Primary syphilis is marked by transmission of the spirochete, ending with development of secondary syphilis (usually two to 12 weeks after transmission). A chancre commonly develops but is often missed by patients because it is painless and can heal spontaneously.7 The chancre is also often confused with two other sources of genital lesions, herpes simplex (genital herpes) and Haemophilus ducreyi (chancroid). In two-thirds of cases of untreated primary syphilis, the infection clears spontaneously, but in the remaining one-third, the disease progresses.8
Secondary syphilis, with or without presence of a chancre, manifests with constitutional symptoms, including lymphadenopathy, fever, headache, and malaise. Patients in this disease phase may also present with a generalized, nonpruritic, macular to maculopapular or pustular rash. The rash can affect the skin of the trunk, the proximal extremities, and the palms and soles. Ocular involvement may occur, especially in patients who are coinfected with HIV.8 In either primary or secondary syphilis, infection can invade the central nervous system.1
During latent syphilis, patients show serologic conversion without overt symptoms. Early latent syphilis is defined as infection within the previous year, as demonstrated by conversion from negative to positive testing, or an increase in titers within the previous year. Any case occurring after one year is defined as late or unknown latent syphilis.8
Tertiary syphilis is marked by complications resulting from untreated syphilis; affected patients commonly experience central nervous system and cardiovascular involvement. Gummatous disease is seen in 15% of patients.1
The early stages of neurosyphilis may be asymptomatic, acute meningeal, and meningovascular.1,4,8,9 Only 5% of patients with early neurosyphilis are symptomatic, with the added potential for cranial neuritis or ocular involvement.1 The late stages of neurosyphilis are detailed in the table.1,4,8
Diagnosis
A diagnosis of syphilis is made by testing blood samples or scrapings from a lesion. In patients with suspected syphilis, rapid plasma reagin (RPR) testing or a VDRL titer is commonly ordered. When results are positive, a serum treponemal test is recommended to confirm a diagnosis of syphilis. Options include the fluorescent treponemal antibody absorption test (FTA-ABS) and the microhemagglutinin assay for antibody to T pallidum (MHA-TP).5
If neurologic symptoms are present, a CSF sample should be obtained, followed by the same testing. A confirmed diagnosis of neurosyphilis is defined by the CDC as syphilis at any stage that meets laboratory criteria for neurosyphilis5; these include increased CSF protein or an elevated CSF leukocyte count with no other known cause, and clinical signs or symptoms without other known causes.7
Treatment
Treatment of syphilis generally consists of penicillin, administered intramuscularly (IM) or IV, depending on the stage. According to 2006 guidelines from the CDC,10,11 treatment for adults with primary and secondary syphilis is a single dose of IM penicillin G, 2.4 million units. If neurosyphilis is suspected, recommended treatment is IV penicillin G, 18 to 24 million units per day divided into six doses (ie, 3 to 4 million units every four hours) or continuous pump infusion for 10 to 14 days.10-12 Follow-up is recommended by monitoring CSF titers to ensure clearance of infection; retreatment may be required if CSF abnormalities persist after two years.11
Patients with a penicillin allergy should undergo desensitization, as penicillin is the preferred agent; the potential exists for cross-reactivity with ceftriaxone, a possible alternative for patients with neurosyphilis.11 All patients diagnosed with syphilis should also be tested for HIV and other sexually transmitted diseases.10-12
The prognosis of patients treated for neurosyphilis is generally good if the condition is diagnosed and treated early. In patients with cerebral atrophy, frontal lesions, dementia, or tabes dorsalis, the potential for recovery decreases.2,13,14
Teaching Points
There are several teaching points to take away from this case:
• Remember to rule out a CVA in any patient who presents with numbness, paresthesias, or slurred speech. In this case, a brain CT and CT angiography of the brain were both obtained in the ED before the patient was admitted. They both yielded negative results; because the patient’s history was consistent with alcohol and drug use and he had a history of seizures, he was monitored closely for signs of withdrawal or further seizure.
• Phenytoin is an antiepileptic agent whose use requires proper patient education and drug level monitoring. Appropriate follow-up must be ensured before phenytoin therapy is begun, as toxicity can result in nystagmus, ataxia, slurred speech, decreased coordination, mental confusion, and possibly death.15,16
• For patients with a suspected acute change in mental status, a workup is required and should be tailored appropriately, based on findings. This should include, but not be limited to, a thorough history and physical exam, CT of the brain (to rule out an acute brain injury17), and, if warranted, MRI of the brain. Also, a urine drug screen and alcohol level, a complete blood count, a TSH level (to evaluate for altered thyroid function that may explain mental status changes), comprehensive panel, RPR testing and/or a VDRL titer should be obtained, depending on the facility’s protocol18,19; at some facilities, a treponemal test, rather than VDRL, is being obtained at the outset.20 Levels of vitamin B12 (as part of the dementia workup), folate, thiamine, and ammonia (in patients with suspected liver disease) can also be obtained in patients with change in mental status.18,19 Urinalysis should not be overlooked to check for a urinary tract infection, especially in elderly patients.21
• If primary syphilis is suspected, treatment must be undertaken.20
Conclusion
Despite the decline seen since the 1940s in cases of primary and secondary syphilis, and the effectiveness of penicillin in treating the infection early, patients with late-stage syphilis, including those with neurosyphilis, may still present to the emergency care, urgent care, or primary care setting. Immediate treatment with penicillin is recommended to achieve an optimal prognosis for the affected patient.
A 54-year-old African-American man was brought by police officers to the emergency department (ED) after he called 911 several times to report seeing a Rottweiler looking into his second-story window. At the scene, the police were unable to confirm his story, thought the man seemed intoxicated, and brought him to the ED for evaluation.
The patient reported that he had been drinking the previous evening but denied current intoxication or illicit drug use. He denied experiencing symptoms of alcohol withdrawal.
Regarding his medical history, the patient admitted to having had seizures, including two episodes that he said required hospitalization. He described these episodes as right-hand “tingling” (paresthesias), accompanied by right-facial numbness and aphasia. The patient said his physician had instructed him to take “a few phenytoin pills” whenever these episodes occurred. He reported that the medication usually helped resolve his symptoms. He said he had taken phenytoin shortly before his current presentation.
According to friends of the patient who were questioned, he had had noticeable memory problems during the previous six to eight months. They said that he often told the same joke, day after day. His speech had become increasingly slurred, even when he was not drinking.
Once the patient’s medical records were retrieved, it was revealed that he had been hospitalized twice for witnessed grand mal seizures about six months before his current admission; he had been drinking alcohol prior to both episodes. He underwent electroencephalography (EEG) during one of these hospitalizations, with results reported as normal. On both occasions, the patient was discharged with phenytoin and was instructed to follow up with his primary care provider and neurologist.
The patient, who reported working in customer service, had no known allergies. He claimed to drink one or two 40-ounce beers twice per week and admitted to occasional cocaine use. Of significance in his family history was a fatal MI in his mother. Although the patient denied any history of rashes or lesions, his current delirium made it impossible to obtain a reliable sexual history; a friend who was questioned, however, described the patient as promiscuous.
On initial physical examination, the man was afebrile, tachycardic, and somewhat combative with the ED staff. He was fully oriented to self but only partially to place and time.
His right pupil was 3+ and his left pupil was 2+, with neither reactive to light. He spoke with tangential speech and his gait was unsteady, but no other significant abnormalities were noted. A full assessment revealed no rashes or other lesions.
Significant laboratory findings included a low level of phenytoin, a negative blood alcohol level, presence of cocaine on urine drug screening, and normal levels of thyroid-stimulating hormone (TSH), vitamin B12, and folate. The patient’s serum VDRL (venereal disease research laboratory) titer was positive at 1:256.
Electroencephalography showed diffuse slowing, and brain CT performed in the ED showed atrophy that was mild but appropriate for a person of the patient’s age, with no evidence of a cerebrovascular accident (CVA). Aneurysm was ruled out by CT angiography of the brain. MRI revealed persistent increased signal in the subarachnoid space.
The patient was admitted with an initial diagnosis of paranoid delusional psychosis and monitored for alcohol withdrawal. He was given lorazepam as needed for agitation. Consultations were arranged with the psychiatry service regarding his delusions, and with neurology to determine whether to continue phenytoin.
The patient showed little response during the next several days. Based on positive results on serum VDRL with high titer, the presence of Argyll-Robertson pupils on exam, and his history of dementia-like symptoms, a lumbar puncture was performed to rule out neurosyphilis. In the patient’s cerebral spinal fluid (CSF) analysis, the first tube was clear and colorless, with 72 cells (28% neutrophils, 59% lymphocytes); glucose, 64 mg/dL; and total protein, 117 mg/dL. The fourth tube had 34 cells (17% neutrophils, 65% lymphocytes) and a positive VDRL titer at 1:128. Results from a serum syphilis immunoglobulin G (IgG) test were positive, and HIV antibody testing was nonreactive, confirming the diagnosis of neurosyphilis.
The hospital’s infectious disease (ID) team recommended treatment with IV penicillin for 14 days. Once this was completed, the patient was discharged with instructions to follow up at the ID clinic in three months for a repeat CSF VDRL titer to monitor for resolution of the disease. His prescription for phenytoin was discontinued.
At the time of discharge, it was noted that the patient showed no evidence of having regained cognitive function. He was deemed by the psychiatry service to lack decision-making capacity—a likely sequelae of untreated neurosyphilis of unknown duration.
He did return to the ID clinic six months after his discharge. At that visit, a VDRL serum titer was drawn with a result of 1:64, a decrease from 1:128. His syphilis IgG remained positive, however.
Discussion
Definition and Epidemiology
Syphilis is commonly known as a sexually transmitted disease with primary, secondary, and tertiary (early and late latent) stages.1 Neurosyphilis is defined as a manifestation of the inflammatory response to invasion over decades by the Treponema pallidum spirochete in the CSF as a result of untreated primary and/or secondary syphilis.2 About one in 10 patients with untreated syphilis will experience neurologic involvement.3,4 Before 2005, neurosyphilis was required to be reported as a specific stage of syphilis (ie, a manifestation of tertiary syphilis4), but now should be reported as syphilis with neurologic manifestations.5
A reportable infectious disease, syphilis was widespread until the advent of penicillin. According to CDC statistics,6 the number of reported cases of primary and secondary syphilis has declined steadily since 1943. In the late 1970s and early 1980s, the number of tertiary cases also began to plateau, likely as a result of earlier diagnosis and more widespread use of penicillin. Recent case reports suggest greater prevalence of syphilis among men than women and increased incidence among men who have sex with men.7
Pathogenesis
Syphilis is most commonly spread by sexual contact or contact with an infected primary lesion (chancre). Less likely routes of transmission are placental passage or blood transfusion. Infectivity is greatest in the early disease stages.8
Primary syphilis is marked by transmission of the spirochete, ending with development of secondary syphilis (usually two to 12 weeks after transmission). A chancre commonly develops but is often missed by patients because it is painless and can heal spontaneously.7 The chancre is also often confused with two other sources of genital lesions, herpes simplex (genital herpes) and Haemophilus ducreyi (chancroid). In two-thirds of cases of untreated primary syphilis, the infection clears spontaneously, but in the remaining one-third, the disease progresses.8
Secondary syphilis, with or without presence of a chancre, manifests with constitutional symptoms, including lymphadenopathy, fever, headache, and malaise. Patients in this disease phase may also present with a generalized, nonpruritic, macular to maculopapular or pustular rash. The rash can affect the skin of the trunk, the proximal extremities, and the palms and soles. Ocular involvement may occur, especially in patients who are coinfected with HIV.8 In either primary or secondary syphilis, infection can invade the central nervous system.1
During latent syphilis, patients show serologic conversion without overt symptoms. Early latent syphilis is defined as infection within the previous year, as demonstrated by conversion from negative to positive testing, or an increase in titers within the previous year. Any case occurring after one year is defined as late or unknown latent syphilis.8
Tertiary syphilis is marked by complications resulting from untreated syphilis; affected patients commonly experience central nervous system and cardiovascular involvement. Gummatous disease is seen in 15% of patients.1
The early stages of neurosyphilis may be asymptomatic, acute meningeal, and meningovascular.1,4,8,9 Only 5% of patients with early neurosyphilis are symptomatic, with the added potential for cranial neuritis or ocular involvement.1 The late stages of neurosyphilis are detailed in the table.1,4,8
Diagnosis
A diagnosis of syphilis is made by testing blood samples or scrapings from a lesion. In patients with suspected syphilis, rapid plasma reagin (RPR) testing or a VDRL titer is commonly ordered. When results are positive, a serum treponemal test is recommended to confirm a diagnosis of syphilis. Options include the fluorescent treponemal antibody absorption test (FTA-ABS) and the microhemagglutinin assay for antibody to T pallidum (MHA-TP).5
If neurologic symptoms are present, a CSF sample should be obtained, followed by the same testing. A confirmed diagnosis of neurosyphilis is defined by the CDC as syphilis at any stage that meets laboratory criteria for neurosyphilis5; these include increased CSF protein or an elevated CSF leukocyte count with no other known cause, and clinical signs or symptoms without other known causes.7
Treatment
Treatment of syphilis generally consists of penicillin, administered intramuscularly (IM) or IV, depending on the stage. According to 2006 guidelines from the CDC,10,11 treatment for adults with primary and secondary syphilis is a single dose of IM penicillin G, 2.4 million units. If neurosyphilis is suspected, recommended treatment is IV penicillin G, 18 to 24 million units per day divided into six doses (ie, 3 to 4 million units every four hours) or continuous pump infusion for 10 to 14 days.10-12 Follow-up is recommended by monitoring CSF titers to ensure clearance of infection; retreatment may be required if CSF abnormalities persist after two years.11
Patients with a penicillin allergy should undergo desensitization, as penicillin is the preferred agent; the potential exists for cross-reactivity with ceftriaxone, a possible alternative for patients with neurosyphilis.11 All patients diagnosed with syphilis should also be tested for HIV and other sexually transmitted diseases.10-12
The prognosis of patients treated for neurosyphilis is generally good if the condition is diagnosed and treated early. In patients with cerebral atrophy, frontal lesions, dementia, or tabes dorsalis, the potential for recovery decreases.2,13,14
Teaching Points
There are several teaching points to take away from this case:
• Remember to rule out a CVA in any patient who presents with numbness, paresthesias, or slurred speech. In this case, a brain CT and CT angiography of the brain were both obtained in the ED before the patient was admitted. They both yielded negative results; because the patient’s history was consistent with alcohol and drug use and he had a history of seizures, he was monitored closely for signs of withdrawal or further seizure.
• Phenytoin is an antiepileptic agent whose use requires proper patient education and drug level monitoring. Appropriate follow-up must be ensured before phenytoin therapy is begun, as toxicity can result in nystagmus, ataxia, slurred speech, decreased coordination, mental confusion, and possibly death.15,16
• For patients with a suspected acute change in mental status, a workup is required and should be tailored appropriately, based on findings. This should include, but not be limited to, a thorough history and physical exam, CT of the brain (to rule out an acute brain injury17), and, if warranted, MRI of the brain. Also, a urine drug screen and alcohol level, a complete blood count, a TSH level (to evaluate for altered thyroid function that may explain mental status changes), comprehensive panel, RPR testing and/or a VDRL titer should be obtained, depending on the facility’s protocol18,19; at some facilities, a treponemal test, rather than VDRL, is being obtained at the outset.20 Levels of vitamin B12 (as part of the dementia workup), folate, thiamine, and ammonia (in patients with suspected liver disease) can also be obtained in patients with change in mental status.18,19 Urinalysis should not be overlooked to check for a urinary tract infection, especially in elderly patients.21
• If primary syphilis is suspected, treatment must be undertaken.20
Conclusion
Despite the decline seen since the 1940s in cases of primary and secondary syphilis, and the effectiveness of penicillin in treating the infection early, patients with late-stage syphilis, including those with neurosyphilis, may still present to the emergency care, urgent care, or primary care setting. Immediate treatment with penicillin is recommended to achieve an optimal prognosis for the affected patient.
1. Golden MR, Marra CM, Holmes KK. Update on syphilis: resurgence of an old problem. JAMA. 2003;290(11):1510-1514.
2. Simon RP. Chapter 20. Neurosyphilis. In: Klausner JD, Hook EW III, eds. Current Diagnosis & Treatment of Sexually Transmitted Diseases. USA: The McGraw-Hill Companies; 2007:130-137.
3. Sanchez FM, Zisselman MH. Treatment of psychiatric symptoms associated with neurosyphilis. Psychosomatics. 2007;48:440-445.
4. Marra CM. Neurosyphilis. Curr Neurol Neurosci Rep. 2004;4(6):435-440.
5. CDC. Sexually transmitted diseases surveillance, 2007: STD surveillance case definitions. www.cdc.gov/std/stats07/app-casedef.htm. Accessed March 23, 2011.
6. CDC. 2008 Sexually Transmitted Diseases Surveillance: Table 1. Cases of sexually transmitted diseases reported by state health departments and rates per 100,000 population: United States, 1941-2008. www.cdc.gov/std/stats08/tables/1.htm. Accessed March 23, 2011.
7. CDC. Sexually transmitted diseases (STDs): Syphilis: CDC fact sheet. www.cdc.gov/std/syphilis/STDfact-syphilis.htm. Accessed March 23, 2011.
8. Tramont EC. Chapter 238. Treponema pallidum (syphilis). In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 7th ed. Philadelphia: Elsevier Churchill Livingstone; 2009.
9. Ghanem KG. Neurosyphilis: a historical perspective and review. CNS Neurosci Ther. 2010; 16(5):e157-e168.
10. Workowski KA, Berman SM; CDC. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep. 2006;55(RR-11):1-94.
11. CDC. Sexually transmitted diseases: treatment guidelines 2006. www.cdc.gov/std/treatment/2006/genital-ulcers.htm#genulc6. Accessed March 29, 2011.
12. Drugs for sexually transmitted infections. Treatment Guidelines from the Medical Letter. 2010;95:95a. http://secure.medicalletter.org. Accessed March 23, 2011.
13. Russouw HG, Roberts MC, Emsley RA, et al. Psychiatric manifestations and magnetic resonance imaging in HIV-negative neurosyphilis. Biol Psychiatry. 1997;41(4):467-473.
14. Hooshmand H, Escobar MR, Kopf SW. Neurosyphylis: a study of 241 patients. JAMA. 1972;219 (6):726-729.
15. Miller CA, Joyce DM. Toxicity, phenytoin. http://emedicine.medscape.com/article/816447-overview. Accessed March 23, 2011.
16. Earnest MP, Marx JA, Drury LR. Complications of intravenous phenytoin for acute treatment of seizures: recommendations for usage. JAMA. 1983; 246(6):762-765.
17. Geschwind MD, Shu H, Haman A, et al. Rapidly progressive dementia. Ann Neurol. 2008;64(1): 97-108.
18. Mechem CC. Chapter 143. Altered mental status and coma. In: Ma J, Cline DM, Tintinalli JE, et al, eds. Emergency Medicine Manual, 6e. www.access emergencymedicine.com/content.aspx?aID=2020. Accessed March 23, 2011.
19. Knopman DS, DeKosky ST, Cummings JL, et al; Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: diagnosis of dementia (an evidence-based review). Neurology. 2001;56(9):1143-1153.
20. CDC. Syphilis testing algorithms using treponemal tests for initial screening—four laboratories, New York City, 2005-2006. MMWR Morb Mortal Wkly Rep. 2008;57(32):872-875.
21. Anderson CA, Filley CM. Chapter 33. Behavioral presentations of medical and neurologic disorders. In: Jacobson JL, Jacobson AM, eds. Psychiatric Secrets. 2nd ed. St. Louis, MO: Hanley & Belfus; 2001.
1. Golden MR, Marra CM, Holmes KK. Update on syphilis: resurgence of an old problem. JAMA. 2003;290(11):1510-1514.
2. Simon RP. Chapter 20. Neurosyphilis. In: Klausner JD, Hook EW III, eds. Current Diagnosis & Treatment of Sexually Transmitted Diseases. USA: The McGraw-Hill Companies; 2007:130-137.
3. Sanchez FM, Zisselman MH. Treatment of psychiatric symptoms associated with neurosyphilis. Psychosomatics. 2007;48:440-445.
4. Marra CM. Neurosyphilis. Curr Neurol Neurosci Rep. 2004;4(6):435-440.
5. CDC. Sexually transmitted diseases surveillance, 2007: STD surveillance case definitions. www.cdc.gov/std/stats07/app-casedef.htm. Accessed March 23, 2011.
6. CDC. 2008 Sexually Transmitted Diseases Surveillance: Table 1. Cases of sexually transmitted diseases reported by state health departments and rates per 100,000 population: United States, 1941-2008. www.cdc.gov/std/stats08/tables/1.htm. Accessed March 23, 2011.
7. CDC. Sexually transmitted diseases (STDs): Syphilis: CDC fact sheet. www.cdc.gov/std/syphilis/STDfact-syphilis.htm. Accessed March 23, 2011.
8. Tramont EC. Chapter 238. Treponema pallidum (syphilis). In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 7th ed. Philadelphia: Elsevier Churchill Livingstone; 2009.
9. Ghanem KG. Neurosyphilis: a historical perspective and review. CNS Neurosci Ther. 2010; 16(5):e157-e168.
10. Workowski KA, Berman SM; CDC. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep. 2006;55(RR-11):1-94.
11. CDC. Sexually transmitted diseases: treatment guidelines 2006. www.cdc.gov/std/treatment/2006/genital-ulcers.htm#genulc6. Accessed March 29, 2011.
12. Drugs for sexually transmitted infections. Treatment Guidelines from the Medical Letter. 2010;95:95a. http://secure.medicalletter.org. Accessed March 23, 2011.
13. Russouw HG, Roberts MC, Emsley RA, et al. Psychiatric manifestations and magnetic resonance imaging in HIV-negative neurosyphilis. Biol Psychiatry. 1997;41(4):467-473.
14. Hooshmand H, Escobar MR, Kopf SW. Neurosyphylis: a study of 241 patients. JAMA. 1972;219 (6):726-729.
15. Miller CA, Joyce DM. Toxicity, phenytoin. http://emedicine.medscape.com/article/816447-overview. Accessed March 23, 2011.
16. Earnest MP, Marx JA, Drury LR. Complications of intravenous phenytoin for acute treatment of seizures: recommendations for usage. JAMA. 1983; 246(6):762-765.
17. Geschwind MD, Shu H, Haman A, et al. Rapidly progressive dementia. Ann Neurol. 2008;64(1): 97-108.
18. Mechem CC. Chapter 143. Altered mental status and coma. In: Ma J, Cline DM, Tintinalli JE, et al, eds. Emergency Medicine Manual, 6e. www.access emergencymedicine.com/content.aspx?aID=2020. Accessed March 23, 2011.
19. Knopman DS, DeKosky ST, Cummings JL, et al; Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: diagnosis of dementia (an evidence-based review). Neurology. 2001;56(9):1143-1153.
20. CDC. Syphilis testing algorithms using treponemal tests for initial screening—four laboratories, New York City, 2005-2006. MMWR Morb Mortal Wkly Rep. 2008;57(32):872-875.
21. Anderson CA, Filley CM. Chapter 33. Behavioral presentations of medical and neurologic disorders. In: Jacobson JL, Jacobson AM, eds. Psychiatric Secrets. 2nd ed. St. Louis, MO: Hanley & Belfus; 2001.
Modified Technique for Unipolar Allograft Ankle Replacement: Midterm Follow-up. A Case Report
Erratum (2011;87:81-84)
Hodgkin Lymphoma Presenting as Generalized Pruritus in an Adolescent
What's Eating You? Hyalomma Ticks
Applying single-incision laparoscopic surgery to gyn practice: What’s involved
- Update on minimally invasive surgery
Amy Garcia, MD (April 2011) - 10 practical, evidence-based suggestions to improve your minimally invasive surgical skills now
Catherine A. Matthews, MD (April 2011)
The benefits of minimally invasive surgery—including less pain, faster recovery, and improved cosmesis—are well known.1,2 Standard laparotomy has been replaced by multiple-port operative laparoscopy for a great array of procedures, and advances in medical technology allow for a minimally invasive surgical approach even when a surgeon is faced with complex pathology.
Single-port laparoscopic surgery (SPLS) represents the latest advance in minimally invasive surgery. Using flexible endoscopes and articulating instruments, the surgeon can complete complex procedures through a single 2-cm incision in the abdomen. The incision is usually placed in the umbilicus, where it is easily hidden.3-8
Since the first laparoscopic hysterectomy through a single incision was performed 20 years ago, SPLS has been used successfully to perform nephrectomy, prostatectomy, hemicolectomy, cholecystectomy, splenectomy, intussusception reduction, gastrostomy tube placement, thoracoscopic lung biopsy, thoracoscopic decortication, and appendectomy.4-7
In gynecology, SPLS has been used to perform oophorectomy, salpingectomy, bilateral tubal ligation, ovarian cystectomy, surgical treatment of ectopic pregnancy, and both total and partial hysterectomy.7-11 At least two recent studies have concluded that SPLS is an acceptable way to treat many benign and malignant gynecologic conditions that are currently treated using multiport laparoscopy.3,11
This article outlines our approach to SPLS in the gynecologic patient and provides an overview of instrumentation, with the aim of allowing you to consider whether this approach might be feasible in your surgical practice, at your institution.
Unique setup required
When SPLS is performed through the umbilicus, the instruments must be held closer to the midline and more cephalad than during conventional laparoscopy to permit adequate visualization and manipulation. For this reason, the surgeon needs to assume a position higher over the torso and thorax of the patient, and both of the patient’s arms need to be tucked. Place the patient in a dorsal lithotomy position with a uterine manipulator in place to facilitate surgery—even when the uterus will be preserved and surgery involves only the adnexae.
With appropriate equipment and positioning, visualization and manipulation of anatomy are comparable to those of standard multiport laparoscopy.
New instruments simplify SPLS
Innovative surgical instruments allow for appropriate hand positioning outside the abdomen and minimize the internal collision of instruments brought through a single midline incision (FIGURE 1). A variety of single-port options are available, each with a unique patented design and method of insertion. In fact, the development of ports with multiple instrument channels has revolutionized SPLS.
FIGURE 1 Setup
Desired triangulation of instruments in SPLS setup.Before true single ports became available, it was necessary to place three 5-mm low-profile trocars in the fascia at three separate sites through a single skin incision. Pneumoperitoneum was established with a Veress needle, but the fascial incisions gradually merged with repeated cannula manipulation, producing air leaks.
Today, multiple-channel ports are placed using an open technique into a single skin and fascial incision. Trocars and instruments of varying size can be exchanged with ease without jeopardizing pneumoperitoneum.
Among the options:
- the SILS Port (Covidien) – a soft, flexible, three-channel port that allows for placement of blunt trocars ranging in size from 5 mm to 12 mm (FIGURE 2)
- the TriPort (Olympus America) – two flexible rings joined by a sleeve and multiple-channel port (FIGURE 3)
- GelPOINT Advanced Access Platform (Applied Medical) – a system constructed of synthetic gel material and consisting of a “GelSeal” cap, cannulas, and seals to accommodate 5-mm to 10-mm instrumentation (FIGURE 4).
We have found that all three devices allow for good range of motion while maintaining pneumoperitoneum.
(A recent article from Korea reports an inventive technique to perform single-incision laparoscopy using standard instrumentation: The authors fitted a self-retaining ring retractor with a surgical glove that had three of the fingers cut off and replaced by trocars.12)
FIGURE 2 SILS Port
The SILS Port is a soft, flexible, three-channel port that allows for placement of blunt trocars ranging in size from 5 mm to 12 mm.
FIGURE 3 TriPort
The TriPort system comprises two flexible rings joined by a sleeve and multiple-channel port.
FIGURE 4 GelPOINT
The GelPOINT Advanced Access Platform is constructed of synthetic gel material and accommodates 5-mm to 10-mm instrumentation.
A flexible laparoscope improves visualization
The ability to visualize the operative field is vital to any surgery, including SPLS. Use of a flexible laparoscope facilitates uncompromised visualization of the entire pelvis (FIGURE 5). Outside the abdomen, the flexible camera can be held laterally and away from the midline to help reduce the clashing of instruments and hands.
FIGURE 5 Flexible-tip laparoscope
A flexible-tip laparoscope ensures good visualization of the surgical field.If a flexible laparoscope is not available, a rigid 30-degree or 45-degree angled scope can be used, although visualization may be limited and adequate triangulation of instruments may be difficult to achieve.
When using a rigid laparoscope, a light cord that inserts into the back of the camera is necessary; otherwise, a 90-degree light cord adapter can be purchased.
Design enhancements facilitate coordination of instruments
One of the disadvantages of SPLS has been the restriction of movement that arises because of the close proximity of instruments and instrument handles. The latest designs have made articulation possible for tissue graspers, scissors, vessel sealers, and scopes.9,10 The value of articulation is apparent inside the abdomen, where it allows perfect positioning of the area of dissection. Outside the abdomen, the handles can be arranged in an angled pattern to allow the surgeon and assistant to operate comfortably (FIGURE 1).
In a four-handed procedure, one hand is on the camera, one on the uterine manipulator, and the remaining two hands operate the articulating grasper, vessel sealer, or needle driver, depending on the task.
Standard straight instruments can also be used for portions of the procedure.
Dissection and hemostasis are achieved in a manner similar to that of conventional laparoscopy. Our instrument of choice is an enhanced bipolar instrument, although harmonic and traditional biopolar energy can be used as well, depending on the preference of the surgeon.
The latest instruments are designed to dissect, cauterize, and cut, thereby decreasing the number of instrument exchanges necessary.
With the right aids, suturing can be simplified
Suturing through a single port can be a challenge. When possible, closure of the vaginal cuff following a total laparoscopic or laparoscopic-assisted vaginal hysterectomy should be performed from below. When endoscopic suturing is required, standard suturing using both intracorporeal and extracorporeal methods is possible.
Suturing aids such as the Endo Stitch (Covidien) or Lapra-Ty (Ethicon) are helpful. One author recommends Quill bidirectional, self-retaining suture with barbs (Angiotech) to avoid the need for knot-tying.6 (For more on self-retaining suture, see “Barbed suture, now in the toolbox of minimally invasive gyn surgery,” by Jon I. Einarsson, MD, MPH, and James A. Greenberg, MD, in the September 2009 issue at obgmanagement.com.)
The MiniLap (Stryker) is a 2.3-mm grasper that is inserted percutaneously directly through the abdominal wall without an incision. It can be used to set the needle on the needle driver or manipulate tissue while suturing. The resulting skin incision is barely visible and does not require closure.
Options are varied for specimen removal
Small specimens can be removed directly through a single-port system that has been opened, or they can be extracted after the system is removed, with rapid desufflation (FIGURE 6).
FIGURE 6 Single-incision oophorectomy
An ovary and tube removed through a single incision using the A) TriPort and B) SILS Port systems.Compared with conventional laparoscopy, the larger incision associated with single-port surgery facilitates specimen removal. Larger or potentially malignant specimens can be placed into an EndoCatch bag (Covidien) inserted through the single-incision 10-mm cannula (FIGURE 7).
FIGURE 7 Specimen removal
In this case, the specimen was placed in a 10-mm EndoCatch bag and removed through the 10-mm cannula of the SILS Port.In total laparoscopic hysterectomy or laparoscopic-assisted vaginal hysterectomy, the uterus is removed through the vagina. In supracervical hysterectomy, a small uterus can be removed through the cul-de-sac or directly through the single incision after placement in a bag.
When morcellation is required, the instrument can be placed through the cul-desac, cervix, or a single port. The morcellator can be placed directly through the SPLS port while utilizing the flexible scope in an angled direction (looking back toward the morcellator) for complete visualization (note: Covidien does not recommend this usage).
Transcervical tissue morcellation has also been described. In this approach, the cervix is dilated once the uterine body has been amputated, and the tissue morcellator is inserted through the cervix while the surgeon maintains visualization from above.6,13
How to master the technique
Many patients desire SPLS for its superior cosmetic outcome, but the approach may not always be appropriate. Depending on the procedure and characteristics of the patient (TABLE), multiple-port laparoscopy may be a better option. When a surgeon first attempts SPLS, we recommend that it be limited to the treatment of adnexal pathology only.
In your early SPlS cases, look for these patient characteristics
|
By using the techniques described in this article and selecting patients carefully, the surgeon can develop expertise in SPLS.11,14 During the learning process, the use of additional ports or Mini-Lap instruments (Stryker) can reduce the challenges of more difficult procedures and should be considered without reservation, as should the use of articulating accessory instruments and flexible or angled laparoscopes.
Although the clinical benefits of SPLS have yet to be determined, the cosmetic advantage of a single, hidden, umbilical incision likely increases patient satisfaction.
Clearly, the goal of SPLS is to use technology in a way that offers all of the benefits of traditional multiport laparoscopy without any of the limitations. Further study is required to determine whether SPLS meets this standard and, more important, whether it has any advantages over conventional techniques.
We want to hear from you! Tell us what you think.
1. Medeiros LR, Rosa DD, Bozzerri MC, et al. Laparoscopy versus laparotomy for benign ovarian tumour. Cochrane Database Syst Rev. 2009;(2):CD004751.-
2. Chapron C, Fauconnier A, Goffinet F, Breart G, Dubuisson JB. Laparoscopic surgery is not inherently dangerous for patients presenting with benign gynecological pathology. Results of a metaanalysis. Hum Reprod. 2002;17(5):1334-1342.
3. Fader AN, Escobar PF. Laparoendoscopic single-site surgery (LESS) in gynecologic oncology: technique and initial report. Gynecol Oncol. 2009;114(2):157-161.
4. Pelosi MA, Pelosi MA 3rd. Laparoscopic hysterectomy with bilateral salpingo-oophorectomy using a single umbilical puncture. N J Med. 1991;88(1):721-726.
5. Curcillo PG, King SA, Podolsky ER, Rottman SJ. Single port access (SPA) minimal access surgery through a single incision. Surg Technol Int. 2009;18:19-25.
6. Romanelli JR, Earle DB. Single-port laparoscopic surgery: an overview. Surg Endosc. 2009;23(7):1419-1427.
7. Ponsky TA. Single port laparoscopic cholecystectomy in adults and children: tools and techniques. J Am Coll Surg. 2009;209(5):e1-6.
8. Kim YW. Single port transumbilical myomectomy and ovarian cystectomy. J Minim Invasive Gynecol. 2009;16(6 suppl):S74.-
9. Ghezzi F, Cromi A, Fasola M, Bolis P. One-trocar salpingectomy for the treatment of tubal pregnancy: a “marionette-like” technique. BJOG. 2005;112(10):1417-1419.
10. Lim MC, Kim TJ, Kang S, Bae DS, Park SY, Seo SS. Embryonic natural orifice transumbilical endoscopic surgery (E-NOTES) for adnexal tumors. Surg Endosc. 2009;23(11):2445-2449.
11. Escobar PF, Starks DC, Fader AN, et al. Single-port risk-reducing salpingo-oophorectomy with and without hysterectomy: surgical outcomes and learning curve analysis. Gynecol Oncol. 2010;119(1):43-47.
12. Jeon HG, Jeong W, Oh CK. Initial experience with 50 laparoendoscopic single site surgeries using a homemade, single port device at a single center. J Urol. 2010;183(5):1866-1871.
13. Yoon G, Kim TJ, Lee YY, et al. Single port access subtotal hysterectomy with transcervical morcellation: a pilot study. J Minim Invasive Gynecol. 2010;17(1):78-81.
14. Ghomi A, Littman P, Prasad A, et al. Assessing the learning curve for laparoscopic supracervical hysterectomy. JSLS. 2007;11(2):190-194.
- Update on minimally invasive surgery
Amy Garcia, MD (April 2011) - 10 practical, evidence-based suggestions to improve your minimally invasive surgical skills now
Catherine A. Matthews, MD (April 2011)
The benefits of minimally invasive surgery—including less pain, faster recovery, and improved cosmesis—are well known.1,2 Standard laparotomy has been replaced by multiple-port operative laparoscopy for a great array of procedures, and advances in medical technology allow for a minimally invasive surgical approach even when a surgeon is faced with complex pathology.
Single-port laparoscopic surgery (SPLS) represents the latest advance in minimally invasive surgery. Using flexible endoscopes and articulating instruments, the surgeon can complete complex procedures through a single 2-cm incision in the abdomen. The incision is usually placed in the umbilicus, where it is easily hidden.3-8
Since the first laparoscopic hysterectomy through a single incision was performed 20 years ago, SPLS has been used successfully to perform nephrectomy, prostatectomy, hemicolectomy, cholecystectomy, splenectomy, intussusception reduction, gastrostomy tube placement, thoracoscopic lung biopsy, thoracoscopic decortication, and appendectomy.4-7
In gynecology, SPLS has been used to perform oophorectomy, salpingectomy, bilateral tubal ligation, ovarian cystectomy, surgical treatment of ectopic pregnancy, and both total and partial hysterectomy.7-11 At least two recent studies have concluded that SPLS is an acceptable way to treat many benign and malignant gynecologic conditions that are currently treated using multiport laparoscopy.3,11
This article outlines our approach to SPLS in the gynecologic patient and provides an overview of instrumentation, with the aim of allowing you to consider whether this approach might be feasible in your surgical practice, at your institution.
Unique setup required
When SPLS is performed through the umbilicus, the instruments must be held closer to the midline and more cephalad than during conventional laparoscopy to permit adequate visualization and manipulation. For this reason, the surgeon needs to assume a position higher over the torso and thorax of the patient, and both of the patient’s arms need to be tucked. Place the patient in a dorsal lithotomy position with a uterine manipulator in place to facilitate surgery—even when the uterus will be preserved and surgery involves only the adnexae.
With appropriate equipment and positioning, visualization and manipulation of anatomy are comparable to those of standard multiport laparoscopy.
New instruments simplify SPLS
Innovative surgical instruments allow for appropriate hand positioning outside the abdomen and minimize the internal collision of instruments brought through a single midline incision (FIGURE 1). A variety of single-port options are available, each with a unique patented design and method of insertion. In fact, the development of ports with multiple instrument channels has revolutionized SPLS.
FIGURE 1 Setup
Desired triangulation of instruments in SPLS setup.Before true single ports became available, it was necessary to place three 5-mm low-profile trocars in the fascia at three separate sites through a single skin incision. Pneumoperitoneum was established with a Veress needle, but the fascial incisions gradually merged with repeated cannula manipulation, producing air leaks.
Today, multiple-channel ports are placed using an open technique into a single skin and fascial incision. Trocars and instruments of varying size can be exchanged with ease without jeopardizing pneumoperitoneum.
Among the options:
- the SILS Port (Covidien) – a soft, flexible, three-channel port that allows for placement of blunt trocars ranging in size from 5 mm to 12 mm (FIGURE 2)
- the TriPort (Olympus America) – two flexible rings joined by a sleeve and multiple-channel port (FIGURE 3)
- GelPOINT Advanced Access Platform (Applied Medical) – a system constructed of synthetic gel material and consisting of a “GelSeal” cap, cannulas, and seals to accommodate 5-mm to 10-mm instrumentation (FIGURE 4).
We have found that all three devices allow for good range of motion while maintaining pneumoperitoneum.
(A recent article from Korea reports an inventive technique to perform single-incision laparoscopy using standard instrumentation: The authors fitted a self-retaining ring retractor with a surgical glove that had three of the fingers cut off and replaced by trocars.12)
FIGURE 2 SILS Port
The SILS Port is a soft, flexible, three-channel port that allows for placement of blunt trocars ranging in size from 5 mm to 12 mm.
FIGURE 3 TriPort
The TriPort system comprises two flexible rings joined by a sleeve and multiple-channel port.
FIGURE 4 GelPOINT
The GelPOINT Advanced Access Platform is constructed of synthetic gel material and accommodates 5-mm to 10-mm instrumentation.
A flexible laparoscope improves visualization
The ability to visualize the operative field is vital to any surgery, including SPLS. Use of a flexible laparoscope facilitates uncompromised visualization of the entire pelvis (FIGURE 5). Outside the abdomen, the flexible camera can be held laterally and away from the midline to help reduce the clashing of instruments and hands.
FIGURE 5 Flexible-tip laparoscope
A flexible-tip laparoscope ensures good visualization of the surgical field.If a flexible laparoscope is not available, a rigid 30-degree or 45-degree angled scope can be used, although visualization may be limited and adequate triangulation of instruments may be difficult to achieve.
When using a rigid laparoscope, a light cord that inserts into the back of the camera is necessary; otherwise, a 90-degree light cord adapter can be purchased.
Design enhancements facilitate coordination of instruments
One of the disadvantages of SPLS has been the restriction of movement that arises because of the close proximity of instruments and instrument handles. The latest designs have made articulation possible for tissue graspers, scissors, vessel sealers, and scopes.9,10 The value of articulation is apparent inside the abdomen, where it allows perfect positioning of the area of dissection. Outside the abdomen, the handles can be arranged in an angled pattern to allow the surgeon and assistant to operate comfortably (FIGURE 1).
In a four-handed procedure, one hand is on the camera, one on the uterine manipulator, and the remaining two hands operate the articulating grasper, vessel sealer, or needle driver, depending on the task.
Standard straight instruments can also be used for portions of the procedure.
Dissection and hemostasis are achieved in a manner similar to that of conventional laparoscopy. Our instrument of choice is an enhanced bipolar instrument, although harmonic and traditional biopolar energy can be used as well, depending on the preference of the surgeon.
The latest instruments are designed to dissect, cauterize, and cut, thereby decreasing the number of instrument exchanges necessary.
With the right aids, suturing can be simplified
Suturing through a single port can be a challenge. When possible, closure of the vaginal cuff following a total laparoscopic or laparoscopic-assisted vaginal hysterectomy should be performed from below. When endoscopic suturing is required, standard suturing using both intracorporeal and extracorporeal methods is possible.
Suturing aids such as the Endo Stitch (Covidien) or Lapra-Ty (Ethicon) are helpful. One author recommends Quill bidirectional, self-retaining suture with barbs (Angiotech) to avoid the need for knot-tying.6 (For more on self-retaining suture, see “Barbed suture, now in the toolbox of minimally invasive gyn surgery,” by Jon I. Einarsson, MD, MPH, and James A. Greenberg, MD, in the September 2009 issue at obgmanagement.com.)
The MiniLap (Stryker) is a 2.3-mm grasper that is inserted percutaneously directly through the abdominal wall without an incision. It can be used to set the needle on the needle driver or manipulate tissue while suturing. The resulting skin incision is barely visible and does not require closure.
Options are varied for specimen removal
Small specimens can be removed directly through a single-port system that has been opened, or they can be extracted after the system is removed, with rapid desufflation (FIGURE 6).
FIGURE 6 Single-incision oophorectomy
An ovary and tube removed through a single incision using the A) TriPort and B) SILS Port systems.Compared with conventional laparoscopy, the larger incision associated with single-port surgery facilitates specimen removal. Larger or potentially malignant specimens can be placed into an EndoCatch bag (Covidien) inserted through the single-incision 10-mm cannula (FIGURE 7).
FIGURE 7 Specimen removal
In this case, the specimen was placed in a 10-mm EndoCatch bag and removed through the 10-mm cannula of the SILS Port.In total laparoscopic hysterectomy or laparoscopic-assisted vaginal hysterectomy, the uterus is removed through the vagina. In supracervical hysterectomy, a small uterus can be removed through the cul-de-sac or directly through the single incision after placement in a bag.
When morcellation is required, the instrument can be placed through the cul-desac, cervix, or a single port. The morcellator can be placed directly through the SPLS port while utilizing the flexible scope in an angled direction (looking back toward the morcellator) for complete visualization (note: Covidien does not recommend this usage).
Transcervical tissue morcellation has also been described. In this approach, the cervix is dilated once the uterine body has been amputated, and the tissue morcellator is inserted through the cervix while the surgeon maintains visualization from above.6,13
How to master the technique
Many patients desire SPLS for its superior cosmetic outcome, but the approach may not always be appropriate. Depending on the procedure and characteristics of the patient (TABLE), multiple-port laparoscopy may be a better option. When a surgeon first attempts SPLS, we recommend that it be limited to the treatment of adnexal pathology only.
In your early SPlS cases, look for these patient characteristics
|
By using the techniques described in this article and selecting patients carefully, the surgeon can develop expertise in SPLS.11,14 During the learning process, the use of additional ports or Mini-Lap instruments (Stryker) can reduce the challenges of more difficult procedures and should be considered without reservation, as should the use of articulating accessory instruments and flexible or angled laparoscopes.
Although the clinical benefits of SPLS have yet to be determined, the cosmetic advantage of a single, hidden, umbilical incision likely increases patient satisfaction.
Clearly, the goal of SPLS is to use technology in a way that offers all of the benefits of traditional multiport laparoscopy without any of the limitations. Further study is required to determine whether SPLS meets this standard and, more important, whether it has any advantages over conventional techniques.
We want to hear from you! Tell us what you think.
- Update on minimally invasive surgery
Amy Garcia, MD (April 2011) - 10 practical, evidence-based suggestions to improve your minimally invasive surgical skills now
Catherine A. Matthews, MD (April 2011)
The benefits of minimally invasive surgery—including less pain, faster recovery, and improved cosmesis—are well known.1,2 Standard laparotomy has been replaced by multiple-port operative laparoscopy for a great array of procedures, and advances in medical technology allow for a minimally invasive surgical approach even when a surgeon is faced with complex pathology.
Single-port laparoscopic surgery (SPLS) represents the latest advance in minimally invasive surgery. Using flexible endoscopes and articulating instruments, the surgeon can complete complex procedures through a single 2-cm incision in the abdomen. The incision is usually placed in the umbilicus, where it is easily hidden.3-8
Since the first laparoscopic hysterectomy through a single incision was performed 20 years ago, SPLS has been used successfully to perform nephrectomy, prostatectomy, hemicolectomy, cholecystectomy, splenectomy, intussusception reduction, gastrostomy tube placement, thoracoscopic lung biopsy, thoracoscopic decortication, and appendectomy.4-7
In gynecology, SPLS has been used to perform oophorectomy, salpingectomy, bilateral tubal ligation, ovarian cystectomy, surgical treatment of ectopic pregnancy, and both total and partial hysterectomy.7-11 At least two recent studies have concluded that SPLS is an acceptable way to treat many benign and malignant gynecologic conditions that are currently treated using multiport laparoscopy.3,11
This article outlines our approach to SPLS in the gynecologic patient and provides an overview of instrumentation, with the aim of allowing you to consider whether this approach might be feasible in your surgical practice, at your institution.
Unique setup required
When SPLS is performed through the umbilicus, the instruments must be held closer to the midline and more cephalad than during conventional laparoscopy to permit adequate visualization and manipulation. For this reason, the surgeon needs to assume a position higher over the torso and thorax of the patient, and both of the patient’s arms need to be tucked. Place the patient in a dorsal lithotomy position with a uterine manipulator in place to facilitate surgery—even when the uterus will be preserved and surgery involves only the adnexae.
With appropriate equipment and positioning, visualization and manipulation of anatomy are comparable to those of standard multiport laparoscopy.
New instruments simplify SPLS
Innovative surgical instruments allow for appropriate hand positioning outside the abdomen and minimize the internal collision of instruments brought through a single midline incision (FIGURE 1). A variety of single-port options are available, each with a unique patented design and method of insertion. In fact, the development of ports with multiple instrument channels has revolutionized SPLS.
FIGURE 1 Setup
Desired triangulation of instruments in SPLS setup.Before true single ports became available, it was necessary to place three 5-mm low-profile trocars in the fascia at three separate sites through a single skin incision. Pneumoperitoneum was established with a Veress needle, but the fascial incisions gradually merged with repeated cannula manipulation, producing air leaks.
Today, multiple-channel ports are placed using an open technique into a single skin and fascial incision. Trocars and instruments of varying size can be exchanged with ease without jeopardizing pneumoperitoneum.
Among the options:
- the SILS Port (Covidien) – a soft, flexible, three-channel port that allows for placement of blunt trocars ranging in size from 5 mm to 12 mm (FIGURE 2)
- the TriPort (Olympus America) – two flexible rings joined by a sleeve and multiple-channel port (FIGURE 3)
- GelPOINT Advanced Access Platform (Applied Medical) – a system constructed of synthetic gel material and consisting of a “GelSeal” cap, cannulas, and seals to accommodate 5-mm to 10-mm instrumentation (FIGURE 4).
We have found that all three devices allow for good range of motion while maintaining pneumoperitoneum.
(A recent article from Korea reports an inventive technique to perform single-incision laparoscopy using standard instrumentation: The authors fitted a self-retaining ring retractor with a surgical glove that had three of the fingers cut off and replaced by trocars.12)
FIGURE 2 SILS Port
The SILS Port is a soft, flexible, three-channel port that allows for placement of blunt trocars ranging in size from 5 mm to 12 mm.
FIGURE 3 TriPort
The TriPort system comprises two flexible rings joined by a sleeve and multiple-channel port.
FIGURE 4 GelPOINT
The GelPOINT Advanced Access Platform is constructed of synthetic gel material and accommodates 5-mm to 10-mm instrumentation.
A flexible laparoscope improves visualization
The ability to visualize the operative field is vital to any surgery, including SPLS. Use of a flexible laparoscope facilitates uncompromised visualization of the entire pelvis (FIGURE 5). Outside the abdomen, the flexible camera can be held laterally and away from the midline to help reduce the clashing of instruments and hands.
FIGURE 5 Flexible-tip laparoscope
A flexible-tip laparoscope ensures good visualization of the surgical field.If a flexible laparoscope is not available, a rigid 30-degree or 45-degree angled scope can be used, although visualization may be limited and adequate triangulation of instruments may be difficult to achieve.
When using a rigid laparoscope, a light cord that inserts into the back of the camera is necessary; otherwise, a 90-degree light cord adapter can be purchased.
Design enhancements facilitate coordination of instruments
One of the disadvantages of SPLS has been the restriction of movement that arises because of the close proximity of instruments and instrument handles. The latest designs have made articulation possible for tissue graspers, scissors, vessel sealers, and scopes.9,10 The value of articulation is apparent inside the abdomen, where it allows perfect positioning of the area of dissection. Outside the abdomen, the handles can be arranged in an angled pattern to allow the surgeon and assistant to operate comfortably (FIGURE 1).
In a four-handed procedure, one hand is on the camera, one on the uterine manipulator, and the remaining two hands operate the articulating grasper, vessel sealer, or needle driver, depending on the task.
Standard straight instruments can also be used for portions of the procedure.
Dissection and hemostasis are achieved in a manner similar to that of conventional laparoscopy. Our instrument of choice is an enhanced bipolar instrument, although harmonic and traditional biopolar energy can be used as well, depending on the preference of the surgeon.
The latest instruments are designed to dissect, cauterize, and cut, thereby decreasing the number of instrument exchanges necessary.
With the right aids, suturing can be simplified
Suturing through a single port can be a challenge. When possible, closure of the vaginal cuff following a total laparoscopic or laparoscopic-assisted vaginal hysterectomy should be performed from below. When endoscopic suturing is required, standard suturing using both intracorporeal and extracorporeal methods is possible.
Suturing aids such as the Endo Stitch (Covidien) or Lapra-Ty (Ethicon) are helpful. One author recommends Quill bidirectional, self-retaining suture with barbs (Angiotech) to avoid the need for knot-tying.6 (For more on self-retaining suture, see “Barbed suture, now in the toolbox of minimally invasive gyn surgery,” by Jon I. Einarsson, MD, MPH, and James A. Greenberg, MD, in the September 2009 issue at obgmanagement.com.)
The MiniLap (Stryker) is a 2.3-mm grasper that is inserted percutaneously directly through the abdominal wall without an incision. It can be used to set the needle on the needle driver or manipulate tissue while suturing. The resulting skin incision is barely visible and does not require closure.
Options are varied for specimen removal
Small specimens can be removed directly through a single-port system that has been opened, or they can be extracted after the system is removed, with rapid desufflation (FIGURE 6).
FIGURE 6 Single-incision oophorectomy
An ovary and tube removed through a single incision using the A) TriPort and B) SILS Port systems.Compared with conventional laparoscopy, the larger incision associated with single-port surgery facilitates specimen removal. Larger or potentially malignant specimens can be placed into an EndoCatch bag (Covidien) inserted through the single-incision 10-mm cannula (FIGURE 7).
FIGURE 7 Specimen removal
In this case, the specimen was placed in a 10-mm EndoCatch bag and removed through the 10-mm cannula of the SILS Port.In total laparoscopic hysterectomy or laparoscopic-assisted vaginal hysterectomy, the uterus is removed through the vagina. In supracervical hysterectomy, a small uterus can be removed through the cul-de-sac or directly through the single incision after placement in a bag.
When morcellation is required, the instrument can be placed through the cul-desac, cervix, or a single port. The morcellator can be placed directly through the SPLS port while utilizing the flexible scope in an angled direction (looking back toward the morcellator) for complete visualization (note: Covidien does not recommend this usage).
Transcervical tissue morcellation has also been described. In this approach, the cervix is dilated once the uterine body has been amputated, and the tissue morcellator is inserted through the cervix while the surgeon maintains visualization from above.6,13
How to master the technique
Many patients desire SPLS for its superior cosmetic outcome, but the approach may not always be appropriate. Depending on the procedure and characteristics of the patient (TABLE), multiple-port laparoscopy may be a better option. When a surgeon first attempts SPLS, we recommend that it be limited to the treatment of adnexal pathology only.
In your early SPlS cases, look for these patient characteristics
|
By using the techniques described in this article and selecting patients carefully, the surgeon can develop expertise in SPLS.11,14 During the learning process, the use of additional ports or Mini-Lap instruments (Stryker) can reduce the challenges of more difficult procedures and should be considered without reservation, as should the use of articulating accessory instruments and flexible or angled laparoscopes.
Although the clinical benefits of SPLS have yet to be determined, the cosmetic advantage of a single, hidden, umbilical incision likely increases patient satisfaction.
Clearly, the goal of SPLS is to use technology in a way that offers all of the benefits of traditional multiport laparoscopy without any of the limitations. Further study is required to determine whether SPLS meets this standard and, more important, whether it has any advantages over conventional techniques.
We want to hear from you! Tell us what you think.
1. Medeiros LR, Rosa DD, Bozzerri MC, et al. Laparoscopy versus laparotomy for benign ovarian tumour. Cochrane Database Syst Rev. 2009;(2):CD004751.-
2. Chapron C, Fauconnier A, Goffinet F, Breart G, Dubuisson JB. Laparoscopic surgery is not inherently dangerous for patients presenting with benign gynecological pathology. Results of a metaanalysis. Hum Reprod. 2002;17(5):1334-1342.
3. Fader AN, Escobar PF. Laparoendoscopic single-site surgery (LESS) in gynecologic oncology: technique and initial report. Gynecol Oncol. 2009;114(2):157-161.
4. Pelosi MA, Pelosi MA 3rd. Laparoscopic hysterectomy with bilateral salpingo-oophorectomy using a single umbilical puncture. N J Med. 1991;88(1):721-726.
5. Curcillo PG, King SA, Podolsky ER, Rottman SJ. Single port access (SPA) minimal access surgery through a single incision. Surg Technol Int. 2009;18:19-25.
6. Romanelli JR, Earle DB. Single-port laparoscopic surgery: an overview. Surg Endosc. 2009;23(7):1419-1427.
7. Ponsky TA. Single port laparoscopic cholecystectomy in adults and children: tools and techniques. J Am Coll Surg. 2009;209(5):e1-6.
8. Kim YW. Single port transumbilical myomectomy and ovarian cystectomy. J Minim Invasive Gynecol. 2009;16(6 suppl):S74.-
9. Ghezzi F, Cromi A, Fasola M, Bolis P. One-trocar salpingectomy for the treatment of tubal pregnancy: a “marionette-like” technique. BJOG. 2005;112(10):1417-1419.
10. Lim MC, Kim TJ, Kang S, Bae DS, Park SY, Seo SS. Embryonic natural orifice transumbilical endoscopic surgery (E-NOTES) for adnexal tumors. Surg Endosc. 2009;23(11):2445-2449.
11. Escobar PF, Starks DC, Fader AN, et al. Single-port risk-reducing salpingo-oophorectomy with and without hysterectomy: surgical outcomes and learning curve analysis. Gynecol Oncol. 2010;119(1):43-47.
12. Jeon HG, Jeong W, Oh CK. Initial experience with 50 laparoendoscopic single site surgeries using a homemade, single port device at a single center. J Urol. 2010;183(5):1866-1871.
13. Yoon G, Kim TJ, Lee YY, et al. Single port access subtotal hysterectomy with transcervical morcellation: a pilot study. J Minim Invasive Gynecol. 2010;17(1):78-81.
14. Ghomi A, Littman P, Prasad A, et al. Assessing the learning curve for laparoscopic supracervical hysterectomy. JSLS. 2007;11(2):190-194.
1. Medeiros LR, Rosa DD, Bozzerri MC, et al. Laparoscopy versus laparotomy for benign ovarian tumour. Cochrane Database Syst Rev. 2009;(2):CD004751.-
2. Chapron C, Fauconnier A, Goffinet F, Breart G, Dubuisson JB. Laparoscopic surgery is not inherently dangerous for patients presenting with benign gynecological pathology. Results of a metaanalysis. Hum Reprod. 2002;17(5):1334-1342.
3. Fader AN, Escobar PF. Laparoendoscopic single-site surgery (LESS) in gynecologic oncology: technique and initial report. Gynecol Oncol. 2009;114(2):157-161.
4. Pelosi MA, Pelosi MA 3rd. Laparoscopic hysterectomy with bilateral salpingo-oophorectomy using a single umbilical puncture. N J Med. 1991;88(1):721-726.
5. Curcillo PG, King SA, Podolsky ER, Rottman SJ. Single port access (SPA) minimal access surgery through a single incision. Surg Technol Int. 2009;18:19-25.
6. Romanelli JR, Earle DB. Single-port laparoscopic surgery: an overview. Surg Endosc. 2009;23(7):1419-1427.
7. Ponsky TA. Single port laparoscopic cholecystectomy in adults and children: tools and techniques. J Am Coll Surg. 2009;209(5):e1-6.
8. Kim YW. Single port transumbilical myomectomy and ovarian cystectomy. J Minim Invasive Gynecol. 2009;16(6 suppl):S74.-
9. Ghezzi F, Cromi A, Fasola M, Bolis P. One-trocar salpingectomy for the treatment of tubal pregnancy: a “marionette-like” technique. BJOG. 2005;112(10):1417-1419.
10. Lim MC, Kim TJ, Kang S, Bae DS, Park SY, Seo SS. Embryonic natural orifice transumbilical endoscopic surgery (E-NOTES) for adnexal tumors. Surg Endosc. 2009;23(11):2445-2449.
11. Escobar PF, Starks DC, Fader AN, et al. Single-port risk-reducing salpingo-oophorectomy with and without hysterectomy: surgical outcomes and learning curve analysis. Gynecol Oncol. 2010;119(1):43-47.
12. Jeon HG, Jeong W, Oh CK. Initial experience with 50 laparoendoscopic single site surgeries using a homemade, single port device at a single center. J Urol. 2010;183(5):1866-1871.
13. Yoon G, Kim TJ, Lee YY, et al. Single port access subtotal hysterectomy with transcervical morcellation: a pilot study. J Minim Invasive Gynecol. 2010;17(1):78-81.
14. Ghomi A, Littman P, Prasad A, et al. Assessing the learning curve for laparoscopic supracervical hysterectomy. JSLS. 2007;11(2):190-194.
Overlooked diagnoses
“Not all mood swings are bipolar disorder” (Current Psychiatry, February 2011, p. 38-52) is a highly relevant and helpful article with a glaring omission. There is no mention of the emotional lability and behavioral dyscontrol associated with abuse, trauma, and invalidation. “Mood swing” symptoms are prominent in developmental trauma disorder and complex posttraumatic stress disorder, although these diagnoses are not yet in the DSM. Unfortunately, the effects of abuse, trauma, and invalidation often are unrecognized in the differential diagnoses of these children and too often the “kneejerk” diagnoses of bipolar disorder, oppositional defiant disorder, and attention-deficit/hyperactivity disorder are inappropriately assigned, delaying the implementation of trauma theory-informed therapy.
Bradford B. Schwartz, MD
Private Practice
York, PA
The authors respond
We thank Dr. Schwartz for his comments regarding emotional lability and behavioral dyscontrol associated with children who have experienced trauma, abuse, and invalidation. An assessment for possible trauma always is part of the initial assessment of each child referred to our program. None of the patients discussed in our article had a history of abuse or trauma. Referrals to our pediatric mood disorders program initially are screened through the Cincinnati Children’s Hospital Psychiatric Intake and Response Center, which functions as triage, gathering psychiatric history, including assessing trauma, and children with a history of abuse and trauma are referred to other clinicians specializing in this area. But Dr. Schwartz’s point is well taken—trauma or abuse always should be part of the differential diagnosis of children and adolescents referred for mood swings.
Robert A. Kowatch, MD, PhD
Professor of Psychiatry and Pediatrics
Erin Monroe, CNS
Clinical Nurse Specialist
Division of Psychiatry
Sergio V. Delgado, MD
Associate Professor of Psychiatry
and Pediatrics
Cincinnati Children’s Hospital Medical Center
Cincinnati, OH
“Not all mood swings are bipolar disorder” (Current Psychiatry, February 2011, p. 38-52) is a highly relevant and helpful article with a glaring omission. There is no mention of the emotional lability and behavioral dyscontrol associated with abuse, trauma, and invalidation. “Mood swing” symptoms are prominent in developmental trauma disorder and complex posttraumatic stress disorder, although these diagnoses are not yet in the DSM. Unfortunately, the effects of abuse, trauma, and invalidation often are unrecognized in the differential diagnoses of these children and too often the “kneejerk” diagnoses of bipolar disorder, oppositional defiant disorder, and attention-deficit/hyperactivity disorder are inappropriately assigned, delaying the implementation of trauma theory-informed therapy.
Bradford B. Schwartz, MD
Private Practice
York, PA
The authors respond
We thank Dr. Schwartz for his comments regarding emotional lability and behavioral dyscontrol associated with children who have experienced trauma, abuse, and invalidation. An assessment for possible trauma always is part of the initial assessment of each child referred to our program. None of the patients discussed in our article had a history of abuse or trauma. Referrals to our pediatric mood disorders program initially are screened through the Cincinnati Children’s Hospital Psychiatric Intake and Response Center, which functions as triage, gathering psychiatric history, including assessing trauma, and children with a history of abuse and trauma are referred to other clinicians specializing in this area. But Dr. Schwartz’s point is well taken—trauma or abuse always should be part of the differential diagnosis of children and adolescents referred for mood swings.
Robert A. Kowatch, MD, PhD
Professor of Psychiatry and Pediatrics
Erin Monroe, CNS
Clinical Nurse Specialist
Division of Psychiatry
Sergio V. Delgado, MD
Associate Professor of Psychiatry
and Pediatrics
Cincinnati Children’s Hospital Medical Center
Cincinnati, OH
“Not all mood swings are bipolar disorder” (Current Psychiatry, February 2011, p. 38-52) is a highly relevant and helpful article with a glaring omission. There is no mention of the emotional lability and behavioral dyscontrol associated with abuse, trauma, and invalidation. “Mood swing” symptoms are prominent in developmental trauma disorder and complex posttraumatic stress disorder, although these diagnoses are not yet in the DSM. Unfortunately, the effects of abuse, trauma, and invalidation often are unrecognized in the differential diagnoses of these children and too often the “kneejerk” diagnoses of bipolar disorder, oppositional defiant disorder, and attention-deficit/hyperactivity disorder are inappropriately assigned, delaying the implementation of trauma theory-informed therapy.
Bradford B. Schwartz, MD
Private Practice
York, PA
The authors respond
We thank Dr. Schwartz for his comments regarding emotional lability and behavioral dyscontrol associated with children who have experienced trauma, abuse, and invalidation. An assessment for possible trauma always is part of the initial assessment of each child referred to our program. None of the patients discussed in our article had a history of abuse or trauma. Referrals to our pediatric mood disorders program initially are screened through the Cincinnati Children’s Hospital Psychiatric Intake and Response Center, which functions as triage, gathering psychiatric history, including assessing trauma, and children with a history of abuse and trauma are referred to other clinicians specializing in this area. But Dr. Schwartz’s point is well taken—trauma or abuse always should be part of the differential diagnosis of children and adolescents referred for mood swings.
Robert A. Kowatch, MD, PhD
Professor of Psychiatry and Pediatrics
Erin Monroe, CNS
Clinical Nurse Specialist
Division of Psychiatry
Sergio V. Delgado, MD
Associate Professor of Psychiatry
and Pediatrics
Cincinnati Children’s Hospital Medical Center
Cincinnati, OH
Subjective cognitive impairment: When to be concerned about ‘senior moments’
MS. F, age 66, requests genetic testing because she is concerned about mild memory difficulties, such as forgetting names and where she puts her keys or checkbook, and fears she may be developing Alzheimer’s disease (AD). Her mother and sister were diagnosed with AD in their early 60s. Ms. F has 20 years of education and reports no problems with driving, managing her finances, remembering to take her medications, or maintaining social activities, which her husband confirms.
Detailed questioning about anxiety and depressive symptoms reveals substantial worries about future cognitive decline and some concerns about her finances and her husband’s health. Ms. F says she occasionally feels down and has low energy but denies other depressive symptoms. She reports no sleep disturbances—including snoring and daytime sleepiness, which could indicate obstructive sleep apnea—which her husband confirms. Ms. F takes levothyroxine for hypothyroidism, atenolol for hypertension, aspirin and clopidogrel for coronary artery disease, and atorvastatin for hyperlipidemia. In addition, she provides a long list of over-the-counter (OTC) supplements—ginkgo, huperzine, ginseng, phosphatidylserine, B1, B12, folate, vitamin D, alpha-lipoic acid, and vinpocetine—that she takes to “protect” her brain from AD.
Subjective cognitive impairment (SCI) in older persons is a common condition with a largely unclear prognosis. Many older adults (age ≥65) express concern about mild cognitive problems—“senior moments”—such as word-finding difficulties and forgetfulness.1 Individuals may wonder if walking into a room only to forget why might be the first sign of dementia. Some older adults try to counteract these memory problems by engaging in brain exercises—including costly computer games—and taking OTC “brain-enhancing” vitamins, herbal remedies, and other supplements.
Although some clinicians may view SCI as benign, that is not always true (Table l).2-5 This article discusses the clinical significance of these mild cognitive complaints by examining:
- age-related cognitive decline (ARCD)
- SCI
- how SCI can be differentiated from more serious conditions, such as mild cognitive impairment (MCI) and early stages of AD and other dementias.
We also will discuss assessing and treating cognitive complaints. Although distinctions between SCI and ARCD may be controversial, evidence suggests clinicians need to adopt a more nuanced clinical approach.
Table 1
Why SCI should be taken seriously
| SCI may create emotional distress because patients are aware of decline in their ‘mental sharpness’ |
| SCI patients might consume unnecessary and potentially harmful OTC supplements touted to promote memory |
| Patients might limit their driving and financial management to avoid making mistakes |
| SCI might impair medication adherence2 |
| SCI may be an early sign of dementia3 |
| Patients’ worry about their self-perceived memory loss might predict dementia4 |
| SCI may predict nursing home placement5 |
| Addressing SCI gives health care providers an opportunity to address anxiety or depression that often accompany SCI |
| Evaluation of potential causes of SCI may uncover reversible conditions that can be treated |
| OTC: over-the-counter; SCI: subjective cognitive impairment |
‘Normal’ cognitive decline
ARCD is subtle decline in cognitive abilities, such as episodic memory, attention, and time needed to complete complex activities.6,7 Individuals with ARCD might not have subjective memory complaints or objective cognitive deficits, and their ability to live independently may not be compromised.7 The degree of decline in ARCD may be smaller than previously thought.8 Park9 summarizes 4 main mechanisms thought to underlie age-related declines in cognition:
- reduced speed of processing
- decreased working memory capabilities
- declining inhibitory control (eg, impaired complex attentional capabilities)
- sensory changes (eg, visual and auditory deficits).
ARCD traditionally is thought to result from predictable changes in the brain associated with aging, such as reduced brain volume in the hippocampus and frontal lobes, loss of myelin, loss of synapses, and cytoskeletal changes.7 However, not all older adults experience ARCD. Some remain highly functional in their later years and continue to actively engage in life well into very old age.6,9
Subjective cognitive impairment
One-quarter to one-half of community-dwelling older adults report subjective cognitive complaints, such as forgetfulness and word-finding difficulties.10 Patients with SCI do not show objective evidence of cognitive impairment on neuropsychological tests and their cognitive problems cause no functional decline.10
Preliminary evidence indicates that SCI may be a harbinger of further cognitive decline. Reisberg et al3 found that compared with patients without SCI, patients with SCI were 4.5 times more likely to develop MCI—cognitive difficulties that can be detected by cognitive tests, but do not cause functional decline—or dementia within 7 years.3 Studies also have suggested that SCI may be a pre-MCI stage of subsequent dementia.11-13 AD generally has a long (10 to 12 years) and progressive prodromal phase before dementia onset and is characterized by successive emergence of cognitive deficits, memory complaints, depressive symptoms, and functional impairment.14
In light of this research, we believe patients with SCI and other risk factors for AD, such as a family history of AD, may be at higher risk of further cognitive and functional decline compared with individuals with ARCD and no AD risk factors. Therefore, patients with SCI and other risk factors for AD (Table 2)15-19 may benefit from annual follow-up to determine if cognitive problems have progressed to MCI or AD.
SCI may be a response to subclinical alterations in neurobiology—a phenomenon known as reverse causality.20 Biomarkers, such as cerebrospinal fluid levels of ß-amyloid and phosphorylated tau, and amyloid imaging using positron emission tomography may help identify AD in SCI patients.21 In these patients, SCI is a misnomer because the cognitive impairment is real—not “subjective”—but current tests are not sensitive enough to detect the cognitive decline the patient has recognized. This group of patients should be differentiated from individuals who may perceive typical cognitive aging (ARCD) as pathologic and complain about it. In the future, biomarkers may help differentiate these 2 groups.
Table 2
Factors that increase SCI patients’ risk for dementia
| Family history of Alzheimer’s disease |
| Mild behavioral impairment |
| Slow gait |
| Depression |
| Rapid weight loss |
| Multiple subtle neurologic abnormalities |
| Vascular disease (eg, peripheral vascular disease, coronary artery disease, cerebrovascular disease) |
| SCI: subjective cognitive impairment Source: References 15-19 |
Mild cognitive impairment
MCI is similar to SCI because MCI patients may present with complaints of memory decline and other cognitive difficulties22 but neither condition is associated with significant impairment of daily activities.23 The key difference is that patients with MCI demonstrate impaired performance on objective cognitive tests whereas SCI patients do not.24 In our experience, office-based tests do not reliably differentiate the 2 conditions because many patients with SCI may show mild impairment in tests such as the Mini-Mental State Exam (MMSE)25 but comprehensive neuropsychological testing reveals no objective cognitive deficits. Neuropsychological testing is essential to reliably differentiate SCI from MCI.
The distinction between SCI and MCI is clinically relevant because evidence suggests that MCI patients have a near-term risk of developing dementia, particularly AD.22,23 In a longitudinal study of 76 individuals with MCI, 12% of patients progressed to AD each year compared with 1% to 2% of healthy older adults.26 Patients with MCI are at increased risk of delirium (especially during hospitalization), falls, medication errors, and difficulty managing their finances.24 Older adults with MCI also have increased mortality compared with older adults with normal cognitive functioning.22 Both SCI and MCI should be differentiated from mild dementia. Common dementias in older adults include:
- AD dementia
- Vascular dementia (may occur with or without AD)
- Lewy body dementia
- Frontotemporal dementia
- Parkinson’s disease dementia.
By definition, all dementia types are associated with impaired ability to perform daily activities and cognitive decline.27
Assessing cognitive complaints
Evaluation of older adults’ cognitive complaints should begin with a thorough history to elicit symptoms of anxiety, depression, physical complaints, and any associated functional decline; a physical exam; and a comprehensive mental status examination. This initial evaluation should be followed by routine and specific investigations as indicated (Table 3).22,24,28,29
In a 6-year study of 100 older adults with and without objective evidence of memory decline, both groups showed similar rates of cognitive complaints.30 Also, researchers found no relationship between individuals’ perception of their cognitive functioning and performance on neuropsychological testing. Mood, education level, and apolipoprotein E epsilon 4 genotype status also did not correlate with participants’ subjective cognitive complaints. These findings highlight the need for objective test data to determine whether older adults’ memory complaints reflect pathologic changes in cognition. After a thorough diagnostic workup, some patients complaining of memory decline will have no detectable evidence of cognitive dysfunction or an identifiable cause. However, others may have identifiable causes of memory impairment (Table 4)28,29,31,32—which could be treated—some will have MCI, and others may be in an early stage of dementia.
Table 3
Investigation of older adults with SCI
| Investigation | Rationale |
|---|---|
| Routine | |
| Neuropsychological testing | Delineation of cognitive syndromes (SCI vs MCI vs AD*) |
| Hematology (full blood count) | Screen for anemia |
| Biochemistry (electrolytes, renal function, liver function, thyroid function, B12, and folate) | Screen for treatable causes of cognitive complaints |
| For specific indication suggested by history, physical exam, or neuropsychological testing | |
| Neuroimaging | Generalized and regional imaging (eg, hippocampal atrophy, space occupying lesions) |
| Electroencephalography | Epilepsy/seizures (especially absence and complex partial) |
| Cardiac (eg, echocardiography) | May reveal cardiac arrhythmia or sources of emboli |
| Inflammatory markers (eg, ESR) | Screen for inflammatory processes |
| Treponemal serology | Tertiary syphilis |
| *Alzheimer’s disease and other dementias AD: Alzheimer’s disease; ESR: erythrocyte sedimentation rate; MCI: mild cognitive impairment; SCI: subjective cognitive impairment Source: References 22,24,28,29 | |
Table 4
Differential diagnosis of SCI
| Cause of cognitive impairment | Potential mechanism |
|---|---|
| ARCD | Allostatic load, ‘wear and tear’ from a lifetime of physiological or psychological stresses and adaptations |
| Anemia | Neuronal hypoxia |
| Alzheimer’s disease | Amyloid and/or tau-mediated neurotoxicity, neuroinflammation |
| Cerebrovascular disease | Neuronal ischemia and hypoxia, neuroinflammation |
| Vitamin deficiencies (eg, B1, B12, folate, D) | Impaired neuronal and neurotransmitter function |
| Inadequate protein intake | Impaired neuronal function |
| Anticholinergic drug use | Decreased cholinergic neurotransmission |
| Alcohol use | Direct neurotoxicity and indirect causes such as malnutrition or head injury |
| Depression, anxiety | Hippocampal dysfunction with or without atrophy |
| Obstructive sleep apnea | Neuronal hypoxia, neuroinflammation |
| Head injury | Neuronal and synaptic loss |
| ARCD: age-related cognitive decline; SCI: subjective cognitive impairment Source: References 28,29,31,32 | |
CASE CONTINUED: No measurable deficits
Ms. F’s medical history is remarkable for coronary artery disease, hypothyroidism, hypertension, hyperlipidemia, cataracts, arthritis, back surgery (secondary to spondylosis), and foot surgery. Ms. F denies a history of alcohol or illicit substance abuse. She smoked tobacco for 30 years (2 packs per day), but quit 5 years ago after her heart attack. Physical exam is unremarkable except for mild obesity (body mass index = 31 kg/m2).
Ms. F’s mental status exam reveals anxious mood and affect. Her recall is 2 out of 3 items. Her MMSE score is 29/30 (1 point lost on recall) and her Geriatric Depression Scale33 score is 2/15, indicating minimal depressive symptoms. On neuropsychological testing, Ms. F demonstrates high average intellectual abilities; compared with others her age, she performs within expectations on all measures. That is, she performs within the above-average to low-average range on measures of attention, working memory, speed of processing, expressive language, learning, memory, visual spatial abilities, executive functioning, and knowledge of basic health and safety information.
Enhancing neuroplasticity
We recommend neuroplasticity-based interventions to treat SCI and promote healthy brain aging.20,29 For a checklist clinicians can use to promote healthy brain aging and thus improve patients’ cognitive health see this article at CurrentPsychiatry. com. Table 51,29 lists cognitive strategies to improve memory and maintain cognitive vitality.
Enhancing brain plasticity and neurogenesis requires engaging older adults in demanding sensory, cognitive, and motor activities on an intensive basis.34 Therapeutic stimulation of neuroplasticity and neurogenesis might contribute to functional “repair” of the diseased adult brain before damage to whole neuronal networks has ensued.29 An important treatment component is reassuring patients with SCI that they do not have AD or MCI. Treating comorbid anxiety and depression and reversible causes of cognitive complaints is key to successful outcomes.
Table 5
Strategies to improve memory and maintain cognitive vitality
| Strategy | Description |
|---|---|
| Mindfulness | Focus on 1 task at a time rather than trying to multitask. Research shows that cognition is more efficient in this manner |
| Cognitive strategies | Use mnemonics (such as ROY G BIV to remember the colors of the rainbow). Make associations for information, such as when meeting someone new, relate their name to someone else you know well. Use cues such as memory notebooks to prompt information recall. Engage in learning new and challenging cognitive activities, such as a new language, a music instrument, or dance. Consider computer-based brain exercises |
| Rehearsal | Practice information you want to remember, such as repeating the information several times or writing it down |
| Be patient | Getting frustrated when you have memory difficulties makes it more challenging to remember information |
| Exercise (mental and physical) | Engage in mental activities, such as reading and crossword puzzles. Do something that you are interested in, rather than making it a chore. Research has demonstrated that physical exercise also aids memory |
| Diet | What is good for the heart is good for the brain. Fruits, vegetables, food rich in omega-3 fatty acids (eg, fatty fish such as salmon), whole grains, spices (eg, turmeric), and small amounts of tree nuts (eg, walnuts) are recommended as part of a balanced diet |
| Source: References 1,29 | |
CASE CONTINUED: Reassurance and risk reduction
Ms. F’s psychiatrist reassures her that she does not have AD. She receives genetic counseling and decides to forgo genetic testing. Her psychiatrist educates Ms. F about the risks of OTC supplements—especially increased risk of bleeding because she takes aspirin and clopidogrel—and lack of data supporting their use. Ms. F is counseled that a healthy lifestyle, including regular exercise, Mediterranean diet with increased intake of omega-3 fatty acids, learning new things, and being socially active, is the safest way to promote brain health. Over 3 months, Ms. F discontinues all supplements except the vitamins and omega-3, starts exercising, resumes piano lessons that she stopped 10 years ago, and becomes a vegetarian. She continues to have mild SCI but she says she is not bothered by it and feels satisfied that she is doing all she can to promote her brain health.
Related Resources
- Desai AK. Healthy brain aging: evidence based methods to preserve brain function and prevent dementia. Philadelphia, PA: W. B. Saunders; 2010.
- Doidge N. The brain that changes itself. New York, NY: Penguin Books; 2007.
- Vance DE, Roberson AJ, McGuinness TM, et al. How neuroplasticity and cognitive reserve protect cognitive functioning. J Psychosoc Nurs Ment Health Serv. 2010; 48: 1-8.
Brain Training Resources
- Weil A, Small G. The healthy brain kit. Boulder, CO: Sounds True, Inc.; 2007. Audio CDs, brain-training cards and workbooks.
- Posit Science. www.positscience.com.
- Sharp Brains. www.sharpbrains.com.
Drug Brand Names
- Atenolol • Tenormin
- Atorvastatin • Lipitor
- Clopidogrel • Plavix
- Levothyroxine • Levoxyl, Synthroid
Disclosures
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Featured Audio
Abhilash K. Desai, MD, discusses emerging research on biomarkers that may help clarify diagnosis.
1. Small GW. What we need to know about age related memory loss. BMJ. 2002;324:1502-1505.
2. Hayes TL, Larimer N, Adami A, et al. Medication adherence in healthy elders. J Aging Health. 2009;21(4):567-580.
3. Reisberg B, Shulman MB, Torossian C, et al. Outcome over seven years of healthy adults with and without subjective cognitive impairment. Alzheimers Dement. 2010;6(1):11-24.
4. Jessen F, Wiese B, Bachmann C, et al. Prediction of dementia by subjective memory impairments: effects of severity and temporal association with cognitive impairment. Arch Gen Psychiatry. 2010;67:414-422.
5. Waldorff FB, Siersma V, Waldemar G. Association between subjective memory complaints and nursing home placement: a four-year follow-up. Int J Geriatr Psychiatry. 2009;24(6):602-609.
6. Salthouse TA. Selective review of cognitive aging. J Int Neuropsychol Soc. 2010;16:754-760.
7. Anderton B. Ageing of the brain. Mech Ageing Dev. 2002;23:811-817.
8. Salthouse TA. Influence of age on practice effects in longitudinal neurocognitive change. Neuropsychology. 2010;24(5):563-572.
9. Park D, Schwarz N. Cognitive aging: a primer. Philadelphia PA: Taylor and Francis Group; 2000.
10. Reisberg B, Shulman MB. Commentary on “a roadmap for the prevention of dementia II: Leon Thal Symposium 2008.” Subjective cognitive impairment as an antecedent of Alzheimer’s dementia: policy import. Alzheimers Dement. 2009;5:154-156.
11. Reisberg B, Gauthier S. Current evidence for subjective cognitive impairment (SCI) as the pre-mild cognitive impairment (MCI) stage of subsequently manifest Alzheimer’s disease. Int Psychogeriatr. 2008;20(1):1-16.
12. Mosconi L, Pupi A, De Leon MJ. Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer’s disease. Ann N Y Acad Sci. 2008;1147:180-195.
13. Ramakers IH, Visser PJ, Aalten P, et al. Symptoms of preclinical dementia in general practice up to five years before dementia diagnosis. Dement Geriatr Cogn Disord. 2007;24(4):300-306.
14. Amieva H, Le Goff M, Millet X, et al. Prodromal Alzheimer’s disease: successive emergence of the clinical symptoms. Ann Neurol. 2008;64(5):492-498.
15. Taragano FE, Allegri RF, Krupitzki H, et al. Mild behavioral impairment and risk of dementia: a prospective cohort study of 358 patients. J Clin Psychiatry. 2009;70(4):584-592.
16. Jayadev S, Steinbart EJ, Chi YY, et al. Conjugal Alzheimer disease: risk in children when both parents have Alzheimer disease. Arch Neurol. 2008;65(3):373-378.
17. Hajjar I, Yang F, Sorond F, et al. A novel aging phenotype of slow gait, impaired executive function, and depressive symptoms: relationship to blood pressure and other cardiovascular risks. J Gerontol A Biol Sci Med Sci. 2009;64(9):994-1001.
18. Yamamoto N, Yamanaka G, Ishikawa M, et al. Cardio-ankle vascular index as a predictor of cognitive impairment in community-dwelling elderly people: four-year follow-up. Dement Geriatr Cogn Disord. 2009;28(2):153-158.
19. Inzitari M, Pozzi C, Ferrucci L, et al. Subtle neurological abnormalities as risk factors for cognitive and functional decline, cerebrovascular events, and mortality in older community-dwelling adults. Arch Intern Med. 2008;168(12):1270-1276.
20. Shineman DW, Salthouse TA, Launer LJ, et al. Therapeutics of cognitive aging. Ann N Y Acad Sci. 2010;1191(suppl 1):E1-E10.
21. Dubois B, Feldman HH, Jacova C, et al. Revising the definition of Alzheimer’s disease: a new lexicon. Lancet Neurol. 2010;9:1118-1127.
22. Chertkow H, Massoud F, Nasreddine Z, et al. Diagnosis and treatment of dementia: 3. Mild cognitive impairment and cognitive impairment without dementia. CMAJ. 2008;178(10):1273-1285.
23. Rosenberg PB, Lyketsos C. Mild cognitive impairment: searching for the prodrome of Alzheimer’s disease. World Psychiatry. 2008;7(2):72-78.
24. Rosenberg PB, Johnston D, Lyketsos CG. A clinical approach to mild cognitive impairment. Am J Psychiatry. 2006;163(11):1884-1890.
25. Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12(3):189-198.
26. Petersen RC, Smith GE, Waring SC, et al. Mild cognitive impairment: clinical characterization and outcome. Arch Neurol. 1999;56(3):303-308.
27. Diagnostic and statistical manual of mental disorders. 4th ed text rev. Washington, DC: American Psychiatric Association; 2000:135–180.
28. Malhotra R, Desai AK. Healthy brain aging: what has sleep got to do with it? Clin Geriatr Med. 2010;26:45-56.
29. Desai AK, Grossberg GT, Chibnall JT. Healthy brain aging: a road map. Clin Geriatr Med. 2010;26:1-16.
30. Weaver Cargin J, Collie A, Masters C, et al. The nature of cognitive complaints in healthy older adults with and without objective memory decline. J Clin Exp Neuropsychol. 2008;30:245-257.
31. Wilson RS, Arnold SE, Schneider JA, et al. Chronic distress, age-related neuropathology, and late-life dementia. Psychosom Med. 2007;69:47-53.
32. Deal JA, Carlson MC, Xue Q, et al. Anemia and 9-year domain-specific cognitive decline in community-dwelling older women: the Women’s Health and Aging Study II. J Am Geriatr Soc. 2009;57(9):1604-1611.
33. Yesavage JA, Brink TL, Rose TL, et al. Development and validation of a geriatric depression scale: a preliminary report. J Psychiatr Res. 1983;17:37-49.
34. Mahncke HW, Bronstone A, Merzenich MM. Brain plasticity and functional losses in the aged: scientific bases for a novel intervention. Prog Brain Res. 2006;157:81-109.
MS. F, age 66, requests genetic testing because she is concerned about mild memory difficulties, such as forgetting names and where she puts her keys or checkbook, and fears she may be developing Alzheimer’s disease (AD). Her mother and sister were diagnosed with AD in their early 60s. Ms. F has 20 years of education and reports no problems with driving, managing her finances, remembering to take her medications, or maintaining social activities, which her husband confirms.
Detailed questioning about anxiety and depressive symptoms reveals substantial worries about future cognitive decline and some concerns about her finances and her husband’s health. Ms. F says she occasionally feels down and has low energy but denies other depressive symptoms. She reports no sleep disturbances—including snoring and daytime sleepiness, which could indicate obstructive sleep apnea—which her husband confirms. Ms. F takes levothyroxine for hypothyroidism, atenolol for hypertension, aspirin and clopidogrel for coronary artery disease, and atorvastatin for hyperlipidemia. In addition, she provides a long list of over-the-counter (OTC) supplements—ginkgo, huperzine, ginseng, phosphatidylserine, B1, B12, folate, vitamin D, alpha-lipoic acid, and vinpocetine—that she takes to “protect” her brain from AD.
Subjective cognitive impairment (SCI) in older persons is a common condition with a largely unclear prognosis. Many older adults (age ≥65) express concern about mild cognitive problems—“senior moments”—such as word-finding difficulties and forgetfulness.1 Individuals may wonder if walking into a room only to forget why might be the first sign of dementia. Some older adults try to counteract these memory problems by engaging in brain exercises—including costly computer games—and taking OTC “brain-enhancing” vitamins, herbal remedies, and other supplements.
Although some clinicians may view SCI as benign, that is not always true (Table l).2-5 This article discusses the clinical significance of these mild cognitive complaints by examining:
- age-related cognitive decline (ARCD)
- SCI
- how SCI can be differentiated from more serious conditions, such as mild cognitive impairment (MCI) and early stages of AD and other dementias.
We also will discuss assessing and treating cognitive complaints. Although distinctions between SCI and ARCD may be controversial, evidence suggests clinicians need to adopt a more nuanced clinical approach.
Table 1
Why SCI should be taken seriously
| SCI may create emotional distress because patients are aware of decline in their ‘mental sharpness’ |
| SCI patients might consume unnecessary and potentially harmful OTC supplements touted to promote memory |
| Patients might limit their driving and financial management to avoid making mistakes |
| SCI might impair medication adherence2 |
| SCI may be an early sign of dementia3 |
| Patients’ worry about their self-perceived memory loss might predict dementia4 |
| SCI may predict nursing home placement5 |
| Addressing SCI gives health care providers an opportunity to address anxiety or depression that often accompany SCI |
| Evaluation of potential causes of SCI may uncover reversible conditions that can be treated |
| OTC: over-the-counter; SCI: subjective cognitive impairment |
‘Normal’ cognitive decline
ARCD is subtle decline in cognitive abilities, such as episodic memory, attention, and time needed to complete complex activities.6,7 Individuals with ARCD might not have subjective memory complaints or objective cognitive deficits, and their ability to live independently may not be compromised.7 The degree of decline in ARCD may be smaller than previously thought.8 Park9 summarizes 4 main mechanisms thought to underlie age-related declines in cognition:
- reduced speed of processing
- decreased working memory capabilities
- declining inhibitory control (eg, impaired complex attentional capabilities)
- sensory changes (eg, visual and auditory deficits).
ARCD traditionally is thought to result from predictable changes in the brain associated with aging, such as reduced brain volume in the hippocampus and frontal lobes, loss of myelin, loss of synapses, and cytoskeletal changes.7 However, not all older adults experience ARCD. Some remain highly functional in their later years and continue to actively engage in life well into very old age.6,9
Subjective cognitive impairment
One-quarter to one-half of community-dwelling older adults report subjective cognitive complaints, such as forgetfulness and word-finding difficulties.10 Patients with SCI do not show objective evidence of cognitive impairment on neuropsychological tests and their cognitive problems cause no functional decline.10
Preliminary evidence indicates that SCI may be a harbinger of further cognitive decline. Reisberg et al3 found that compared with patients without SCI, patients with SCI were 4.5 times more likely to develop MCI—cognitive difficulties that can be detected by cognitive tests, but do not cause functional decline—or dementia within 7 years.3 Studies also have suggested that SCI may be a pre-MCI stage of subsequent dementia.11-13 AD generally has a long (10 to 12 years) and progressive prodromal phase before dementia onset and is characterized by successive emergence of cognitive deficits, memory complaints, depressive symptoms, and functional impairment.14
In light of this research, we believe patients with SCI and other risk factors for AD, such as a family history of AD, may be at higher risk of further cognitive and functional decline compared with individuals with ARCD and no AD risk factors. Therefore, patients with SCI and other risk factors for AD (Table 2)15-19 may benefit from annual follow-up to determine if cognitive problems have progressed to MCI or AD.
SCI may be a response to subclinical alterations in neurobiology—a phenomenon known as reverse causality.20 Biomarkers, such as cerebrospinal fluid levels of ß-amyloid and phosphorylated tau, and amyloid imaging using positron emission tomography may help identify AD in SCI patients.21 In these patients, SCI is a misnomer because the cognitive impairment is real—not “subjective”—but current tests are not sensitive enough to detect the cognitive decline the patient has recognized. This group of patients should be differentiated from individuals who may perceive typical cognitive aging (ARCD) as pathologic and complain about it. In the future, biomarkers may help differentiate these 2 groups.
Table 2
Factors that increase SCI patients’ risk for dementia
| Family history of Alzheimer’s disease |
| Mild behavioral impairment |
| Slow gait |
| Depression |
| Rapid weight loss |
| Multiple subtle neurologic abnormalities |
| Vascular disease (eg, peripheral vascular disease, coronary artery disease, cerebrovascular disease) |
| SCI: subjective cognitive impairment Source: References 15-19 |
Mild cognitive impairment
MCI is similar to SCI because MCI patients may present with complaints of memory decline and other cognitive difficulties22 but neither condition is associated with significant impairment of daily activities.23 The key difference is that patients with MCI demonstrate impaired performance on objective cognitive tests whereas SCI patients do not.24 In our experience, office-based tests do not reliably differentiate the 2 conditions because many patients with SCI may show mild impairment in tests such as the Mini-Mental State Exam (MMSE)25 but comprehensive neuropsychological testing reveals no objective cognitive deficits. Neuropsychological testing is essential to reliably differentiate SCI from MCI.
The distinction between SCI and MCI is clinically relevant because evidence suggests that MCI patients have a near-term risk of developing dementia, particularly AD.22,23 In a longitudinal study of 76 individuals with MCI, 12% of patients progressed to AD each year compared with 1% to 2% of healthy older adults.26 Patients with MCI are at increased risk of delirium (especially during hospitalization), falls, medication errors, and difficulty managing their finances.24 Older adults with MCI also have increased mortality compared with older adults with normal cognitive functioning.22 Both SCI and MCI should be differentiated from mild dementia. Common dementias in older adults include:
- AD dementia
- Vascular dementia (may occur with or without AD)
- Lewy body dementia
- Frontotemporal dementia
- Parkinson’s disease dementia.
By definition, all dementia types are associated with impaired ability to perform daily activities and cognitive decline.27
Assessing cognitive complaints
Evaluation of older adults’ cognitive complaints should begin with a thorough history to elicit symptoms of anxiety, depression, physical complaints, and any associated functional decline; a physical exam; and a comprehensive mental status examination. This initial evaluation should be followed by routine and specific investigations as indicated (Table 3).22,24,28,29
In a 6-year study of 100 older adults with and without objective evidence of memory decline, both groups showed similar rates of cognitive complaints.30 Also, researchers found no relationship between individuals’ perception of their cognitive functioning and performance on neuropsychological testing. Mood, education level, and apolipoprotein E epsilon 4 genotype status also did not correlate with participants’ subjective cognitive complaints. These findings highlight the need for objective test data to determine whether older adults’ memory complaints reflect pathologic changes in cognition. After a thorough diagnostic workup, some patients complaining of memory decline will have no detectable evidence of cognitive dysfunction or an identifiable cause. However, others may have identifiable causes of memory impairment (Table 4)28,29,31,32—which could be treated—some will have MCI, and others may be in an early stage of dementia.
Table 3
Investigation of older adults with SCI
| Investigation | Rationale |
|---|---|
| Routine | |
| Neuropsychological testing | Delineation of cognitive syndromes (SCI vs MCI vs AD*) |
| Hematology (full blood count) | Screen for anemia |
| Biochemistry (electrolytes, renal function, liver function, thyroid function, B12, and folate) | Screen for treatable causes of cognitive complaints |
| For specific indication suggested by history, physical exam, or neuropsychological testing | |
| Neuroimaging | Generalized and regional imaging (eg, hippocampal atrophy, space occupying lesions) |
| Electroencephalography | Epilepsy/seizures (especially absence and complex partial) |
| Cardiac (eg, echocardiography) | May reveal cardiac arrhythmia or sources of emboli |
| Inflammatory markers (eg, ESR) | Screen for inflammatory processes |
| Treponemal serology | Tertiary syphilis |
| *Alzheimer’s disease and other dementias AD: Alzheimer’s disease; ESR: erythrocyte sedimentation rate; MCI: mild cognitive impairment; SCI: subjective cognitive impairment Source: References 22,24,28,29 | |
Table 4
Differential diagnosis of SCI
| Cause of cognitive impairment | Potential mechanism |
|---|---|
| ARCD | Allostatic load, ‘wear and tear’ from a lifetime of physiological or psychological stresses and adaptations |
| Anemia | Neuronal hypoxia |
| Alzheimer’s disease | Amyloid and/or tau-mediated neurotoxicity, neuroinflammation |
| Cerebrovascular disease | Neuronal ischemia and hypoxia, neuroinflammation |
| Vitamin deficiencies (eg, B1, B12, folate, D) | Impaired neuronal and neurotransmitter function |
| Inadequate protein intake | Impaired neuronal function |
| Anticholinergic drug use | Decreased cholinergic neurotransmission |
| Alcohol use | Direct neurotoxicity and indirect causes such as malnutrition or head injury |
| Depression, anxiety | Hippocampal dysfunction with or without atrophy |
| Obstructive sleep apnea | Neuronal hypoxia, neuroinflammation |
| Head injury | Neuronal and synaptic loss |
| ARCD: age-related cognitive decline; SCI: subjective cognitive impairment Source: References 28,29,31,32 | |
CASE CONTINUED: No measurable deficits
Ms. F’s medical history is remarkable for coronary artery disease, hypothyroidism, hypertension, hyperlipidemia, cataracts, arthritis, back surgery (secondary to spondylosis), and foot surgery. Ms. F denies a history of alcohol or illicit substance abuse. She smoked tobacco for 30 years (2 packs per day), but quit 5 years ago after her heart attack. Physical exam is unremarkable except for mild obesity (body mass index = 31 kg/m2).
Ms. F’s mental status exam reveals anxious mood and affect. Her recall is 2 out of 3 items. Her MMSE score is 29/30 (1 point lost on recall) and her Geriatric Depression Scale33 score is 2/15, indicating minimal depressive symptoms. On neuropsychological testing, Ms. F demonstrates high average intellectual abilities; compared with others her age, she performs within expectations on all measures. That is, she performs within the above-average to low-average range on measures of attention, working memory, speed of processing, expressive language, learning, memory, visual spatial abilities, executive functioning, and knowledge of basic health and safety information.
Enhancing neuroplasticity
We recommend neuroplasticity-based interventions to treat SCI and promote healthy brain aging.20,29 For a checklist clinicians can use to promote healthy brain aging and thus improve patients’ cognitive health see this article at CurrentPsychiatry. com. Table 51,29 lists cognitive strategies to improve memory and maintain cognitive vitality.
Enhancing brain plasticity and neurogenesis requires engaging older adults in demanding sensory, cognitive, and motor activities on an intensive basis.34 Therapeutic stimulation of neuroplasticity and neurogenesis might contribute to functional “repair” of the diseased adult brain before damage to whole neuronal networks has ensued.29 An important treatment component is reassuring patients with SCI that they do not have AD or MCI. Treating comorbid anxiety and depression and reversible causes of cognitive complaints is key to successful outcomes.
Table 5
Strategies to improve memory and maintain cognitive vitality
| Strategy | Description |
|---|---|
| Mindfulness | Focus on 1 task at a time rather than trying to multitask. Research shows that cognition is more efficient in this manner |
| Cognitive strategies | Use mnemonics (such as ROY G BIV to remember the colors of the rainbow). Make associations for information, such as when meeting someone new, relate their name to someone else you know well. Use cues such as memory notebooks to prompt information recall. Engage in learning new and challenging cognitive activities, such as a new language, a music instrument, or dance. Consider computer-based brain exercises |
| Rehearsal | Practice information you want to remember, such as repeating the information several times or writing it down |
| Be patient | Getting frustrated when you have memory difficulties makes it more challenging to remember information |
| Exercise (mental and physical) | Engage in mental activities, such as reading and crossword puzzles. Do something that you are interested in, rather than making it a chore. Research has demonstrated that physical exercise also aids memory |
| Diet | What is good for the heart is good for the brain. Fruits, vegetables, food rich in omega-3 fatty acids (eg, fatty fish such as salmon), whole grains, spices (eg, turmeric), and small amounts of tree nuts (eg, walnuts) are recommended as part of a balanced diet |
| Source: References 1,29 | |
CASE CONTINUED: Reassurance and risk reduction
Ms. F’s psychiatrist reassures her that she does not have AD. She receives genetic counseling and decides to forgo genetic testing. Her psychiatrist educates Ms. F about the risks of OTC supplements—especially increased risk of bleeding because she takes aspirin and clopidogrel—and lack of data supporting their use. Ms. F is counseled that a healthy lifestyle, including regular exercise, Mediterranean diet with increased intake of omega-3 fatty acids, learning new things, and being socially active, is the safest way to promote brain health. Over 3 months, Ms. F discontinues all supplements except the vitamins and omega-3, starts exercising, resumes piano lessons that she stopped 10 years ago, and becomes a vegetarian. She continues to have mild SCI but she says she is not bothered by it and feels satisfied that she is doing all she can to promote her brain health.
Related Resources
- Desai AK. Healthy brain aging: evidence based methods to preserve brain function and prevent dementia. Philadelphia, PA: W. B. Saunders; 2010.
- Doidge N. The brain that changes itself. New York, NY: Penguin Books; 2007.
- Vance DE, Roberson AJ, McGuinness TM, et al. How neuroplasticity and cognitive reserve protect cognitive functioning. J Psychosoc Nurs Ment Health Serv. 2010; 48: 1-8.
Brain Training Resources
- Weil A, Small G. The healthy brain kit. Boulder, CO: Sounds True, Inc.; 2007. Audio CDs, brain-training cards and workbooks.
- Posit Science. www.positscience.com.
- Sharp Brains. www.sharpbrains.com.
Drug Brand Names
- Atenolol • Tenormin
- Atorvastatin • Lipitor
- Clopidogrel • Plavix
- Levothyroxine • Levoxyl, Synthroid
Disclosures
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Featured Audio
Abhilash K. Desai, MD, discusses emerging research on biomarkers that may help clarify diagnosis.
MS. F, age 66, requests genetic testing because she is concerned about mild memory difficulties, such as forgetting names and where she puts her keys or checkbook, and fears she may be developing Alzheimer’s disease (AD). Her mother and sister were diagnosed with AD in their early 60s. Ms. F has 20 years of education and reports no problems with driving, managing her finances, remembering to take her medications, or maintaining social activities, which her husband confirms.
Detailed questioning about anxiety and depressive symptoms reveals substantial worries about future cognitive decline and some concerns about her finances and her husband’s health. Ms. F says she occasionally feels down and has low energy but denies other depressive symptoms. She reports no sleep disturbances—including snoring and daytime sleepiness, which could indicate obstructive sleep apnea—which her husband confirms. Ms. F takes levothyroxine for hypothyroidism, atenolol for hypertension, aspirin and clopidogrel for coronary artery disease, and atorvastatin for hyperlipidemia. In addition, she provides a long list of over-the-counter (OTC) supplements—ginkgo, huperzine, ginseng, phosphatidylserine, B1, B12, folate, vitamin D, alpha-lipoic acid, and vinpocetine—that she takes to “protect” her brain from AD.
Subjective cognitive impairment (SCI) in older persons is a common condition with a largely unclear prognosis. Many older adults (age ≥65) express concern about mild cognitive problems—“senior moments”—such as word-finding difficulties and forgetfulness.1 Individuals may wonder if walking into a room only to forget why might be the first sign of dementia. Some older adults try to counteract these memory problems by engaging in brain exercises—including costly computer games—and taking OTC “brain-enhancing” vitamins, herbal remedies, and other supplements.
Although some clinicians may view SCI as benign, that is not always true (Table l).2-5 This article discusses the clinical significance of these mild cognitive complaints by examining:
- age-related cognitive decline (ARCD)
- SCI
- how SCI can be differentiated from more serious conditions, such as mild cognitive impairment (MCI) and early stages of AD and other dementias.
We also will discuss assessing and treating cognitive complaints. Although distinctions between SCI and ARCD may be controversial, evidence suggests clinicians need to adopt a more nuanced clinical approach.
Table 1
Why SCI should be taken seriously
| SCI may create emotional distress because patients are aware of decline in their ‘mental sharpness’ |
| SCI patients might consume unnecessary and potentially harmful OTC supplements touted to promote memory |
| Patients might limit their driving and financial management to avoid making mistakes |
| SCI might impair medication adherence2 |
| SCI may be an early sign of dementia3 |
| Patients’ worry about their self-perceived memory loss might predict dementia4 |
| SCI may predict nursing home placement5 |
| Addressing SCI gives health care providers an opportunity to address anxiety or depression that often accompany SCI |
| Evaluation of potential causes of SCI may uncover reversible conditions that can be treated |
| OTC: over-the-counter; SCI: subjective cognitive impairment |
‘Normal’ cognitive decline
ARCD is subtle decline in cognitive abilities, such as episodic memory, attention, and time needed to complete complex activities.6,7 Individuals with ARCD might not have subjective memory complaints or objective cognitive deficits, and their ability to live independently may not be compromised.7 The degree of decline in ARCD may be smaller than previously thought.8 Park9 summarizes 4 main mechanisms thought to underlie age-related declines in cognition:
- reduced speed of processing
- decreased working memory capabilities
- declining inhibitory control (eg, impaired complex attentional capabilities)
- sensory changes (eg, visual and auditory deficits).
ARCD traditionally is thought to result from predictable changes in the brain associated with aging, such as reduced brain volume in the hippocampus and frontal lobes, loss of myelin, loss of synapses, and cytoskeletal changes.7 However, not all older adults experience ARCD. Some remain highly functional in their later years and continue to actively engage in life well into very old age.6,9
Subjective cognitive impairment
One-quarter to one-half of community-dwelling older adults report subjective cognitive complaints, such as forgetfulness and word-finding difficulties.10 Patients with SCI do not show objective evidence of cognitive impairment on neuropsychological tests and their cognitive problems cause no functional decline.10
Preliminary evidence indicates that SCI may be a harbinger of further cognitive decline. Reisberg et al3 found that compared with patients without SCI, patients with SCI were 4.5 times more likely to develop MCI—cognitive difficulties that can be detected by cognitive tests, but do not cause functional decline—or dementia within 7 years.3 Studies also have suggested that SCI may be a pre-MCI stage of subsequent dementia.11-13 AD generally has a long (10 to 12 years) and progressive prodromal phase before dementia onset and is characterized by successive emergence of cognitive deficits, memory complaints, depressive symptoms, and functional impairment.14
In light of this research, we believe patients with SCI and other risk factors for AD, such as a family history of AD, may be at higher risk of further cognitive and functional decline compared with individuals with ARCD and no AD risk factors. Therefore, patients with SCI and other risk factors for AD (Table 2)15-19 may benefit from annual follow-up to determine if cognitive problems have progressed to MCI or AD.
SCI may be a response to subclinical alterations in neurobiology—a phenomenon known as reverse causality.20 Biomarkers, such as cerebrospinal fluid levels of ß-amyloid and phosphorylated tau, and amyloid imaging using positron emission tomography may help identify AD in SCI patients.21 In these patients, SCI is a misnomer because the cognitive impairment is real—not “subjective”—but current tests are not sensitive enough to detect the cognitive decline the patient has recognized. This group of patients should be differentiated from individuals who may perceive typical cognitive aging (ARCD) as pathologic and complain about it. In the future, biomarkers may help differentiate these 2 groups.
Table 2
Factors that increase SCI patients’ risk for dementia
| Family history of Alzheimer’s disease |
| Mild behavioral impairment |
| Slow gait |
| Depression |
| Rapid weight loss |
| Multiple subtle neurologic abnormalities |
| Vascular disease (eg, peripheral vascular disease, coronary artery disease, cerebrovascular disease) |
| SCI: subjective cognitive impairment Source: References 15-19 |
Mild cognitive impairment
MCI is similar to SCI because MCI patients may present with complaints of memory decline and other cognitive difficulties22 but neither condition is associated with significant impairment of daily activities.23 The key difference is that patients with MCI demonstrate impaired performance on objective cognitive tests whereas SCI patients do not.24 In our experience, office-based tests do not reliably differentiate the 2 conditions because many patients with SCI may show mild impairment in tests such as the Mini-Mental State Exam (MMSE)25 but comprehensive neuropsychological testing reveals no objective cognitive deficits. Neuropsychological testing is essential to reliably differentiate SCI from MCI.
The distinction between SCI and MCI is clinically relevant because evidence suggests that MCI patients have a near-term risk of developing dementia, particularly AD.22,23 In a longitudinal study of 76 individuals with MCI, 12% of patients progressed to AD each year compared with 1% to 2% of healthy older adults.26 Patients with MCI are at increased risk of delirium (especially during hospitalization), falls, medication errors, and difficulty managing their finances.24 Older adults with MCI also have increased mortality compared with older adults with normal cognitive functioning.22 Both SCI and MCI should be differentiated from mild dementia. Common dementias in older adults include:
- AD dementia
- Vascular dementia (may occur with or without AD)
- Lewy body dementia
- Frontotemporal dementia
- Parkinson’s disease dementia.
By definition, all dementia types are associated with impaired ability to perform daily activities and cognitive decline.27
Assessing cognitive complaints
Evaluation of older adults’ cognitive complaints should begin with a thorough history to elicit symptoms of anxiety, depression, physical complaints, and any associated functional decline; a physical exam; and a comprehensive mental status examination. This initial evaluation should be followed by routine and specific investigations as indicated (Table 3).22,24,28,29
In a 6-year study of 100 older adults with and without objective evidence of memory decline, both groups showed similar rates of cognitive complaints.30 Also, researchers found no relationship between individuals’ perception of their cognitive functioning and performance on neuropsychological testing. Mood, education level, and apolipoprotein E epsilon 4 genotype status also did not correlate with participants’ subjective cognitive complaints. These findings highlight the need for objective test data to determine whether older adults’ memory complaints reflect pathologic changes in cognition. After a thorough diagnostic workup, some patients complaining of memory decline will have no detectable evidence of cognitive dysfunction or an identifiable cause. However, others may have identifiable causes of memory impairment (Table 4)28,29,31,32—which could be treated—some will have MCI, and others may be in an early stage of dementia.
Table 3
Investigation of older adults with SCI
| Investigation | Rationale |
|---|---|
| Routine | |
| Neuropsychological testing | Delineation of cognitive syndromes (SCI vs MCI vs AD*) |
| Hematology (full blood count) | Screen for anemia |
| Biochemistry (electrolytes, renal function, liver function, thyroid function, B12, and folate) | Screen for treatable causes of cognitive complaints |
| For specific indication suggested by history, physical exam, or neuropsychological testing | |
| Neuroimaging | Generalized and regional imaging (eg, hippocampal atrophy, space occupying lesions) |
| Electroencephalography | Epilepsy/seizures (especially absence and complex partial) |
| Cardiac (eg, echocardiography) | May reveal cardiac arrhythmia or sources of emboli |
| Inflammatory markers (eg, ESR) | Screen for inflammatory processes |
| Treponemal serology | Tertiary syphilis |
| *Alzheimer’s disease and other dementias AD: Alzheimer’s disease; ESR: erythrocyte sedimentation rate; MCI: mild cognitive impairment; SCI: subjective cognitive impairment Source: References 22,24,28,29 | |
Table 4
Differential diagnosis of SCI
| Cause of cognitive impairment | Potential mechanism |
|---|---|
| ARCD | Allostatic load, ‘wear and tear’ from a lifetime of physiological or psychological stresses and adaptations |
| Anemia | Neuronal hypoxia |
| Alzheimer’s disease | Amyloid and/or tau-mediated neurotoxicity, neuroinflammation |
| Cerebrovascular disease | Neuronal ischemia and hypoxia, neuroinflammation |
| Vitamin deficiencies (eg, B1, B12, folate, D) | Impaired neuronal and neurotransmitter function |
| Inadequate protein intake | Impaired neuronal function |
| Anticholinergic drug use | Decreased cholinergic neurotransmission |
| Alcohol use | Direct neurotoxicity and indirect causes such as malnutrition or head injury |
| Depression, anxiety | Hippocampal dysfunction with or without atrophy |
| Obstructive sleep apnea | Neuronal hypoxia, neuroinflammation |
| Head injury | Neuronal and synaptic loss |
| ARCD: age-related cognitive decline; SCI: subjective cognitive impairment Source: References 28,29,31,32 | |
CASE CONTINUED: No measurable deficits
Ms. F’s medical history is remarkable for coronary artery disease, hypothyroidism, hypertension, hyperlipidemia, cataracts, arthritis, back surgery (secondary to spondylosis), and foot surgery. Ms. F denies a history of alcohol or illicit substance abuse. She smoked tobacco for 30 years (2 packs per day), but quit 5 years ago after her heart attack. Physical exam is unremarkable except for mild obesity (body mass index = 31 kg/m2).
Ms. F’s mental status exam reveals anxious mood and affect. Her recall is 2 out of 3 items. Her MMSE score is 29/30 (1 point lost on recall) and her Geriatric Depression Scale33 score is 2/15, indicating minimal depressive symptoms. On neuropsychological testing, Ms. F demonstrates high average intellectual abilities; compared with others her age, she performs within expectations on all measures. That is, she performs within the above-average to low-average range on measures of attention, working memory, speed of processing, expressive language, learning, memory, visual spatial abilities, executive functioning, and knowledge of basic health and safety information.
Enhancing neuroplasticity
We recommend neuroplasticity-based interventions to treat SCI and promote healthy brain aging.20,29 For a checklist clinicians can use to promote healthy brain aging and thus improve patients’ cognitive health see this article at CurrentPsychiatry. com. Table 51,29 lists cognitive strategies to improve memory and maintain cognitive vitality.
Enhancing brain plasticity and neurogenesis requires engaging older adults in demanding sensory, cognitive, and motor activities on an intensive basis.34 Therapeutic stimulation of neuroplasticity and neurogenesis might contribute to functional “repair” of the diseased adult brain before damage to whole neuronal networks has ensued.29 An important treatment component is reassuring patients with SCI that they do not have AD or MCI. Treating comorbid anxiety and depression and reversible causes of cognitive complaints is key to successful outcomes.
Table 5
Strategies to improve memory and maintain cognitive vitality
| Strategy | Description |
|---|---|
| Mindfulness | Focus on 1 task at a time rather than trying to multitask. Research shows that cognition is more efficient in this manner |
| Cognitive strategies | Use mnemonics (such as ROY G BIV to remember the colors of the rainbow). Make associations for information, such as when meeting someone new, relate their name to someone else you know well. Use cues such as memory notebooks to prompt information recall. Engage in learning new and challenging cognitive activities, such as a new language, a music instrument, or dance. Consider computer-based brain exercises |
| Rehearsal | Practice information you want to remember, such as repeating the information several times or writing it down |
| Be patient | Getting frustrated when you have memory difficulties makes it more challenging to remember information |
| Exercise (mental and physical) | Engage in mental activities, such as reading and crossword puzzles. Do something that you are interested in, rather than making it a chore. Research has demonstrated that physical exercise also aids memory |
| Diet | What is good for the heart is good for the brain. Fruits, vegetables, food rich in omega-3 fatty acids (eg, fatty fish such as salmon), whole grains, spices (eg, turmeric), and small amounts of tree nuts (eg, walnuts) are recommended as part of a balanced diet |
| Source: References 1,29 | |
CASE CONTINUED: Reassurance and risk reduction
Ms. F’s psychiatrist reassures her that she does not have AD. She receives genetic counseling and decides to forgo genetic testing. Her psychiatrist educates Ms. F about the risks of OTC supplements—especially increased risk of bleeding because she takes aspirin and clopidogrel—and lack of data supporting their use. Ms. F is counseled that a healthy lifestyle, including regular exercise, Mediterranean diet with increased intake of omega-3 fatty acids, learning new things, and being socially active, is the safest way to promote brain health. Over 3 months, Ms. F discontinues all supplements except the vitamins and omega-3, starts exercising, resumes piano lessons that she stopped 10 years ago, and becomes a vegetarian. She continues to have mild SCI but she says she is not bothered by it and feels satisfied that she is doing all she can to promote her brain health.
Related Resources
- Desai AK. Healthy brain aging: evidence based methods to preserve brain function and prevent dementia. Philadelphia, PA: W. B. Saunders; 2010.
- Doidge N. The brain that changes itself. New York, NY: Penguin Books; 2007.
- Vance DE, Roberson AJ, McGuinness TM, et al. How neuroplasticity and cognitive reserve protect cognitive functioning. J Psychosoc Nurs Ment Health Serv. 2010; 48: 1-8.
Brain Training Resources
- Weil A, Small G. The healthy brain kit. Boulder, CO: Sounds True, Inc.; 2007. Audio CDs, brain-training cards and workbooks.
- Posit Science. www.positscience.com.
- Sharp Brains. www.sharpbrains.com.
Drug Brand Names
- Atenolol • Tenormin
- Atorvastatin • Lipitor
- Clopidogrel • Plavix
- Levothyroxine • Levoxyl, Synthroid
Disclosures
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Featured Audio
Abhilash K. Desai, MD, discusses emerging research on biomarkers that may help clarify diagnosis.
1. Small GW. What we need to know about age related memory loss. BMJ. 2002;324:1502-1505.
2. Hayes TL, Larimer N, Adami A, et al. Medication adherence in healthy elders. J Aging Health. 2009;21(4):567-580.
3. Reisberg B, Shulman MB, Torossian C, et al. Outcome over seven years of healthy adults with and without subjective cognitive impairment. Alzheimers Dement. 2010;6(1):11-24.
4. Jessen F, Wiese B, Bachmann C, et al. Prediction of dementia by subjective memory impairments: effects of severity and temporal association with cognitive impairment. Arch Gen Psychiatry. 2010;67:414-422.
5. Waldorff FB, Siersma V, Waldemar G. Association between subjective memory complaints and nursing home placement: a four-year follow-up. Int J Geriatr Psychiatry. 2009;24(6):602-609.
6. Salthouse TA. Selective review of cognitive aging. J Int Neuropsychol Soc. 2010;16:754-760.
7. Anderton B. Ageing of the brain. Mech Ageing Dev. 2002;23:811-817.
8. Salthouse TA. Influence of age on practice effects in longitudinal neurocognitive change. Neuropsychology. 2010;24(5):563-572.
9. Park D, Schwarz N. Cognitive aging: a primer. Philadelphia PA: Taylor and Francis Group; 2000.
10. Reisberg B, Shulman MB. Commentary on “a roadmap for the prevention of dementia II: Leon Thal Symposium 2008.” Subjective cognitive impairment as an antecedent of Alzheimer’s dementia: policy import. Alzheimers Dement. 2009;5:154-156.
11. Reisberg B, Gauthier S. Current evidence for subjective cognitive impairment (SCI) as the pre-mild cognitive impairment (MCI) stage of subsequently manifest Alzheimer’s disease. Int Psychogeriatr. 2008;20(1):1-16.
12. Mosconi L, Pupi A, De Leon MJ. Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer’s disease. Ann N Y Acad Sci. 2008;1147:180-195.
13. Ramakers IH, Visser PJ, Aalten P, et al. Symptoms of preclinical dementia in general practice up to five years before dementia diagnosis. Dement Geriatr Cogn Disord. 2007;24(4):300-306.
14. Amieva H, Le Goff M, Millet X, et al. Prodromal Alzheimer’s disease: successive emergence of the clinical symptoms. Ann Neurol. 2008;64(5):492-498.
15. Taragano FE, Allegri RF, Krupitzki H, et al. Mild behavioral impairment and risk of dementia: a prospective cohort study of 358 patients. J Clin Psychiatry. 2009;70(4):584-592.
16. Jayadev S, Steinbart EJ, Chi YY, et al. Conjugal Alzheimer disease: risk in children when both parents have Alzheimer disease. Arch Neurol. 2008;65(3):373-378.
17. Hajjar I, Yang F, Sorond F, et al. A novel aging phenotype of slow gait, impaired executive function, and depressive symptoms: relationship to blood pressure and other cardiovascular risks. J Gerontol A Biol Sci Med Sci. 2009;64(9):994-1001.
18. Yamamoto N, Yamanaka G, Ishikawa M, et al. Cardio-ankle vascular index as a predictor of cognitive impairment in community-dwelling elderly people: four-year follow-up. Dement Geriatr Cogn Disord. 2009;28(2):153-158.
19. Inzitari M, Pozzi C, Ferrucci L, et al. Subtle neurological abnormalities as risk factors for cognitive and functional decline, cerebrovascular events, and mortality in older community-dwelling adults. Arch Intern Med. 2008;168(12):1270-1276.
20. Shineman DW, Salthouse TA, Launer LJ, et al. Therapeutics of cognitive aging. Ann N Y Acad Sci. 2010;1191(suppl 1):E1-E10.
21. Dubois B, Feldman HH, Jacova C, et al. Revising the definition of Alzheimer’s disease: a new lexicon. Lancet Neurol. 2010;9:1118-1127.
22. Chertkow H, Massoud F, Nasreddine Z, et al. Diagnosis and treatment of dementia: 3. Mild cognitive impairment and cognitive impairment without dementia. CMAJ. 2008;178(10):1273-1285.
23. Rosenberg PB, Lyketsos C. Mild cognitive impairment: searching for the prodrome of Alzheimer’s disease. World Psychiatry. 2008;7(2):72-78.
24. Rosenberg PB, Johnston D, Lyketsos CG. A clinical approach to mild cognitive impairment. Am J Psychiatry. 2006;163(11):1884-1890.
25. Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12(3):189-198.
26. Petersen RC, Smith GE, Waring SC, et al. Mild cognitive impairment: clinical characterization and outcome. Arch Neurol. 1999;56(3):303-308.
27. Diagnostic and statistical manual of mental disorders. 4th ed text rev. Washington, DC: American Psychiatric Association; 2000:135–180.
28. Malhotra R, Desai AK. Healthy brain aging: what has sleep got to do with it? Clin Geriatr Med. 2010;26:45-56.
29. Desai AK, Grossberg GT, Chibnall JT. Healthy brain aging: a road map. Clin Geriatr Med. 2010;26:1-16.
30. Weaver Cargin J, Collie A, Masters C, et al. The nature of cognitive complaints in healthy older adults with and without objective memory decline. J Clin Exp Neuropsychol. 2008;30:245-257.
31. Wilson RS, Arnold SE, Schneider JA, et al. Chronic distress, age-related neuropathology, and late-life dementia. Psychosom Med. 2007;69:47-53.
32. Deal JA, Carlson MC, Xue Q, et al. Anemia and 9-year domain-specific cognitive decline in community-dwelling older women: the Women’s Health and Aging Study II. J Am Geriatr Soc. 2009;57(9):1604-1611.
33. Yesavage JA, Brink TL, Rose TL, et al. Development and validation of a geriatric depression scale: a preliminary report. J Psychiatr Res. 1983;17:37-49.
34. Mahncke HW, Bronstone A, Merzenich MM. Brain plasticity and functional losses in the aged: scientific bases for a novel intervention. Prog Brain Res. 2006;157:81-109.
1. Small GW. What we need to know about age related memory loss. BMJ. 2002;324:1502-1505.
2. Hayes TL, Larimer N, Adami A, et al. Medication adherence in healthy elders. J Aging Health. 2009;21(4):567-580.
3. Reisberg B, Shulman MB, Torossian C, et al. Outcome over seven years of healthy adults with and without subjective cognitive impairment. Alzheimers Dement. 2010;6(1):11-24.
4. Jessen F, Wiese B, Bachmann C, et al. Prediction of dementia by subjective memory impairments: effects of severity and temporal association with cognitive impairment. Arch Gen Psychiatry. 2010;67:414-422.
5. Waldorff FB, Siersma V, Waldemar G. Association between subjective memory complaints and nursing home placement: a four-year follow-up. Int J Geriatr Psychiatry. 2009;24(6):602-609.
6. Salthouse TA. Selective review of cognitive aging. J Int Neuropsychol Soc. 2010;16:754-760.
7. Anderton B. Ageing of the brain. Mech Ageing Dev. 2002;23:811-817.
8. Salthouse TA. Influence of age on practice effects in longitudinal neurocognitive change. Neuropsychology. 2010;24(5):563-572.
9. Park D, Schwarz N. Cognitive aging: a primer. Philadelphia PA: Taylor and Francis Group; 2000.
10. Reisberg B, Shulman MB. Commentary on “a roadmap for the prevention of dementia II: Leon Thal Symposium 2008.” Subjective cognitive impairment as an antecedent of Alzheimer’s dementia: policy import. Alzheimers Dement. 2009;5:154-156.
11. Reisberg B, Gauthier S. Current evidence for subjective cognitive impairment (SCI) as the pre-mild cognitive impairment (MCI) stage of subsequently manifest Alzheimer’s disease. Int Psychogeriatr. 2008;20(1):1-16.
12. Mosconi L, Pupi A, De Leon MJ. Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer’s disease. Ann N Y Acad Sci. 2008;1147:180-195.
13. Ramakers IH, Visser PJ, Aalten P, et al. Symptoms of preclinical dementia in general practice up to five years before dementia diagnosis. Dement Geriatr Cogn Disord. 2007;24(4):300-306.
14. Amieva H, Le Goff M, Millet X, et al. Prodromal Alzheimer’s disease: successive emergence of the clinical symptoms. Ann Neurol. 2008;64(5):492-498.
15. Taragano FE, Allegri RF, Krupitzki H, et al. Mild behavioral impairment and risk of dementia: a prospective cohort study of 358 patients. J Clin Psychiatry. 2009;70(4):584-592.
16. Jayadev S, Steinbart EJ, Chi YY, et al. Conjugal Alzheimer disease: risk in children when both parents have Alzheimer disease. Arch Neurol. 2008;65(3):373-378.
17. Hajjar I, Yang F, Sorond F, et al. A novel aging phenotype of slow gait, impaired executive function, and depressive symptoms: relationship to blood pressure and other cardiovascular risks. J Gerontol A Biol Sci Med Sci. 2009;64(9):994-1001.
18. Yamamoto N, Yamanaka G, Ishikawa M, et al. Cardio-ankle vascular index as a predictor of cognitive impairment in community-dwelling elderly people: four-year follow-up. Dement Geriatr Cogn Disord. 2009;28(2):153-158.
19. Inzitari M, Pozzi C, Ferrucci L, et al. Subtle neurological abnormalities as risk factors for cognitive and functional decline, cerebrovascular events, and mortality in older community-dwelling adults. Arch Intern Med. 2008;168(12):1270-1276.
20. Shineman DW, Salthouse TA, Launer LJ, et al. Therapeutics of cognitive aging. Ann N Y Acad Sci. 2010;1191(suppl 1):E1-E10.
21. Dubois B, Feldman HH, Jacova C, et al. Revising the definition of Alzheimer’s disease: a new lexicon. Lancet Neurol. 2010;9:1118-1127.
22. Chertkow H, Massoud F, Nasreddine Z, et al. Diagnosis and treatment of dementia: 3. Mild cognitive impairment and cognitive impairment without dementia. CMAJ. 2008;178(10):1273-1285.
23. Rosenberg PB, Lyketsos C. Mild cognitive impairment: searching for the prodrome of Alzheimer’s disease. World Psychiatry. 2008;7(2):72-78.
24. Rosenberg PB, Johnston D, Lyketsos CG. A clinical approach to mild cognitive impairment. Am J Psychiatry. 2006;163(11):1884-1890.
25. Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12(3):189-198.
26. Petersen RC, Smith GE, Waring SC, et al. Mild cognitive impairment: clinical characterization and outcome. Arch Neurol. 1999;56(3):303-308.
27. Diagnostic and statistical manual of mental disorders. 4th ed text rev. Washington, DC: American Psychiatric Association; 2000:135–180.
28. Malhotra R, Desai AK. Healthy brain aging: what has sleep got to do with it? Clin Geriatr Med. 2010;26:45-56.
29. Desai AK, Grossberg GT, Chibnall JT. Healthy brain aging: a road map. Clin Geriatr Med. 2010;26:1-16.
30. Weaver Cargin J, Collie A, Masters C, et al. The nature of cognitive complaints in healthy older adults with and without objective memory decline. J Clin Exp Neuropsychol. 2008;30:245-257.
31. Wilson RS, Arnold SE, Schneider JA, et al. Chronic distress, age-related neuropathology, and late-life dementia. Psychosom Med. 2007;69:47-53.
32. Deal JA, Carlson MC, Xue Q, et al. Anemia and 9-year domain-specific cognitive decline in community-dwelling older women: the Women’s Health and Aging Study II. J Am Geriatr Soc. 2009;57(9):1604-1611.
33. Yesavage JA, Brink TL, Rose TL, et al. Development and validation of a geriatric depression scale: a preliminary report. J Psychiatr Res. 1983;17:37-49.
34. Mahncke HW, Bronstone A, Merzenich MM. Brain plasticity and functional losses in the aged: scientific bases for a novel intervention. Prog Brain Res. 2006;157:81-109.
Managing ADHD in children: Are you doing enough?
• Side effects of psychostimulants can often be managed with monitoring, dose adjustment, a switch to another drug, or adjunctive therapy. A
• Weigh and measure a child being treated for ADHD twice a year; aberrant growth may indicate a need for a change in medication regimen. A
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Untreated attention deficit hyperactivity disorder (ADHD) can have serious academic, social, and psychological consequences, both for young patients and their parents. Diagnosis is based on criteria detailed in the Diagnostic and Statistical Manual of Mental Health Disorders, Fourth Edition Text Revision (DSM-IV-TR), with observations of the child’s behavior obtained from more than one setting.
Physicians should also consider the possibility of coexisting conditions, which could complicate diagnosis and subsequent attempts to treat the signs and symptoms of ADHD. Treatment is multifaceted, and will vary depending on severity, comorbidities, and the degree of compliance with nonpharmacologic modalities.
A comprehensive approach is called for
Managing pediatric ADHD in a primary care setting requires a comprehensive, goal-oriented treatment plan. The primary goal, as noted in the American Academy of Child and Adolescent Psychiatry (AACAP)’s ADHD guideline,1 is to maximize the child’s functioning, both in terms of an improvement in relationships and academic performance and a reduction of disruptive behavior. Parents and children should be integrated into community supports and school resources, the guideline recommends1 (strength of recommendation [SOR]: A).
Additional recommendations focus on patient (and parental) education, and on medication, monitoring, and follow-up (SOR: A). Physicians should:
Educate parents and patients about common ADHD symptoms and treatment strategies.
Initiate pharmacotherapy. Select an agent that is approved by the US Food and Drug Administration (FDA) for ADHD. These include the psychostimulants dextroamphetamine, D- and DL-methylphenidate, and mixed salts amphetamine; and atomoxetine, a noradrenergic reuptake inhibitor. (Central nervous system stimulants should be avoided in children with cardiac abnormalities, who are at increased risk of experiencing sympathomimetic effects.)
Familiarize themselves with medication side effects. Decreased appetite, insomnia, headache, abdominal pain, and irritable mood are the most common side effects of psychostimulants. Common side effects of atomoxetine include somnolence, anorexia, nausea, skin rash, and a mild increase in blood pressure or heart rate. Notably, there is a small risk of suicide associated with atomoxetine.
Monitor patients for the emergence and severity of side effects. Many of the side effects of stimulants are transient and can be managed through monitoring, as long as it does not compromise the patient’s health or interfere with daily living. Side effects can also be managed with dose adjustment, change of drug treatment, or adjunctive therapy.
Measure height and weight of the patient twice yearly. If a child’s height or weight crosses 2 percentiles on his or her growth curve, it may be an indication of aberrant growth—and a drug holiday or switching to a different medication should be considered.
Evaluate treatment success several times a year. The review should include behavior, academic progress, emergence of comorbid disorders, and the need for behavioral therapy and continuing pharmacotherapy. A lack of response to one psychostimulant is not predictive of the patient’s response to another, the AACAP emphasizes, and it is important to keep trying to find another medication until treatment goals are reached.1
If none of the FDA-approved ADHD medications has the desired results, the AACAP recommends (SOR: B):
- a referral to a cognitive behavioral therapist or child psychologist
- a trial with a medication that is not FDA-approved for ADHD, such as bupropion, a tricyclic antidepressant, or an alpha-agonist
- a reevaluation of the ADHD diagnosis, adherence to the treatment plan, and the presence of comorbid conditions.1
AAP stresses hands-on behavioral intervention
The American Academy of Pediatrics (AAP) also has a clinical practice guideline for the treatment of ADHD, issued in 2001.2 Its recommendations are similar to those of the AACAP. But AAP puts additional emphasis on parental training in behavioral therapy and classroom behavioral interventions, and considers both to be more effective than cognitive behavioral therapy (CBT).2
Virtual reality: A viable option?
Although conventional treatment of childhood ADHD has had considerable clinical success, other forms of treatment may be needed in some cases—if a child’s parents reject psychopharmacologic treatment, for example, or medication trials and traditional behavioral therapies, such as CBT, fail to bring the desired results.
Virtual reality (VR), a computer-generated 3-dimensional interactive system, is an emerging clinical tool. VR programs such as The Virtual Classroom3,4—in which a child is “immersed” in a simulated classroom setting—have shown promise for ADHD assessment and treatment.
Perhaps the biggest benefit of VR as an ADHD intervention is the opportunity for a clinician to place a patient in a virtual classroom, with tasks that require the child’s attention as well as distractors, such as conversation, ambient noise, and moving objects. Another advantage is the ability to integrate traditional assessment tools (Continuous Performance Tasks, for example) and treatment modalities, such as CBT.5 This can be accomplished through a graphic display of a child’s performance during a VR session, which the therapist can use as part of the therapeutic process.3 And VR has no side effects.
Several facilities are either using or experimenting with VR for ADHD. More information is available from the Virtual Reality Medical Center at http://www.vrphobia.com/adhd.htm.
CORRESPONDENCE
Keith B. Holten, MD, Berger Health System, 600 North Pickaway Street, Circleville, OH 43113; [email protected]
1. Pliszka S. AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2007;46:894-921.
2. American Academy of Pediatrics. Subcommittee on Attention-Deficit/Hyperactivity Disorder. Clinical practice guideline: treatment of the school-aged child with attention-deficit/hyperactivity disorder. Pediatrics. 2001;108:1033-1044.
3. Rizzo AA, Buckwalter JG, Humphrey L, et al. The virtual classroom: a virtual environment for the assessment and rehabilitation of attention deficits. CyberPsych Behav. 2000;3:483-499.
4. Rizzo AA, Klimchuk D, Mitura R, et al. A virtual reality scenario for all seasons: the virtual classroom. CNS Spectr. 2006;11:35-44.
5. Pollak Y, Weiss PL, Rizzo AA, et al. The utility of a continuous performance test embedded in virtual reality in measuring ADHD-related deficits. J Dev Behav Pediatr. 2009;30:2-6.
• Side effects of psychostimulants can often be managed with monitoring, dose adjustment, a switch to another drug, or adjunctive therapy. A
• Weigh and measure a child being treated for ADHD twice a year; aberrant growth may indicate a need for a change in medication regimen. A
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Untreated attention deficit hyperactivity disorder (ADHD) can have serious academic, social, and psychological consequences, both for young patients and their parents. Diagnosis is based on criteria detailed in the Diagnostic and Statistical Manual of Mental Health Disorders, Fourth Edition Text Revision (DSM-IV-TR), with observations of the child’s behavior obtained from more than one setting.
Physicians should also consider the possibility of coexisting conditions, which could complicate diagnosis and subsequent attempts to treat the signs and symptoms of ADHD. Treatment is multifaceted, and will vary depending on severity, comorbidities, and the degree of compliance with nonpharmacologic modalities.
A comprehensive approach is called for
Managing pediatric ADHD in a primary care setting requires a comprehensive, goal-oriented treatment plan. The primary goal, as noted in the American Academy of Child and Adolescent Psychiatry (AACAP)’s ADHD guideline,1 is to maximize the child’s functioning, both in terms of an improvement in relationships and academic performance and a reduction of disruptive behavior. Parents and children should be integrated into community supports and school resources, the guideline recommends1 (strength of recommendation [SOR]: A).
Additional recommendations focus on patient (and parental) education, and on medication, monitoring, and follow-up (SOR: A). Physicians should:
Educate parents and patients about common ADHD symptoms and treatment strategies.
Initiate pharmacotherapy. Select an agent that is approved by the US Food and Drug Administration (FDA) for ADHD. These include the psychostimulants dextroamphetamine, D- and DL-methylphenidate, and mixed salts amphetamine; and atomoxetine, a noradrenergic reuptake inhibitor. (Central nervous system stimulants should be avoided in children with cardiac abnormalities, who are at increased risk of experiencing sympathomimetic effects.)
Familiarize themselves with medication side effects. Decreased appetite, insomnia, headache, abdominal pain, and irritable mood are the most common side effects of psychostimulants. Common side effects of atomoxetine include somnolence, anorexia, nausea, skin rash, and a mild increase in blood pressure or heart rate. Notably, there is a small risk of suicide associated with atomoxetine.
Monitor patients for the emergence and severity of side effects. Many of the side effects of stimulants are transient and can be managed through monitoring, as long as it does not compromise the patient’s health or interfere with daily living. Side effects can also be managed with dose adjustment, change of drug treatment, or adjunctive therapy.
Measure height and weight of the patient twice yearly. If a child’s height or weight crosses 2 percentiles on his or her growth curve, it may be an indication of aberrant growth—and a drug holiday or switching to a different medication should be considered.
Evaluate treatment success several times a year. The review should include behavior, academic progress, emergence of comorbid disorders, and the need for behavioral therapy and continuing pharmacotherapy. A lack of response to one psychostimulant is not predictive of the patient’s response to another, the AACAP emphasizes, and it is important to keep trying to find another medication until treatment goals are reached.1
If none of the FDA-approved ADHD medications has the desired results, the AACAP recommends (SOR: B):
- a referral to a cognitive behavioral therapist or child psychologist
- a trial with a medication that is not FDA-approved for ADHD, such as bupropion, a tricyclic antidepressant, or an alpha-agonist
- a reevaluation of the ADHD diagnosis, adherence to the treatment plan, and the presence of comorbid conditions.1
AAP stresses hands-on behavioral intervention
The American Academy of Pediatrics (AAP) also has a clinical practice guideline for the treatment of ADHD, issued in 2001.2 Its recommendations are similar to those of the AACAP. But AAP puts additional emphasis on parental training in behavioral therapy and classroom behavioral interventions, and considers both to be more effective than cognitive behavioral therapy (CBT).2
Virtual reality: A viable option?
Although conventional treatment of childhood ADHD has had considerable clinical success, other forms of treatment may be needed in some cases—if a child’s parents reject psychopharmacologic treatment, for example, or medication trials and traditional behavioral therapies, such as CBT, fail to bring the desired results.
Virtual reality (VR), a computer-generated 3-dimensional interactive system, is an emerging clinical tool. VR programs such as The Virtual Classroom3,4—in which a child is “immersed” in a simulated classroom setting—have shown promise for ADHD assessment and treatment.
Perhaps the biggest benefit of VR as an ADHD intervention is the opportunity for a clinician to place a patient in a virtual classroom, with tasks that require the child’s attention as well as distractors, such as conversation, ambient noise, and moving objects. Another advantage is the ability to integrate traditional assessment tools (Continuous Performance Tasks, for example) and treatment modalities, such as CBT.5 This can be accomplished through a graphic display of a child’s performance during a VR session, which the therapist can use as part of the therapeutic process.3 And VR has no side effects.
Several facilities are either using or experimenting with VR for ADHD. More information is available from the Virtual Reality Medical Center at http://www.vrphobia.com/adhd.htm.
CORRESPONDENCE
Keith B. Holten, MD, Berger Health System, 600 North Pickaway Street, Circleville, OH 43113; [email protected]
• Side effects of psychostimulants can often be managed with monitoring, dose adjustment, a switch to another drug, or adjunctive therapy. A
• Weigh and measure a child being treated for ADHD twice a year; aberrant growth may indicate a need for a change in medication regimen. A
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Untreated attention deficit hyperactivity disorder (ADHD) can have serious academic, social, and psychological consequences, both for young patients and their parents. Diagnosis is based on criteria detailed in the Diagnostic and Statistical Manual of Mental Health Disorders, Fourth Edition Text Revision (DSM-IV-TR), with observations of the child’s behavior obtained from more than one setting.
Physicians should also consider the possibility of coexisting conditions, which could complicate diagnosis and subsequent attempts to treat the signs and symptoms of ADHD. Treatment is multifaceted, and will vary depending on severity, comorbidities, and the degree of compliance with nonpharmacologic modalities.
A comprehensive approach is called for
Managing pediatric ADHD in a primary care setting requires a comprehensive, goal-oriented treatment plan. The primary goal, as noted in the American Academy of Child and Adolescent Psychiatry (AACAP)’s ADHD guideline,1 is to maximize the child’s functioning, both in terms of an improvement in relationships and academic performance and a reduction of disruptive behavior. Parents and children should be integrated into community supports and school resources, the guideline recommends1 (strength of recommendation [SOR]: A).
Additional recommendations focus on patient (and parental) education, and on medication, monitoring, and follow-up (SOR: A). Physicians should:
Educate parents and patients about common ADHD symptoms and treatment strategies.
Initiate pharmacotherapy. Select an agent that is approved by the US Food and Drug Administration (FDA) for ADHD. These include the psychostimulants dextroamphetamine, D- and DL-methylphenidate, and mixed salts amphetamine; and atomoxetine, a noradrenergic reuptake inhibitor. (Central nervous system stimulants should be avoided in children with cardiac abnormalities, who are at increased risk of experiencing sympathomimetic effects.)
Familiarize themselves with medication side effects. Decreased appetite, insomnia, headache, abdominal pain, and irritable mood are the most common side effects of psychostimulants. Common side effects of atomoxetine include somnolence, anorexia, nausea, skin rash, and a mild increase in blood pressure or heart rate. Notably, there is a small risk of suicide associated with atomoxetine.
Monitor patients for the emergence and severity of side effects. Many of the side effects of stimulants are transient and can be managed through monitoring, as long as it does not compromise the patient’s health or interfere with daily living. Side effects can also be managed with dose adjustment, change of drug treatment, or adjunctive therapy.
Measure height and weight of the patient twice yearly. If a child’s height or weight crosses 2 percentiles on his or her growth curve, it may be an indication of aberrant growth—and a drug holiday or switching to a different medication should be considered.
Evaluate treatment success several times a year. The review should include behavior, academic progress, emergence of comorbid disorders, and the need for behavioral therapy and continuing pharmacotherapy. A lack of response to one psychostimulant is not predictive of the patient’s response to another, the AACAP emphasizes, and it is important to keep trying to find another medication until treatment goals are reached.1
If none of the FDA-approved ADHD medications has the desired results, the AACAP recommends (SOR: B):
- a referral to a cognitive behavioral therapist or child psychologist
- a trial with a medication that is not FDA-approved for ADHD, such as bupropion, a tricyclic antidepressant, or an alpha-agonist
- a reevaluation of the ADHD diagnosis, adherence to the treatment plan, and the presence of comorbid conditions.1
AAP stresses hands-on behavioral intervention
The American Academy of Pediatrics (AAP) also has a clinical practice guideline for the treatment of ADHD, issued in 2001.2 Its recommendations are similar to those of the AACAP. But AAP puts additional emphasis on parental training in behavioral therapy and classroom behavioral interventions, and considers both to be more effective than cognitive behavioral therapy (CBT).2
Virtual reality: A viable option?
Although conventional treatment of childhood ADHD has had considerable clinical success, other forms of treatment may be needed in some cases—if a child’s parents reject psychopharmacologic treatment, for example, or medication trials and traditional behavioral therapies, such as CBT, fail to bring the desired results.
Virtual reality (VR), a computer-generated 3-dimensional interactive system, is an emerging clinical tool. VR programs such as The Virtual Classroom3,4—in which a child is “immersed” in a simulated classroom setting—have shown promise for ADHD assessment and treatment.
Perhaps the biggest benefit of VR as an ADHD intervention is the opportunity for a clinician to place a patient in a virtual classroom, with tasks that require the child’s attention as well as distractors, such as conversation, ambient noise, and moving objects. Another advantage is the ability to integrate traditional assessment tools (Continuous Performance Tasks, for example) and treatment modalities, such as CBT.5 This can be accomplished through a graphic display of a child’s performance during a VR session, which the therapist can use as part of the therapeutic process.3 And VR has no side effects.
Several facilities are either using or experimenting with VR for ADHD. More information is available from the Virtual Reality Medical Center at http://www.vrphobia.com/adhd.htm.
CORRESPONDENCE
Keith B. Holten, MD, Berger Health System, 600 North Pickaway Street, Circleville, OH 43113; [email protected]
1. Pliszka S. AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2007;46:894-921.
2. American Academy of Pediatrics. Subcommittee on Attention-Deficit/Hyperactivity Disorder. Clinical practice guideline: treatment of the school-aged child with attention-deficit/hyperactivity disorder. Pediatrics. 2001;108:1033-1044.
3. Rizzo AA, Buckwalter JG, Humphrey L, et al. The virtual classroom: a virtual environment for the assessment and rehabilitation of attention deficits. CyberPsych Behav. 2000;3:483-499.
4. Rizzo AA, Klimchuk D, Mitura R, et al. A virtual reality scenario for all seasons: the virtual classroom. CNS Spectr. 2006;11:35-44.
5. Pollak Y, Weiss PL, Rizzo AA, et al. The utility of a continuous performance test embedded in virtual reality in measuring ADHD-related deficits. J Dev Behav Pediatr. 2009;30:2-6.
1. Pliszka S. AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2007;46:894-921.
2. American Academy of Pediatrics. Subcommittee on Attention-Deficit/Hyperactivity Disorder. Clinical practice guideline: treatment of the school-aged child with attention-deficit/hyperactivity disorder. Pediatrics. 2001;108:1033-1044.
3. Rizzo AA, Buckwalter JG, Humphrey L, et al. The virtual classroom: a virtual environment for the assessment and rehabilitation of attention deficits. CyberPsych Behav. 2000;3:483-499.
4. Rizzo AA, Klimchuk D, Mitura R, et al. A virtual reality scenario for all seasons: the virtual classroom. CNS Spectr. 2006;11:35-44.
5. Pollak Y, Weiss PL, Rizzo AA, et al. The utility of a continuous performance test embedded in virtual reality in measuring ADHD-related deficits. J Dev Behav Pediatr. 2009;30:2-6.