CASE REPORT

Topiramate Improves Psychiatric Symptoms in a Patient with Lewy Body Dementia Juan G. Ochoa, MD

Abstract: Many patients with Lewy body dementia develop visual hallucinations and other psychiatric symptoms. These patients are hypersensitive to antipsychotic drugs. Although patients tolerate atypical better than typical antipsychotics, both types can cause major extrapyramidal side effects. The anticonvulsant mood stabilizer topiramate, which does not cause parkinsonism, has been used as adjuvant therapy for both the positive and negative symptoms of schizophrenia; these symptoms can resemble those of Lewy body dementia. This report documents a 65-year-old woman with a 3-year history of progressive dementia that over the past 2 years had become complicated by severe extrapyramidal symptoms and agitated hallucinations. Her hallucinations became daily and were disrupting to her family. She was given a clinical diagnosis of Lewy body dementia after imaging and laboratory studies ruled out other etiologies. Treatment with olanzapine relieved her psychotic symptoms but caused severe dystonias, daily myoclonic jerks, and tremors. Stopping the olanzapine and starting topiramate 25 mg daily eliminated the hallucinations and agitation without worsening her extrapyramidal side effects. However, the topiramate was stopped because the patient reportedly developed anorexia and significant weight loss. Her hallucinations returned. When topiramate was reinstated at 12.5 mg a day, her agitation resolved, although her hallucinations continued. After 6 months on this dose, her agitation was still fairly well controlled without serious side effects or worsening of her parkinsonian symptoms. Key Words: topiramate, dementia, Lewy body, parkinsonism, hallucinations (Cogn Behav Neurol 2014;27:222–223)

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bout 10% to 15% of patients who develop a late-onset dementia have Lewy bodies (Ballard et al, 2011). Many of these patients have associated parkinsonism and neuropsychiatric symptoms, most often persistent visual hallucinations (Ballard et al, 2011). Patients with Lewy body dementia have much worse neuropsychiatric symptoms and

cause more stress for caregivers than do patients with Alzheimer disease (Bjoerke-Bertheussen et al, 2012). Unfortunately, patients with Lewy body dementia are hypersensitive to antipsychotic drugs, which can cause severe reactions and even death (Kaufer, 2004). However, atypical antipsychotics cause less severe extrapyramidal side effects than do typical antipsychotics (Calvo´-Perxas et al, 2012). Despite the still-reported risks of atypical antipsychotics, they are given to many patients who have dementia and psychiatric symptoms, including those with Lewy body dementia (Calvo´-Perxas et al, 2012). The neuropsychiatric symptoms of patients with Lewy body dementia have been shown to improve modestly with cholinesterase inhibitors and memantine (Ballard et al, 2011). A review of anticonvulsant mood stabilizers reported that carbamazepine helped control behavioral and psychological symptoms in some patients with dementia (Konovalov et al, 2008); however, the authors recommended against routine use of the drug class because most studies showed either no benefit or actual worsening of symptoms, and the treated groups had significantly higher rates of adverse effects than did placebo groups. The anticonvulsant mood stabilizer topiramate has been effective as an adjuvant drug in controlling the positive and negative symptoms of schizophrenia (Afshar et al, 2009; Hahn et al, 2013). Positive psychiatric symptoms have been associated with high-frequency thalamocortical oscillations, and it is plausible that topiramate reduces these oscillations through a GABAergic effect (Schulman et al, 2011). Topiramate does not cause extrapyramidal dysfunction. I cared for a patient who did not respond to any of the routine drug treatments for the neuropsychiatric complications of progressive dementia. When her standard options ran out, I tried her on topiramate, and here describe her response.

CASE REPORT

Received for publication December 3, 2013; accepted February 18, 2014. From the Department of Neurology, University of South Alabama, Mobile, Alabama. The author declares no conflicts of interest. Reprints: Juan G. Ochoa, MD, Department of Neurology, University of South Alabama, 2451 Fillingim Street, Suite 10-E, Mobile, Alabama 36617-2293 (e-mail: [email protected]). Copyright r 2014 by Lippincott Williams & Wilkins

A 65-year-old woman with a 3-year history of progressive dementia was referred to my clinic at the University of South Alabama with severe hallucinations and parkinsonism. Her local neurologist had been treating her dementia with memantine and rivastigmine, but she had not shown any noteworthy improvement. Two years earlier, she had started having visual hallucinations, which she described as seeing people talking to her. The hallucinations gradually became daily,

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Cogn Behav Neurol



Volume 27, Number 4, December 2014

Cogn Behav Neurol

Volume 27, Number 4, December 2014

Topiramate for Psychiatric Symptoms in Lewy Body Dementia

sometimes with severe agitation. They were being treated with olanzapine 5 mg 3 times a day. She had become severely rigid, with gait imbalance, frequent falls, and prominent bradykinesia. She also had dizziness, difficulty swallowing, and severe insomnia. Neither trazodone nor sertraline improved her psychiatric symptoms or sleep disturbance. She suffered 2 unprovoked generalized seizures. The seizures were being controlled with lamotrigine 25 mg twice a day. She had frequent daily myoclonic jerks, which had become progressively worse over the last year. She also had episodes of stiffness in both legs, lasting several minutes. At this point her neurologist referred her to me for further evaluation. On neurologic examination at my clinic, she was alert, had fluent speech, and followed commands fairly well. She had a prominent bradykinesia with severe rigidity and bilateral hand tremors that worsened when she walked. She also had akathisia. She needed help to stand up from a chair. She walked with a stooped posture, shuffling gait, and poor balance. Even so, she was able to move about without an assistive device. Video electroencephalographic monitoring revealed myoclonic activity and frequent dystonic reactions without electroencephalographic correlate. Magnetic resonance imaging of her brain showed global atrophy but no localized abnormalities. Blood test results excluded metabolic, infectious, nutritional, and toxic disorders. With other etiologies ruled out, I gave her a clinical diagnosis of Lewy body dementia based on her presentation. I stopped her olanzapine and trazodone, and started her on topiramate 25 mg a day. When I saw her 2 weeks later, her extrapyramidal dysfunction was much improved, with many fewer tremors and disappearance of her myoclonus and dystonia. She could move faster and her akathisia was less pronounced. Her agitation and visual hallucinations had disappeared. She had persistent bradykinesia and still needed help getting up from a seated position. During those 2 weeks, the patient’s family reported that she had a drop in her appetite and had lost considerable weight. Because these can be serious side effects of topiramate, I stopped the drug. Without topiramate, the patient’s hallucinations and severe agitation returned. I tried reinstating the topiramate at 12.5 mg a day. On this halved dose, the patient’s agitation resolved, but she still had daily hallucinations. Her family reported that her appetite and weight improved. At a follow-up examination after the patient had been on the lower dose of topiramate for 6 months, her

agitation remained under control, without major side effects. Her hallucinations continued.

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2014 Lippincott Williams & Wilkins

DISCUSSION First, a note about this patient’s myoclonus. Myoclonus is rare in Lewy body dementia. This patient’s myoclonus was probably caused by her olanzapine therapy, because the myoclonus resolved after the drug was stopped. Another cause of myoclonus such as Creutzfeldt-Jakob disease was unlikely, given the patient’s relatively stable course over the past 2 years. Psychiatric symptoms in patients with Lewy body dementia are difficult to manage, and treatment options are limited. The psychiatric symptoms in our patient were not controlled by the atypical antipsychotic drug olanzapine. Lamotrigine, which she had started after her seizures, had no effect on her psychotic symptoms. Topiramate, which has been shown to help improve both positive and negative symptoms in schizophrenia (Afshar et al, 2009; Hahn et al, 2013), thus became a rational alternative for this patient. The span of

Topiramate improves psychiatric symptoms in a patient with Lewy body dementia.

Many patients with Lewy body dementia develop visual hallucinations and other psychiatric symptoms. These patients are hypersensitive to antipsychotic...
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