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Malignant Catatonia and Aphasia Follow Multiple-Drug Overdose Neeta Shenai, MD, Crystal White, MD, Pierre Azzam, MD, Priya Gopalan, MD, and Lalithkumar K

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Malignant Catatonia and Aphasia Follow Multiple-Drug Overdose Neeta Shenai, MD, Crystal White, MD, Pierre Azzam, MD, Priya Gopalan, MD, and Lalithkumar K Cases That Test Your Skills Malignant catatonia and aphasia follow multiple-drug overdose Neeta Shenai, MD, Crystal White, MD, Pierre Azzam, MD, Priya Gopalan, MD, and LalithKumar K. Solai, MD Two weeks after an overdose, Ms. M, age 37, develops malignant How would you catatonia. Although her catatonic symptoms resolve with ECT, handle this case? Answer the challenge she shows word-finding difficulty. How would you proceed? questions throughout this article CASE Improvement, then decline 2 Weeks later. Ms. M is brought to the Ms. M, age 37, is brought to the hospi- emergency department after a progressive tal after her husband found her at home, decrease in social interaction, limited oral after an unknown duration of impaired intake, decline in activities of daily living, and consciousness. Her husband reports that urinary incontinence. Results from laboratory Ms. M had normal cognitive functioning studies are within normal limits; brain MRI is before this event, with no difficulty complet- negative; EEG shows generalized moderate ing activities of daily living. Ms. M’s medi- slowing. cal and psychiatric histories are notable for During psychiatric evaluation, Ms. M is type 2 diabetes mellitus, unspecified bipolar mute and staring continuously. Examination disorder, and opioid, cocaine, and alcohol use reveals oppositional paratonia (gegen- disorders. Her medications include parox- halten), catalepsy, prominent negativism, etine, 40 mg/d, and gabapentin, 1,200 mg/d. and waxy flexibility, all suggestive of cata- tonia. IV lorazepam is initiated at 1 mg every First admission. Poor inspiratory effort 8 hours, titrated to 2 mg, 3 times a day. and oxygen saturation of 70% leads to Ms. M is transferred to a psychiatric hospi- emergent intubation. Serum laboratory tal for further treatment of catatonia. studies reveal a white blood cell (WBC) count at 10,900/μL and creatinine phos- Second admission. Evaluation with the phokinase level of 25,000 U/L. Urine drug Bush-Francis Catatonia Rating Scale supported screen is positive for tetrahydrocannabinol, a diagnosis of catatonia, with the presence of cocaine, and opioids. >3 features from the 14-item screen and a score Ms. M is admitted to the ICU for manage- of 16 on the 23-item rating scale.1 After titrat- ment of rhabdomyolysis and multi-organ ing lorazepam to 9 mg/d with minimal thera- system failure, including acute hypoxic kid- peutic impact, the psychiatry team consults the ney injury. By hospital Day 7, the tube is extubated Dr. Shenai is a Fourth-Year Resident, Dr. White is Assistant Professor, Dr. Azzam is Assistant Professor, Dr. Gopalan is Assistant Professor, with no recorded physical neurologic defi- and Dr. Solai is Associate Professor, Department of Psychiatry, cits. Mental status exam is normal, except for University of Pittsburgh, Pittsburgh, Pennsylvania. impaired memory of events surrounding the Disclosures admission. Ms. M is discharged home with a The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers Current Psychiatry recommendation for outpatient follow-up. of competing products. Vol. 14, No. 12 51 Cases That Test Your Skills TableTable 1 1 Differential diagnosis and workup for Ms. M Possible diagnosis Evaluation Dementia Initial studies: B12, folate, thyroid-stimulating hormone; brain MRI Delirium Initial studies: CBC with differential, complete metabolic panel, urinalysis Toxins Urine drug screen; comprehensive drug screen; history • Heroin inhalation encephalopathy Brain MRI • Carbon monoxide poisoning • Heavy metals Infection Lumbar puncture with cytology (protein, glucose, cell count, • Viral encephalopathy bacterial cultures) Clinical Point • Pneumonia Chest radiography, CBC with differential • Urinary tract infection Urinalysis with culture In approximately 25% • HIV • Neurosyphilis Rapid HIV test of cases, catatonia is Rapid plasma reagin test caused by a general Multiple sclerosis Lumbar puncture, brain MRI medical condition; as Nutritional deficiencies B12, folate such, a comprehensive Nonconvulsive status epilepticus EEG Seizures medical workup is vital Stroke (hemorrhagic vs ischemic) Brain MRI Tumor/metastasis Brain MRI Posterior reversible encephalopathy Brain MRI syndrome Autoimmune Brain MRI • Vasculitis • Acute disseminated encephalomyelitis Creutzfeldt-Jakob disease CSF analysis, EEG, and (rarely) brain biopsy CBC: complete blood count; CSF: cerebrospinal fluid electroconvulsive therapy (ECT) service, who autonomic instability or psychomotor fea- deems Ms. M to be an appropriate candidate tures of catatonia. Despite these improve- and petitions for court-ordered ECT. ments, she is noted to have persistent On hospital Day 8, Ms. M has a fever of 104°F, word-finding difficulty. tachycardia at 180 beats per minute, increased rigidity, and a WBC count of 17,800/μL. She Which test would you order as the next step in is transferred to the ICU, with a presumptive your work up? diagnosis of malignant catatonia. a) EEG Discuss this article at The medical evaluation, including general b) lumbar puncture www.facebook.com/ laboratory studies, EEG, and spinal fluid anal- c) MRI CurrentPsychiatry ysis, is unremarkable. Because of vital sign d) CT instability, 2 ECT treatments are completed in the general hospital before Ms. M resumes psychiatric inpatient care. The authors’ observations The authors‘ observations By the tenth ECT treatment, Ms. M is no In approximately 25% of cases, catatonia Current Psychiatry 52 December 2015 longer febrile and experiences no further is caused by a general medical condition2; Cases That Test Your Skills as such, a comprehensive medical workup TableTable 2 2 is vital for assessment and management of Mechanisms of anoxic injury catatonic patients. In Ms. M’s case, we con- Anoxic anoxia Low environmental oxygen sidered several medical causes, including tension or pulmonary nutritional deficiency, infection, a toxin, renal function or hepatic impairment, hypothyroidism, sei- Anemic anoxia Low oxygen-carrying zure, and stroke. Evaluation included mea- capacity of blood surement of thyroid-stimulating hormone, Ischemic anoxia Failure of cerebral blood flow vitamin B12, and folic acid levels; urinalysis Source: Reference 7 and urine drug screen; chest radiography; lumbar puncture; neuroimaging; and EEG (Table 1). Several conditions in the differen- Etiology and pathophysiology Clinical Point tial diagnosis were noteworthy. Ms. M’s First described in 1979, DPHL is rare, pos- severe and sudden neurologic decline, ing diagnostic challenges for clinical pro- Although the exact along with a positive urine drug screen for viders.6 Although the exact incidence of incidence of DPHL substances of abuse, raised concern about DPHL is unknown, the precipitating event is unknown, overdose leading to toxic encephalopathy typically involves cerebral anoxia, which the precipitating event or hypoxic brain injury. Ms. M’s oxygen can occur through carbon monoxide (CO) typically involves saturation when she was found was mod- poisoning, strangulation, cardiac arrest, cerebral anoxia erately hypoxic at 70%, which is not a level respiratory failure, and overdose from sed- associated with hypoxic brain damage. atives and narcotics (Table 2).7 DPHL was We also considered posterior reversible first observed in a small percentage (2.75%) encephalopathy syndrome (PRES), which of patients suffering from CO poison- presents variably with nausea, visual ing.8,9 Progression of the disease generally impairment, disturbance in conscious- includes a period of unconsciousness, then ness, seizures, and focal neurologic signs.3 a lucid interval that can last 2 to 40 days, Although 67% to 80% of patients with followed by the abrupt onset of neuropsy- PRES also have acute hypertension, blood chiatric symptoms.10 The specific patho- pressure elevation is not necessary for the physiologic mechanism is unknown, but diagnosis.4 Similar to toxic leukoencepha- has been hypothesized to involve inferior lopathy, PRES is diagnosed by brain MRI, with classic signs of posterior white-matter COMING NEXT MONTH edema. Case reports also describe an uncom- Follow the challenging narratives mon demyelinating syndrome, delayed of 3 patients, in a compilation of new post-hypoxic leukoencephalopathy (DPHL), CASES THAT TEST YOUR SKILLS which develops several weeks or months • A girl, age 11, refuses solid food for fear after a cerebral anoxic insult.5 In Ms. M’s of choking and is losing weight case, brain MRI performed during her sec- • A woman, age 58, with bipolar mania is being ond medical hospitalization, 7 days after treated for breast cancer the initial neuropsychiatric decline, was • A man, age 42, slowly deteriorating with schizophrenia, reports a throbbing headache; unremarkable. Using this result to rule out his family fears that he might grow violent DPHL would have been premature because How would you proceed with their care? pathognomonic abnormalities can appear as long as 40 days after the anoxic insult. All 3 “Cases” in the January 2016 Given our differential diagnosis, we ordered issue of Current Psychiatry a repeat MRI. Vol. 14, No. 12 53 Cases That Test Your Skills FigureFigure 1 Second brain MRI (T2/FLAIR) Clinical Point DPHL is a diagnosis of exclusion. A careful history is critical to establish the possibility Diffuse hyperintensities are seen in the white matter of a recent anoxic event compensatory response to decreased oxy- Early reports of DPHL suggested an genation in the white matter.
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