Catatonia in a patient with Alzheimer’s dementia

Alzheimer’s disease (AD), is one of the most prevalent dementias, affecting two-thirds of individuals over the age of 65 years.1,2 Behavioral and Psychological symptoms (BPSD) are common in patients with AD and include delusions, hallucinations, and affective symptoms.3 Catatonia is a syndrome characterized by abnormal motor movements, behaviors, or social withdrawal. Although catatonia has been noted in association with dementia, it is relatively uncommon. Delirium, depression, or underlying medical conditions can lead to confusion and diagnostic delays.4 A 63-year-old female was brought to the emergency with one month history of posturing, mutism, refusal to eat or drink, and staring. She had bipolar affective disorder for the last 30 years with five manic episodes and two depressive episodes, the last occurring four years ago. There was a family history of bipolar disorder in siblings and dementia in her father. She was on sodium valproate, Quetiapine, and Olanzapine. Since, 3 years family noted she was forgetting, misplacing items, had difficulty recognizing relatives and progressive impairment in performing daily chores. She received treatment elsewhere for the above symptoms for 2 weeks with antibiotics, and haloperidol 5 mg intravenously on multiple occasions. Her symptoms did not improve, leading to a referral to our center. On examination, she was mute, had posturing, rigidity, negativism, and tachycardia. Routine investigations, electroencephalogram, and Magnetic resonance imaging of the brain was conducted on admission. Labs showed leukocytosis (12,000/cumm) and elevated creatine phosphokinase (CPK 1345 IU/L). EEG was unremarkable. MRI showed cerebral atrophy with chronic ischemic changes. Given the recent haloperidol exposure, neuroleptic malignant syndrome (NMS) was suspected. Bromocriptine (5 mg/day) was started, and other medications were withheld. Supportive care and Ryle’s tube feeding were started. Although CPK levels gradually reduced, there was no clinical improvement, the elevated CPK was attributed to antipsychotic use. NMS was ruled out and Catatonia became the diagnosis. Bush–Francis Catatonia Rating Scale score was 35/69. A lorazepam challenge (2 mg IV) produced partial improvement, but scheduled dosing caused excessive sedation, necessitating discontinuation. With family consent, modified electroconvulsive therapy (mECT) was initiated. After four treatments, BFCRS improved to 28/69, and after ten sessions, her catatonia resolved. However, significant cognitive and functional deficits persisted, including impaired attention, memory, abstraction, verbal fluency, and executive function. Apraxia’s and inhibitory control deficits were present. APOE genotyping revealed APOE3/APOE4 alleles, indicating elevated risk for AD. There was no temporal association between mood symptoms and the catatonic presentation, and cognition remained impaired after catatonia resolved, she was diagnosed with AD with BPSD (catatonia) and a history of bipolar disorder. Donepezil was initiated. She was discharged with outpatient follow-up. Catatonia can manifest as retarded or excited motor symptoms. Early diagnosis is essential, especially in older adults, where the risk is four times higher than in younger patients.5 Delayed recognition may lead to serious complications, including NMS.6 In this case, the patient was diagnosed with catatonia only after weeks of medical intervention. Although catatonia is a DSM-5 specifier for mood episodes in bipolar disorder, this patient exhibited no mood symptoms before or after the catatonic state.7 Hence the catatonic symptoms were a part of BPSD. Catatonia associated with AD is uncommon, with reported prevalence in dementia ranging from 4.8% to 42.8%, and is more often linked with frontotemporal dementia, Lewy body dementia, and Parkinson’s disease. Benzodiazepines remain first-line therapy, but ECT is highly effective in refractory cases.8 This case highlights that catatonia can be a presenting feature of BPSD in Alzheimer’s dementia and underscores the need for heightened clinical suspicion in older adults with atypical neuropsychiatric presentations. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.