EEG and video documentation of benzodiazepine challenge in catatonic stupor: A case report.

INTRODUCTION: Catatonia, a psychomotor disorder characterized by diverse clinical signs, including stupor and mutism, remains elusive in its causes and a challenge to diagnose. Moreover, it is often underrecognized due to its resemblance to disorders of consciousness. However, when diagnosing catatonia, an antipsychotic medication may exacerbate the condition. The first-line treatment typically includes benzodiazepines and/or electroconvulsive therapy (ECT). CASE REPORT: A 60-year-old woman with systemic lupus erythematosus (SLE) and epilepsy presented with catatonic stupor. Despite stable treatment, she experienced an acute deterioration in consciousness, requiring hospitalization. Her condition improved markedly following a benzodiazepine challenge, as documented on EEG. This improvement was short-lived, but a second benzodiazepine challenge restored her from E1V1M1 (stupor) to E4V5M6 within minutes, as documented by a video recording. The patient was treated with lorazepam 1.5 mg/day orally and did not experience further relapses. DISCUSSION: The diagnosis of catatonia had been based on her scores on the Bush-Francis Catatonia Rating Scale (BFCRS; Screening, 6/14; Severity, 19), despite meeting only two DSM-5 criteria for catatonia (stupor and mutism). The diagnosis was supported by EEG and video documentation, excluding other potential differential diagnoses such as nonconvulsive status epilepticus and encephalopathy. Additional quantitative EEG analyses indicated that benzodiazepine administration increased brainwide alpha and beta band power significantly, suggesting that the benzodiazepine normalized attention, consciousness, and long-range synchronization. This report additionally emphasizes the significance of video recordings in managing catatonia, and it helps in accurately tracking symptoms, documenting comprehensively, and improving patient understanding, which is crucial for treatment adherence.

Anti-SARS-CoV-2 antibodies in the CSF, blood-brain barrier dysfunction, and neurological outcome: Studies in 8 stuporous and comatose patients.

OBJECTIVE: To investigate the pathophysiologic mechanism of encephalopathy and prolonged comatose or stuporous state in severally ill patients with coronavirus disease 2019 (COVID-19). METHODS: Eight COVID-19 patients with signs of encephalopathy were tested for antibodies to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the serum and CSF using a Food and Drug Administration-approved and independently validated ELISA. Blood-brain barrier (BBB) integrity and immunoglobulin G (IgG) intrathecal synthesis were further tested using albumin and IgG indices. The CSF was also tested for autoimmune encephalitis antibodies and 14-3-3, a marker of ongoing neurodegeneration. RESULTS: All patients had anti-SARS-CoV-2 antibodies in their CSF, and 4 of 8 patients had high titers, comparable to high serum values. One patient had anti-SARS-CoV-2 IgG intrathecal synthesis, and 3 others had disruption of the blood-brain barrier. The CSF in 4 patients was positive for 14-3-3-protein suggesting ongoing neurodegeneration. In all patients, the CSF was negative for autoimmune encephalitis antibodies and SARS-CoV-2 by PCR. None of the patients, apart from persistent encephalopathic signs, had any focal neurologic signs or history or specific neurologic disease. CONCLUSIONS: High-titer anti-SARS-CoV-2 antibodies were detected in the CSF of comatose or encephalopathic patients demonstrating intrathecal IgG synthesis or BBB disruption. A disrupted BBB may facilitate the entry of cytokines and inflammatory mediators into the CNS enhancing neuroinflammation and neurodegeneration. The observations highlight the need for prospective CSF studies to determine the pathogenic role of anti-SARS-CoV-2 antibodies and identify early therapeutic interventions.

Segmental Hair Testing of Triazolam to Unmask a Suspected Case of Idiopathic Recurrent Stupor.

ABSTRACT: Stupor is a diagnostic challenge at emergency department. Differential diagnosis includes idiopathic recurrent stupor, formerly attributed to "endozepine-4" accumulation. This condition has been recently questioned because many suspected cases resulted in exogenous benzodiazepine intake that eludes the conventional toxicological assay. In case of unexplained recurrent stupor, to extend the benzodiazepine search in nonconventional matrices can allow unmasking of hidden toxic behavior.

[Psychiatric emergencies]. / Notfälle aufgrund psychischer Störungen.

Psychiatric emergencies present a frequent and interdisciplinary challenge. Clinical diagnosis and management are complicated by the acuity, and the patient's compliance is often limited by the illness. Psychiatric emergencies include states of acute agitation, suicidality, delirium, stupor, and drug-induced emergencies. Sometimes interventions such as conversational contact, responding empathically to patients, or "talking down" are sufficient. If pharmacotherapy is necessary, benzodiazepines and antipsychotic drugs are the primary agents of choice.

[Unconsciousness and clouded awareness]. / Bewusstseinsstörung oder -trübung.

Stupor and coma are clinical states in which patients have impaired responsiveness or are unresponsive to external stimulation and are either difficult to arouse or are unarousable. The term stupor refer to states between alertness and coma. An alteration in arousal represents an acute life-threatening emergency, requiring prompt intervention for preservation of life and brain function.

Steak and Stupor: seizures and E. coli O157 infection.

Neurological complications of haemolytic uraemic syndrome (HUS) include altered states of consciousness, seizures, ischaemic stroke and encephalopathy. Adult-onset HUS is uncommon, and there is only a limited literature reporting neurological complications in this population. We report an adult with Shiga toxin-associated HUS complicated by focal-onset non-convulsive status epilepticus, who made a full neurological recovery.

Neuroleptic malignant syndrome masked by cerebral malaria.

A 38-year-old man with an underlying psychiatric illness presented with altered sensorium and abnormal behaviour. He was febrile at 38°C and weak looking; otherwise no other abnormalities were detected. A blood film conducted for malarial parasite (BFMP) revealed Plasmodium falciparum; hence a diagnosis of cerebral malaria was made. He was treated with antimalarial drugs for 2 days prior to being transferred out to the ward following clinical improvement. He subsequently developed episodes of stupor and refusal of feeding. Following an evaluation by the psychiatrist, a diagnosis of catatonic schizophrenia was made and he was started on oral sulpiride and benhexol. Unfortunately, he developed high-grade fever at 40°C with muscle rigidity and fasciculation. The diagnosis of neuroleptic malignant syndrome (NMS) was clinched and the antipsychotics were discontinued. However he succumbed to NMS several days later due to multiorgan failure.

Tiagabine-induced stupor in patients with psychogenic nonepileptic seizures: nonconvulsive status epilepticus or encephalopathy?

BACKGROUND: Nonconvulsive status epilepticus has been rarely reported with tiagabine (TGB) use. METHODS: We report findings from continuous video-EEG monitoring and serial neurological examinations during prolonged episodes of stupor associated with TGB use in three patients who did not have epilepsy. RESULTS: All three patients had emergence of new type of events after starting TGB treatment. All three patients had gradual decline in responsiveness to verbal stimuli, intermittent twitching of the upper extremities, and urinary incontinence. The corresponding EEG showed gradual build-up of generalized bisynchronous delta-wave activity with subsequent intermingled sharp transients. Two patients did not respond to IV lorazepam, one of whom also did not respond to IV phenytoin. The EEG slowly normalized in conjunction with associated clinical improvement. Habitual seizures were found to be psychogenic, with no interictal evidence for epilepsy. CONCLUSION: Tiagabine-related stupor may represent a form of toxic encephalopathy in some cases rather than nonconvulsive status epilepticus.

Altered mental status in older patients in the emergency department.

Altered mental status is a common chief compliant among older patients in the emergency department (ED). Acute changes in mental status are more concerning and are usually secondary to delirium, stupor, and coma. Although stupor and coma are easily identifiable, the clinical presentation of delirium can be subtle and is often missed without actively screening for it. For patients with acute changes in mental status the ED evaluation should focus on searching for the underlying etiology. Infection is one of the most common precipitants of delirium, but multiple causes may exist concurrently.

Stupor due to possible interaction between Lorazepam and valproic acid: report of two cases.

Valproate (VPA) and lorazepam are excreted mainly by glucuronide conjugation. VPA reduces the excretion of lorazepam as a result of the administration of these two medications together. As a result of these interactions, even if rarely, serious adverse effects such as coma may develop. Herein, we present two cases of stupor which developed after the addition of lorazepam to treatment administered with VPA. The first patient was being followed for five years with a diagnosis of schizoaffective disorder. She was subjected to a treatment of VPA at 1000 mg/day and an antipsychotic drug. On the twentieth day of the treatment, Lorazepam 2.5 mg was administered as an anxiolytic. The second patient was being followed with a diagnosis of schizophrenia for nine years. A VPA treatment of 750 mg/day was initiated together with an antipsychotic treatment. On the eighth day of the treatment, Lorazepam 2.5 mg was administered. A few hours later, a stupor manifestation developed in both of the patients. Administration of the entire medication to the patients was terminated and parenteral liquid administration was initiated. The clinical profile was back to normal approximately 24-36 hours following the termination of the medication. Studies about the clinical reflections of the VPA and Lorazepam interaction are limited. However, it must be remembered that as a result of the interaction of these two medications, conditions that vary between stupor and coma may arise.

Seizures and postictal stupor in a patient with uncontrolled Graves' hyperthyroidism.

A 16-year-old girl with a history of Graves' disease presented with two episodes of generalised tonic-clonic seizures, necessitating intensive care admission. Laboratory examination demonstrated a suppressed thyroid-stimulating hormone level with dramatically elevated free triiodothyronine, free thyroxine and thyroid-stimulating immunoglobulins. Cerebrospinal fluid analysis showed oligoclonal banding in the absence of pleocytosis, thyroid peroxidase antibodies or infection. Neuroimaging revealed the presence of a congenital arachnoid cyst in the right temporal lobe. Despite restoration of euthyroidism and administration of antiepileptic and antiviral drugs, neurological features persisted. Subsequently, intravenous corticoids were administered to exclude the contribution of an underlying autoimmune encephalopathy. The patient gradually recovered and, in retrospect, elevated serum N-methyl-D-aspartic acid-receptor (NMDA-R) antibodies were detected. Although this patient presented with an intracerebral arachnoid cyst that can act epileptogenic per se, the combination of prolonged postictal encephalopathy with unresponsiveness to antiepileptic measures, absence of focal epileptiform activity on EEG, response to corticoids and serum NMDA-R antibody positivity favours the diagnosis of autoimmune NMDA-R encephalitis in this case.