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Although the peak age of onset of bipolar disorder (BD) is between 20 and 40 years,1 some patients develop BD later in life. The International Society for Bipolar Disorders Task Force has classified the illness into 3 categories:
- early-onset bipolar disorder (EOBD), in which the first manic episode occurs before age 40
- late-onset bipolar disorder (LOBD), in which the initial manic/hypomanic episode occurs after age 50
- older-age bipolar disorder (OABD), in which the first manic/hypomanic episode occurs after age 60.2
OABD represents 25% of the population with BD.3 OABD differs from EOBD in its clinical presentation, biological factors, and psychiatric and somatic comorbidities.4 Studies suggest OABD warrants a more extensive workup to rule out organic causes because symptoms are often attributable to a variety of organic etiologies.
This article describes 3 cases of OABD, including treatments and outcomes. We discuss general treatment recommendations for patients with OABD as cited in the literature. Further research is needed to expand our ability to better care for this unique population.
CASE 1
Mr. D was a 66-year-old African American male with no psychiatric history. His medical history was significant for hypertension, poorly controlled diabetes mellitus, and chronic kidney disease. One year ago, he was diagnosed with cholangiocarcinoma, and underwent uncomplicated right trisegmentectomy, resection of extrahepatic biliary tree, and complete portal lymphadenectomy, with Roux-en-Y hepaticojejunostomy to 2 intrahepatic ducts. He presented to the emergency department (ED) with disorganized behavior for 3 weeks. During that time, Mr. D reported increased distractibility, irritability, hyper-religiosity, racing thoughts, decreased appetite, and decreased need for sleep. There was no pertinent family history.
On mental status examination, Mr. D was agitated, noncooperative, and guarded. His speech was loud and pressured. Mr. D was distractible, tangential, and goal-directed. His Young Mania Rating Scale (YMRS) score was 31, which is highly indicative of mania.5 Computed tomography (CT) scan of the head (Figure 1)
CASE 2
Mr. M was a 63-year-old African American male with no psychiatric history and a medical history significant for hypertension and hypercholesterolemia. He presented to the ED with behavioral changes for 2 weeks. During this time, he experienced decreased need for sleep, agitation, excessive spending, self-conversing, hypersexuality, and paranoia. His family history was significant for schizoaffective disorder, bipolar type.
A mental status examination revealed pressured speech, grandiose delusions, hyper-religiosity, flight of ideas, looseness of association, auditory hallucinations, and tangential thought processes. Mr. M’s initial YMRS score was 56. A CT scan of the head revealed no acute abnormality, but MRI of the brain (Figure 2) showed chronic microvascular ischemic change. Mr. M was diagnosed with bipolar I disorder and admitted. He was started on quetiapine extended release, which was titrated to 600 mg nightly. Divalproex sodium extended release was titrated to 1,500 mg nightly, with subsequent improvement. At discharge, his YMRS score was 15.
Continue to: CASE 3
CASE 3
Ms. F was a 69-year-old White female with no psychiatric history. Her medical history was significant for hypertension, osteoarthritis, and stage III-C ovarian adenocarcinoma with a debulking surgical procedure 5 years earlier. After that, she received adjuvant therapy with paclitaxel and carboplatin, which resulted in a 10-month disease-free interval. Subsequent progression led to cycles of doxorubicin liposomal and gemcitabine. She was in remission until 1 week earlier, when a CT scan of the abdomen/pelvis showed recurrence. She presented to the hospital after disrobing in the street due to hyper-religiosity and divine instruction. She endorsed elevated mood and increased energy despite sleeping only 2 hours daily. Her family psychiatric history was significant for her daughter’s suicide attempt.
A mental status examination revealed disorganized behavior and agitation. Her speech was loud and pressured. She described a “great” mood with congruent affect. Her thought process was circumstantial and illogical. She displayed flight of ideas, grandiose delusions, and paranoia. Ms. F’s initial YMRS score was 38. Vital signs were significant for an elevated blood pressure of 153/113 mm Hg. A CT scan of the head (Figure 3) showed age-related change with no acute findings. Ms. F was admitted with a diagnosis of bipolar I disorder and prescribed olanzapine, 2.5 mg nightly. Due to continued manic symptoms, olanzapine was discontinued, and Ms. F was started on quetiapine, 300 mg nightly, with subsequent improvement. At discharge, her YMRS score was 10.
Differences between EOBD and OABD
BD has always been considered a multi-system illness; however, comorbidity is much more common in OABD than in EOBD. Comorbid conditions are 3 to 4 times more common in patients with OABD.2 Common comorbidities include metabolic syndrome, allergic rhinitis, arthritis, asthma, and cardiovascular disease.
Compared with younger individuals, older patients with BD score lower on the YMRS in the areas of increased activity-energy, language-thought disorder, and sexual interest.6 Psychotic symptoms are less common or less severe in OABD. Although symptom severity is lower, the prevalence of rapid cycling illness is 20% higher in patients with OABD.6 OABD is less commonly associated with a family history.7 This may suggest a difference from the popular genetic component typically found in patients with EOBD.
Cognitive impairment is more commonly found in OABD. Patients with OABD suffer from neuropsychological deficits even during euthymic phases.8 While these deficits may also be found in patients with EOBD, compared with younger patients, older adults are more susceptible to accelerated decline in cognition. OABD can first present within the context of cardiovascular or neuropsychological impairment. It has also been linked to a greater prevalence of white matter hyperintensities compared with EOBD.9,10
Continue to: Treatment is not specific to OABD
Treatment is not specific to OABD
No established treatment guidelines specifically address OABD. It has been treated similarly to EOBD, with antipsychotics, mood stabilizers, antidepressants, and electroconvulsive therapy (ECT). Although lithium is effective, special precautions should be taken when prescribing it to older adults because these patients may be more sensitive to adverse events.11 Drug–drug interactions may also be more likely due to concomitant use of medications for common medical issues such as hypertension.
Treatment with antipsychotics in older patients carries risks. Use of antipsychotics may result in higher rates of morbidity and mortality related to cardiovascular, metabolic, and infectious etiologies. Some literature recommends the use of antipsychotics for OABD; however, the potential benefits must outweigh the risks.6 Monotherapy followed by combination therapy has demonstrated effectiveness in OABD.11 Because symptoms of OABD are often less severe, it may be best to avoid maintenance antipsychotic therapy when possible. With a higher prevalence of depressed mood following manic episodes, use of antidepressant therapy is common in OABD.6 ECT should be considered for patients with treatment-refractory BD.11
Lessons from our case series
Our case series included 3 patients with OABD. These patients’ comorbid conditions included hypertension, hypercholesteremia, and diabetes mellitus. Two patients had a history of cancer, but there was no metastasis to the brain in either case. However, we considered the possibility of structural changes in the brain or cognitive impairment secondary to cancer or its treatment. A literature review confirmed that adult patients treated for noncentral nervous system cancer experienced cancer-related cognitive impairment (CRCI).12 New research suggests that CRCI could be related to altered neuronal integrity along with a disturbance of brain structure networks that process and integrate information.13
We used the YMRS to compare symptom severity and treatment response (Figure 4). Two patients were treated with atypical antipsychotics with a mood stabilizer, and the third patient was prescribed an antipsychotic only. We avoided lithium and carbamazepine as mood stabilizers due to their adverse effect profiles and potential for drug–drug interactions. Each patient responded well to treatment without adverse events.
Future studies are needed to clearly define the safest and most effective treatment guidelines in patients with OABD. We believe that OABD may require the development of a unique treatment algorithm due to the high likelihood of medical comorbidity and age-related variations in treatment response.
Continue to: Etiology of OABD may be different
Etiology of OABD may be different
OABD may be associated with manic presentations and vascular risk factors. MRI imaging that found more white matter hyperintensities and cerebrovascular lesions in patients with OABD compared with younger patients provides evidence of possible differing etiologies.14 Cassidy and Carroll15 found a higher incidence of smoking, hypertension, diabetes mellitus, coronary heart disease, and atrial fibrillation in patients in the older onset group. Bellivier et al16 proposed 3 subgroups of bipolar I disorder; the late-onset subgroup’s etiology was multifactorial. EOBD and OABD subgroups have similar gender ratios,17 first-episode descriptions, and alcohol use rates; however, OABD subgroups have more neurological comorbidity, lesser severe psychosis, and less genetic predisposition.
Although 25% of BD cases are late onset,3 there is still little consensus regarding subgroups and etiological causes. Therefore, additional research specifically focusing on vascular risks may provide much-needed information. Controlling and mitigating vascular risks in OABD may affect its development and course. Despite debated etiologies, the treatment of BD remains consistent, with anticonvulsants preferred over lithium in older individuals.
The Table summarizes clinical pearls about the features and treatment of OABD.
Bottom Line
Compared with younger patients with bipolar disorder (BD), those who develop BD later in life may be more likely to have rapid cycling, medical comorbidities, and cognitive impairment. Older patients with BD also may be more likely to experience adverse effects of the medications commonly used to treat BD, including antipsychotics, lithium, and carbamazepine.
Related Resources
- Carlino AR, Stinnett JL, Kim DR. New onset of bipolar disorder in late life. Psychosomatics. 2013;54(1):94-97.
- Sajatovic M, Kales HC, Mulsant BH. Prescribing antipsychotics in geriatric patients: Focus on schizophrenia and bipolar disorder. Current Psychiatry. 2017;16(10):20-26,28.
Drug Brand Names
Carbamazepine • Carbatrol, Tegretol
Carboplatin • Paraplatin
Divalproex sodium • Depakote
Doxorubicin liposome injection • Doxil
Gemcitabine injection • Gemzar
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Paclitaxel injection • Abraxane
Quetiapine • Seroquel
1. Prabhakar D, Balon R. Late-onset bipolar disorder: a case for careful appraisal. Psychiatry (Edgmont). 2010;7(1):34-37.
2. Sajatovic M, Strejilevich SA, Gildengers AG, et al. A report on older-age bipolar disorder from the International Society for Bipolar Disorders Task Force. Bipolar Disord. 2015;17(7):689-704.
3. Arciniegas DB. New-onset bipolar disorder in late life: a case of mistaken identity. Am J Psychiatry. 2006;163(2):198-203.
4. Chou P-H, Tseng W-J, Chen L-M, et al. Late onset bipolar disorder: a case report and review of the literature. Journal of Clinical Gerontology and Geriatrics. 2015;6(1):27-29.
5. Lukasiewicz M, Gerard S, Besnard A, et al; Emblem Study Group. Young Mania Rating Scale: how to interpret the numbers? Determination of a severity threshold and of the minimal clinically significant difference in the EMBLEM cohort. Int J Methods Psychiatr Res. 2013;22(1):46-58.
6. Oostervink F, Boomsma MM, Nolen WA; EMBLEM Advisory Board. Bipolar disorder in the elderly; different effects of age and of age of onset. J Affect Disord. 2009;116(3):176-183.
7. Depp CA, Jeste D V. Bipolar disorder in older adults: A critical review. Bipolar Disord. 2004;6(5):343-367.8.
8. Gildengers AG, Butters MA, et al. Cognitive functioning in late-life bipolar disorder. Am J Psychiatry. 2004. doi:10.1176/appi.ajp.161.4.736
9. Steffens DC, Krishnan KR. Structural neuroimaging and mood disorders: Recent findings, implications for classification, and future directions. Biological Psychiatry. 1998;43(10):705-712.
10. Tamashiro JH, Zung S, Zanetti MV, et al. Increased rates of white matter hyperintensities in late-onset bipolar disorder. Bipolar Disord. 2008;10(7):765-775.
11. Aziz R, Lorberg B, Tampi RR. Treatments for late-life bipolar disorder. Am J Geriatr Pharmacother. 2006;4(4):347-364.
12. Wefel JS, Kesler SR, Noll KR, et al. Clinical characteristics, pathophysiology, and management of noncentral nervous system cancer-related cognitive impairment in adults. CA Cancer J Clin. 2015;65(2):123-138.
13. Amidi A, Hosseini SMH, Leemans A, et al. Changes in brain structural networks and cognitive functions in testicular cancer patients receiving cisplatin-based chemotherapy. J Natl Cancer Inst. 2017;109(12). doi: 10.1093/jnci/djx085.
14. Torrence C, Jackson J. New onset mania in late life: case report and literature review. J Mississippi Acad Sci. 2016;61(1):159.
15. Cassidy F, Carroll BJ. Vascular risk factors in late onset mania. Psychol Med. 2002;32(2):359-362.
16. Bellivier F, Golmard JL, Rietschel M, et al. Age at onset in bipolar I affective disorder: further evidence for three subgroups. Am J Psychiatry. 2003;160(5):999-1001.
17. Almeida OP, Fenner S. Bipolar disorder: similarities and differences between patients with illness onset before and after 65 years of age. Int Psychogeriatr. 2002;14(3):311-322.
18. Schürhoff F, Bellivier F, Jouvent R, et al. Early and late onset bipolar disorders: two different forms of manic-depressive illness? J Affect Disord. 2000;58(3):215-21.
Although the peak age of onset of bipolar disorder (BD) is between 20 and 40 years,1 some patients develop BD later in life. The International Society for Bipolar Disorders Task Force has classified the illness into 3 categories:
- early-onset bipolar disorder (EOBD), in which the first manic episode occurs before age 40
- late-onset bipolar disorder (LOBD), in which the initial manic/hypomanic episode occurs after age 50
- older-age bipolar disorder (OABD), in which the first manic/hypomanic episode occurs after age 60.2
OABD represents 25% of the population with BD.3 OABD differs from EOBD in its clinical presentation, biological factors, and psychiatric and somatic comorbidities.4 Studies suggest OABD warrants a more extensive workup to rule out organic causes because symptoms are often attributable to a variety of organic etiologies.
This article describes 3 cases of OABD, including treatments and outcomes. We discuss general treatment recommendations for patients with OABD as cited in the literature. Further research is needed to expand our ability to better care for this unique population.
CASE 1
Mr. D was a 66-year-old African American male with no psychiatric history. His medical history was significant for hypertension, poorly controlled diabetes mellitus, and chronic kidney disease. One year ago, he was diagnosed with cholangiocarcinoma, and underwent uncomplicated right trisegmentectomy, resection of extrahepatic biliary tree, and complete portal lymphadenectomy, with Roux-en-Y hepaticojejunostomy to 2 intrahepatic ducts. He presented to the emergency department (ED) with disorganized behavior for 3 weeks. During that time, Mr. D reported increased distractibility, irritability, hyper-religiosity, racing thoughts, decreased appetite, and decreased need for sleep. There was no pertinent family history.
On mental status examination, Mr. D was agitated, noncooperative, and guarded. His speech was loud and pressured. Mr. D was distractible, tangential, and goal-directed. His Young Mania Rating Scale (YMRS) score was 31, which is highly indicative of mania.5 Computed tomography (CT) scan of the head (Figure 1)
CASE 2
Mr. M was a 63-year-old African American male with no psychiatric history and a medical history significant for hypertension and hypercholesterolemia. He presented to the ED with behavioral changes for 2 weeks. During this time, he experienced decreased need for sleep, agitation, excessive spending, self-conversing, hypersexuality, and paranoia. His family history was significant for schizoaffective disorder, bipolar type.
A mental status examination revealed pressured speech, grandiose delusions, hyper-religiosity, flight of ideas, looseness of association, auditory hallucinations, and tangential thought processes. Mr. M’s initial YMRS score was 56. A CT scan of the head revealed no acute abnormality, but MRI of the brain (Figure 2) showed chronic microvascular ischemic change. Mr. M was diagnosed with bipolar I disorder and admitted. He was started on quetiapine extended release, which was titrated to 600 mg nightly. Divalproex sodium extended release was titrated to 1,500 mg nightly, with subsequent improvement. At discharge, his YMRS score was 15.
Continue to: CASE 3
CASE 3
Ms. F was a 69-year-old White female with no psychiatric history. Her medical history was significant for hypertension, osteoarthritis, and stage III-C ovarian adenocarcinoma with a debulking surgical procedure 5 years earlier. After that, she received adjuvant therapy with paclitaxel and carboplatin, which resulted in a 10-month disease-free interval. Subsequent progression led to cycles of doxorubicin liposomal and gemcitabine. She was in remission until 1 week earlier, when a CT scan of the abdomen/pelvis showed recurrence. She presented to the hospital after disrobing in the street due to hyper-religiosity and divine instruction. She endorsed elevated mood and increased energy despite sleeping only 2 hours daily. Her family psychiatric history was significant for her daughter’s suicide attempt.
A mental status examination revealed disorganized behavior and agitation. Her speech was loud and pressured. She described a “great” mood with congruent affect. Her thought process was circumstantial and illogical. She displayed flight of ideas, grandiose delusions, and paranoia. Ms. F’s initial YMRS score was 38. Vital signs were significant for an elevated blood pressure of 153/113 mm Hg. A CT scan of the head (Figure 3) showed age-related change with no acute findings. Ms. F was admitted with a diagnosis of bipolar I disorder and prescribed olanzapine, 2.5 mg nightly. Due to continued manic symptoms, olanzapine was discontinued, and Ms. F was started on quetiapine, 300 mg nightly, with subsequent improvement. At discharge, her YMRS score was 10.
Differences between EOBD and OABD
BD has always been considered a multi-system illness; however, comorbidity is much more common in OABD than in EOBD. Comorbid conditions are 3 to 4 times more common in patients with OABD.2 Common comorbidities include metabolic syndrome, allergic rhinitis, arthritis, asthma, and cardiovascular disease.
Compared with younger individuals, older patients with BD score lower on the YMRS in the areas of increased activity-energy, language-thought disorder, and sexual interest.6 Psychotic symptoms are less common or less severe in OABD. Although symptom severity is lower, the prevalence of rapid cycling illness is 20% higher in patients with OABD.6 OABD is less commonly associated with a family history.7 This may suggest a difference from the popular genetic component typically found in patients with EOBD.
Cognitive impairment is more commonly found in OABD. Patients with OABD suffer from neuropsychological deficits even during euthymic phases.8 While these deficits may also be found in patients with EOBD, compared with younger patients, older adults are more susceptible to accelerated decline in cognition. OABD can first present within the context of cardiovascular or neuropsychological impairment. It has also been linked to a greater prevalence of white matter hyperintensities compared with EOBD.9,10
Continue to: Treatment is not specific to OABD
Treatment is not specific to OABD
No established treatment guidelines specifically address OABD. It has been treated similarly to EOBD, with antipsychotics, mood stabilizers, antidepressants, and electroconvulsive therapy (ECT). Although lithium is effective, special precautions should be taken when prescribing it to older adults because these patients may be more sensitive to adverse events.11 Drug–drug interactions may also be more likely due to concomitant use of medications for common medical issues such as hypertension.
Treatment with antipsychotics in older patients carries risks. Use of antipsychotics may result in higher rates of morbidity and mortality related to cardiovascular, metabolic, and infectious etiologies. Some literature recommends the use of antipsychotics for OABD; however, the potential benefits must outweigh the risks.6 Monotherapy followed by combination therapy has demonstrated effectiveness in OABD.11 Because symptoms of OABD are often less severe, it may be best to avoid maintenance antipsychotic therapy when possible. With a higher prevalence of depressed mood following manic episodes, use of antidepressant therapy is common in OABD.6 ECT should be considered for patients with treatment-refractory BD.11
Lessons from our case series
Our case series included 3 patients with OABD. These patients’ comorbid conditions included hypertension, hypercholesteremia, and diabetes mellitus. Two patients had a history of cancer, but there was no metastasis to the brain in either case. However, we considered the possibility of structural changes in the brain or cognitive impairment secondary to cancer or its treatment. A literature review confirmed that adult patients treated for noncentral nervous system cancer experienced cancer-related cognitive impairment (CRCI).12 New research suggests that CRCI could be related to altered neuronal integrity along with a disturbance of brain structure networks that process and integrate information.13
We used the YMRS to compare symptom severity and treatment response (Figure 4). Two patients were treated with atypical antipsychotics with a mood stabilizer, and the third patient was prescribed an antipsychotic only. We avoided lithium and carbamazepine as mood stabilizers due to their adverse effect profiles and potential for drug–drug interactions. Each patient responded well to treatment without adverse events.
Future studies are needed to clearly define the safest and most effective treatment guidelines in patients with OABD. We believe that OABD may require the development of a unique treatment algorithm due to the high likelihood of medical comorbidity and age-related variations in treatment response.
Continue to: Etiology of OABD may be different
Etiology of OABD may be different
OABD may be associated with manic presentations and vascular risk factors. MRI imaging that found more white matter hyperintensities and cerebrovascular lesions in patients with OABD compared with younger patients provides evidence of possible differing etiologies.14 Cassidy and Carroll15 found a higher incidence of smoking, hypertension, diabetes mellitus, coronary heart disease, and atrial fibrillation in patients in the older onset group. Bellivier et al16 proposed 3 subgroups of bipolar I disorder; the late-onset subgroup’s etiology was multifactorial. EOBD and OABD subgroups have similar gender ratios,17 first-episode descriptions, and alcohol use rates; however, OABD subgroups have more neurological comorbidity, lesser severe psychosis, and less genetic predisposition.
Although 25% of BD cases are late onset,3 there is still little consensus regarding subgroups and etiological causes. Therefore, additional research specifically focusing on vascular risks may provide much-needed information. Controlling and mitigating vascular risks in OABD may affect its development and course. Despite debated etiologies, the treatment of BD remains consistent, with anticonvulsants preferred over lithium in older individuals.
The Table summarizes clinical pearls about the features and treatment of OABD.
Bottom Line
Compared with younger patients with bipolar disorder (BD), those who develop BD later in life may be more likely to have rapid cycling, medical comorbidities, and cognitive impairment. Older patients with BD also may be more likely to experience adverse effects of the medications commonly used to treat BD, including antipsychotics, lithium, and carbamazepine.
Related Resources
- Carlino AR, Stinnett JL, Kim DR. New onset of bipolar disorder in late life. Psychosomatics. 2013;54(1):94-97.
- Sajatovic M, Kales HC, Mulsant BH. Prescribing antipsychotics in geriatric patients: Focus on schizophrenia and bipolar disorder. Current Psychiatry. 2017;16(10):20-26,28.
Drug Brand Names
Carbamazepine • Carbatrol, Tegretol
Carboplatin • Paraplatin
Divalproex sodium • Depakote
Doxorubicin liposome injection • Doxil
Gemcitabine injection • Gemzar
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Paclitaxel injection • Abraxane
Quetiapine • Seroquel
Although the peak age of onset of bipolar disorder (BD) is between 20 and 40 years,1 some patients develop BD later in life. The International Society for Bipolar Disorders Task Force has classified the illness into 3 categories:
- early-onset bipolar disorder (EOBD), in which the first manic episode occurs before age 40
- late-onset bipolar disorder (LOBD), in which the initial manic/hypomanic episode occurs after age 50
- older-age bipolar disorder (OABD), in which the first manic/hypomanic episode occurs after age 60.2
OABD represents 25% of the population with BD.3 OABD differs from EOBD in its clinical presentation, biological factors, and psychiatric and somatic comorbidities.4 Studies suggest OABD warrants a more extensive workup to rule out organic causes because symptoms are often attributable to a variety of organic etiologies.
This article describes 3 cases of OABD, including treatments and outcomes. We discuss general treatment recommendations for patients with OABD as cited in the literature. Further research is needed to expand our ability to better care for this unique population.
CASE 1
Mr. D was a 66-year-old African American male with no psychiatric history. His medical history was significant for hypertension, poorly controlled diabetes mellitus, and chronic kidney disease. One year ago, he was diagnosed with cholangiocarcinoma, and underwent uncomplicated right trisegmentectomy, resection of extrahepatic biliary tree, and complete portal lymphadenectomy, with Roux-en-Y hepaticojejunostomy to 2 intrahepatic ducts. He presented to the emergency department (ED) with disorganized behavior for 3 weeks. During that time, Mr. D reported increased distractibility, irritability, hyper-religiosity, racing thoughts, decreased appetite, and decreased need for sleep. There was no pertinent family history.
On mental status examination, Mr. D was agitated, noncooperative, and guarded. His speech was loud and pressured. Mr. D was distractible, tangential, and goal-directed. His Young Mania Rating Scale (YMRS) score was 31, which is highly indicative of mania.5 Computed tomography (CT) scan of the head (Figure 1)
CASE 2
Mr. M was a 63-year-old African American male with no psychiatric history and a medical history significant for hypertension and hypercholesterolemia. He presented to the ED with behavioral changes for 2 weeks. During this time, he experienced decreased need for sleep, agitation, excessive spending, self-conversing, hypersexuality, and paranoia. His family history was significant for schizoaffective disorder, bipolar type.
A mental status examination revealed pressured speech, grandiose delusions, hyper-religiosity, flight of ideas, looseness of association, auditory hallucinations, and tangential thought processes. Mr. M’s initial YMRS score was 56. A CT scan of the head revealed no acute abnormality, but MRI of the brain (Figure 2) showed chronic microvascular ischemic change. Mr. M was diagnosed with bipolar I disorder and admitted. He was started on quetiapine extended release, which was titrated to 600 mg nightly. Divalproex sodium extended release was titrated to 1,500 mg nightly, with subsequent improvement. At discharge, his YMRS score was 15.
Continue to: CASE 3
CASE 3
Ms. F was a 69-year-old White female with no psychiatric history. Her medical history was significant for hypertension, osteoarthritis, and stage III-C ovarian adenocarcinoma with a debulking surgical procedure 5 years earlier. After that, she received adjuvant therapy with paclitaxel and carboplatin, which resulted in a 10-month disease-free interval. Subsequent progression led to cycles of doxorubicin liposomal and gemcitabine. She was in remission until 1 week earlier, when a CT scan of the abdomen/pelvis showed recurrence. She presented to the hospital after disrobing in the street due to hyper-religiosity and divine instruction. She endorsed elevated mood and increased energy despite sleeping only 2 hours daily. Her family psychiatric history was significant for her daughter’s suicide attempt.
A mental status examination revealed disorganized behavior and agitation. Her speech was loud and pressured. She described a “great” mood with congruent affect. Her thought process was circumstantial and illogical. She displayed flight of ideas, grandiose delusions, and paranoia. Ms. F’s initial YMRS score was 38. Vital signs were significant for an elevated blood pressure of 153/113 mm Hg. A CT scan of the head (Figure 3) showed age-related change with no acute findings. Ms. F was admitted with a diagnosis of bipolar I disorder and prescribed olanzapine, 2.5 mg nightly. Due to continued manic symptoms, olanzapine was discontinued, and Ms. F was started on quetiapine, 300 mg nightly, with subsequent improvement. At discharge, her YMRS score was 10.
Differences between EOBD and OABD
BD has always been considered a multi-system illness; however, comorbidity is much more common in OABD than in EOBD. Comorbid conditions are 3 to 4 times more common in patients with OABD.2 Common comorbidities include metabolic syndrome, allergic rhinitis, arthritis, asthma, and cardiovascular disease.
Compared with younger individuals, older patients with BD score lower on the YMRS in the areas of increased activity-energy, language-thought disorder, and sexual interest.6 Psychotic symptoms are less common or less severe in OABD. Although symptom severity is lower, the prevalence of rapid cycling illness is 20% higher in patients with OABD.6 OABD is less commonly associated with a family history.7 This may suggest a difference from the popular genetic component typically found in patients with EOBD.
Cognitive impairment is more commonly found in OABD. Patients with OABD suffer from neuropsychological deficits even during euthymic phases.8 While these deficits may also be found in patients with EOBD, compared with younger patients, older adults are more susceptible to accelerated decline in cognition. OABD can first present within the context of cardiovascular or neuropsychological impairment. It has also been linked to a greater prevalence of white matter hyperintensities compared with EOBD.9,10
Continue to: Treatment is not specific to OABD
Treatment is not specific to OABD
No established treatment guidelines specifically address OABD. It has been treated similarly to EOBD, with antipsychotics, mood stabilizers, antidepressants, and electroconvulsive therapy (ECT). Although lithium is effective, special precautions should be taken when prescribing it to older adults because these patients may be more sensitive to adverse events.11 Drug–drug interactions may also be more likely due to concomitant use of medications for common medical issues such as hypertension.
Treatment with antipsychotics in older patients carries risks. Use of antipsychotics may result in higher rates of morbidity and mortality related to cardiovascular, metabolic, and infectious etiologies. Some literature recommends the use of antipsychotics for OABD; however, the potential benefits must outweigh the risks.6 Monotherapy followed by combination therapy has demonstrated effectiveness in OABD.11 Because symptoms of OABD are often less severe, it may be best to avoid maintenance antipsychotic therapy when possible. With a higher prevalence of depressed mood following manic episodes, use of antidepressant therapy is common in OABD.6 ECT should be considered for patients with treatment-refractory BD.11
Lessons from our case series
Our case series included 3 patients with OABD. These patients’ comorbid conditions included hypertension, hypercholesteremia, and diabetes mellitus. Two patients had a history of cancer, but there was no metastasis to the brain in either case. However, we considered the possibility of structural changes in the brain or cognitive impairment secondary to cancer or its treatment. A literature review confirmed that adult patients treated for noncentral nervous system cancer experienced cancer-related cognitive impairment (CRCI).12 New research suggests that CRCI could be related to altered neuronal integrity along with a disturbance of brain structure networks that process and integrate information.13
We used the YMRS to compare symptom severity and treatment response (Figure 4). Two patients were treated with atypical antipsychotics with a mood stabilizer, and the third patient was prescribed an antipsychotic only. We avoided lithium and carbamazepine as mood stabilizers due to their adverse effect profiles and potential for drug–drug interactions. Each patient responded well to treatment without adverse events.
Future studies are needed to clearly define the safest and most effective treatment guidelines in patients with OABD. We believe that OABD may require the development of a unique treatment algorithm due to the high likelihood of medical comorbidity and age-related variations in treatment response.
Continue to: Etiology of OABD may be different
Etiology of OABD may be different
OABD may be associated with manic presentations and vascular risk factors. MRI imaging that found more white matter hyperintensities and cerebrovascular lesions in patients with OABD compared with younger patients provides evidence of possible differing etiologies.14 Cassidy and Carroll15 found a higher incidence of smoking, hypertension, diabetes mellitus, coronary heart disease, and atrial fibrillation in patients in the older onset group. Bellivier et al16 proposed 3 subgroups of bipolar I disorder; the late-onset subgroup’s etiology was multifactorial. EOBD and OABD subgroups have similar gender ratios,17 first-episode descriptions, and alcohol use rates; however, OABD subgroups have more neurological comorbidity, lesser severe psychosis, and less genetic predisposition.
Although 25% of BD cases are late onset,3 there is still little consensus regarding subgroups and etiological causes. Therefore, additional research specifically focusing on vascular risks may provide much-needed information. Controlling and mitigating vascular risks in OABD may affect its development and course. Despite debated etiologies, the treatment of BD remains consistent, with anticonvulsants preferred over lithium in older individuals.
The Table summarizes clinical pearls about the features and treatment of OABD.
Bottom Line
Compared with younger patients with bipolar disorder (BD), those who develop BD later in life may be more likely to have rapid cycling, medical comorbidities, and cognitive impairment. Older patients with BD also may be more likely to experience adverse effects of the medications commonly used to treat BD, including antipsychotics, lithium, and carbamazepine.
Related Resources
- Carlino AR, Stinnett JL, Kim DR. New onset of bipolar disorder in late life. Psychosomatics. 2013;54(1):94-97.
- Sajatovic M, Kales HC, Mulsant BH. Prescribing antipsychotics in geriatric patients: Focus on schizophrenia and bipolar disorder. Current Psychiatry. 2017;16(10):20-26,28.
Drug Brand Names
Carbamazepine • Carbatrol, Tegretol
Carboplatin • Paraplatin
Divalproex sodium • Depakote
Doxorubicin liposome injection • Doxil
Gemcitabine injection • Gemzar
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Paclitaxel injection • Abraxane
Quetiapine • Seroquel
1. Prabhakar D, Balon R. Late-onset bipolar disorder: a case for careful appraisal. Psychiatry (Edgmont). 2010;7(1):34-37.
2. Sajatovic M, Strejilevich SA, Gildengers AG, et al. A report on older-age bipolar disorder from the International Society for Bipolar Disorders Task Force. Bipolar Disord. 2015;17(7):689-704.
3. Arciniegas DB. New-onset bipolar disorder in late life: a case of mistaken identity. Am J Psychiatry. 2006;163(2):198-203.
4. Chou P-H, Tseng W-J, Chen L-M, et al. Late onset bipolar disorder: a case report and review of the literature. Journal of Clinical Gerontology and Geriatrics. 2015;6(1):27-29.
5. Lukasiewicz M, Gerard S, Besnard A, et al; Emblem Study Group. Young Mania Rating Scale: how to interpret the numbers? Determination of a severity threshold and of the minimal clinically significant difference in the EMBLEM cohort. Int J Methods Psychiatr Res. 2013;22(1):46-58.
6. Oostervink F, Boomsma MM, Nolen WA; EMBLEM Advisory Board. Bipolar disorder in the elderly; different effects of age and of age of onset. J Affect Disord. 2009;116(3):176-183.
7. Depp CA, Jeste D V. Bipolar disorder in older adults: A critical review. Bipolar Disord. 2004;6(5):343-367.8.
8. Gildengers AG, Butters MA, et al. Cognitive functioning in late-life bipolar disorder. Am J Psychiatry. 2004. doi:10.1176/appi.ajp.161.4.736
9. Steffens DC, Krishnan KR. Structural neuroimaging and mood disorders: Recent findings, implications for classification, and future directions. Biological Psychiatry. 1998;43(10):705-712.
10. Tamashiro JH, Zung S, Zanetti MV, et al. Increased rates of white matter hyperintensities in late-onset bipolar disorder. Bipolar Disord. 2008;10(7):765-775.
11. Aziz R, Lorberg B, Tampi RR. Treatments for late-life bipolar disorder. Am J Geriatr Pharmacother. 2006;4(4):347-364.
12. Wefel JS, Kesler SR, Noll KR, et al. Clinical characteristics, pathophysiology, and management of noncentral nervous system cancer-related cognitive impairment in adults. CA Cancer J Clin. 2015;65(2):123-138.
13. Amidi A, Hosseini SMH, Leemans A, et al. Changes in brain structural networks and cognitive functions in testicular cancer patients receiving cisplatin-based chemotherapy. J Natl Cancer Inst. 2017;109(12). doi: 10.1093/jnci/djx085.
14. Torrence C, Jackson J. New onset mania in late life: case report and literature review. J Mississippi Acad Sci. 2016;61(1):159.
15. Cassidy F, Carroll BJ. Vascular risk factors in late onset mania. Psychol Med. 2002;32(2):359-362.
16. Bellivier F, Golmard JL, Rietschel M, et al. Age at onset in bipolar I affective disorder: further evidence for three subgroups. Am J Psychiatry. 2003;160(5):999-1001.
17. Almeida OP, Fenner S. Bipolar disorder: similarities and differences between patients with illness onset before and after 65 years of age. Int Psychogeriatr. 2002;14(3):311-322.
18. Schürhoff F, Bellivier F, Jouvent R, et al. Early and late onset bipolar disorders: two different forms of manic-depressive illness? J Affect Disord. 2000;58(3):215-21.
1. Prabhakar D, Balon R. Late-onset bipolar disorder: a case for careful appraisal. Psychiatry (Edgmont). 2010;7(1):34-37.
2. Sajatovic M, Strejilevich SA, Gildengers AG, et al. A report on older-age bipolar disorder from the International Society for Bipolar Disorders Task Force. Bipolar Disord. 2015;17(7):689-704.
3. Arciniegas DB. New-onset bipolar disorder in late life: a case of mistaken identity. Am J Psychiatry. 2006;163(2):198-203.
4. Chou P-H, Tseng W-J, Chen L-M, et al. Late onset bipolar disorder: a case report and review of the literature. Journal of Clinical Gerontology and Geriatrics. 2015;6(1):27-29.
5. Lukasiewicz M, Gerard S, Besnard A, et al; Emblem Study Group. Young Mania Rating Scale: how to interpret the numbers? Determination of a severity threshold and of the minimal clinically significant difference in the EMBLEM cohort. Int J Methods Psychiatr Res. 2013;22(1):46-58.
6. Oostervink F, Boomsma MM, Nolen WA; EMBLEM Advisory Board. Bipolar disorder in the elderly; different effects of age and of age of onset. J Affect Disord. 2009;116(3):176-183.
7. Depp CA, Jeste D V. Bipolar disorder in older adults: A critical review. Bipolar Disord. 2004;6(5):343-367.8.
8. Gildengers AG, Butters MA, et al. Cognitive functioning in late-life bipolar disorder. Am J Psychiatry. 2004. doi:10.1176/appi.ajp.161.4.736
9. Steffens DC, Krishnan KR. Structural neuroimaging and mood disorders: Recent findings, implications for classification, and future directions. Biological Psychiatry. 1998;43(10):705-712.
10. Tamashiro JH, Zung S, Zanetti MV, et al. Increased rates of white matter hyperintensities in late-onset bipolar disorder. Bipolar Disord. 2008;10(7):765-775.
11. Aziz R, Lorberg B, Tampi RR. Treatments for late-life bipolar disorder. Am J Geriatr Pharmacother. 2006;4(4):347-364.
12. Wefel JS, Kesler SR, Noll KR, et al. Clinical characteristics, pathophysiology, and management of noncentral nervous system cancer-related cognitive impairment in adults. CA Cancer J Clin. 2015;65(2):123-138.
13. Amidi A, Hosseini SMH, Leemans A, et al. Changes in brain structural networks and cognitive functions in testicular cancer patients receiving cisplatin-based chemotherapy. J Natl Cancer Inst. 2017;109(12). doi: 10.1093/jnci/djx085.
14. Torrence C, Jackson J. New onset mania in late life: case report and literature review. J Mississippi Acad Sci. 2016;61(1):159.
15. Cassidy F, Carroll BJ. Vascular risk factors in late onset mania. Psychol Med. 2002;32(2):359-362.
16. Bellivier F, Golmard JL, Rietschel M, et al. Age at onset in bipolar I affective disorder: further evidence for three subgroups. Am J Psychiatry. 2003;160(5):999-1001.
17. Almeida OP, Fenner S. Bipolar disorder: similarities and differences between patients with illness onset before and after 65 years of age. Int Psychogeriatr. 2002;14(3):311-322.
18. Schürhoff F, Bellivier F, Jouvent R, et al. Early and late onset bipolar disorders: two different forms of manic-depressive illness? J Affect Disord. 2000;58(3):215-21.
