Benzodiazepine Withdrawal Catatonia, Delirium, and Seizures in a Patient With Schizoaffective Disorder.

Benzodiazepine withdrawal symptoms vary from mild anxiety to life-threatening delirium or seizures. In susceptible individuals, such as those with mood disorders, benzodiazepine withdrawal may also precipitate catatonia. A 26-year-old man with schizoaffective disorder (depressed type with catatonia) ran out of lorazepam and presented with catatonia, delirium, and seizures. He was taking olanzapine, venlafaxine, and trazodone for schizoaffective disorder. Lorazepam 2 mg twice daily kept him free of catatonia for 6 months. Besides catatonia and delirium, lorazepam withdrawal also triggered convulsive seizures and nonconvulsive status epilepticus. He was admitted to the intensive care unit where he underwent continuous video-EEG monitoring. Catatonia resolved with lorazepam on day 2. Seizures stopped with levetiracetam, lacosamide, and propofol on day 4. His mental status was normal when he was discharged on day 6. If not immediately recognized and treated, catatonia and delirium can lead to significant morbidity or mortality. Unfortunately, physicians tend to overlook catatonia and delirium, especially if both syndromes are present. At first, we suspected that our patient had ictal catatonia, but video-EEG showed no clear-cut correlation between catatonia, seizures, and epileptiform activity. As with prior observations, the patient's catatonia was more sensitive to benzodiazepine withdrawal and treatment than his seizures. The efficacy of benzodiazepines in aborting catatonia, seizures, and mixed delirium-catatonia syndromes suggests a key pathogenetic role of abnormal GABA neurotransmission in these brain disorders.

Stroke-Onset Seizures During Midbrain Infarction in a Patient With Top of the Basilar Syndrome.

Risk factors for early-onset seizures in acute ischemic stroke include anterior circulation stroke, infarction of the cerebral cortex, large infarct size, and ischemic-to-hemorrhagic transformation. We define stroke-onset seizures as seizures occurring within 2 hours of stroke onset. A 64-year-old woman presented with top of the basilar artery syndrome-thalamic infarction occurred first and midbrain infarction 12 days later. She manifested stroke-onset seizures during midbrain infarction, which was heralded by stupor. Within 2 hours of the onset of stupor, she had a clonic seizure of the lower extremities, electroencephalography (EEG) revealed nonconvulsive status epilepticus, and an episode of convulsive movements of all extremities was recorded on video and on EEG. Continuous EEG recording showed epileptiform discharges that would appear, disappear, and reappear over a 3-week period. It took 3 weeks and 4 antiepileptic drugs to fully suppress cortical hyperexcitability, perhaps because injury to some midbrain structures resulted in global lowering of the seizure threshold. The most important risk factor for stroke-onset seizures appears to be posterior circulation stroke, particularly brainstem infarction. The difference in risk profile between stroke-onset seizures and other forms of early-onset seizures suggest that their pathophysiology is not exactly the same. Focusing some of the research spotlight on stroke-onset seizures can help us better understand their unique clinical, electrographic, radiologic, and pathophysiologic features.

Full Recovery From Cocaine-Induced Toxic Leukoencephalopathy: Emphasizing the Role of Neuroinflammation and Brain Edema.

Toxic leukoencephalopathy (TL) is characterized by white matter disease on magnetic resonance imaging (MRI) and evidence of exposure to a neurotoxic agent. We describe a case of cocaine-induced TL in which extensive white matter disease did not preclude full recovery. A 57-year-old man with substance abuse disorder presented with a 5-day history of strange behavior. On admission, he was alert but had difficulty concentrating, psychomotor retardation, and diffuse hyperreflexia. Brain MRI revealed confluent subcortical white matter hyperintensities with restricted diffusion in some but not in other areas. Electroencephalography (EEG) showed mild diffuse slowing. Blood tests were normal except for mild hyperammonemia. Urine screen was positive for cocaine and benzodiazepine but quantitative analysis was significant only for cocaine. Prednisone 60-mg qd was initiated on day 4, tapered over a 5-day period, and discontinued on day 9. He was discharged after 3 weeks. Cognitive function returned to normal 2 weeks after discharge. Five months later, neurologic exam and EEG were normal and MRI showed near-100% resolution of white matter lesions. TL has been attributed to white matter ischemia/hypoxia resulting in demyelination/axonal injury. The clinical, EEG, and MRI findings and time course of recovery of our patient suggest that cocaine-induced inflammation/edema resulted in TL but not in ischemic/hypoxic injury. While inflammation/edema may have regressed when cocaine was discontinued, we cannot exclude a role for prednisone in protecting the patient from the ischemic/hypoxic sequelae of inflammation/edema. MRI is indispensable for diagnosing TL but EEG may provide additional useful diagnostic and prognostic information.

Fetal-Type Variants of the Posterior Cerebral Artery and Concurrent Infarction in the Major Arterial Territories of the Cerebral Hemisphere.

Fetal-type or fetal posterior cerebral artery (FPCA) is a variant of cerebrovascular anatomy in which the distal posterior cerebral artery (PCA) territory is perfused by a branch of the internal carotid artery (ICA). In the presence of FPCA, thromboembolism in the anterior circulation may result in paradoxical PCA territory infarction with or without concomitant infarction in the territories of the middle (MCA) or the anterior (ACA) cerebral artery. We describe 2 cases of FPCA and concurrent acute infarction in the PCA and ICA territories-right PCA and MCA in Patient 1 and left PCA, MCA, and ACA in Patient 2. Noninvasive angiography detected a left FPCA in both patients. While FPCA was clearly the mechanism of paradoxical infarction in Patient 2, it turned out to be an incidental finding in Patient 1 when evidence of a classic right PCA was uncovered from an old computed tomography scan image. Differences in anatomical details of the FPCA in each patient suggest that the 2 FPCAs are developmentally different. The FPCA of Patient 1 appeared to be an extension of the embryonic left posterior communicating artery (PcomA). Patient 2 had 2 PCAs on the left (PCA duplication), classic bilateral PCAs, and PcomAs, and absent left anterior choroidal artery (AchoA), suggesting developmental AchoA-to-FPCA transformation on the left. These 2 cases underscore the variable anatomy, clinical significance, and embryological origins of FPCA variants.

Acute renal failure is associated with higher death and disability in patients with acute ischemic stroke: analysis of nationwide inpatient sample.

BACKGROUND AND PURPOSE: Acute renal failure (ARF) in setting of acute ischemic stroke (AIS) is associated with worse outcome. We sought to determine the prevalence of ARF and effect on outcomes of patients with AIS. METHODS: Data from all patients admitted to US hospitals between 2002 and 2010 with a primary discharge diagnosis of ischemic stroke and secondary diagnosis of ARF were included. The effect of ARF on rates of intracerebral hemorrhage and discharge outcomes was analyzed after adjusting for potential confounders using logistic regression analysis. RESULTS: Of 7,068,334 patients with AIS, 372,223 (5.3%) had ARF during hospitalization. Dialysis was required in 2364 (0.6%) of 372,223 patients. Patients with AIS with ARF had higher rates of moderate to severe disability (41.3% versus 30%; P<0.0001), intracerebral hemorrhage (1.0% versus 0.5%; P<0.0001), and in-hospital mortality (8.4% versus 2.9%; P<0.0001) compared with those without ARF. After adjusting for confounding factors, patients with AIS with ARF had higher odds of moderate to severe disability (odds ratio, 1.3; 95% confidence interval, 1.3-1.4; P<0.0001), intracerebral hemorrhage (odds ratio, 1.4; 95% confidence interval, 1.3-1.6; P<0.0001), and death (odds ratio, 2.2; 95% confidence interval, 2.0-2.2; P<0.0001). CONCLUSIONS: ARF in patients with AIS is associated with significantly higher rates of moderate to severe disability at discharge and in-hospital mortality.