Public health efforts have decreased the incidence of gonorrhea over the past several decades, but this progress is threatened by emergent bacteria resistance to the few remaining antibiotics available to treat it.

Gonococcal resistance to penicillin and tetracycline began in the 1970s and was widespread by the 1980s. Resistance to fluoroquinolones developed during the last decade and led the Centers for Disease Control and Prevention (CDC) in 2007 to stop recommending this class of antibiotics for treatment of gonorrhea.¹ (See “The decline of gonorrhea: A success story now threatened by antibiotic resistance”.)

Given the speed with which gonococci developed resistance to fluoroquinolones, the CDC sees as inevitable the eventual development of resistance to cephalosporins—the currently favored agents for gonorrhea.² This is the main reason behind the new recommendations for treating all cases of gonorrhea with both a cephalosporin and azithromycin, whether or not co-infection with Chlamydia trachomatis is documented or suspected.³

FIGURE 1
A decline in gonorrhea that began in the mid-1970s*

FIGURE 2
Gonorrhea prevalence, 2010

FIGURE 3
Gonorrhea prevalence by age and sex, 2010

Augment therapy, follow up thoroughly

Family physicians can assist with public health efforts to control gonorrhea and delay the development of cephalosporin resistance by screening for and detecting the infection, diagnosing those with symptoms, and treating according to newer recommendations. It’s also essential to report cases to local public health departments, assist with finding and treating sexual contacts of infected individuals, and immediately report suspected treatment failures.

A 2-drug regimen is imperative. The latest recommendation for treating gonorrhea is ceftriaxone 250 mg IM in a single dose and azithromycin 1 g orally in a single dose. Until 2010, the dose of ceftriaxone had been 125 mg. This dual drug regimen is recommended for several reasons: As with using multiple drugs to treat tuberculosis, it is hoped dual drug therapy will slow development of resistance to both cephalosporins and azithromycin; co-infection with C trachomatis remains a significant problem; and the combination may be more effective against pharyngeal gonorrhea, which is hard to detect.

Alternative regimens. Cefixime 400 mg orally as a single dose is an option in lieu of ceftriaxone, but is not preferred because of the higher number of reported failures of treatment with oral cephalosporins and less efficacy against pharyngeal disease.³ Other injectable cephalosporins are also an option, but less is known about their effectiveness in treating pharyngeal infection. Injectable options include ceftizoxime 500 mg IM, cefoxitin 2 g IM with probenecid 1 g orally, and cefotaxime 500 mg IM.

Regardless of the cephalosporin chosen, always administer azithromycin. If necessary, an alternative to azithromycin is doxycycline 100 mg orally twice a day. But doxycycline is not preferred because it has a multiple daily dosing requirement and higher levels of gonococcal resistance than is seen with azithromycin.

Necessary follow-up. Although routine testing for cure is not advocated for those treated with a recommended antibiotic regimen, a gonococcal culture and testing for antibiotic susceptibility should be done for any patient whose symptoms persist after treatment. Rapid tests using nucleic acid amplification are unsuitable for testing antibiotic susceptibility. The CDC does recommend retesting patients 3 months after treatment is completed because of a high prevalence of reinfection.³ If cephalosporin resistance becomes prevalent, routine tests of cure might become a recommended standard.

Report all patients with gonorrhea to the local public health department so that sexual contacts within the past 60 days can be notified, tested, and treated presumptively with the dual drug regimen. Recommend simultaneous treatment for all current sex partners, and discourage sexual intercourse until symptoms have resolved. Promptly report any patient with suspected treatment failure to the local health department, and consult the local or state health department for recommendations on subsequent treatment regimens.

The US Preventive Services Task Force (USPSTF) recommends routine screening for asymptomatic infection in women at risk, as per the details in the TABLE.⁴ While the USPSTF found insufficient evidence to recommend screening of high-risk men, physicians might still consider screening men who have sex with multiple male partners.

TABLE
USPSTF recommendations on screening for gonorrhea⁴

Doing our best in the face of uncertainty
Although evidence is lacking that dual drug therapy will delay the progression of resistance, the strategy makes empirical sense. If gonorrhea develops resistance to cephalosporins, it will seriously challenge public health efforts to control this infection. Family physicians have an important role in controlling this sexually transmitted infection and helping to prevent drug resistance.

Public health efforts have decreased the incidence of gonorrhea over the past several decades, but this progress is threatened by emergent bacteria resistance to the few remaining antibiotics available to treat it.

Gonococcal resistance to penicillin and tetracycline began in the 1970s and was widespread by the 1980s. Resistance to fluoroquinolones developed during the last decade and led the Centers for Disease Control and Prevention (CDC) in 2007 to stop recommending this class of antibiotics for treatment of gonorrhea.¹ (See “The decline of gonorrhea: A success story now threatened by antibiotic resistance”.)

Given the speed with which gonococci developed resistance to fluoroquinolones, the CDC sees as inevitable the eventual development of resistance to cephalosporins—the currently favored agents for gonorrhea.² This is the main reason behind the new recommendations for treating all cases of gonorrhea with both a cephalosporin and azithromycin, whether or not co-infection with Chlamydia trachomatis is documented or suspected.³

FIGURE 1
A decline in gonorrhea that began in the mid-1970s*

FIGURE 2
Gonorrhea prevalence, 2010

FIGURE 3
Gonorrhea prevalence by age and sex, 2010

Augment therapy, follow up thoroughly

Family physicians can assist with public health efforts to control gonorrhea and delay the development of cephalosporin resistance by screening for and detecting the infection, diagnosing those with symptoms, and treating according to newer recommendations. It’s also essential to report cases to local public health departments, assist with finding and treating sexual contacts of infected individuals, and immediately report suspected treatment failures.

A 2-drug regimen is imperative. The latest recommendation for treating gonorrhea is ceftriaxone 250 mg IM in a single dose and azithromycin 1 g orally in a single dose. Until 2010, the dose of ceftriaxone had been 125 mg. This dual drug regimen is recommended for several reasons: As with using multiple drugs to treat tuberculosis, it is hoped dual drug therapy will slow development of resistance to both cephalosporins and azithromycin; co-infection with C trachomatis remains a significant problem; and the combination may be more effective against pharyngeal gonorrhea, which is hard to detect.

Alternative regimens. Cefixime 400 mg orally as a single dose is an option in lieu of ceftriaxone, but is not preferred because of the higher number of reported failures of treatment with oral cephalosporins and less efficacy against pharyngeal disease.³ Other injectable cephalosporins are also an option, but less is known about their effectiveness in treating pharyngeal infection. Injectable options include ceftizoxime 500 mg IM, cefoxitin 2 g IM with probenecid 1 g orally, and cefotaxime 500 mg IM.

Regardless of the cephalosporin chosen, always administer azithromycin. If necessary, an alternative to azithromycin is doxycycline 100 mg orally twice a day. But doxycycline is not preferred because it has a multiple daily dosing requirement and higher levels of gonococcal resistance than is seen with azithromycin.

Necessary follow-up. Although routine testing for cure is not advocated for those treated with a recommended antibiotic regimen, a gonococcal culture and testing for antibiotic susceptibility should be done for any patient whose symptoms persist after treatment. Rapid tests using nucleic acid amplification are unsuitable for testing antibiotic susceptibility. The CDC does recommend retesting patients 3 months after treatment is completed because of a high prevalence of reinfection.³ If cephalosporin resistance becomes prevalent, routine tests of cure might become a recommended standard.

Report all patients with gonorrhea to the local public health department so that sexual contacts within the past 60 days can be notified, tested, and treated presumptively with the dual drug regimen. Recommend simultaneous treatment for all current sex partners, and discourage sexual intercourse until symptoms have resolved. Promptly report any patient with suspected treatment failure to the local health department, and consult the local or state health department for recommendations on subsequent treatment regimens.

The US Preventive Services Task Force (USPSTF) recommends routine screening for asymptomatic infection in women at risk, as per the details in the TABLE.⁴ While the USPSTF found insufficient evidence to recommend screening of high-risk men, physicians might still consider screening men who have sex with multiple male partners.

TABLE
USPSTF recommendations on screening for gonorrhea⁴

Doing our best in the face of uncertainty
Although evidence is lacking that dual drug therapy will delay the progression of resistance, the strategy makes empirical sense. If gonorrhea develops resistance to cephalosporins, it will seriously challenge public health efforts to control this infection. Family physicians have an important role in controlling this sexually transmitted infection and helping to prevent drug resistance.

Public health efforts have decreased the incidence of gonorrhea over the past several decades, but this progress is threatened by emergent bacteria resistance to the few remaining antibiotics available to treat it.

Gonococcal resistance to penicillin and tetracycline began in the 1970s and was widespread by the 1980s. Resistance to fluoroquinolones developed during the last decade and led the Centers for Disease Control and Prevention (CDC) in 2007 to stop recommending this class of antibiotics for treatment of gonorrhea.¹ (See “The decline of gonorrhea: A success story now threatened by antibiotic resistance”.)

Given the speed with which gonococci developed resistance to fluoroquinolones, the CDC sees as inevitable the eventual development of resistance to cephalosporins—the currently favored agents for gonorrhea.² This is the main reason behind the new recommendations for treating all cases of gonorrhea with both a cephalosporin and azithromycin, whether or not co-infection with Chlamydia trachomatis is documented or suspected.³

FIGURE 1
A decline in gonorrhea that began in the mid-1970s*

FIGURE 2
Gonorrhea prevalence, 2010

FIGURE 3
Gonorrhea prevalence by age and sex, 2010

Augment therapy, follow up thoroughly

Family physicians can assist with public health efforts to control gonorrhea and delay the development of cephalosporin resistance by screening for and detecting the infection, diagnosing those with symptoms, and treating according to newer recommendations. It’s also essential to report cases to local public health departments, assist with finding and treating sexual contacts of infected individuals, and immediately report suspected treatment failures.

A 2-drug regimen is imperative. The latest recommendation for treating gonorrhea is ceftriaxone 250 mg IM in a single dose and azithromycin 1 g orally in a single dose. Until 2010, the dose of ceftriaxone had been 125 mg. This dual drug regimen is recommended for several reasons: As with using multiple drugs to treat tuberculosis, it is hoped dual drug therapy will slow development of resistance to both cephalosporins and azithromycin; co-infection with C trachomatis remains a significant problem; and the combination may be more effective against pharyngeal gonorrhea, which is hard to detect.

Alternative regimens. Cefixime 400 mg orally as a single dose is an option in lieu of ceftriaxone, but is not preferred because of the higher number of reported failures of treatment with oral cephalosporins and less efficacy against pharyngeal disease.³ Other injectable cephalosporins are also an option, but less is known about their effectiveness in treating pharyngeal infection. Injectable options include ceftizoxime 500 mg IM, cefoxitin 2 g IM with probenecid 1 g orally, and cefotaxime 500 mg IM.

Regardless of the cephalosporin chosen, always administer azithromycin. If necessary, an alternative to azithromycin is doxycycline 100 mg orally twice a day. But doxycycline is not preferred because it has a multiple daily dosing requirement and higher levels of gonococcal resistance than is seen with azithromycin.

Necessary follow-up. Although routine testing for cure is not advocated for those treated with a recommended antibiotic regimen, a gonococcal culture and testing for antibiotic susceptibility should be done for any patient whose symptoms persist after treatment. Rapid tests using nucleic acid amplification are unsuitable for testing antibiotic susceptibility. The CDC does recommend retesting patients 3 months after treatment is completed because of a high prevalence of reinfection.³ If cephalosporin resistance becomes prevalent, routine tests of cure might become a recommended standard.

Report all patients with gonorrhea to the local public health department so that sexual contacts within the past 60 days can be notified, tested, and treated presumptively with the dual drug regimen. Recommend simultaneous treatment for all current sex partners, and discourage sexual intercourse until symptoms have resolved. Promptly report any patient with suspected treatment failure to the local health department, and consult the local or state health department for recommendations on subsequent treatment regimens.

The US Preventive Services Task Force (USPSTF) recommends routine screening for asymptomatic infection in women at risk, as per the details in the TABLE.⁴ While the USPSTF found insufficient evidence to recommend screening of high-risk men, physicians might still consider screening men who have sex with multiple male partners.

TABLE
USPSTF recommendations on screening for gonorrhea⁴

Doing our best in the face of uncertainty
Although evidence is lacking that dual drug therapy will delay the progression of resistance, the strategy makes empirical sense. If gonorrhea develops resistance to cephalosporins, it will seriously challenge public health efforts to control this infection. Family physicians have an important role in controlling this sexually transmitted infection and helping to prevent drug resistance.

CASE Mr. D, a 75-year-old patient with a history of hypertension and congestive heart failure, sustained a femoral neck fracture and was admitted to the hospital for surgery. He underwent open reduction and internal fixation and was doing well postoperatively, until Day 2—when his primary care physician made morning rounds and noted that Mr. D was somnolent. The nurse on duty assured the physician that Mr. D was fine and “was awake and alert earlier,” and attributed his somnolence to the oxycodone (10 mg) the patient was taking for pain. The physician ordered a reduction in dosage.

If Mr. D had been your patient, would you have considered other possible causes of his somnolence? Or do you think the physician’s action was sufficient?

Derived from Latin, the word delirium literally means “off the [ploughed] track.”¹ Dozens of terms have been used to describe delirium, with acute confusion state, organic brain syndrome, acute brain syndrome, and toxic psychosis among them.

Delirium has been reported to occur in 15% to 30% of patients on general medical units,² about 40% of postoperative patients, and up to 70% of terminally ill patients.³ The true prevalence is hard to determine, as up to 66% of cases may be missed.⁴

Delirium is being diagnosed more frequently, however—a likely result of a growing geriatric population, increased longevity, and greater awareness of the condition. Each year, an estimated 2.3 million US residents are affected, leading to prolonged hospitalization; poor functional outcomes; the development or worsening of dementia; increased nursing home placement; and a significant burden for families and the US health care system.⁵

Delirium is also associated with an increase in mortality.^6,7 The mortality rate among hospitalized patients who develop delirium is reported to be 18%, rising to an estimated 47% within the first 3 months after discharge.⁶ Greater awareness of risk factors, rapid recognition of signs and symptoms of delirium, and early intervention—detailed in the text and tables that follow—will lead to better outcomes.

Assessing risk, evaluating mental status

In addition to advanced age, risk factors for delirium (TABLE 1)^8-14 include alcohol use, brain dysfunction, comorbidities, hypertension, malignancy, anticholinergic medications, anemia, metabolic abnormalities, and male sex. In patients who, like Mr. D, have numerous risk factors, early—and frequent—evaluation of mental status is needed. One way to do this is to treat mental status as a vital sign, to be included in the assessment of every elderly patient.¹⁵

The Confusion Assessment Method, a quick and easy-to-use delirium screening tool (TABLE 2), has a sensitivity of 94% to 100% and a specificity of 90% to 95%.^16,17 There are a number of other screening tools, including the widely used Mini-Mental State Exam (MMSE), as well as the Delirium Rating Scale, Delirium Symptom Interview, and Delirium Severity Scale.

TABLE 1
Risk factors for delirium^8-14

TABLE 2
Screening for delirium: The Confusion Assessment Method*^16,17

Arriving at a delirium diagnosis

The clinical presentation of delirium is characterized by acute—and reversible—impairment of cognition, attention, orientation, and memory, and disruption of the normal sleep/wake cycle. The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) criteria for a delirium diagnosis include all of the following:

• disturbance of consciousness, with a reduced ability to focus, sustain, or shift attention
• change in cognition, or a perceptual disturbance, that is not accounted for by a preexisting or developing dementia
• rapid onset of cognitive impairment, with fluctuation likely during the course of the day
• evidence from the history, physical exam, or laboratory findings that the disturbed consciousness is a direct physiological consequence of a general medical condition.¹⁷

There are 3 basic types of delirium, each associated with a different psychomotor disturbance.

1. Hyperactive delirium—the least common—is characterized by restlessness and agitation, and is therefore the easiest to diagnose.
2. Hypoactive delirium is characterized by psychomotor retardation and hypoalertness. It is often misdiagnosed as depression, and has the poorest prognosis.
3. Mixed delirium—the most common—is characterized by symptoms that fluctuate between hyper- and hypoactivity.¹⁸

CASE By lunchtime, Mr. D had awakened; however, he needed help with his meal. After eating, he slept for the rest of the day. At night, a nurse paged the resident to report that the patient’s blood pressure was 82/60 mm Hg and his heart rate was 115. The physician ordered an intravenous fluid bolus, which corrected the patient’s hypotension, but only temporarily.

The fluctuating nature of delirium—most notably, in patients’ level of alertness—is helpful in establishing a diagnosis. The history and physical exam are the gold standard tools, both for diagnosing delirium and identifying the underlying cause (TABLE 3).^19,20 A review of the patient’s medications should be a key component of the medical history, as drugs—particularly those with anticholinergic properties—are often associated with delirium. Environmental shifts, including hospitalization and a disruption of the normal sleep/wake cycle, endocrine disorders, infection, and nutritional deficiencies are also potential causes of delirium, among others.

If history and physical exam fail to identify the underlying cause, laboratory testing, including complete blood count, complete metabolic profile, and urinalysis, should be done. Brain imaging is usually not needed for individuals with symptoms of delirium, but computed tomography (CT) may be indicated if a patient’s condition continues to deteriorate while the underlying cause remains unidentified.²¹ Electroencephalography (EEG) may be used to confirm a delirium diagnosis that’s uncertain, in a patient with underlying dementia, for instance. (In more than 16% of cases of delirium, the cause is unknown.²²)

The most common structural abnormalities found in patients with delirium are brain atrophy and increased white matter lesions, as well as basal ganglia lesions.²³ Single-photon emission CT (SPECT) shows a reduction of regional cerebral perfusion by 50%,²⁴ while EEG shows slowing of the posterior dominant rhythm and increased generalized slow-wave activity.²⁵

TABLE 3
A DELIRIUM mnemonic to get to the heart of the problem^19,20

Treating (or preventing) delirium: Start with these steps

Nonpharmacologic interventions are the mainstay of treatment for patients with delirium, and may also help to prevent the development of delirium in patients at risk. One key measure is to correct, or avoid, disruptions in the patient’s normal sleep/wake cycle—eg, restoring circadian rhythm by avoiding,
to the extent possible, awakening the patient at night for medication or vital signs. Preventing sensory deprivation, by ensuring that the patient’s eyeglasses and hearing aid are nearby and that there is a clock and calendar nearby and adequate light, is also helpful. Other key interventions (TABLE 4)^26-28 include:

• limiting medications associated with delirium (and eliminating any nonessential medication)
• improving nutrition and ambulation
• correcting electrolyte and fluid disturbances
• treating infection
• involving family members in patient care
• ensuring that patients receive adequate pain management
• avoiding transfers (if the patient is hospitalized) and trying to secure a single room.

Several studies have evaluated the effectiveness of nonpharmacologic interventions in preventing or lowering the incidence of delirium. A large multicomponent delirium prevention study of patients >70 years on general medical units focused on managing risk factors. The interventions studied included (1) avoidance of sensory deprivation, (2) early mobilization, (3) treating dehydration, (4) implementing noise reduction strategies and sleep enhancement programs, and (5) avoiding the use of sleep medications. These interventions proved to be effective not only in lowering the incidence of delirium, but in shortening the duration of delirium in affected patients (NNT=20).²⁷

One study found that proactively using a geriatric consultation model (ie, implementing standardized protocols for the management of 6 risk factors) for elderly hospitalized patients led to a reduction in the incidence of delirium by more than a third.²⁶ Admission to a specialized geriatric unit is associated with a lower incidence of delirium compared with being hospitalized on a general medical unit.²⁹

Reducing the incidence of postoperative delirium. Bright light therapy (a light intensity of 5000 lux with a distance from the light source of 100 cm), implemented postoperatively, may play a role in reducing the incidence of delirium, research suggests.³⁰ Music may be helpful, as well. An RCT involving patients (>65 years) undergoing elective knee or hip surgery found that those who listened to classical music postoperatively had a lower incidence of delirium.³¹ Similarly, playing music in nursing homes has been shown to decrease aggressive behavior and agitation.³²

TABLE 4
Helpful interventions in the hospital or at home^26-28

When medication is needed, proceed with caution

None of the medications currently used to treat delirium are approved by the US Food and Drug Administration for this indication, and many of them have substantial side effects. Nonetheless, palliative or symptomatic treatment requires some form of sedation for agitated patients with delirium. Thus, it is necessary to strike a balance in order to manage the symptoms of delirium and avoid potential side effects (primarily, sedation). Overly sedating patients can confuse the clinical picture of delirium and make it difficult to differentiate between ongoing delirium and medication side effects. Medication should be started at a low, but frequent, dose to achieve an effective therapeutic level, after which a lower maintenance dose can be used until the cause of delirium is resolved.

Antipsychotics are the cornerstone of drug treatment
Haloperidol has traditionally been used to treat delirium³³ and has proven effectiveness. However, it is associated with increased risk of extrapyramidal manifestations compared with atypical antipsychotics.

Atypical antipsychotics (olanzapine, risperidone, quetiapine) are increasingly being used to treat delirium because they have fewer extrapyramidal side effects.³⁴ With the exception of olanzapine (available in intramuscular and oral disintegrating form), atypical antipsychotics are available only in oral form, which may limit their usefulness as a treatment for agitated, delirious patients.

Risperidone (at a dose ranging from 0.25 to 1 mg/d) and olanzapine (1.25 to 2.5 mg/d) have shown similar efficacy to haloperidol (0.75 to 1.5 mg/d) in both the prevention and treatment of delirium, but with fewer extrapyramidal side effects.^35-39 Quetiapine, a second-generation antipsychotic, is widely used to treat inpatient delirium, although there are no large RCTs comparing it with placebo. One pilot study and another open-label trial found the drug to be beneficial for patients with delirium, with fewer extrapyramidal side effects than haloperidol.^40,41

Do a risk-benefit analysis. The use of antipsychotics in elderly patients with delirium has been associated with increased morbidity and mortality. The incidence of stroke and death were higher for community-dwelling patients (NNH=100) and patients in long-term care (N=67) who received typical or atypical antipsychotics for 6 months compared with that of patients who did not receive any antipsychotics.^42,43 Thus, a risk-benefit analysis should be done before prescribing antipsychotics for elderly patients. Both typical and atypical antipsychotics carry black box warnings of increased mortality rates in the elderly.

Other drugs for delirium? More research is needed
Cholinesterase inhibitors. Procholinergic agents would be expected to be helpful in treating delirium, as cholinergic deficiency has been implicated as a predisposing factor for delirium and medications with anticholinergic effects have been shown to induce delirium. However, several studies of cholinesterase inhibitors have not found this to be the case.^44-47

Benzodiazepines. There is no evidence to support the use of benzodiazepines in the treatment of delirium, except when the delirium is related to alcohol withdrawal.⁴⁸ When indicated, the use of a short-acting benzodiazepine such as lorazepam is preferred for elderly patients (vs long-acting agents like diazepam) because of its shorter half-life and better side effect profile.² Drowsiness, ataxia, and disinhibition are common side effects of benzodiazepines.

Gabapentin. A pilot study conducted to assess the efficacy of gabapentin (900 mg/d) for the prevention of postoperative delirium found a significantly lower incidence of delirium among patients who received gabapentin compared with placebo. This may be associated with gabapentin’s opioid-sparing effect.⁴⁹ Larger studies are needed to recommend for or against the use of gabapentin in patients receiving opiates.

Further study of the pathophysiology of delirium is needed, as well, to increase our ability to prevent and treat it.

CASE After receiving the IV fluid bolus, Mr. D became increasingly short of breath and required more oxygen to keep his oxygen saturation in the 90s. Labs were ordered during morning rounds, and the patient was found to have urosepsis. He was admitted to the ICU in septic shock, and was intubated and died several days later.

In retrospect, it was determined that Mr. D had developed hypoactive delirium brought on by the infection—and that his somnolence on the second postoperative day was not a sign of overmedication. Had this been recognized early on through the use of an appropriate screening tool, the outcome would likely have been more favorable.

CORRESPONDENCE Abdulraouf Ghandour, MD, Green Meadows Clinic University Physicians, 3217 Providence Road, Columbia, MO 65203; [email protected]

CASE Mr. D, a 75-year-old patient with a history of hypertension and congestive heart failure, sustained a femoral neck fracture and was admitted to the hospital for surgery. He underwent open reduction and internal fixation and was doing well postoperatively, until Day 2—when his primary care physician made morning rounds and noted that Mr. D was somnolent. The nurse on duty assured the physician that Mr. D was fine and “was awake and alert earlier,” and attributed his somnolence to the oxycodone (10 mg) the patient was taking for pain. The physician ordered a reduction in dosage.

If Mr. D had been your patient, would you have considered other possible causes of his somnolence? Or do you think the physician’s action was sufficient?

Derived from Latin, the word delirium literally means “off the [ploughed] track.”¹ Dozens of terms have been used to describe delirium, with acute confusion state, organic brain syndrome, acute brain syndrome, and toxic psychosis among them.

Delirium has been reported to occur in 15% to 30% of patients on general medical units,² about 40% of postoperative patients, and up to 70% of terminally ill patients.³ The true prevalence is hard to determine, as up to 66% of cases may be missed.⁴

Delirium is being diagnosed more frequently, however—a likely result of a growing geriatric population, increased longevity, and greater awareness of the condition. Each year, an estimated 2.3 million US residents are affected, leading to prolonged hospitalization; poor functional outcomes; the development or worsening of dementia; increased nursing home placement; and a significant burden for families and the US health care system.⁵

Delirium is also associated with an increase in mortality.^6,7 The mortality rate among hospitalized patients who develop delirium is reported to be 18%, rising to an estimated 47% within the first 3 months after discharge.⁶ Greater awareness of risk factors, rapid recognition of signs and symptoms of delirium, and early intervention—detailed in the text and tables that follow—will lead to better outcomes.

Assessing risk, evaluating mental status

In addition to advanced age, risk factors for delirium (TABLE 1)^8-14 include alcohol use, brain dysfunction, comorbidities, hypertension, malignancy, anticholinergic medications, anemia, metabolic abnormalities, and male sex. In patients who, like Mr. D, have numerous risk factors, early—and frequent—evaluation of mental status is needed. One way to do this is to treat mental status as a vital sign, to be included in the assessment of every elderly patient.¹⁵

The Confusion Assessment Method, a quick and easy-to-use delirium screening tool (TABLE 2), has a sensitivity of 94% to 100% and a specificity of 90% to 95%.^16,17 There are a number of other screening tools, including the widely used Mini-Mental State Exam (MMSE), as well as the Delirium Rating Scale, Delirium Symptom Interview, and Delirium Severity Scale.

TABLE 1
Risk factors for delirium^8-14

TABLE 2
Screening for delirium: The Confusion Assessment Method*^16,17

Arriving at a delirium diagnosis

The clinical presentation of delirium is characterized by acute—and reversible—impairment of cognition, attention, orientation, and memory, and disruption of the normal sleep/wake cycle. The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) criteria for a delirium diagnosis include all of the following:

• disturbance of consciousness, with a reduced ability to focus, sustain, or shift attention
• change in cognition, or a perceptual disturbance, that is not accounted for by a preexisting or developing dementia
• rapid onset of cognitive impairment, with fluctuation likely during the course of the day
• evidence from the history, physical exam, or laboratory findings that the disturbed consciousness is a direct physiological consequence of a general medical condition.¹⁷

There are 3 basic types of delirium, each associated with a different psychomotor disturbance.

1. Hyperactive delirium—the least common—is characterized by restlessness and agitation, and is therefore the easiest to diagnose.
2. Hypoactive delirium is characterized by psychomotor retardation and hypoalertness. It is often misdiagnosed as depression, and has the poorest prognosis.
3. Mixed delirium—the most common—is characterized by symptoms that fluctuate between hyper- and hypoactivity.¹⁸

CASE By lunchtime, Mr. D had awakened; however, he needed help with his meal. After eating, he slept for the rest of the day. At night, a nurse paged the resident to report that the patient’s blood pressure was 82/60 mm Hg and his heart rate was 115. The physician ordered an intravenous fluid bolus, which corrected the patient’s hypotension, but only temporarily.

The fluctuating nature of delirium—most notably, in patients’ level of alertness—is helpful in establishing a diagnosis. The history and physical exam are the gold standard tools, both for diagnosing delirium and identifying the underlying cause (TABLE 3).^19,20 A review of the patient’s medications should be a key component of the medical history, as drugs—particularly those with anticholinergic properties—are often associated with delirium. Environmental shifts, including hospitalization and a disruption of the normal sleep/wake cycle, endocrine disorders, infection, and nutritional deficiencies are also potential causes of delirium, among others.

If history and physical exam fail to identify the underlying cause, laboratory testing, including complete blood count, complete metabolic profile, and urinalysis, should be done. Brain imaging is usually not needed for individuals with symptoms of delirium, but computed tomography (CT) may be indicated if a patient’s condition continues to deteriorate while the underlying cause remains unidentified.²¹ Electroencephalography (EEG) may be used to confirm a delirium diagnosis that’s uncertain, in a patient with underlying dementia, for instance. (In more than 16% of cases of delirium, the cause is unknown.²²)

The most common structural abnormalities found in patients with delirium are brain atrophy and increased white matter lesions, as well as basal ganglia lesions.²³ Single-photon emission CT (SPECT) shows a reduction of regional cerebral perfusion by 50%,²⁴ while EEG shows slowing of the posterior dominant rhythm and increased generalized slow-wave activity.²⁵

TABLE 3
A DELIRIUM mnemonic to get to the heart of the problem^19,20

Treating (or preventing) delirium: Start with these steps

Nonpharmacologic interventions are the mainstay of treatment for patients with delirium, and may also help to prevent the development of delirium in patients at risk. One key measure is to correct, or avoid, disruptions in the patient’s normal sleep/wake cycle—eg, restoring circadian rhythm by avoiding,
to the extent possible, awakening the patient at night for medication or vital signs. Preventing sensory deprivation, by ensuring that the patient’s eyeglasses and hearing aid are nearby and that there is a clock and calendar nearby and adequate light, is also helpful. Other key interventions (TABLE 4)^26-28 include:

• limiting medications associated with delirium (and eliminating any nonessential medication)
• improving nutrition and ambulation
• correcting electrolyte and fluid disturbances
• treating infection
• involving family members in patient care
• ensuring that patients receive adequate pain management
• avoiding transfers (if the patient is hospitalized) and trying to secure a single room.

Several studies have evaluated the effectiveness of nonpharmacologic interventions in preventing or lowering the incidence of delirium. A large multicomponent delirium prevention study of patients >70 years on general medical units focused on managing risk factors. The interventions studied included (1) avoidance of sensory deprivation, (2) early mobilization, (3) treating dehydration, (4) implementing noise reduction strategies and sleep enhancement programs, and (5) avoiding the use of sleep medications. These interventions proved to be effective not only in lowering the incidence of delirium, but in shortening the duration of delirium in affected patients (NNT=20).²⁷

One study found that proactively using a geriatric consultation model (ie, implementing standardized protocols for the management of 6 risk factors) for elderly hospitalized patients led to a reduction in the incidence of delirium by more than a third.²⁶ Admission to a specialized geriatric unit is associated with a lower incidence of delirium compared with being hospitalized on a general medical unit.²⁹

Reducing the incidence of postoperative delirium. Bright light therapy (a light intensity of 5000 lux with a distance from the light source of 100 cm), implemented postoperatively, may play a role in reducing the incidence of delirium, research suggests.³⁰ Music may be helpful, as well. An RCT involving patients (>65 years) undergoing elective knee or hip surgery found that those who listened to classical music postoperatively had a lower incidence of delirium.³¹ Similarly, playing music in nursing homes has been shown to decrease aggressive behavior and agitation.³²

TABLE 4
Helpful interventions in the hospital or at home^26-28

When medication is needed, proceed with caution

None of the medications currently used to treat delirium are approved by the US Food and Drug Administration for this indication, and many of them have substantial side effects. Nonetheless, palliative or symptomatic treatment requires some form of sedation for agitated patients with delirium. Thus, it is necessary to strike a balance in order to manage the symptoms of delirium and avoid potential side effects (primarily, sedation). Overly sedating patients can confuse the clinical picture of delirium and make it difficult to differentiate between ongoing delirium and medication side effects. Medication should be started at a low, but frequent, dose to achieve an effective therapeutic level, after which a lower maintenance dose can be used until the cause of delirium is resolved.

Antipsychotics are the cornerstone of drug treatment
Haloperidol has traditionally been used to treat delirium³³ and has proven effectiveness. However, it is associated with increased risk of extrapyramidal manifestations compared with atypical antipsychotics.

Atypical antipsychotics (olanzapine, risperidone, quetiapine) are increasingly being used to treat delirium because they have fewer extrapyramidal side effects.³⁴ With the exception of olanzapine (available in intramuscular and oral disintegrating form), atypical antipsychotics are available only in oral form, which may limit their usefulness as a treatment for agitated, delirious patients.

Risperidone (at a dose ranging from 0.25 to 1 mg/d) and olanzapine (1.25 to 2.5 mg/d) have shown similar efficacy to haloperidol (0.75 to 1.5 mg/d) in both the prevention and treatment of delirium, but with fewer extrapyramidal side effects.^35-39 Quetiapine, a second-generation antipsychotic, is widely used to treat inpatient delirium, although there are no large RCTs comparing it with placebo. One pilot study and another open-label trial found the drug to be beneficial for patients with delirium, with fewer extrapyramidal side effects than haloperidol.^40,41

Do a risk-benefit analysis. The use of antipsychotics in elderly patients with delirium has been associated with increased morbidity and mortality. The incidence of stroke and death were higher for community-dwelling patients (NNH=100) and patients in long-term care (N=67) who received typical or atypical antipsychotics for 6 months compared with that of patients who did not receive any antipsychotics.^42,43 Thus, a risk-benefit analysis should be done before prescribing antipsychotics for elderly patients. Both typical and atypical antipsychotics carry black box warnings of increased mortality rates in the elderly.

Other drugs for delirium? More research is needed
Cholinesterase inhibitors. Procholinergic agents would be expected to be helpful in treating delirium, as cholinergic deficiency has been implicated as a predisposing factor for delirium and medications with anticholinergic effects have been shown to induce delirium. However, several studies of cholinesterase inhibitors have not found this to be the case.^44-47

Benzodiazepines. There is no evidence to support the use of benzodiazepines in the treatment of delirium, except when the delirium is related to alcohol withdrawal.⁴⁸ When indicated, the use of a short-acting benzodiazepine such as lorazepam is preferred for elderly patients (vs long-acting agents like diazepam) because of its shorter half-life and better side effect profile.² Drowsiness, ataxia, and disinhibition are common side effects of benzodiazepines.

Gabapentin. A pilot study conducted to assess the efficacy of gabapentin (900 mg/d) for the prevention of postoperative delirium found a significantly lower incidence of delirium among patients who received gabapentin compared with placebo. This may be associated with gabapentin’s opioid-sparing effect.⁴⁹ Larger studies are needed to recommend for or against the use of gabapentin in patients receiving opiates.

Further study of the pathophysiology of delirium is needed, as well, to increase our ability to prevent and treat it.

CASE After receiving the IV fluid bolus, Mr. D became increasingly short of breath and required more oxygen to keep his oxygen saturation in the 90s. Labs were ordered during morning rounds, and the patient was found to have urosepsis. He was admitted to the ICU in septic shock, and was intubated and died several days later.

In retrospect, it was determined that Mr. D had developed hypoactive delirium brought on by the infection—and that his somnolence on the second postoperative day was not a sign of overmedication. Had this been recognized early on through the use of an appropriate screening tool, the outcome would likely have been more favorable.

CORRESPONDENCE Abdulraouf Ghandour, MD, Green Meadows Clinic University Physicians, 3217 Providence Road, Columbia, MO 65203; [email protected]

CASE Mr. D, a 75-year-old patient with a history of hypertension and congestive heart failure, sustained a femoral neck fracture and was admitted to the hospital for surgery. He underwent open reduction and internal fixation and was doing well postoperatively, until Day 2—when his primary care physician made morning rounds and noted that Mr. D was somnolent. The nurse on duty assured the physician that Mr. D was fine and “was awake and alert earlier,” and attributed his somnolence to the oxycodone (10 mg) the patient was taking for pain. The physician ordered a reduction in dosage.

If Mr. D had been your patient, would you have considered other possible causes of his somnolence? Or do you think the physician’s action was sufficient?

Derived from Latin, the word delirium literally means “off the [ploughed] track.”¹ Dozens of terms have been used to describe delirium, with acute confusion state, organic brain syndrome, acute brain syndrome, and toxic psychosis among them.

Delirium has been reported to occur in 15% to 30% of patients on general medical units,² about 40% of postoperative patients, and up to 70% of terminally ill patients.³ The true prevalence is hard to determine, as up to 66% of cases may be missed.⁴

Delirium is being diagnosed more frequently, however—a likely result of a growing geriatric population, increased longevity, and greater awareness of the condition. Each year, an estimated 2.3 million US residents are affected, leading to prolonged hospitalization; poor functional outcomes; the development or worsening of dementia; increased nursing home placement; and a significant burden for families and the US health care system.⁵

Delirium is also associated with an increase in mortality.^6,7 The mortality rate among hospitalized patients who develop delirium is reported to be 18%, rising to an estimated 47% within the first 3 months after discharge.⁶ Greater awareness of risk factors, rapid recognition of signs and symptoms of delirium, and early intervention—detailed in the text and tables that follow—will lead to better outcomes.

Assessing risk, evaluating mental status

In addition to advanced age, risk factors for delirium (TABLE 1)^8-14 include alcohol use, brain dysfunction, comorbidities, hypertension, malignancy, anticholinergic medications, anemia, metabolic abnormalities, and male sex. In patients who, like Mr. D, have numerous risk factors, early—and frequent—evaluation of mental status is needed. One way to do this is to treat mental status as a vital sign, to be included in the assessment of every elderly patient.¹⁵

The Confusion Assessment Method, a quick and easy-to-use delirium screening tool (TABLE 2), has a sensitivity of 94% to 100% and a specificity of 90% to 95%.^16,17 There are a number of other screening tools, including the widely used Mini-Mental State Exam (MMSE), as well as the Delirium Rating Scale, Delirium Symptom Interview, and Delirium Severity Scale.

TABLE 1
Risk factors for delirium^8-14

TABLE 2
Screening for delirium: The Confusion Assessment Method*^16,17

Arriving at a delirium diagnosis

The clinical presentation of delirium is characterized by acute—and reversible—impairment of cognition, attention, orientation, and memory, and disruption of the normal sleep/wake cycle. The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) criteria for a delirium diagnosis include all of the following:

• disturbance of consciousness, with a reduced ability to focus, sustain, or shift attention
• change in cognition, or a perceptual disturbance, that is not accounted for by a preexisting or developing dementia
• rapid onset of cognitive impairment, with fluctuation likely during the course of the day
• evidence from the history, physical exam, or laboratory findings that the disturbed consciousness is a direct physiological consequence of a general medical condition.¹⁷

There are 3 basic types of delirium, each associated with a different psychomotor disturbance.

1. Hyperactive delirium—the least common—is characterized by restlessness and agitation, and is therefore the easiest to diagnose.
2. Hypoactive delirium is characterized by psychomotor retardation and hypoalertness. It is often misdiagnosed as depression, and has the poorest prognosis.
3. Mixed delirium—the most common—is characterized by symptoms that fluctuate between hyper- and hypoactivity.¹⁸

CASE By lunchtime, Mr. D had awakened; however, he needed help with his meal. After eating, he slept for the rest of the day. At night, a nurse paged the resident to report that the patient’s blood pressure was 82/60 mm Hg and his heart rate was 115. The physician ordered an intravenous fluid bolus, which corrected the patient’s hypotension, but only temporarily.

The fluctuating nature of delirium—most notably, in patients’ level of alertness—is helpful in establishing a diagnosis. The history and physical exam are the gold standard tools, both for diagnosing delirium and identifying the underlying cause (TABLE 3).^19,20 A review of the patient’s medications should be a key component of the medical history, as drugs—particularly those with anticholinergic properties—are often associated with delirium. Environmental shifts, including hospitalization and a disruption of the normal sleep/wake cycle, endocrine disorders, infection, and nutritional deficiencies are also potential causes of delirium, among others.

If history and physical exam fail to identify the underlying cause, laboratory testing, including complete blood count, complete metabolic profile, and urinalysis, should be done. Brain imaging is usually not needed for individuals with symptoms of delirium, but computed tomography (CT) may be indicated if a patient’s condition continues to deteriorate while the underlying cause remains unidentified.²¹ Electroencephalography (EEG) may be used to confirm a delirium diagnosis that’s uncertain, in a patient with underlying dementia, for instance. (In more than 16% of cases of delirium, the cause is unknown.²²)

The most common structural abnormalities found in patients with delirium are brain atrophy and increased white matter lesions, as well as basal ganglia lesions.²³ Single-photon emission CT (SPECT) shows a reduction of regional cerebral perfusion by 50%,²⁴ while EEG shows slowing of the posterior dominant rhythm and increased generalized slow-wave activity.²⁵

TABLE 3
A DELIRIUM mnemonic to get to the heart of the problem^19,20

Treating (or preventing) delirium: Start with these steps

Nonpharmacologic interventions are the mainstay of treatment for patients with delirium, and may also help to prevent the development of delirium in patients at risk. One key measure is to correct, or avoid, disruptions in the patient’s normal sleep/wake cycle—eg, restoring circadian rhythm by avoiding,
to the extent possible, awakening the patient at night for medication or vital signs. Preventing sensory deprivation, by ensuring that the patient’s eyeglasses and hearing aid are nearby and that there is a clock and calendar nearby and adequate light, is also helpful. Other key interventions (TABLE 4)^26-28 include:

• limiting medications associated with delirium (and eliminating any nonessential medication)
• improving nutrition and ambulation
• correcting electrolyte and fluid disturbances
• treating infection
• involving family members in patient care
• ensuring that patients receive adequate pain management
• avoiding transfers (if the patient is hospitalized) and trying to secure a single room.

Several studies have evaluated the effectiveness of nonpharmacologic interventions in preventing or lowering the incidence of delirium. A large multicomponent delirium prevention study of patients >70 years on general medical units focused on managing risk factors. The interventions studied included (1) avoidance of sensory deprivation, (2) early mobilization, (3) treating dehydration, (4) implementing noise reduction strategies and sleep enhancement programs, and (5) avoiding the use of sleep medications. These interventions proved to be effective not only in lowering the incidence of delirium, but in shortening the duration of delirium in affected patients (NNT=20).²⁷

One study found that proactively using a geriatric consultation model (ie, implementing standardized protocols for the management of 6 risk factors) for elderly hospitalized patients led to a reduction in the incidence of delirium by more than a third.²⁶ Admission to a specialized geriatric unit is associated with a lower incidence of delirium compared with being hospitalized on a general medical unit.²⁹

Reducing the incidence of postoperative delirium. Bright light therapy (a light intensity of 5000 lux with a distance from the light source of 100 cm), implemented postoperatively, may play a role in reducing the incidence of delirium, research suggests.³⁰ Music may be helpful, as well. An RCT involving patients (>65 years) undergoing elective knee or hip surgery found that those who listened to classical music postoperatively had a lower incidence of delirium.³¹ Similarly, playing music in nursing homes has been shown to decrease aggressive behavior and agitation.³²

TABLE 4
Helpful interventions in the hospital or at home^26-28

When medication is needed, proceed with caution

None of the medications currently used to treat delirium are approved by the US Food and Drug Administration for this indication, and many of them have substantial side effects. Nonetheless, palliative or symptomatic treatment requires some form of sedation for agitated patients with delirium. Thus, it is necessary to strike a balance in order to manage the symptoms of delirium and avoid potential side effects (primarily, sedation). Overly sedating patients can confuse the clinical picture of delirium and make it difficult to differentiate between ongoing delirium and medication side effects. Medication should be started at a low, but frequent, dose to achieve an effective therapeutic level, after which a lower maintenance dose can be used until the cause of delirium is resolved.

Antipsychotics are the cornerstone of drug treatment
Haloperidol has traditionally been used to treat delirium³³ and has proven effectiveness. However, it is associated with increased risk of extrapyramidal manifestations compared with atypical antipsychotics.

Atypical antipsychotics (olanzapine, risperidone, quetiapine) are increasingly being used to treat delirium because they have fewer extrapyramidal side effects.³⁴ With the exception of olanzapine (available in intramuscular and oral disintegrating form), atypical antipsychotics are available only in oral form, which may limit their usefulness as a treatment for agitated, delirious patients.

Risperidone (at a dose ranging from 0.25 to 1 mg/d) and olanzapine (1.25 to 2.5 mg/d) have shown similar efficacy to haloperidol (0.75 to 1.5 mg/d) in both the prevention and treatment of delirium, but with fewer extrapyramidal side effects.^35-39 Quetiapine, a second-generation antipsychotic, is widely used to treat inpatient delirium, although there are no large RCTs comparing it with placebo. One pilot study and another open-label trial found the drug to be beneficial for patients with delirium, with fewer extrapyramidal side effects than haloperidol.^40,41

Do a risk-benefit analysis. The use of antipsychotics in elderly patients with delirium has been associated with increased morbidity and mortality. The incidence of stroke and death were higher for community-dwelling patients (NNH=100) and patients in long-term care (N=67) who received typical or atypical antipsychotics for 6 months compared with that of patients who did not receive any antipsychotics.^42,43 Thus, a risk-benefit analysis should be done before prescribing antipsychotics for elderly patients. Both typical and atypical antipsychotics carry black box warnings of increased mortality rates in the elderly.

Other drugs for delirium? More research is needed
Cholinesterase inhibitors. Procholinergic agents would be expected to be helpful in treating delirium, as cholinergic deficiency has been implicated as a predisposing factor for delirium and medications with anticholinergic effects have been shown to induce delirium. However, several studies of cholinesterase inhibitors have not found this to be the case.^44-47

Benzodiazepines. There is no evidence to support the use of benzodiazepines in the treatment of delirium, except when the delirium is related to alcohol withdrawal.⁴⁸ When indicated, the use of a short-acting benzodiazepine such as lorazepam is preferred for elderly patients (vs long-acting agents like diazepam) because of its shorter half-life and better side effect profile.² Drowsiness, ataxia, and disinhibition are common side effects of benzodiazepines.

Gabapentin. A pilot study conducted to assess the efficacy of gabapentin (900 mg/d) for the prevention of postoperative delirium found a significantly lower incidence of delirium among patients who received gabapentin compared with placebo. This may be associated with gabapentin’s opioid-sparing effect.⁴⁹ Larger studies are needed to recommend for or against the use of gabapentin in patients receiving opiates.

Further study of the pathophysiology of delirium is needed, as well, to increase our ability to prevent and treat it.

CASE After receiving the IV fluid bolus, Mr. D became increasingly short of breath and required more oxygen to keep his oxygen saturation in the 90s. Labs were ordered during morning rounds, and the patient was found to have urosepsis. He was admitted to the ICU in septic shock, and was intubated and died several days later.

In retrospect, it was determined that Mr. D had developed hypoactive delirium brought on by the infection—and that his somnolence on the second postoperative day was not a sign of overmedication. Had this been recognized early on through the use of an appropriate screening tool, the outcome would likely have been more favorable.

CORRESPONDENCE Abdulraouf Ghandour, MD, Green Meadows Clinic University Physicians, 3217 Providence Road, Columbia, MO 65203; [email protected]

Movement disorders often require consultation with a neurologist, and a working knowledge of established and novel treatments can set the stage for optimal long-term cooperative management.¹ In this article, we review therapeutic options for common movement disorders, including hypokinetic, hyperkinetic, and dyskinetic disturbances.

Parkinson’s disease treatment: MAO-B inhibitor, levodopa are mainstays

Parkinson’s disease, the most common hypokinetic movement disorder, is a chronic, progressive, neurodegenerative disease. It affects 1% of individuals older than 65 years and 4% to 5% of individuals older than 85 years. Its cardinal symptoms are resting tremor, bradykinesia, rigidity, a flexed posture, and loss of postural reflexes. Resting tremor, referred to as “pill rolling” tremor, is 4 to 6 Hz and usually begins unilaterally.^2,3 Associated symptoms can include dystonia, dementia, psychiatric disorders, sleep disorders, and autonomic symptoms.

Neuroprotective therapy is used to slow the progression of the disease, particularly in its early stage. The monoamine oxidase B (MAO-B) inhibitor selegiline has proven effective in this regard² (strength of recommendation [SOR]: A). In randomized controlled studies, selegiline has delayed the need for levodopa for 9 to 12 months⁴ (SOR: A). Another MAO-B inhibitor, rasagiline, has demonstrated neuroprotective effects as well⁵ (SOR: B). These medications may also be used with levodopa for symptom control and as adjuvant therapy in patients with motor fluctuations.² A conventional dose of selegiline is 10 mg/d (5 mg at breakfast; 5 mg at lunch). Rasagiline is given at 1 mg/d. Concomitant use of ciprofloxacin or other CYP1A2 inhibitors limits its effectiveness.^6,7

Symptomatic therapy is indicated at the onset of functional impairment. The dopamine precursor levodopa is the most widely used and effective drug for Parkinson’s disease symptoms, especially bradykinesia and rigidity. Use the lowest possible dose to control symptoms (eg, 100 mg twice daily) and protect against motor complications of the drug^7-9 (SOR: A). To prevent conversion of levodopa to dopamine outside the blood-brain barrier, combine it with the decarboxylase inhibitor carbidopa. Dietary restriction of proteins may be needed, because amino acids can interfere with the absorption of levodopa.

Especially with prolonged use, levodopa can cause disturbing adverse effects, such as nausea, vomiting, psychosis, cardiac arrhythmia, and orthostatic hypotension. Dyskinesias and motor fluctuations are complications of long-term treatment and are irreversible. Adding a cathecol-O-methyltransferase (COMT) inhibitor, such as entacapone, to increase levodopa’s effectiveness has been shown to reduce motor fluctuations^2,3,10 (SOR: B). Dopamine agonists such as bromocriptine, ropinirole, and pramipexole used in early Parkinson’s disease can also reduce dyskinesias and motor fluctuations. Dopamine agonists may be preferred to levodopa in early Parkinson’s disease because they are better tolerated and cause fewer adverse effects. Or they may be used as adjuncts for patients whose response to levodopa is deteriorating or fluctuating^3,7,8 (SOR: B). In advanced disease, motor complications can also be managed by augmenting levodopa therapy with a dopamine agonist, MAO-B inhibitor, or COMT inhibitor^7,8 (SOR: A).

Anticholinergics, mainly benztropine and trihexyphenidyl, may be used as symptomatic treatment, especially in young people with early Parkinson’s disease and severe tremor. However, they are not the first drugs of choice due to limited efficacy and the potential for neuropsychiatric side effects⁸ (SOR: C). Amantadine can reduce dyskinesia in people with advanced Parkinson’s disease⁸ (SOR: C). For patients who have Parkinson’s disease with severe motor complications, intermittent apomorphine injections can help reduce “off time” periods in the daily treatment cycle when the efficacy of drugs wanes⁹ (SOR: B).

Deep brain stimulation of the subthalamic nucleus has only SOR C support for reducing dyskinesias and off time.⁹

Treating nonmotor symptoms of Parkinson’s disease can be challenging. For dementia in these patients, consider cholinesterase inhibitors^6,8 (SOR: C). For depression, selective serotonin reuptake inhibitors are effective^6,8,9 (SOR: C). For psychosis, preferred agents are low-dose clozapine or quetiapine^6,8-10 (SOR: C). Plan for supportive and symptomatic management of constipation, dysphagia, sialorrhea, orthostatic hypotension, sleep disturbances, and urinary urgency.^2,3

Tremor

Tremor is a common form of hyperkinesia, presenting either as a primary disorder or as a symptom of another condition.¹¹ By definition, it is a rhythmical, involuntary, oscillatory movement of 1 or more body parts. Tremors are classified as rest or action tremors, with the latter being further categorized as postural (occurring while the patient maintains a position against gravity) or kinetic (occurring during voluntary movement).^2,10

Physiologic tremor: Pharmacologic Tx is usually not needed
Physiologic tremor is benign, high frequency (8-12 Hz), low amplitude, and postural. An exaggerated form of this tremor may result from anxiety, hyperthyroidism, pheochromocytoma, hypoglycemia, excessive caffeine consumption, fever, withdrawal from opioids and sedatives, and some medications. No drug treatment is necessary unless symptoms become bothersome. Correct the underlying cause or have the patient avoid the triggering factor, and offer reassurance that the condition is not pathological or progressive.^2,12 For anxiety, consider cognitive-behavioral/relaxation therapy or benzodiazepines (if tremor did not result from withdrawal of benzodiazepines) or beta-adrenergic antagonists (eg, propranolol).^12,13

Essential tremor: Try propranolol or primidone first
Essential tremor (ET) is the most common movement disorder. It often results in functional disability and leads to many physical and emotional difficulties. ET is bilateral, usually symmetric (although mild asymmetry is possible), and postural or kinetic, typically affecting hands and forearms. The frequency of ET is 4 to 12 Hz. Cranial musculature may be involved in 30% of cases, affecting the head and voice.³ Prevalence ranges from 4 to 40 cases per 1000 people. The age-adjusted incidence is 17.5/100,000 per year; it peaks during the teen years and the fifth decade.^2,3

Autosomal dominant type of inheritance is common, and a family history of ET is often present, particularly with younger patients. The differential diagnosis includes Parkinson’s disease tremor; dystonic, cerebellar, rubral, and psychogenic tremors; and asterixis.³ Unlike ET, many of these disorders have associated neurologic, psychiatric, or systemic signs.

Treatment with propranolol or primidone is indicated if ET causes functional impairment or social or emotional problems for the patient.^2,3,10,13 Both propranolol and primidone reduce limb tremor^2,10,13 (SOR: B), but only propranolol is approved by the US Food and Drug Administration (FDA) for treatment of ET. Propranolol is more effective for hand and forearm tremor than for head and voice tremor. Start propranolol at 20 to 40 mg twice a day and increase the dose as needed to achieve symptom relief.¹⁴

A maintenance dose of 240 to 320 mg/d may be needed. Major adverse effects are fatigue, sedation, depression, and erectile dysfunction. Contraindications to propranolol include asthma, second-degree atrioventricular block, and insulin-dependent diabetes.

If starting with primidone alone, prescribe at a dose <25 mg at bedtime and increase the dose slowly over several weeks to prevent onset of nausea, vomiting, sedation, confusion, or ataxia. The maximum allowable dose is 750 mg/d in 3 divided doses.¹⁰ Primidone and propranolol may be used in combination to treat limb tremor when monotherapy is insufficient (SOR: B).¹³

Thirty percent of patients with ET will not respond to propranolol or primidone. An alternative choice is the anticonvulsant gabapentin^10,12-14 (SOR: C). However, clinical experience with it is limited. Lethargy, fatigue, decreased libido, dizziness, nervousness, and shortness of breath are adverse effects of gabapentin; they are usually mild and tolerable.¹³ Topiramate is another option that seems to be as effective as gabapentin^10,13 (SOR: C), but studies of long-term outcomes are lacking. Topiramate’s side effects include weight loss and paresthesias. Additionally, alprazolam, clonazepam, clozapine, olanzapine, atenolol, sotalol, nadolol, and nimodipine may reduce limb tremor² (SOR: C). Alcohol reduces tremor amplitude in 50% to 90% of patients, but tremor may worsen after the effect of alcohol has worn off.¹⁵

For patients with essential hand tremor that fails to respond to oral agents, consider botulinum toxin A¹⁶ (SOR: B). However, it is also associated with dose-dependent hand weakness¹⁶ (SOR: C). Botulinum toxin may reduce head and voice tremor¹⁶ (SOR: C), but hoarseness and swallowing difficulties may occur after use for voice tremor.¹⁶

Invasive therapies may benefit patients with refractory tremor. Deep brain stimulation and thalamotomy are highly effective in reducing limb tremor¹³ (SOR: C). Each carries a small risk of major complications. Some deep brain stimulation adverse events may resolve with time. Other adverse events may resolve with adjustment of stimulator settings. No evidence exists for surgical treatment for voice and head tremor or for gamma-knife thalamotomy.¹³

Drug-induced tremor
Drugs with the potential to cause postural tremor, intention tremor, or rest tremor include the following: ¹⁵

• alcohol (chronic)
• amiodarone
• amphetamines
• beta-adrenergic agonists
• caffeine
• calcitonin
• carbamazepine
• cocaine
• cyclosporine
• dopamine
• lithium
• metoclopramide
• neuroleptics
• procainamide
• steroids
• theophylline
• thyroid hormones
• tricyclic antidepressants
• trifluoperazine
• valproic acid

With drug-induced tremor, carefully evaluate a patient’s need for the drug. Discontinue the offending agent if possible, or try lowering the dose.

Psychogenic tremor: A history of somatization is a clue
Psychogenic tremor can occur at rest or during postural or kinetic movement. Clinical features include an abrupt onset, a static course, spontaneous remission, and unclassifiable tremors.¹⁷ Psychogenic tremor increases under direct observation and decreases with distraction. Patients with psychogenic tremor often have a history of somatization.¹⁸ Electrophysiologic testing can help confirm the diagnosis. If remission does not occur spontaneously, patients may find relief with psychotherapy or placebo.¹⁹

Tic disorders: Opt for dopamine receptor blockers

Tics are involuntary or semivoluntary movements or sounds that are sudden, brief, intermittent, repetitive, nonrhythmic, unpredictable, and purposeless. Tics can occur in any part of the body.²⁰

The most common tic disorder is Tourette syndrome—a combination of motor and phonic tics with onset before age 21. It affects approximately 5 to 10 children out of 10,000. Boys are more commonly affected than girls. Attention deficit hyperactivity disorder frequently accompanies this syndrome.²

The goal of treatment with any tic disorder is to improve social functioning, self-esteem, and quality of life. Education and support of patients is important. Tic disorders, including Tourette, rarely require drugs. But if tics become too distressing, first-line treatment would be a dopamine modulator, tetrabenazine, or clonidine. Randomized controlled trials with various neuroleptics have revealed dramatic reductions in tic severity. However, many patients do not tolerate the acute adverse effects (most commonly sedation, weight gain, depression, lethargy, and akathisia), and prolonged treatment confers a small risk of tardive dyskinesia. Behavioral therapy is an important part of management.²⁰

Dopamine-receptor blocking drugs such as haloperidol, pimozide, and fluphenazine are the most effective treatment for tics²⁰ (SOR: B). Tetrabenazine is a promising new dopamine-depleting drug; controlled trials are ongoing^2,20 (SOR: B). Clonidine, an alpha 2-adrenergic agonist, is useful in treating patients with Tourette syndrome, helping to improve sleep and attention^2,21 (SOR: C). Medically refractory motor and disabling phonic tics such as coprolalia can be ameliorated by botulinum toxin injections²¹ (SOR: B). Deep brain stimulation is being used at an increasing rate for medically refractory tics in Tourette syndrome²¹ (SOR: B).

Restless legs syndrome: Dopamine agonists are preferred

Restless legs syndrome (RLS) is a disorder characterized by sensory symptoms and motor disturbances of the legs, mainly during rest. Treatment may not be necessary for patients with mild or sporadic symptoms. For moderate to severe RLS with significant impairment, dopamine agonists are the preferred agents²² (SOR: A). RLS can also occur secondary to such conditions as iron deficiency and uremia, and correction of the underlying disorder is the goal. Prescribe iron replacement for patients with a ferritin level <50 ng/mL²² (SOR: C). Medications known to cause or exacerbate the symptoms of RLS are anti-dopaminergic agents (such as neuroleptics), diphenhydramine, tricyclic antidepressants, alcohol, caffeine, lithium, and beta-blockers. If a patient is taking medications that exacerbate symptoms of RLS, discontinue them and use appropriate substitutes²² (SOR: C).

Myoclonus: Clonazepam for essential disorder

Myoclonus is a brief, sudden, shock-like movement caused by involuntary muscle contractions or lapse of muscle contraction (asterixis). Given the complex origins of myoclonus, multiple drugs may be needed. Essential myoclonus is disabling and can be treated with clonazepam. Start with 0.25 mg orally twice daily, and increase the dosage over 3 days to 1 mg/d²³ (SOR: C). Most cases of myoclonus are secondary due to drugs such as lithium, toxins, advanced liver disease, infections including human immunodeficiency virus, dementia, and brain lesions. Treatment should also address the underlying disorder.^2,23

Chorea

Chorea is an abnormal involuntary movement disorder described as “a state of excessive, spontaneous movements, irregularly timed, nonrepetitive, randomly distributed, and abrupt in character.”²⁴

Treatment of chorea is symptomatic, aiming to reduce morbidity and prevent complications. Haloperidol and fluphenazine are effective but can impair voluntary movements^2,10,25 (SOR: C). The dopamine-depleting drugs reserpine and tetrabenazine are also effective^2,10,25 (SOR: C). GABAergic drugs, such as clonazepam, gabapentin, and valproate, can be used adjunctively.^10,25

Dystonia

Dystonia is a syndrome involving sustained contractions of opposing muscles that cause twisting, repetitive movements and abnormal postures. Primary dystonia can be treated successfully with high doses of trihexyphenidyl alone, starting with 1 mg orally per day and increasing gradually to 6 to 80 mg/d until symptoms are controlled; or in combination with baclofen, starting with 10 mg orally once daily and increasing to a maximum dose of 30 to 120 mg/d^1,2 (SOR: C).

Consider botulinum neurotoxin injection for focal upper extremity dystonia and adductor spasmodic dysphonia¹⁶ (SOR: B).

Ataxia

Ataxia is an unsteady gait associated with cerebellar dysfunction, proprioceptive defects, or both. Ataxia may be primary (Friedreich ataxia and spinocerebellar ataxia) or secondary to stroke, trauma, alcoholic degeneration, multiple sclerosis, vitamin B12 deficiency, and hydrocephalus. Treatment, when possible, should target the underlying cause.^1,2

CORRESPONDENCE Hakan Yaman, MD, Akdeniz University, Department of Family Medicine, Antalya, Turkey 07058; [email protected]

Movement disorders often require consultation with a neurologist, and a working knowledge of established and novel treatments can set the stage for optimal long-term cooperative management.¹ In this article, we review therapeutic options for common movement disorders, including hypokinetic, hyperkinetic, and dyskinetic disturbances.

Parkinson’s disease treatment: MAO-B inhibitor, levodopa are mainstays

Parkinson’s disease, the most common hypokinetic movement disorder, is a chronic, progressive, neurodegenerative disease. It affects 1% of individuals older than 65 years and 4% to 5% of individuals older than 85 years. Its cardinal symptoms are resting tremor, bradykinesia, rigidity, a flexed posture, and loss of postural reflexes. Resting tremor, referred to as “pill rolling” tremor, is 4 to 6 Hz and usually begins unilaterally.^2,3 Associated symptoms can include dystonia, dementia, psychiatric disorders, sleep disorders, and autonomic symptoms.

Neuroprotective therapy is used to slow the progression of the disease, particularly in its early stage. The monoamine oxidase B (MAO-B) inhibitor selegiline has proven effective in this regard² (strength of recommendation [SOR]: A). In randomized controlled studies, selegiline has delayed the need for levodopa for 9 to 12 months⁴ (SOR: A). Another MAO-B inhibitor, rasagiline, has demonstrated neuroprotective effects as well⁵ (SOR: B). These medications may also be used with levodopa for symptom control and as adjuvant therapy in patients with motor fluctuations.² A conventional dose of selegiline is 10 mg/d (5 mg at breakfast; 5 mg at lunch). Rasagiline is given at 1 mg/d. Concomitant use of ciprofloxacin or other CYP1A2 inhibitors limits its effectiveness.^6,7

Symptomatic therapy is indicated at the onset of functional impairment. The dopamine precursor levodopa is the most widely used and effective drug for Parkinson’s disease symptoms, especially bradykinesia and rigidity. Use the lowest possible dose to control symptoms (eg, 100 mg twice daily) and protect against motor complications of the drug^7-9 (SOR: A). To prevent conversion of levodopa to dopamine outside the blood-brain barrier, combine it with the decarboxylase inhibitor carbidopa. Dietary restriction of proteins may be needed, because amino acids can interfere with the absorption of levodopa.

Especially with prolonged use, levodopa can cause disturbing adverse effects, such as nausea, vomiting, psychosis, cardiac arrhythmia, and orthostatic hypotension. Dyskinesias and motor fluctuations are complications of long-term treatment and are irreversible. Adding a cathecol-O-methyltransferase (COMT) inhibitor, such as entacapone, to increase levodopa’s effectiveness has been shown to reduce motor fluctuations^2,3,10 (SOR: B). Dopamine agonists such as bromocriptine, ropinirole, and pramipexole used in early Parkinson’s disease can also reduce dyskinesias and motor fluctuations. Dopamine agonists may be preferred to levodopa in early Parkinson’s disease because they are better tolerated and cause fewer adverse effects. Or they may be used as adjuncts for patients whose response to levodopa is deteriorating or fluctuating^3,7,8 (SOR: B). In advanced disease, motor complications can also be managed by augmenting levodopa therapy with a dopamine agonist, MAO-B inhibitor, or COMT inhibitor^7,8 (SOR: A).

Anticholinergics, mainly benztropine and trihexyphenidyl, may be used as symptomatic treatment, especially in young people with early Parkinson’s disease and severe tremor. However, they are not the first drugs of choice due to limited efficacy and the potential for neuropsychiatric side effects⁸ (SOR: C). Amantadine can reduce dyskinesia in people with advanced Parkinson’s disease⁸ (SOR: C). For patients who have Parkinson’s disease with severe motor complications, intermittent apomorphine injections can help reduce “off time” periods in the daily treatment cycle when the efficacy of drugs wanes⁹ (SOR: B).

Deep brain stimulation of the subthalamic nucleus has only SOR C support for reducing dyskinesias and off time.⁹

Treating nonmotor symptoms of Parkinson’s disease can be challenging. For dementia in these patients, consider cholinesterase inhibitors^6,8 (SOR: C). For depression, selective serotonin reuptake inhibitors are effective^6,8,9 (SOR: C). For psychosis, preferred agents are low-dose clozapine or quetiapine^6,8-10 (SOR: C). Plan for supportive and symptomatic management of constipation, dysphagia, sialorrhea, orthostatic hypotension, sleep disturbances, and urinary urgency.^2,3

Tremor

Tremor is a common form of hyperkinesia, presenting either as a primary disorder or as a symptom of another condition.¹¹ By definition, it is a rhythmical, involuntary, oscillatory movement of 1 or more body parts. Tremors are classified as rest or action tremors, with the latter being further categorized as postural (occurring while the patient maintains a position against gravity) or kinetic (occurring during voluntary movement).^2,10

Physiologic tremor: Pharmacologic Tx is usually not needed
Physiologic tremor is benign, high frequency (8-12 Hz), low amplitude, and postural. An exaggerated form of this tremor may result from anxiety, hyperthyroidism, pheochromocytoma, hypoglycemia, excessive caffeine consumption, fever, withdrawal from opioids and sedatives, and some medications. No drug treatment is necessary unless symptoms become bothersome. Correct the underlying cause or have the patient avoid the triggering factor, and offer reassurance that the condition is not pathological or progressive.^2,12 For anxiety, consider cognitive-behavioral/relaxation therapy or benzodiazepines (if tremor did not result from withdrawal of benzodiazepines) or beta-adrenergic antagonists (eg, propranolol).^12,13

Essential tremor: Try propranolol or primidone first
Essential tremor (ET) is the most common movement disorder. It often results in functional disability and leads to many physical and emotional difficulties. ET is bilateral, usually symmetric (although mild asymmetry is possible), and postural or kinetic, typically affecting hands and forearms. The frequency of ET is 4 to 12 Hz. Cranial musculature may be involved in 30% of cases, affecting the head and voice.³ Prevalence ranges from 4 to 40 cases per 1000 people. The age-adjusted incidence is 17.5/100,000 per year; it peaks during the teen years and the fifth decade.^2,3

Autosomal dominant type of inheritance is common, and a family history of ET is often present, particularly with younger patients. The differential diagnosis includes Parkinson’s disease tremor; dystonic, cerebellar, rubral, and psychogenic tremors; and asterixis.³ Unlike ET, many of these disorders have associated neurologic, psychiatric, or systemic signs.

Treatment with propranolol or primidone is indicated if ET causes functional impairment or social or emotional problems for the patient.^2,3,10,13 Both propranolol and primidone reduce limb tremor^2,10,13 (SOR: B), but only propranolol is approved by the US Food and Drug Administration (FDA) for treatment of ET. Propranolol is more effective for hand and forearm tremor than for head and voice tremor. Start propranolol at 20 to 40 mg twice a day and increase the dose as needed to achieve symptom relief.¹⁴

A maintenance dose of 240 to 320 mg/d may be needed. Major adverse effects are fatigue, sedation, depression, and erectile dysfunction. Contraindications to propranolol include asthma, second-degree atrioventricular block, and insulin-dependent diabetes.

If starting with primidone alone, prescribe at a dose <25 mg at bedtime and increase the dose slowly over several weeks to prevent onset of nausea, vomiting, sedation, confusion, or ataxia. The maximum allowable dose is 750 mg/d in 3 divided doses.¹⁰ Primidone and propranolol may be used in combination to treat limb tremor when monotherapy is insufficient (SOR: B).¹³

Thirty percent of patients with ET will not respond to propranolol or primidone. An alternative choice is the anticonvulsant gabapentin^10,12-14 (SOR: C). However, clinical experience with it is limited. Lethargy, fatigue, decreased libido, dizziness, nervousness, and shortness of breath are adverse effects of gabapentin; they are usually mild and tolerable.¹³ Topiramate is another option that seems to be as effective as gabapentin^10,13 (SOR: C), but studies of long-term outcomes are lacking. Topiramate’s side effects include weight loss and paresthesias. Additionally, alprazolam, clonazepam, clozapine, olanzapine, atenolol, sotalol, nadolol, and nimodipine may reduce limb tremor² (SOR: C). Alcohol reduces tremor amplitude in 50% to 90% of patients, but tremor may worsen after the effect of alcohol has worn off.¹⁵

For patients with essential hand tremor that fails to respond to oral agents, consider botulinum toxin A¹⁶ (SOR: B). However, it is also associated with dose-dependent hand weakness¹⁶ (SOR: C). Botulinum toxin may reduce head and voice tremor¹⁶ (SOR: C), but hoarseness and swallowing difficulties may occur after use for voice tremor.¹⁶

Invasive therapies may benefit patients with refractory tremor. Deep brain stimulation and thalamotomy are highly effective in reducing limb tremor¹³ (SOR: C). Each carries a small risk of major complications. Some deep brain stimulation adverse events may resolve with time. Other adverse events may resolve with adjustment of stimulator settings. No evidence exists for surgical treatment for voice and head tremor or for gamma-knife thalamotomy.¹³

Drug-induced tremor
Drugs with the potential to cause postural tremor, intention tremor, or rest tremor include the following: ¹⁵

• alcohol (chronic)
• amiodarone
• amphetamines
• beta-adrenergic agonists
• caffeine
• calcitonin
• carbamazepine
• cocaine
• cyclosporine
• dopamine
• lithium
• metoclopramide
• neuroleptics
• procainamide
• steroids
• theophylline
• thyroid hormones
• tricyclic antidepressants
• trifluoperazine
• valproic acid

With drug-induced tremor, carefully evaluate a patient’s need for the drug. Discontinue the offending agent if possible, or try lowering the dose.

Psychogenic tremor: A history of somatization is a clue
Psychogenic tremor can occur at rest or during postural or kinetic movement. Clinical features include an abrupt onset, a static course, spontaneous remission, and unclassifiable tremors.¹⁷ Psychogenic tremor increases under direct observation and decreases with distraction. Patients with psychogenic tremor often have a history of somatization.¹⁸ Electrophysiologic testing can help confirm the diagnosis. If remission does not occur spontaneously, patients may find relief with psychotherapy or placebo.¹⁹

Tic disorders: Opt for dopamine receptor blockers

Tics are involuntary or semivoluntary movements or sounds that are sudden, brief, intermittent, repetitive, nonrhythmic, unpredictable, and purposeless. Tics can occur in any part of the body.²⁰

The most common tic disorder is Tourette syndrome—a combination of motor and phonic tics with onset before age 21. It affects approximately 5 to 10 children out of 10,000. Boys are more commonly affected than girls. Attention deficit hyperactivity disorder frequently accompanies this syndrome.²

The goal of treatment with any tic disorder is to improve social functioning, self-esteem, and quality of life. Education and support of patients is important. Tic disorders, including Tourette, rarely require drugs. But if tics become too distressing, first-line treatment would be a dopamine modulator, tetrabenazine, or clonidine. Randomized controlled trials with various neuroleptics have revealed dramatic reductions in tic severity. However, many patients do not tolerate the acute adverse effects (most commonly sedation, weight gain, depression, lethargy, and akathisia), and prolonged treatment confers a small risk of tardive dyskinesia. Behavioral therapy is an important part of management.²⁰

Dopamine-receptor blocking drugs such as haloperidol, pimozide, and fluphenazine are the most effective treatment for tics²⁰ (SOR: B). Tetrabenazine is a promising new dopamine-depleting drug; controlled trials are ongoing^2,20 (SOR: B). Clonidine, an alpha 2-adrenergic agonist, is useful in treating patients with Tourette syndrome, helping to improve sleep and attention^2,21 (SOR: C). Medically refractory motor and disabling phonic tics such as coprolalia can be ameliorated by botulinum toxin injections²¹ (SOR: B). Deep brain stimulation is being used at an increasing rate for medically refractory tics in Tourette syndrome²¹ (SOR: B).

Restless legs syndrome: Dopamine agonists are preferred

Restless legs syndrome (RLS) is a disorder characterized by sensory symptoms and motor disturbances of the legs, mainly during rest. Treatment may not be necessary for patients with mild or sporadic symptoms. For moderate to severe RLS with significant impairment, dopamine agonists are the preferred agents²² (SOR: A). RLS can also occur secondary to such conditions as iron deficiency and uremia, and correction of the underlying disorder is the goal. Prescribe iron replacement for patients with a ferritin level <50 ng/mL²² (SOR: C). Medications known to cause or exacerbate the symptoms of RLS are anti-dopaminergic agents (such as neuroleptics), diphenhydramine, tricyclic antidepressants, alcohol, caffeine, lithium, and beta-blockers. If a patient is taking medications that exacerbate symptoms of RLS, discontinue them and use appropriate substitutes²² (SOR: C).

Myoclonus: Clonazepam for essential disorder

Myoclonus is a brief, sudden, shock-like movement caused by involuntary muscle contractions or lapse of muscle contraction (asterixis). Given the complex origins of myoclonus, multiple drugs may be needed. Essential myoclonus is disabling and can be treated with clonazepam. Start with 0.25 mg orally twice daily, and increase the dosage over 3 days to 1 mg/d²³ (SOR: C). Most cases of myoclonus are secondary due to drugs such as lithium, toxins, advanced liver disease, infections including human immunodeficiency virus, dementia, and brain lesions. Treatment should also address the underlying disorder.^2,23

Chorea

Chorea is an abnormal involuntary movement disorder described as “a state of excessive, spontaneous movements, irregularly timed, nonrepetitive, randomly distributed, and abrupt in character.”²⁴

Treatment of chorea is symptomatic, aiming to reduce morbidity and prevent complications. Haloperidol and fluphenazine are effective but can impair voluntary movements^2,10,25 (SOR: C). The dopamine-depleting drugs reserpine and tetrabenazine are also effective^2,10,25 (SOR: C). GABAergic drugs, such as clonazepam, gabapentin, and valproate, can be used adjunctively.^10,25

Dystonia

Dystonia is a syndrome involving sustained contractions of opposing muscles that cause twisting, repetitive movements and abnormal postures. Primary dystonia can be treated successfully with high doses of trihexyphenidyl alone, starting with 1 mg orally per day and increasing gradually to 6 to 80 mg/d until symptoms are controlled; or in combination with baclofen, starting with 10 mg orally once daily and increasing to a maximum dose of 30 to 120 mg/d^1,2 (SOR: C).

Consider botulinum neurotoxin injection for focal upper extremity dystonia and adductor spasmodic dysphonia¹⁶ (SOR: B).

Ataxia

Ataxia is an unsteady gait associated with cerebellar dysfunction, proprioceptive defects, or both. Ataxia may be primary (Friedreich ataxia and spinocerebellar ataxia) or secondary to stroke, trauma, alcoholic degeneration, multiple sclerosis, vitamin B12 deficiency, and hydrocephalus. Treatment, when possible, should target the underlying cause.^1,2

CORRESPONDENCE Hakan Yaman, MD, Akdeniz University, Department of Family Medicine, Antalya, Turkey 07058; [email protected]

Movement disorders often require consultation with a neurologist, and a working knowledge of established and novel treatments can set the stage for optimal long-term cooperative management.¹ In this article, we review therapeutic options for common movement disorders, including hypokinetic, hyperkinetic, and dyskinetic disturbances.

Parkinson’s disease treatment: MAO-B inhibitor, levodopa are mainstays

Parkinson’s disease, the most common hypokinetic movement disorder, is a chronic, progressive, neurodegenerative disease. It affects 1% of individuals older than 65 years and 4% to 5% of individuals older than 85 years. Its cardinal symptoms are resting tremor, bradykinesia, rigidity, a flexed posture, and loss of postural reflexes. Resting tremor, referred to as “pill rolling” tremor, is 4 to 6 Hz and usually begins unilaterally.^2,3 Associated symptoms can include dystonia, dementia, psychiatric disorders, sleep disorders, and autonomic symptoms.

Neuroprotective therapy is used to slow the progression of the disease, particularly in its early stage. The monoamine oxidase B (MAO-B) inhibitor selegiline has proven effective in this regard² (strength of recommendation [SOR]: A). In randomized controlled studies, selegiline has delayed the need for levodopa for 9 to 12 months⁴ (SOR: A). Another MAO-B inhibitor, rasagiline, has demonstrated neuroprotective effects as well⁵ (SOR: B). These medications may also be used with levodopa for symptom control and as adjuvant therapy in patients with motor fluctuations.² A conventional dose of selegiline is 10 mg/d (5 mg at breakfast; 5 mg at lunch). Rasagiline is given at 1 mg/d. Concomitant use of ciprofloxacin or other CYP1A2 inhibitors limits its effectiveness.^6,7

Symptomatic therapy is indicated at the onset of functional impairment. The dopamine precursor levodopa is the most widely used and effective drug for Parkinson’s disease symptoms, especially bradykinesia and rigidity. Use the lowest possible dose to control symptoms (eg, 100 mg twice daily) and protect against motor complications of the drug^7-9 (SOR: A). To prevent conversion of levodopa to dopamine outside the blood-brain barrier, combine it with the decarboxylase inhibitor carbidopa. Dietary restriction of proteins may be needed, because amino acids can interfere with the absorption of levodopa.

Especially with prolonged use, levodopa can cause disturbing adverse effects, such as nausea, vomiting, psychosis, cardiac arrhythmia, and orthostatic hypotension. Dyskinesias and motor fluctuations are complications of long-term treatment and are irreversible. Adding a cathecol-O-methyltransferase (COMT) inhibitor, such as entacapone, to increase levodopa’s effectiveness has been shown to reduce motor fluctuations^2,3,10 (SOR: B). Dopamine agonists such as bromocriptine, ropinirole, and pramipexole used in early Parkinson’s disease can also reduce dyskinesias and motor fluctuations. Dopamine agonists may be preferred to levodopa in early Parkinson’s disease because they are better tolerated and cause fewer adverse effects. Or they may be used as adjuncts for patients whose response to levodopa is deteriorating or fluctuating^3,7,8 (SOR: B). In advanced disease, motor complications can also be managed by augmenting levodopa therapy with a dopamine agonist, MAO-B inhibitor, or COMT inhibitor^7,8 (SOR: A).

Anticholinergics, mainly benztropine and trihexyphenidyl, may be used as symptomatic treatment, especially in young people with early Parkinson’s disease and severe tremor. However, they are not the first drugs of choice due to limited efficacy and the potential for neuropsychiatric side effects⁸ (SOR: C). Amantadine can reduce dyskinesia in people with advanced Parkinson’s disease⁸ (SOR: C). For patients who have Parkinson’s disease with severe motor complications, intermittent apomorphine injections can help reduce “off time” periods in the daily treatment cycle when the efficacy of drugs wanes⁹ (SOR: B).

Deep brain stimulation of the subthalamic nucleus has only SOR C support for reducing dyskinesias and off time.⁹

Treating nonmotor symptoms of Parkinson’s disease can be challenging. For dementia in these patients, consider cholinesterase inhibitors^6,8 (SOR: C). For depression, selective serotonin reuptake inhibitors are effective^6,8,9 (SOR: C). For psychosis, preferred agents are low-dose clozapine or quetiapine^6,8-10 (SOR: C). Plan for supportive and symptomatic management of constipation, dysphagia, sialorrhea, orthostatic hypotension, sleep disturbances, and urinary urgency.^2,3

Tremor

Tremor is a common form of hyperkinesia, presenting either as a primary disorder or as a symptom of another condition.¹¹ By definition, it is a rhythmical, involuntary, oscillatory movement of 1 or more body parts. Tremors are classified as rest or action tremors, with the latter being further categorized as postural (occurring while the patient maintains a position against gravity) or kinetic (occurring during voluntary movement).^2,10

Physiologic tremor: Pharmacologic Tx is usually not needed
Physiologic tremor is benign, high frequency (8-12 Hz), low amplitude, and postural. An exaggerated form of this tremor may result from anxiety, hyperthyroidism, pheochromocytoma, hypoglycemia, excessive caffeine consumption, fever, withdrawal from opioids and sedatives, and some medications. No drug treatment is necessary unless symptoms become bothersome. Correct the underlying cause or have the patient avoid the triggering factor, and offer reassurance that the condition is not pathological or progressive.^2,12 For anxiety, consider cognitive-behavioral/relaxation therapy or benzodiazepines (if tremor did not result from withdrawal of benzodiazepines) or beta-adrenergic antagonists (eg, propranolol).^12,13

Essential tremor: Try propranolol or primidone first
Essential tremor (ET) is the most common movement disorder. It often results in functional disability and leads to many physical and emotional difficulties. ET is bilateral, usually symmetric (although mild asymmetry is possible), and postural or kinetic, typically affecting hands and forearms. The frequency of ET is 4 to 12 Hz. Cranial musculature may be involved in 30% of cases, affecting the head and voice.³ Prevalence ranges from 4 to 40 cases per 1000 people. The age-adjusted incidence is 17.5/100,000 per year; it peaks during the teen years and the fifth decade.^2,3

Autosomal dominant type of inheritance is common, and a family history of ET is often present, particularly with younger patients. The differential diagnosis includes Parkinson’s disease tremor; dystonic, cerebellar, rubral, and psychogenic tremors; and asterixis.³ Unlike ET, many of these disorders have associated neurologic, psychiatric, or systemic signs.

Treatment with propranolol or primidone is indicated if ET causes functional impairment or social or emotional problems for the patient.^2,3,10,13 Both propranolol and primidone reduce limb tremor^2,10,13 (SOR: B), but only propranolol is approved by the US Food and Drug Administration (FDA) for treatment of ET. Propranolol is more effective for hand and forearm tremor than for head and voice tremor. Start propranolol at 20 to 40 mg twice a day and increase the dose as needed to achieve symptom relief.¹⁴

A maintenance dose of 240 to 320 mg/d may be needed. Major adverse effects are fatigue, sedation, depression, and erectile dysfunction. Contraindications to propranolol include asthma, second-degree atrioventricular block, and insulin-dependent diabetes.

If starting with primidone alone, prescribe at a dose <25 mg at bedtime and increase the dose slowly over several weeks to prevent onset of nausea, vomiting, sedation, confusion, or ataxia. The maximum allowable dose is 750 mg/d in 3 divided doses.¹⁰ Primidone and propranolol may be used in combination to treat limb tremor when monotherapy is insufficient (SOR: B).¹³

Thirty percent of patients with ET will not respond to propranolol or primidone. An alternative choice is the anticonvulsant gabapentin^10,12-14 (SOR: C). However, clinical experience with it is limited. Lethargy, fatigue, decreased libido, dizziness, nervousness, and shortness of breath are adverse effects of gabapentin; they are usually mild and tolerable.¹³ Topiramate is another option that seems to be as effective as gabapentin^10,13 (SOR: C), but studies of long-term outcomes are lacking. Topiramate’s side effects include weight loss and paresthesias. Additionally, alprazolam, clonazepam, clozapine, olanzapine, atenolol, sotalol, nadolol, and nimodipine may reduce limb tremor² (SOR: C). Alcohol reduces tremor amplitude in 50% to 90% of patients, but tremor may worsen after the effect of alcohol has worn off.¹⁵

For patients with essential hand tremor that fails to respond to oral agents, consider botulinum toxin A¹⁶ (SOR: B). However, it is also associated with dose-dependent hand weakness¹⁶ (SOR: C). Botulinum toxin may reduce head and voice tremor¹⁶ (SOR: C), but hoarseness and swallowing difficulties may occur after use for voice tremor.¹⁶

Invasive therapies may benefit patients with refractory tremor. Deep brain stimulation and thalamotomy are highly effective in reducing limb tremor¹³ (SOR: C). Each carries a small risk of major complications. Some deep brain stimulation adverse events may resolve with time. Other adverse events may resolve with adjustment of stimulator settings. No evidence exists for surgical treatment for voice and head tremor or for gamma-knife thalamotomy.¹³

Drug-induced tremor
Drugs with the potential to cause postural tremor, intention tremor, or rest tremor include the following: ¹⁵

• alcohol (chronic)
• amiodarone
• amphetamines
• beta-adrenergic agonists
• caffeine
• calcitonin
• carbamazepine
• cocaine
• cyclosporine
• dopamine
• lithium
• metoclopramide
• neuroleptics
• procainamide
• steroids
• theophylline
• thyroid hormones
• tricyclic antidepressants
• trifluoperazine
• valproic acid

With drug-induced tremor, carefully evaluate a patient’s need for the drug. Discontinue the offending agent if possible, or try lowering the dose.

Psychogenic tremor: A history of somatization is a clue
Psychogenic tremor can occur at rest or during postural or kinetic movement. Clinical features include an abrupt onset, a static course, spontaneous remission, and unclassifiable tremors.¹⁷ Psychogenic tremor increases under direct observation and decreases with distraction. Patients with psychogenic tremor often have a history of somatization.¹⁸ Electrophysiologic testing can help confirm the diagnosis. If remission does not occur spontaneously, patients may find relief with psychotherapy or placebo.¹⁹

Tic disorders: Opt for dopamine receptor blockers

Tics are involuntary or semivoluntary movements or sounds that are sudden, brief, intermittent, repetitive, nonrhythmic, unpredictable, and purposeless. Tics can occur in any part of the body.²⁰

The most common tic disorder is Tourette syndrome—a combination of motor and phonic tics with onset before age 21. It affects approximately 5 to 10 children out of 10,000. Boys are more commonly affected than girls. Attention deficit hyperactivity disorder frequently accompanies this syndrome.²

The goal of treatment with any tic disorder is to improve social functioning, self-esteem, and quality of life. Education and support of patients is important. Tic disorders, including Tourette, rarely require drugs. But if tics become too distressing, first-line treatment would be a dopamine modulator, tetrabenazine, or clonidine. Randomized controlled trials with various neuroleptics have revealed dramatic reductions in tic severity. However, many patients do not tolerate the acute adverse effects (most commonly sedation, weight gain, depression, lethargy, and akathisia), and prolonged treatment confers a small risk of tardive dyskinesia. Behavioral therapy is an important part of management.²⁰

Dopamine-receptor blocking drugs such as haloperidol, pimozide, and fluphenazine are the most effective treatment for tics²⁰ (SOR: B). Tetrabenazine is a promising new dopamine-depleting drug; controlled trials are ongoing^2,20 (SOR: B). Clonidine, an alpha 2-adrenergic agonist, is useful in treating patients with Tourette syndrome, helping to improve sleep and attention^2,21 (SOR: C). Medically refractory motor and disabling phonic tics such as coprolalia can be ameliorated by botulinum toxin injections²¹ (SOR: B). Deep brain stimulation is being used at an increasing rate for medically refractory tics in Tourette syndrome²¹ (SOR: B).

Restless legs syndrome: Dopamine agonists are preferred

Restless legs syndrome (RLS) is a disorder characterized by sensory symptoms and motor disturbances of the legs, mainly during rest. Treatment may not be necessary for patients with mild or sporadic symptoms. For moderate to severe RLS with significant impairment, dopamine agonists are the preferred agents²² (SOR: A). RLS can also occur secondary to such conditions as iron deficiency and uremia, and correction of the underlying disorder is the goal. Prescribe iron replacement for patients with a ferritin level <50 ng/mL²² (SOR: C). Medications known to cause or exacerbate the symptoms of RLS are anti-dopaminergic agents (such as neuroleptics), diphenhydramine, tricyclic antidepressants, alcohol, caffeine, lithium, and beta-blockers. If a patient is taking medications that exacerbate symptoms of RLS, discontinue them and use appropriate substitutes²² (SOR: C).

Myoclonus: Clonazepam for essential disorder

Myoclonus is a brief, sudden, shock-like movement caused by involuntary muscle contractions or lapse of muscle contraction (asterixis). Given the complex origins of myoclonus, multiple drugs may be needed. Essential myoclonus is disabling and can be treated with clonazepam. Start with 0.25 mg orally twice daily, and increase the dosage over 3 days to 1 mg/d²³ (SOR: C). Most cases of myoclonus are secondary due to drugs such as lithium, toxins, advanced liver disease, infections including human immunodeficiency virus, dementia, and brain lesions. Treatment should also address the underlying disorder.^2,23

Chorea

Chorea is an abnormal involuntary movement disorder described as “a state of excessive, spontaneous movements, irregularly timed, nonrepetitive, randomly distributed, and abrupt in character.”²⁴

Treatment of chorea is symptomatic, aiming to reduce morbidity and prevent complications. Haloperidol and fluphenazine are effective but can impair voluntary movements^2,10,25 (SOR: C). The dopamine-depleting drugs reserpine and tetrabenazine are also effective^2,10,25 (SOR: C). GABAergic drugs, such as clonazepam, gabapentin, and valproate, can be used adjunctively.^10,25

Dystonia

Dystonia is a syndrome involving sustained contractions of opposing muscles that cause twisting, repetitive movements and abnormal postures. Primary dystonia can be treated successfully with high doses of trihexyphenidyl alone, starting with 1 mg orally per day and increasing gradually to 6 to 80 mg/d until symptoms are controlled; or in combination with baclofen, starting with 10 mg orally once daily and increasing to a maximum dose of 30 to 120 mg/d^1,2 (SOR: C).

Consider botulinum neurotoxin injection for focal upper extremity dystonia and adductor spasmodic dysphonia¹⁶ (SOR: B).

Ataxia

Ataxia is an unsteady gait associated with cerebellar dysfunction, proprioceptive defects, or both. Ataxia may be primary (Friedreich ataxia and spinocerebellar ataxia) or secondary to stroke, trauma, alcoholic degeneration, multiple sclerosis, vitamin B12 deficiency, and hydrocephalus. Treatment, when possible, should target the underlying cause.^1,2

CORRESPONDENCE Hakan Yaman, MD, Akdeniz University, Department of Family Medicine, Antalya, Turkey 07058; [email protected]

For patients with asthma or chronic obstructive pulmonary disease (COPD), inhalation therapy is the foundation of treatment. Yet all too often, patients don’t get the full value of their inhaled medications because they use their inhaler incorrectly. When technique is markedly flawed, suboptimal outcomes typically result.

Given the number of Americans with asthma (at least 22 million)¹ and COPD (more than 13 million adults),² faulty inhaler technique is a major public health problem. In fact, the number of people suffering from COPD may be even larger: Close to 24 million US adults are believed to have impaired lung function.^3,4 For patients with asthma or COPD—many of whom are treated by family physicians—comprehensive education with a focus on correct use of an inhaler is essential.

In this review, we present evidence of frequent inhaler errors (from clinical studies) and highlight some of the more common mistakes (based on our clinical experience [TABLE]⁵). Finally, we offer ‘‘time-efficient’’ solutions to inhaler problems—steps that physicians in busy primary care practices can take to ensure that patients with asthma or COPD get the maximum benefit from inhalation therapy.

TABLE
Caution patients about these device-specific mistakes*

Inhaler error is well documented

Since 1965, when it was first reported that many patients used metered dose inhalers (MDIs) incorrectly,⁶ evidence has accumulated supporting the magnitude of the problem.^7-12 (Studies conducted in family practice settings are described in “Researchers look at inhaler problems in primary care” and in TABLE W1.^13-20)

Error rates vary widely from one clinical trial to another, depending on study criteria, type of device, and extent of patient education, among other factors. Nonetheless, several studies (spanning 3 decades) found the error rate to be close to, or greater than, 90%.^7,10,21

The most recent of these, published in 2009,²¹ was based on observation of the inhaler technique used by patients with asthma or COPD directly following appointments in an outpatient clinic. The authors found that, although >98% of the study participants claimed to know how to use their inhalers, 94% committed at least one error. In this study and a number of others, user error was more likely in patients using MDIs.^13,18,21,22

Breath-activated dry powder inhalers (DPIs)—such as the Flexhaler, HandiHaler, Aerolizer, and Diskus—also reduce the likelihood of error. DPIs eliminate a step that MDI users often struggle with: the need to simultaneously press down on the canister and begin a slow, deep inhalation.

What’s more, DPIs do not have to be shaken before use. Nonetheless, using a DPI still involves a series of actions. For the HandiHaler and Aerolizer, patients must load the dose, and some patients fail to read the directions and swallow the capsule instead of loading it into the device. Patients must remember to exhale away from the device (ie, not into the dry powder) before inhaling, then hold their breath for approximately 10 seconds. There is potential for error at each step.

Stress the need to exhale before using the inhaler
Forgetting to exhale before inhaling is a common, and significant, mistake regardless of the type of device. It is paramount to stress the need to exhale gently for a few seconds before inhaling (slowly and deeply for patients using an MDI, rapidly and deeply with most DPIs). For MDI users, poor timing, described earlier, is another common and serious mistake. Patients using an MDI with a valved holding chamber sometimes inhale for too long before pressing down on the inhaler, then are unable to continue inhaling although the aerosol is still in the chamber. A common error made by patients using multidose DPIs is simply to forget to load the dose.

Physicians need to brush up on their skills, too

It’s not just patients who lack proficiency in inhaler technique. Numerous studies have demonstrated poor skill among physicians and other health care professionals.^27-34 Evidence also shows that targeted education results in substantial improvement.^32,35

In one study undertaken to evaluate family medicine residents’ proficiency in using asthma inhalers, participants (an intervention group at one clinic and a control group at another) all were given a pretest. The intervention group then received educational materials and a tutorial, as well as the opportunity for hands-on practice, after which both groups were given a post-test. The residents who received the training had a 170% jump, on average, in proficiency score, vs a 55% increase for the control group (P<.001).³⁵

WATCH THE VIDEOS

Inhaled Medication Instructional Videos
Courtesy of: National Jewish Health

Go to http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos

Another study—this one involving first-year interns—looked at level of improvement based on the type of education provided. Initially, only 5% of the interns could use an MDI without error. After a lecture and demonstration, 13% had an error-free technique. But when each intern participated in an intensive one-on-one session, the error-free rate reached 73%. The researchers’ conclusion: Lectures are relatively ineffective in teaching interns inhaler technique compared with a one-on-one approach.³²

The Chicago Breathe Project,³⁶ a new program aimed at improving education in the use of asthma inhalers for physicians and minority patients, provides further evidence of the value of clinician education. After a series of workshops for residents at 5 academic institutions, the physicians’ knowledge of proper use of inhalers rose dramatically—from just 5% preprogram to 91% postprogram (P<.001). Six months after the educational activity, the residents (n=161) were more likely (44% vs 11% preprogram) to assess patients’ inhaler technique.³⁶

Teaching patients when time is tight

National and international guidelines stress the need to teach patients correct use of asthma and COPD inhalers.^1,37,38 Providing the requisite education includes observation of each patient’s inhaler technique with proper use demonstrated, as needed.

The problem, of course, is how to provide that level of patient education within the time constraints of a busy family practice. We recommend these time-efficient solutions:

Enlist the help of other clinicians. While it is important that someone in your office be well trained and able to instruct patients in the proper use of inhalers, that individual need not be you. The National Institutes of Health recommends that the “principal clinician” introduce key educational messages, which can be reinforced and expanded on by other members of the health care team.¹

After you advise patients that it is crucial for them to be trained in and adhere to proper inhaler technique, another health care professional—often a clinic nurse or pharmacist who has had special training—can provide the hands-on education. Studies have shown that when pharmacists who are competent in asthma management, including inhaler technique, work with physicians to optimize the education and overall management of patients with asthma, better outcomes often result, including a reduction in both emergency department visits and hospitalizations.^1,39,40

Use videos to demonstrate correct technique. Videos are an effective teaching tool,⁹ and many of them are device-specific. National Jewish Health, which is world renowned for its asthma care, has a set of instructional videos posted on You-Tube and accessible from its Web site (http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos). In addition to videos that demonstrate the use of an MDI alone and an MDI plus a valved holding chamber, the site has links to 6 DPI videos, each covering a different device.

Use intermittent observation. After the patient views the appropriate video, you or a member of your staff will still need to observe the patient’s inhaler technique to ensure correct use. Ideally, this should occur at every visit.^1,37 When that’s not possible, use intermittent observation, starting with the first 2 or 3 visits after the introduction of inhalation therapy and then switching to periodic observation to ensure that the patient is maintaining good technique.

In determining how often observation is necessary, keep in mind that simply asking patients whether they are having inhaler problems is not sufficient.¹ Patients tend to say they have little or no trouble when, in fact, most struggle, at times, with the devices. What’s more, good technique tends to decrease over time, and repetitive education is important.

To motivate patients, try this communication technique
Motivational interviewing, a technique that has been used to help patients battle obesity, quit smoking, and control hypertension,^41-43 among other health problems, can help you identify inhaler problems that need to be addressed. It involves the use of open-ended questions (eg, “What worries you most about your asthma?”), affirmations (“You’ve done a great job testing your peak flow level every morning”), reflective listening (“You’re tired of taking medicine every day”), and summary statements (“You know you should take your medicine every day but you’re having trouble remembering it. Is that right?”).

A pilot study⁴⁴ showed that when this technique was incorporated into an asthma education session, patient motivation increased. The ratio of perceived advantages vs disadvantages of taking asthma medication correctly improved, as well. Another study⁴⁵ found that when motivational interviewing was used during home visits to inner-city African American adolescents for asthma care, the patients’ motivation, readiness to adhere to treatment, and asthma-related quality of life improved, although self-reported adherence to asthma medication did not. Further studies involving patients with asthma are under way (www.clinicaltrials.gov/ct2/results?term=asthma).

It is important to note that the use of motivational interviewing does not require a lengthy visit. One study found that on average, visits in which primary care physicians used this communication technique lasted less than 10 minutes.⁴⁶

CORRESPONDENCE Timothy H. Self, PharmD, University of Tennessee Health Science Center, 881 Madison Avenue, Room 235, Memphis, TN 38163; [email protected]

For patients with asthma or chronic obstructive pulmonary disease (COPD), inhalation therapy is the foundation of treatment. Yet all too often, patients don’t get the full value of their inhaled medications because they use their inhaler incorrectly. When technique is markedly flawed, suboptimal outcomes typically result.

Given the number of Americans with asthma (at least 22 million)¹ and COPD (more than 13 million adults),² faulty inhaler technique is a major public health problem. In fact, the number of people suffering from COPD may be even larger: Close to 24 million US adults are believed to have impaired lung function.^3,4 For patients with asthma or COPD—many of whom are treated by family physicians—comprehensive education with a focus on correct use of an inhaler is essential.

In this review, we present evidence of frequent inhaler errors (from clinical studies) and highlight some of the more common mistakes (based on our clinical experience [TABLE]⁵). Finally, we offer ‘‘time-efficient’’ solutions to inhaler problems—steps that physicians in busy primary care practices can take to ensure that patients with asthma or COPD get the maximum benefit from inhalation therapy.

TABLE
Caution patients about these device-specific mistakes*

Inhaler error is well documented

Since 1965, when it was first reported that many patients used metered dose inhalers (MDIs) incorrectly,⁶ evidence has accumulated supporting the magnitude of the problem.^7-12 (Studies conducted in family practice settings are described in “Researchers look at inhaler problems in primary care” and in TABLE W1.^13-20)

Error rates vary widely from one clinical trial to another, depending on study criteria, type of device, and extent of patient education, among other factors. Nonetheless, several studies (spanning 3 decades) found the error rate to be close to, or greater than, 90%.^7,10,21

The most recent of these, published in 2009,²¹ was based on observation of the inhaler technique used by patients with asthma or COPD directly following appointments in an outpatient clinic. The authors found that, although >98% of the study participants claimed to know how to use their inhalers, 94% committed at least one error. In this study and a number of others, user error was more likely in patients using MDIs.^13,18,21,22

Breath-activated dry powder inhalers (DPIs)—such as the Flexhaler, HandiHaler, Aerolizer, and Diskus—also reduce the likelihood of error. DPIs eliminate a step that MDI users often struggle with: the need to simultaneously press down on the canister and begin a slow, deep inhalation.

What’s more, DPIs do not have to be shaken before use. Nonetheless, using a DPI still involves a series of actions. For the HandiHaler and Aerolizer, patients must load the dose, and some patients fail to read the directions and swallow the capsule instead of loading it into the device. Patients must remember to exhale away from the device (ie, not into the dry powder) before inhaling, then hold their breath for approximately 10 seconds. There is potential for error at each step.

Stress the need to exhale before using the inhaler
Forgetting to exhale before inhaling is a common, and significant, mistake regardless of the type of device. It is paramount to stress the need to exhale gently for a few seconds before inhaling (slowly and deeply for patients using an MDI, rapidly and deeply with most DPIs). For MDI users, poor timing, described earlier, is another common and serious mistake. Patients using an MDI with a valved holding chamber sometimes inhale for too long before pressing down on the inhaler, then are unable to continue inhaling although the aerosol is still in the chamber. A common error made by patients using multidose DPIs is simply to forget to load the dose.

Physicians need to brush up on their skills, too

It’s not just patients who lack proficiency in inhaler technique. Numerous studies have demonstrated poor skill among physicians and other health care professionals.^27-34 Evidence also shows that targeted education results in substantial improvement.^32,35

In one study undertaken to evaluate family medicine residents’ proficiency in using asthma inhalers, participants (an intervention group at one clinic and a control group at another) all were given a pretest. The intervention group then received educational materials and a tutorial, as well as the opportunity for hands-on practice, after which both groups were given a post-test. The residents who received the training had a 170% jump, on average, in proficiency score, vs a 55% increase for the control group (P<.001).³⁵

WATCH THE VIDEOS

Inhaled Medication Instructional Videos
Courtesy of: National Jewish Health

Go to http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos

Another study—this one involving first-year interns—looked at level of improvement based on the type of education provided. Initially, only 5% of the interns could use an MDI without error. After a lecture and demonstration, 13% had an error-free technique. But when each intern participated in an intensive one-on-one session, the error-free rate reached 73%. The researchers’ conclusion: Lectures are relatively ineffective in teaching interns inhaler technique compared with a one-on-one approach.³²

The Chicago Breathe Project,³⁶ a new program aimed at improving education in the use of asthma inhalers for physicians and minority patients, provides further evidence of the value of clinician education. After a series of workshops for residents at 5 academic institutions, the physicians’ knowledge of proper use of inhalers rose dramatically—from just 5% preprogram to 91% postprogram (P<.001). Six months after the educational activity, the residents (n=161) were more likely (44% vs 11% preprogram) to assess patients’ inhaler technique.³⁶

Teaching patients when time is tight

National and international guidelines stress the need to teach patients correct use of asthma and COPD inhalers.^1,37,38 Providing the requisite education includes observation of each patient’s inhaler technique with proper use demonstrated, as needed.

The problem, of course, is how to provide that level of patient education within the time constraints of a busy family practice. We recommend these time-efficient solutions:

Enlist the help of other clinicians. While it is important that someone in your office be well trained and able to instruct patients in the proper use of inhalers, that individual need not be you. The National Institutes of Health recommends that the “principal clinician” introduce key educational messages, which can be reinforced and expanded on by other members of the health care team.¹

After you advise patients that it is crucial for them to be trained in and adhere to proper inhaler technique, another health care professional—often a clinic nurse or pharmacist who has had special training—can provide the hands-on education. Studies have shown that when pharmacists who are competent in asthma management, including inhaler technique, work with physicians to optimize the education and overall management of patients with asthma, better outcomes often result, including a reduction in both emergency department visits and hospitalizations.^1,39,40

Use videos to demonstrate correct technique. Videos are an effective teaching tool,⁹ and many of them are device-specific. National Jewish Health, which is world renowned for its asthma care, has a set of instructional videos posted on You-Tube and accessible from its Web site (http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos). In addition to videos that demonstrate the use of an MDI alone and an MDI plus a valved holding chamber, the site has links to 6 DPI videos, each covering a different device.

Use intermittent observation. After the patient views the appropriate video, you or a member of your staff will still need to observe the patient’s inhaler technique to ensure correct use. Ideally, this should occur at every visit.^1,37 When that’s not possible, use intermittent observation, starting with the first 2 or 3 visits after the introduction of inhalation therapy and then switching to periodic observation to ensure that the patient is maintaining good technique.

In determining how often observation is necessary, keep in mind that simply asking patients whether they are having inhaler problems is not sufficient.¹ Patients tend to say they have little or no trouble when, in fact, most struggle, at times, with the devices. What’s more, good technique tends to decrease over time, and repetitive education is important.

To motivate patients, try this communication technique
Motivational interviewing, a technique that has been used to help patients battle obesity, quit smoking, and control hypertension,^41-43 among other health problems, can help you identify inhaler problems that need to be addressed. It involves the use of open-ended questions (eg, “What worries you most about your asthma?”), affirmations (“You’ve done a great job testing your peak flow level every morning”), reflective listening (“You’re tired of taking medicine every day”), and summary statements (“You know you should take your medicine every day but you’re having trouble remembering it. Is that right?”).

A pilot study⁴⁴ showed that when this technique was incorporated into an asthma education session, patient motivation increased. The ratio of perceived advantages vs disadvantages of taking asthma medication correctly improved, as well. Another study⁴⁵ found that when motivational interviewing was used during home visits to inner-city African American adolescents for asthma care, the patients’ motivation, readiness to adhere to treatment, and asthma-related quality of life improved, although self-reported adherence to asthma medication did not. Further studies involving patients with asthma are under way (www.clinicaltrials.gov/ct2/results?term=asthma).

It is important to note that the use of motivational interviewing does not require a lengthy visit. One study found that on average, visits in which primary care physicians used this communication technique lasted less than 10 minutes.⁴⁶

CORRESPONDENCE Timothy H. Self, PharmD, University of Tennessee Health Science Center, 881 Madison Avenue, Room 235, Memphis, TN 38163; [email protected]

For patients with asthma or chronic obstructive pulmonary disease (COPD), inhalation therapy is the foundation of treatment. Yet all too often, patients don’t get the full value of their inhaled medications because they use their inhaler incorrectly. When technique is markedly flawed, suboptimal outcomes typically result.

Given the number of Americans with asthma (at least 22 million)¹ and COPD (more than 13 million adults),² faulty inhaler technique is a major public health problem. In fact, the number of people suffering from COPD may be even larger: Close to 24 million US adults are believed to have impaired lung function.^3,4 For patients with asthma or COPD—many of whom are treated by family physicians—comprehensive education with a focus on correct use of an inhaler is essential.

In this review, we present evidence of frequent inhaler errors (from clinical studies) and highlight some of the more common mistakes (based on our clinical experience [TABLE]⁵). Finally, we offer ‘‘time-efficient’’ solutions to inhaler problems—steps that physicians in busy primary care practices can take to ensure that patients with asthma or COPD get the maximum benefit from inhalation therapy.

TABLE
Caution patients about these device-specific mistakes*

Inhaler error is well documented

Since 1965, when it was first reported that many patients used metered dose inhalers (MDIs) incorrectly,⁶ evidence has accumulated supporting the magnitude of the problem.^7-12 (Studies conducted in family practice settings are described in “Researchers look at inhaler problems in primary care” and in TABLE W1.^13-20)

Error rates vary widely from one clinical trial to another, depending on study criteria, type of device, and extent of patient education, among other factors. Nonetheless, several studies (spanning 3 decades) found the error rate to be close to, or greater than, 90%.^7,10,21

The most recent of these, published in 2009,²¹ was based on observation of the inhaler technique used by patients with asthma or COPD directly following appointments in an outpatient clinic. The authors found that, although >98% of the study participants claimed to know how to use their inhalers, 94% committed at least one error. In this study and a number of others, user error was more likely in patients using MDIs.^13,18,21,22

Breath-activated dry powder inhalers (DPIs)—such as the Flexhaler, HandiHaler, Aerolizer, and Diskus—also reduce the likelihood of error. DPIs eliminate a step that MDI users often struggle with: the need to simultaneously press down on the canister and begin a slow, deep inhalation.

What’s more, DPIs do not have to be shaken before use. Nonetheless, using a DPI still involves a series of actions. For the HandiHaler and Aerolizer, patients must load the dose, and some patients fail to read the directions and swallow the capsule instead of loading it into the device. Patients must remember to exhale away from the device (ie, not into the dry powder) before inhaling, then hold their breath for approximately 10 seconds. There is potential for error at each step.

Stress the need to exhale before using the inhaler
Forgetting to exhale before inhaling is a common, and significant, mistake regardless of the type of device. It is paramount to stress the need to exhale gently for a few seconds before inhaling (slowly and deeply for patients using an MDI, rapidly and deeply with most DPIs). For MDI users, poor timing, described earlier, is another common and serious mistake. Patients using an MDI with a valved holding chamber sometimes inhale for too long before pressing down on the inhaler, then are unable to continue inhaling although the aerosol is still in the chamber. A common error made by patients using multidose DPIs is simply to forget to load the dose.

Physicians need to brush up on their skills, too

It’s not just patients who lack proficiency in inhaler technique. Numerous studies have demonstrated poor skill among physicians and other health care professionals.^27-34 Evidence also shows that targeted education results in substantial improvement.^32,35

In one study undertaken to evaluate family medicine residents’ proficiency in using asthma inhalers, participants (an intervention group at one clinic and a control group at another) all were given a pretest. The intervention group then received educational materials and a tutorial, as well as the opportunity for hands-on practice, after which both groups were given a post-test. The residents who received the training had a 170% jump, on average, in proficiency score, vs a 55% increase for the control group (P<.001).³⁵

WATCH THE VIDEOS

Inhaled Medication Instructional Videos
Courtesy of: National Jewish Health

Go to http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos

Another study—this one involving first-year interns—looked at level of improvement based on the type of education provided. Initially, only 5% of the interns could use an MDI without error. After a lecture and demonstration, 13% had an error-free technique. But when each intern participated in an intensive one-on-one session, the error-free rate reached 73%. The researchers’ conclusion: Lectures are relatively ineffective in teaching interns inhaler technique compared with a one-on-one approach.³²

The Chicago Breathe Project,³⁶ a new program aimed at improving education in the use of asthma inhalers for physicians and minority patients, provides further evidence of the value of clinician education. After a series of workshops for residents at 5 academic institutions, the physicians’ knowledge of proper use of inhalers rose dramatically—from just 5% preprogram to 91% postprogram (P<.001). Six months after the educational activity, the residents (n=161) were more likely (44% vs 11% preprogram) to assess patients’ inhaler technique.³⁶

Teaching patients when time is tight

National and international guidelines stress the need to teach patients correct use of asthma and COPD inhalers.^1,37,38 Providing the requisite education includes observation of each patient’s inhaler technique with proper use demonstrated, as needed.

The problem, of course, is how to provide that level of patient education within the time constraints of a busy family practice. We recommend these time-efficient solutions:

Enlist the help of other clinicians. While it is important that someone in your office be well trained and able to instruct patients in the proper use of inhalers, that individual need not be you. The National Institutes of Health recommends that the “principal clinician” introduce key educational messages, which can be reinforced and expanded on by other members of the health care team.¹

After you advise patients that it is crucial for them to be trained in and adhere to proper inhaler technique, another health care professional—often a clinic nurse or pharmacist who has had special training—can provide the hands-on education. Studies have shown that when pharmacists who are competent in asthma management, including inhaler technique, work with physicians to optimize the education and overall management of patients with asthma, better outcomes often result, including a reduction in both emergency department visits and hospitalizations.^1,39,40

Use videos to demonstrate correct technique. Videos are an effective teaching tool,⁹ and many of them are device-specific. National Jewish Health, which is world renowned for its asthma care, has a set of instructional videos posted on You-Tube and accessible from its Web site (http://www.nationaljewish.org/healthinfo/medications/lung-diseases/devices/instructional-videos). In addition to videos that demonstrate the use of an MDI alone and an MDI plus a valved holding chamber, the site has links to 6 DPI videos, each covering a different device.

Use intermittent observation. After the patient views the appropriate video, you or a member of your staff will still need to observe the patient’s inhaler technique to ensure correct use. Ideally, this should occur at every visit.^1,37 When that’s not possible, use intermittent observation, starting with the first 2 or 3 visits after the introduction of inhalation therapy and then switching to periodic observation to ensure that the patient is maintaining good technique.

In determining how often observation is necessary, keep in mind that simply asking patients whether they are having inhaler problems is not sufficient.¹ Patients tend to say they have little or no trouble when, in fact, most struggle, at times, with the devices. What’s more, good technique tends to decrease over time, and repetitive education is important.

To motivate patients, try this communication technique
Motivational interviewing, a technique that has been used to help patients battle obesity, quit smoking, and control hypertension,^41-43 among other health problems, can help you identify inhaler problems that need to be addressed. It involves the use of open-ended questions (eg, “What worries you most about your asthma?”), affirmations (“You’ve done a great job testing your peak flow level every morning”), reflective listening (“You’re tired of taking medicine every day”), and summary statements (“You know you should take your medicine every day but you’re having trouble remembering it. Is that right?”).

A pilot study⁴⁴ showed that when this technique was incorporated into an asthma education session, patient motivation increased. The ratio of perceived advantages vs disadvantages of taking asthma medication correctly improved, as well. Another study⁴⁵ found that when motivational interviewing was used during home visits to inner-city African American adolescents for asthma care, the patients’ motivation, readiness to adhere to treatment, and asthma-related quality of life improved, although self-reported adherence to asthma medication did not. Further studies involving patients with asthma are under way (www.clinicaltrials.gov/ct2/results?term=asthma).

It is important to note that the use of motivational interviewing does not require a lengthy visit. One study found that on average, visits in which primary care physicians used this communication technique lasted less than 10 minutes.⁴⁶

CORRESPONDENCE Timothy H. Self, PharmD, University of Tennessee Health Science Center, 881 Madison Avenue, Room 235, Memphis, TN 38163; [email protected]

Technological developments—most notably, the increasing popularity of social networking sites such as Facebook—have led to a resurgence in the prevalence of bullying.1,2 The unlimited reach and anonymity of “cyber” bullying has introduced new challenges for pediatricians and child psychiatrists. Traditional bullying—defined as a specific form of aggression that is intentional, repeated, and involves a disparity of power between the victim and perpetrators—remains more common, with 54% of middle school students reporting verbal bullying, compared with 14% reporting at least 1 episode of electronic bullying over 2 months.2 Compared with students who weren’t bullied, middle and high school students who were bullied were 3 times more likely to report seriously considering suicide, engaging in intentional self-harm, being physically hurt by a family member, and witnessing violence in their families.3

Although bullying occurs frequently and is closely associated with several psychiatric conditions, including attention-deficit/hyperactivity disorder,⁴ depression,¹ and anxiety,¹ clinicians often don’t thoroughly assess patients to determine if they’ve been bullied and rarely intervene. The mnemonic HURT may aid in the clinical assessment and management of bullied children.

Help empower the child who is being bullied by encouraging him or her to find appropriate help from teachers, school counselors, or other resources, which may decrease the likelihood of psychological and physical consequences.

Understand the risk factors for being bullied, including less parental support,² violent family encounters,³ and obesity,³ that may contribute to a child’s emotional experiences or behavior in ways that make him or her an easy target for bullying.²

Recognize a child who is at risk for being bullied and ask about his or her peer relations at school and use of online social networks. At-risk children warrant further evaluation for depression, anxiety, loneliness, and low self-esteem.

Teach the child why others engage in bullying so he or she may avoid actions and words that instigate or provoke a bully, and discuss techniques for dealing with confrontations.

Disclosures

Dr. Madaan is a consultant for The NOW Coalition for Bipolar Disorder and Avanir Pharmaceuticals and has pending research support from Merck and Otsuka.

Ms. Kepple reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgement

The authors would like to thank Sara Kepple for her assistance with this article.

Technological developments—most notably, the increasing popularity of social networking sites such as Facebook—have led to a resurgence in the prevalence of bullying.1,2 The unlimited reach and anonymity of “cyber” bullying has introduced new challenges for pediatricians and child psychiatrists. Traditional bullying—defined as a specific form of aggression that is intentional, repeated, and involves a disparity of power between the victim and perpetrators—remains more common, with 54% of middle school students reporting verbal bullying, compared with 14% reporting at least 1 episode of electronic bullying over 2 months.2 Compared with students who weren’t bullied, middle and high school students who were bullied were 3 times more likely to report seriously considering suicide, engaging in intentional self-harm, being physically hurt by a family member, and witnessing violence in their families.3

Although bullying occurs frequently and is closely associated with several psychiatric conditions, including attention-deficit/hyperactivity disorder,⁴ depression,¹ and anxiety,¹ clinicians often don’t thoroughly assess patients to determine if they’ve been bullied and rarely intervene. The mnemonic HURT may aid in the clinical assessment and management of bullied children.

Help empower the child who is being bullied by encouraging him or her to find appropriate help from teachers, school counselors, or other resources, which may decrease the likelihood of psychological and physical consequences.

Understand the risk factors for being bullied, including less parental support,² violent family encounters,³ and obesity,³ that may contribute to a child’s emotional experiences or behavior in ways that make him or her an easy target for bullying.²

Recognize a child who is at risk for being bullied and ask about his or her peer relations at school and use of online social networks. At-risk children warrant further evaluation for depression, anxiety, loneliness, and low self-esteem.

Teach the child why others engage in bullying so he or she may avoid actions and words that instigate or provoke a bully, and discuss techniques for dealing with confrontations.

Disclosures

Dr. Madaan is a consultant for The NOW Coalition for Bipolar Disorder and Avanir Pharmaceuticals and has pending research support from Merck and Otsuka.

Ms. Kepple reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgement

The authors would like to thank Sara Kepple for her assistance with this article.

Technological developments—most notably, the increasing popularity of social networking sites such as Facebook—have led to a resurgence in the prevalence of bullying.1,2 The unlimited reach and anonymity of “cyber” bullying has introduced new challenges for pediatricians and child psychiatrists. Traditional bullying—defined as a specific form of aggression that is intentional, repeated, and involves a disparity of power between the victim and perpetrators—remains more common, with 54% of middle school students reporting verbal bullying, compared with 14% reporting at least 1 episode of electronic bullying over 2 months.2 Compared with students who weren’t bullied, middle and high school students who were bullied were 3 times more likely to report seriously considering suicide, engaging in intentional self-harm, being physically hurt by a family member, and witnessing violence in their families.3

Although bullying occurs frequently and is closely associated with several psychiatric conditions, including attention-deficit/hyperactivity disorder,⁴ depression,¹ and anxiety,¹ clinicians often don’t thoroughly assess patients to determine if they’ve been bullied and rarely intervene. The mnemonic HURT may aid in the clinical assessment and management of bullied children.

Help empower the child who is being bullied by encouraging him or her to find appropriate help from teachers, school counselors, or other resources, which may decrease the likelihood of psychological and physical consequences.

Understand the risk factors for being bullied, including less parental support,² violent family encounters,³ and obesity,³ that may contribute to a child’s emotional experiences or behavior in ways that make him or her an easy target for bullying.²

Recognize a child who is at risk for being bullied and ask about his or her peer relations at school and use of online social networks. At-risk children warrant further evaluation for depression, anxiety, loneliness, and low self-esteem.

Teach the child why others engage in bullying so he or she may avoid actions and words that instigate or provoke a bully, and discuss techniques for dealing with confrontations.

Disclosures

Dr. Madaan is a consultant for The NOW Coalition for Bipolar Disorder and Avanir Pharmaceuticals and has pending research support from Merck and Otsuka.

Ms. Kepple reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgement

The authors would like to thank Sara Kepple for her assistance with this article.

Discuss this article at www.facebook.com/CurrentPsychiatry

Xerostomia, commonly known as “dry mouth,” is a reported side effect of >1,800 drugs from >80 classes.¹ This condition often goes unrecognized and untreated, but it can significantly affect patients’ quality of life and cause oral and medical health problems.^2,3 Although psychotropic medications are not the only offenders, they comprise a large portion of the agents that can cause dry mouth. Antidepressants, anticonvulsants, anxiolytics, antipsychotics, anticholinergics, and alpha agonists can cause xerostomia.⁴ The risk of salivary hypofunction increases with polypharmacy and may be especially likely when ≥3 drugs are taken per day.⁵

Among all reported side effects of antidepressants and antipsychotics, dry mouth often is the most prevalent complaint. For example, in a study of 5 antidepressants 35% to 46% of patients reported dry mouth.⁶ Rates are similar in users of various antipsychotics. Patients with severe, persistent mental illness often cite side effects as the primary reason for psychotropic noncompliance.^7-9

Few psychiatrists routinely screen patients for xerostomia, and if a patient reports this side effect, they may be unlikely to address it or understand its implications because of more pressing concerns such as psychosis or risk of suicide. Historically, education in general medical training about the effects of oral health on a patient’s overall health has been limited. It is crucial for psychiatrists to be aware of potential problems related to dry mouth and the impact it can have on their patients. In this article, we:

• describe how dry mouth can impact a patient’s oral, medical, and psychiatric health
• provide psychiatrists with an understanding of pathology related to xerostomia
• explain how psychiatrists can screen for xerostomia
• discuss the benefits patients may receive when psychiatrists collaborate with dental clinicians to manage this condition.

Implications of xerostomia

Saliva provides a protective function. It is an antimicrobial, buffering, and lubricating agent that aids cleansing and removal of food debris within the mouth. It also helps maintain oral mucosa and remineralizing of tooth structure.¹⁰

Psychotropics can affect the amount of saliva secreted and may alter the composition of saliva via their receptor affects on the dual sympathetic and parasympathetic innervations of the salivary glands.¹¹ When the protective environment produced by saliva is altered, patients may start to develop oral problems before experiencing dryness. A 50% reduction in saliva flow may occur before they become aware of the problem.^12,13

Patients may not taste food properly, experience cracked lips, or have trouble eating, oral pain, or dentures that no longer fit well.¹⁴ Additionally, oral diseases such as dental decay and periodontal disease (Photos 1 and 2), inflamed soft tissue, and candidiasis (Photo 3) also may occur.^10,15 Patients may begin to notice dry mouth when they wake at night, which could disrupt sleep. Patients with xerostomia can accumulate excessive amounts of plaque on their teeth and the dorsum of the tongue. The increased bacterial count and release of volatile sulfide gases that occur with dry mouth may explain some cases of halitosis.^16,17 Patients also may have difficulty swallowing or speaking and be unaware of the oral health destruction occurring as a result of reduced saliva. Some experts report oral bacteria levels can skyrocket as much as 10-fold in people who take medications that cause dry mouth.¹⁸

Infections of the mouth can create havoc elsewhere in the body. The evidence base that establishes an association between periodontal disease and other chronic inflammatory conditions such as diabetes, cardiovascular disease, cancer, and rheumatoid arthritis is steadily growing.^19-22 Periodontal disease also is a risk factor for preeclampsia and other illnesses that can negatively affect neonatal health.^23,24

Failure to recognize xerostomia caused by psychotropic medications may lead to an increase in cavities, periodontal disease, and chronic systemic inflammatory conditions that can shorten a patient’s life span. Recognizing and treating causes of xerostomia is vital because doing so may halt this chain of events.

Photo 1
This patient complained of dry mouth and exhibits decay (a) and evidence of periodontal disease. Plaque and calculus is present (b), along with gingival recession from the loss of attachment and bone (c). This patient was taking venlafaxine, zolpidem, and alprazolam

Photo 2
Dental cavities were restored with tooth-colored restorations (arrows) on this patient, who has xerostomia. Every effort must be made to manage this patient’s dry mouth or the restorations may fail due to recurrent decay

Photo 3
This partial denture wearer, who complained of dry mouth, has evidence of palatal irritation and sores as a result of xerostomia and use of a partial denture. This patient was taking bupropion, esomeprazole, and tolterodine

Psychiatric patients’ oral health

Psychiatric patients’ oral health status often is poor. Several studies found that compared with the general population, patients who have severe, persistent mental illness are at higher risk to be missing teeth, schedule fewer visits to the dentist, and neglect oral hygiene.^25-28 Periodontal disease also could be a problem in these patients.²⁹ Although some evidence suggests mental illness may make patients less likely to go to the dentist, psychotropic medications also may contribute to their dental difficulties.

Screening for xerostomia

Simply advising patients of the problems related to xerostomia and asking several questions may help prevent pain and deterioration in function within the oral cavity (Table 1).^14,30

You can perform a simple in-office assessment of the oral cavity by visual inspection and by placing a dry tongue blade against the inside of the cheek mucosa. If the blade sticks to the mucosa and a gentle tug is needed to lift it away, xerostomia may be present.³⁰ Conversely, a healthy mouth will have a collection of saliva on the floor of the oral cavity, and pulling a tongue blade away from the inside of the cheek will not require any effort (Photos 4 and 5).

Table 1

Screening questions for xerostomia

Photo 4
The arrow shows the normal appearance of saliva collecting on the floor of the mouth

Photo 5
This patient complained of dry mouth. Note the floor of the mouth is free of saliva (a). Decay is present (b), and the patient is missing posterior teeth (c). This patient was taking clonidine, metoprolol, hydrochlorothiazide, amlodipine, and irbesartan

Treatment options

Patients who have reduced salivary flow as a result of a medication may become so affected by dryness that their drug regimen may need to be changed. However, the greatest concern is for deteriorating oral health among patients who may be unaware xerostomia is occurring.³¹

Counsel patients who take medications that can affect their salivary function about the importance of seeing a dentist regularly, and provide referrals when appropriate. Depending upon the patient’s oral health, dentists recommend patients with xerostomia have their teeth cleaned/examined 3 or 4 times per year, rather than the 2 times per year allowed by third-party payers (ie, insurance companies). Also advise patients to be diligent in their oral hygiene practices, including flossing and brushing the teeth and tongue, and to avoid foods that are sticky and/or have high sucrose content (Table 2). Recommend using a toothpaste containing fluoride—preferably one free of sodium lauryl sulfate, which could contribute to mouth sores¹⁴—and drinking fluoridated water. Explain to patients that their dentist may recommend in-office high-fluoride applications, high-fluoride prescription toothpaste, and/or “mouth trays” that contain high fluoride gel. Tell patients to avoid cigarettes and caffeinated beverages, which can increase dryness. Alcohol use should be minimized and mouth rinses containing alcohol should not be used.

Many over-the-counter products are available to address xerostomia, including toothpastes, mouth rinses, and gels. Salivary substitutes—which are available as sprays, liquids, tablets, and swab sticks—imitate saliva and may provide a temporary reprieve from dryness. Although none of these products will cure dry mouth, they may help manage the condition. Advise patients to eat foods that stimulate saliva production, such as carrots, apples, and celery, and to chew sugarless gum and candies, which also will stimulate salivary flow.

The FDA has approved 2 prescription drugs for treating xerostomia: cevimeline and pilocarpine. Cevimeline is approved for treating dry mouth associated with Sjögren’s syndrome and pilocarpine is approved for treating dry mouth caused by head and neck radiation therapy; however, these medications’ role in treating dry mouth in psychiatric patients has not been investigated. Both agents are contraindicated in patients with narrow-angle glaucoma, uncontrolled asthma, or liver disease, and should be prescribed with caution for patients with cardiovascular disease, chronic respiratory conditions, or kidney disease.³²

Acupuncture and electrostimulation are being studied as a treatment for xerostomia. Trials have found acupuncture improves symptoms of xerostomia,^33,34 and 1 study found electrostimulation improved xerostomia in patients with Sjögren’s syndrome.³⁵ Both approaches require more study to confirm their effectiveness.^33-35

Table 2

Managing dry mouth: What to tell patients

Related Resources

• Persson K, Axtelius B, Söderfeldt B, et al. Monitoring oral health and dental attendance in an outpatient psychiatric population. J Psychiatr Ment Health Nurs. 2009;16(3):263-271.
• Keene JJ Jr, Galasko GT, Land MF. Antidepressant use in psychiatry and medicine: importance for dental practice. J Am Dent Assoc. 2003;134(1):71-79.

Drug Brand Names

• Alprazolam • Xanax
• Amlodipine • Norvasc
• Bupropion • Wellbutrin, Zyban
• Cevimeline • Evoxac
• Clonidine • Catapres, Kapvay, others
• Esomeprazole • Nexium
• Irbesartan • Avapro
• Metoprolol • Lopressor, Toprol
• Pilocarpine • Salagen
• Tolterodine • Detrol
• Venlafaxine • Effexor
• Zolpidem • Ambien

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Xerostomia, commonly known as “dry mouth,” is a reported side effect of >1,800 drugs from >80 classes.¹ This condition often goes unrecognized and untreated, but it can significantly affect patients’ quality of life and cause oral and medical health problems.^2,3 Although psychotropic medications are not the only offenders, they comprise a large portion of the agents that can cause dry mouth. Antidepressants, anticonvulsants, anxiolytics, antipsychotics, anticholinergics, and alpha agonists can cause xerostomia.⁴ The risk of salivary hypofunction increases with polypharmacy and may be especially likely when ≥3 drugs are taken per day.⁵

Among all reported side effects of antidepressants and antipsychotics, dry mouth often is the most prevalent complaint. For example, in a study of 5 antidepressants 35% to 46% of patients reported dry mouth.⁶ Rates are similar in users of various antipsychotics. Patients with severe, persistent mental illness often cite side effects as the primary reason for psychotropic noncompliance.^7-9

Few psychiatrists routinely screen patients for xerostomia, and if a patient reports this side effect, they may be unlikely to address it or understand its implications because of more pressing concerns such as psychosis or risk of suicide. Historically, education in general medical training about the effects of oral health on a patient’s overall health has been limited. It is crucial for psychiatrists to be aware of potential problems related to dry mouth and the impact it can have on their patients. In this article, we:

• describe how dry mouth can impact a patient’s oral, medical, and psychiatric health
• provide psychiatrists with an understanding of pathology related to xerostomia
• explain how psychiatrists can screen for xerostomia
• discuss the benefits patients may receive when psychiatrists collaborate with dental clinicians to manage this condition.

Implications of xerostomia

Saliva provides a protective function. It is an antimicrobial, buffering, and lubricating agent that aids cleansing and removal of food debris within the mouth. It also helps maintain oral mucosa and remineralizing of tooth structure.¹⁰

Psychotropics can affect the amount of saliva secreted and may alter the composition of saliva via their receptor affects on the dual sympathetic and parasympathetic innervations of the salivary glands.¹¹ When the protective environment produced by saliva is altered, patients may start to develop oral problems before experiencing dryness. A 50% reduction in saliva flow may occur before they become aware of the problem.^12,13

Patients may not taste food properly, experience cracked lips, or have trouble eating, oral pain, or dentures that no longer fit well.¹⁴ Additionally, oral diseases such as dental decay and periodontal disease (Photos 1 and 2), inflamed soft tissue, and candidiasis (Photo 3) also may occur.^10,15 Patients may begin to notice dry mouth when they wake at night, which could disrupt sleep. Patients with xerostomia can accumulate excessive amounts of plaque on their teeth and the dorsum of the tongue. The increased bacterial count and release of volatile sulfide gases that occur with dry mouth may explain some cases of halitosis.^16,17 Patients also may have difficulty swallowing or speaking and be unaware of the oral health destruction occurring as a result of reduced saliva. Some experts report oral bacteria levels can skyrocket as much as 10-fold in people who take medications that cause dry mouth.¹⁸

Infections of the mouth can create havoc elsewhere in the body. The evidence base that establishes an association between periodontal disease and other chronic inflammatory conditions such as diabetes, cardiovascular disease, cancer, and rheumatoid arthritis is steadily growing.^19-22 Periodontal disease also is a risk factor for preeclampsia and other illnesses that can negatively affect neonatal health.^23,24

Failure to recognize xerostomia caused by psychotropic medications may lead to an increase in cavities, periodontal disease, and chronic systemic inflammatory conditions that can shorten a patient’s life span. Recognizing and treating causes of xerostomia is vital because doing so may halt this chain of events.

Photo 1
This patient complained of dry mouth and exhibits decay (a) and evidence of periodontal disease. Plaque and calculus is present (b), along with gingival recession from the loss of attachment and bone (c). This patient was taking venlafaxine, zolpidem, and alprazolam

Photo 2
Dental cavities were restored with tooth-colored restorations (arrows) on this patient, who has xerostomia. Every effort must be made to manage this patient’s dry mouth or the restorations may fail due to recurrent decay

Photo 3
This partial denture wearer, who complained of dry mouth, has evidence of palatal irritation and sores as a result of xerostomia and use of a partial denture. This patient was taking bupropion, esomeprazole, and tolterodine

Psychiatric patients’ oral health

Psychiatric patients’ oral health status often is poor. Several studies found that compared with the general population, patients who have severe, persistent mental illness are at higher risk to be missing teeth, schedule fewer visits to the dentist, and neglect oral hygiene.^25-28 Periodontal disease also could be a problem in these patients.²⁹ Although some evidence suggests mental illness may make patients less likely to go to the dentist, psychotropic medications also may contribute to their dental difficulties.

Screening for xerostomia

Simply advising patients of the problems related to xerostomia and asking several questions may help prevent pain and deterioration in function within the oral cavity (Table 1).^14,30

You can perform a simple in-office assessment of the oral cavity by visual inspection and by placing a dry tongue blade against the inside of the cheek mucosa. If the blade sticks to the mucosa and a gentle tug is needed to lift it away, xerostomia may be present.³⁰ Conversely, a healthy mouth will have a collection of saliva on the floor of the oral cavity, and pulling a tongue blade away from the inside of the cheek will not require any effort (Photos 4 and 5).

Table 1

Screening questions for xerostomia

Photo 4
The arrow shows the normal appearance of saliva collecting on the floor of the mouth

Photo 5
This patient complained of dry mouth. Note the floor of the mouth is free of saliva (a). Decay is present (b), and the patient is missing posterior teeth (c). This patient was taking clonidine, metoprolol, hydrochlorothiazide, amlodipine, and irbesartan

Treatment options

Patients who have reduced salivary flow as a result of a medication may become so affected by dryness that their drug regimen may need to be changed. However, the greatest concern is for deteriorating oral health among patients who may be unaware xerostomia is occurring.³¹

Counsel patients who take medications that can affect their salivary function about the importance of seeing a dentist regularly, and provide referrals when appropriate. Depending upon the patient’s oral health, dentists recommend patients with xerostomia have their teeth cleaned/examined 3 or 4 times per year, rather than the 2 times per year allowed by third-party payers (ie, insurance companies). Also advise patients to be diligent in their oral hygiene practices, including flossing and brushing the teeth and tongue, and to avoid foods that are sticky and/or have high sucrose content (Table 2). Recommend using a toothpaste containing fluoride—preferably one free of sodium lauryl sulfate, which could contribute to mouth sores¹⁴—and drinking fluoridated water. Explain to patients that their dentist may recommend in-office high-fluoride applications, high-fluoride prescription toothpaste, and/or “mouth trays” that contain high fluoride gel. Tell patients to avoid cigarettes and caffeinated beverages, which can increase dryness. Alcohol use should be minimized and mouth rinses containing alcohol should not be used.

Many over-the-counter products are available to address xerostomia, including toothpastes, mouth rinses, and gels. Salivary substitutes—which are available as sprays, liquids, tablets, and swab sticks—imitate saliva and may provide a temporary reprieve from dryness. Although none of these products will cure dry mouth, they may help manage the condition. Advise patients to eat foods that stimulate saliva production, such as carrots, apples, and celery, and to chew sugarless gum and candies, which also will stimulate salivary flow.

The FDA has approved 2 prescription drugs for treating xerostomia: cevimeline and pilocarpine. Cevimeline is approved for treating dry mouth associated with Sjögren’s syndrome and pilocarpine is approved for treating dry mouth caused by head and neck radiation therapy; however, these medications’ role in treating dry mouth in psychiatric patients has not been investigated. Both agents are contraindicated in patients with narrow-angle glaucoma, uncontrolled asthma, or liver disease, and should be prescribed with caution for patients with cardiovascular disease, chronic respiratory conditions, or kidney disease.³²

Acupuncture and electrostimulation are being studied as a treatment for xerostomia. Trials have found acupuncture improves symptoms of xerostomia,^33,34 and 1 study found electrostimulation improved xerostomia in patients with Sjögren’s syndrome.³⁵ Both approaches require more study to confirm their effectiveness.^33-35

Table 2

Managing dry mouth: What to tell patients

Related Resources

• Persson K, Axtelius B, Söderfeldt B, et al. Monitoring oral health and dental attendance in an outpatient psychiatric population. J Psychiatr Ment Health Nurs. 2009;16(3):263-271.
• Keene JJ Jr, Galasko GT, Land MF. Antidepressant use in psychiatry and medicine: importance for dental practice. J Am Dent Assoc. 2003;134(1):71-79.

Drug Brand Names

• Alprazolam • Xanax
• Amlodipine • Norvasc
• Bupropion • Wellbutrin, Zyban
• Cevimeline • Evoxac
• Clonidine • Catapres, Kapvay, others
• Esomeprazole • Nexium
• Irbesartan • Avapro
• Metoprolol • Lopressor, Toprol
• Pilocarpine • Salagen
• Tolterodine • Detrol
• Venlafaxine • Effexor
• Zolpidem • Ambien

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Discuss this article at www.facebook.com/CurrentPsychiatry

Xerostomia, commonly known as “dry mouth,” is a reported side effect of >1,800 drugs from >80 classes.¹ This condition often goes unrecognized and untreated, but it can significantly affect patients’ quality of life and cause oral and medical health problems.^2,3 Although psychotropic medications are not the only offenders, they comprise a large portion of the agents that can cause dry mouth. Antidepressants, anticonvulsants, anxiolytics, antipsychotics, anticholinergics, and alpha agonists can cause xerostomia.⁴ The risk of salivary hypofunction increases with polypharmacy and may be especially likely when ≥3 drugs are taken per day.⁵

Among all reported side effects of antidepressants and antipsychotics, dry mouth often is the most prevalent complaint. For example, in a study of 5 antidepressants 35% to 46% of patients reported dry mouth.⁶ Rates are similar in users of various antipsychotics. Patients with severe, persistent mental illness often cite side effects as the primary reason for psychotropic noncompliance.^7-9

Few psychiatrists routinely screen patients for xerostomia, and if a patient reports this side effect, they may be unlikely to address it or understand its implications because of more pressing concerns such as psychosis or risk of suicide. Historically, education in general medical training about the effects of oral health on a patient’s overall health has been limited. It is crucial for psychiatrists to be aware of potential problems related to dry mouth and the impact it can have on their patients. In this article, we:

• describe how dry mouth can impact a patient’s oral, medical, and psychiatric health
• provide psychiatrists with an understanding of pathology related to xerostomia
• explain how psychiatrists can screen for xerostomia
• discuss the benefits patients may receive when psychiatrists collaborate with dental clinicians to manage this condition.

Implications of xerostomia

Saliva provides a protective function. It is an antimicrobial, buffering, and lubricating agent that aids cleansing and removal of food debris within the mouth. It also helps maintain oral mucosa and remineralizing of tooth structure.¹⁰

Psychotropics can affect the amount of saliva secreted and may alter the composition of saliva via their receptor affects on the dual sympathetic and parasympathetic innervations of the salivary glands.¹¹ When the protective environment produced by saliva is altered, patients may start to develop oral problems before experiencing dryness. A 50% reduction in saliva flow may occur before they become aware of the problem.^12,13

Patients may not taste food properly, experience cracked lips, or have trouble eating, oral pain, or dentures that no longer fit well.¹⁴ Additionally, oral diseases such as dental decay and periodontal disease (Photos 1 and 2), inflamed soft tissue, and candidiasis (Photo 3) also may occur.^10,15 Patients may begin to notice dry mouth when they wake at night, which could disrupt sleep. Patients with xerostomia can accumulate excessive amounts of plaque on their teeth and the dorsum of the tongue. The increased bacterial count and release of volatile sulfide gases that occur with dry mouth may explain some cases of halitosis.^16,17 Patients also may have difficulty swallowing or speaking and be unaware of the oral health destruction occurring as a result of reduced saliva. Some experts report oral bacteria levels can skyrocket as much as 10-fold in people who take medications that cause dry mouth.¹⁸

Infections of the mouth can create havoc elsewhere in the body. The evidence base that establishes an association between periodontal disease and other chronic inflammatory conditions such as diabetes, cardiovascular disease, cancer, and rheumatoid arthritis is steadily growing.^19-22 Periodontal disease also is a risk factor for preeclampsia and other illnesses that can negatively affect neonatal health.^23,24

Failure to recognize xerostomia caused by psychotropic medications may lead to an increase in cavities, periodontal disease, and chronic systemic inflammatory conditions that can shorten a patient’s life span. Recognizing and treating causes of xerostomia is vital because doing so may halt this chain of events.

Photo 1
This patient complained of dry mouth and exhibits decay (a) and evidence of periodontal disease. Plaque and calculus is present (b), along with gingival recession from the loss of attachment and bone (c). This patient was taking venlafaxine, zolpidem, and alprazolam

Photo 2
Dental cavities were restored with tooth-colored restorations (arrows) on this patient, who has xerostomia. Every effort must be made to manage this patient’s dry mouth or the restorations may fail due to recurrent decay

Photo 3
This partial denture wearer, who complained of dry mouth, has evidence of palatal irritation and sores as a result of xerostomia and use of a partial denture. This patient was taking bupropion, esomeprazole, and tolterodine

Psychiatric patients’ oral health

Psychiatric patients’ oral health status often is poor. Several studies found that compared with the general population, patients who have severe, persistent mental illness are at higher risk to be missing teeth, schedule fewer visits to the dentist, and neglect oral hygiene.^25-28 Periodontal disease also could be a problem in these patients.²⁹ Although some evidence suggests mental illness may make patients less likely to go to the dentist, psychotropic medications also may contribute to their dental difficulties.

Screening for xerostomia

Simply advising patients of the problems related to xerostomia and asking several questions may help prevent pain and deterioration in function within the oral cavity (Table 1).^14,30

You can perform a simple in-office assessment of the oral cavity by visual inspection and by placing a dry tongue blade against the inside of the cheek mucosa. If the blade sticks to the mucosa and a gentle tug is needed to lift it away, xerostomia may be present.³⁰ Conversely, a healthy mouth will have a collection of saliva on the floor of the oral cavity, and pulling a tongue blade away from the inside of the cheek will not require any effort (Photos 4 and 5).

Table 1

Screening questions for xerostomia

Photo 4
The arrow shows the normal appearance of saliva collecting on the floor of the mouth

Photo 5
This patient complained of dry mouth. Note the floor of the mouth is free of saliva (a). Decay is present (b), and the patient is missing posterior teeth (c). This patient was taking clonidine, metoprolol, hydrochlorothiazide, amlodipine, and irbesartan

Treatment options

Patients who have reduced salivary flow as a result of a medication may become so affected by dryness that their drug regimen may need to be changed. However, the greatest concern is for deteriorating oral health among patients who may be unaware xerostomia is occurring.³¹

Counsel patients who take medications that can affect their salivary function about the importance of seeing a dentist regularly, and provide referrals when appropriate. Depending upon the patient’s oral health, dentists recommend patients with xerostomia have their teeth cleaned/examined 3 or 4 times per year, rather than the 2 times per year allowed by third-party payers (ie, insurance companies). Also advise patients to be diligent in their oral hygiene practices, including flossing and brushing the teeth and tongue, and to avoid foods that are sticky and/or have high sucrose content (Table 2). Recommend using a toothpaste containing fluoride—preferably one free of sodium lauryl sulfate, which could contribute to mouth sores¹⁴—and drinking fluoridated water. Explain to patients that their dentist may recommend in-office high-fluoride applications, high-fluoride prescription toothpaste, and/or “mouth trays” that contain high fluoride gel. Tell patients to avoid cigarettes and caffeinated beverages, which can increase dryness. Alcohol use should be minimized and mouth rinses containing alcohol should not be used.

Many over-the-counter products are available to address xerostomia, including toothpastes, mouth rinses, and gels. Salivary substitutes—which are available as sprays, liquids, tablets, and swab sticks—imitate saliva and may provide a temporary reprieve from dryness. Although none of these products will cure dry mouth, they may help manage the condition. Advise patients to eat foods that stimulate saliva production, such as carrots, apples, and celery, and to chew sugarless gum and candies, which also will stimulate salivary flow.

The FDA has approved 2 prescription drugs for treating xerostomia: cevimeline and pilocarpine. Cevimeline is approved for treating dry mouth associated with Sjögren’s syndrome and pilocarpine is approved for treating dry mouth caused by head and neck radiation therapy; however, these medications’ role in treating dry mouth in psychiatric patients has not been investigated. Both agents are contraindicated in patients with narrow-angle glaucoma, uncontrolled asthma, or liver disease, and should be prescribed with caution for patients with cardiovascular disease, chronic respiratory conditions, or kidney disease.³²

Acupuncture and electrostimulation are being studied as a treatment for xerostomia. Trials have found acupuncture improves symptoms of xerostomia,^33,34 and 1 study found electrostimulation improved xerostomia in patients with Sjögren’s syndrome.³⁵ Both approaches require more study to confirm their effectiveness.^33-35

Table 2

Managing dry mouth: What to tell patients

Related Resources

• Persson K, Axtelius B, Söderfeldt B, et al. Monitoring oral health and dental attendance in an outpatient psychiatric population. J Psychiatr Ment Health Nurs. 2009;16(3):263-271.
• Keene JJ Jr, Galasko GT, Land MF. Antidepressant use in psychiatry and medicine: importance for dental practice. J Am Dent Assoc. 2003;134(1):71-79.

Drug Brand Names

• Alprazolam • Xanax
• Amlodipine • Norvasc
• Bupropion • Wellbutrin, Zyban
• Cevimeline • Evoxac
• Clonidine • Catapres, Kapvay, others
• Esomeprazole • Nexium
• Irbesartan • Avapro
• Metoprolol • Lopressor, Toprol
• Pilocarpine • Salagen
• Tolterodine • Detrol
• Venlafaxine • Effexor
• Zolpidem • Ambien

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dear Dr. Mossman:

I practice in a region with few psychiatrists and very little public transportation. For many patients, coming to my office is inconvenient, expensive, or time-consuming. Sometimes, their emotional problems make it hard for them to travel, and sometimes, bad weather makes travel difficult. I am considering providing remote treatment via Skype. Is this a reasonable idea? What are the risks of using this technology in my practice? — Submitted by “Dr. A”

Diagnosing and treating patients without a face-to-face encounter is not new. Doctors have provided “remote treatment” since shortly after telephones were invented.¹ Until recently, however, forensic psychiatrists advised colleagues not to diagnose patients or start treatment based on phone contact alone.²

The Internet has revolutionized our attitudes about many things. Communication technologies that seemed miraculous a generation ago have become commonplace and have transformed standards for ordinary and “acceptable” human contact. A quick Internet search of “telephone psychotherapy” turns up hundreds of mental health professionals who offer remote treatment services to patients via computers and Web cams.

Physicians in many specialties practice telemedicine, often with the support and encouragement of state governments and third-party payers. To decide whether to include telepsychiatry in your psychiatric practice, you should know:

• what “telemedicine” means and includes
• the possible advantages of offering remote health care
• potential risks and ambiguity about legal matters.

Defining telemedicine

Studies of remote, closed-circuit “telediagnosis” extend back more than 4 decades, closely following mid-20^th century advancements in audio and video relay technologies that made space broadcasts possible.³ Then as now, “telemedicine” simply means conveying health-related information from 1 site to another for diagnostic or treatment purposes.⁴ It’s an adaptation of available technology to deliver care more easily, with the goal of improving patients’ access to care and health status.

Telemedicine usage accelerated as the Internet and related technologies developed. Telemedicine programs in the United States increased by 1,500% from 1993 to 1998.⁴ Telemedicine use has grown 10% annually in recent years and has become a $4 billion per year industry in the United States.⁵ Recently enacted federal legislation is likely to extend health care coverage to 36 million Americans and require coverage of pre-existing conditions. To make these changes affordable, health care delivery will need to exploit new, efficiency-enhancing technologies.⁶

Advantages of telemedicine

State governments and some third-party payers have recognized that telemedicine can overcome geographic and cost barriers to health services and patient education.^5,7-9 Although closed-circuit video transmission has served this purpose for some time, Skype—free software that allows individuals to make video phone calls over the Internet using their computers—is an option that doctors are using to treat patients.^10-12

Research suggests that telepsychiatry may provide huge benefits to medically underserved areas while reducing health care costs.⁴ Telepsychiatry can reduce travel time and expenses for professionals and patients, and it also may lower wait times and “no-show” rates (Table 1).⁴ Telepsychiatry lets patients see caregivers when winter weather makes roads unsafe. It may allow geriatric patients who can no longer drive to access psychiatric care and it lowers health care’s “carbon footprint,” making it “eco-friendly.”¹³

Social media strategies are playing an expanding role in medical education,^14,15 and this probably will help practitioners feel more at ease about incorporating the underlying technologies into work with patients. Increased use of laptops and mobile phones lends itself well to telepsychiatry applications,¹³ and studies have examined the feasibility of psychotherapies delivered via remote communication devices.¹⁶ Smartphone apps are being designed to assist mental health professionals¹⁷ and consumers.¹⁸

Table 1

Potential benefits of telemedicine

Potential pitfalls and drawbacks

Although convenience, access, cost, and fossil fuel savings may favor video-chat doctor visits, telemedicine has downsides, some of which apply specifically to psychiatry. First, no current technology provides psychiatrists with “the rich multidimensional aspects of a person-to-person encounter,”¹⁹ and remote communication may change what patients tell us, how they feel when they tell us things, and how they feel when we respond. Often, an inherent awkwardness affects many forms of Internet communication.²⁰

Also uncertain is whether Skype is compliant with the Health Insurance Portability and Accountability Act and protects doctor-patient privacy well enough to satisfy ethical standards—although it probably is far better than e-mail in this regard. Third-party payers often will not reimburse for telephone calls and may balk at paying for Skype-based therapy, even in states that require insurers to reimburse for telemedicine.

Psychiatrists typically have limited physical contact with patients, but we often check weight and vital signs when we prescribe certain psychotropic medications. Results from home- and drugstore-based blood pressure monitors may not be accurate enough for treatment purposes. Remote communication also reduces the quality of visual information,²⁰ which can be crucial—for example, when good lighting and visual resolution is needed to decide whether a skin rash might be drug-induced.

Telemedicine raises concerns about licensure and meeting adequate standards of care. Medical care usually is deemed to have occurred in the state where the patient is located. For example, only physicians licensed to practice medicine in California are legally permitted to treat patients in California. As is the case with any treatment, care delivered via telemedicine must include appropriate patient examination and diagnosis.²¹

Help and guidance

Despite these potential drawbacks, many state agencies recognize the promise of telemedicine, and have developed networks to promote it (Table 2).^7-9,22,23 These networks have various goals but share a common pattern of establishing infrastructure, policies, and organized results. In the future, states may adopt laws or regulations that address conflicts in malpractice standards and liability coverage, licensing, accreditation, reimbursement, privacy, and data protection policies that now may impede or inhibit use of telepsychiatric services across jurisdictional boundaries. Last year, Ohio produced regulations to guide psychiatrists in prescribing medication remotely without an in-person examination. The University of Hawaii suggested steps that its state legislature might take to help providers predict the potential legal ramifications of telemedicine.⁶

Further help for telepsychiatry practitioners may be found in practice standards and guidelines developed by the American Telemedicine Association.^24,25 These documents gave guidance and support for the practice of telemedicine and for providing appropriate telepsychiatry health services.

Table 2

Telemedicine services available in different states

What should Dr. A do?

In answer to Dr. A’s question, many factors favor including telepsychiatry in her practice. Yet we know little about the accuracy and reliability of psychiatric assessments made solely via Skype or other remote video technology in ordinary practice. Legislation and legal rules about acceptable practices are ambiguous, although in the absence of clear guidance, psychiatrists should assume that all usual professional standards and expectations about adequate care apply to treatment via Skype or other remote communication methods.

Related Resources

• Skype. www.skype.com.
• American Telemedicine Association. www.americantelemed.org.