[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.

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.

[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.

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.

Case Report of Retarded Catatonia: Always Consider Catatonia as a Differential Diagnosis of Altered Mental Status.

BACKGROUND: Catatonia is a rare neuropsychiatric condition; it is estimated that around 10% of patients with mood disorders present signs and symptoms of catatonia. A catatonic syndrome is characterised by mutism, negativism, rigidity, and stupor. CASE REPORT: We report the case of a 59-year-old patient with a medical history of bipolar disorder who was admitted to the internal medicine service due to a seizure episode. During hospitalisation, the patient presented significant worsening of her clinical condition, showing marked symptoms of stupor and catatonia. Once the neurological and metabolic etiologies of altered mental status had been ruled out, pharmacological treatment with high doses of lorazepam was started. The patient had a complete clinical remission, and her evolution was favourable without any complications. Electroconvulsive therapy was recommended as a definitive treatment. CONCLUSIONS: The diagnosis of catatonia is a challenge for both hospitalists and psychiatrists due to the clinical presentation of catatonia. In reporting this clinical case, we want to emphasise the importance of taking into account the catatonic syndrome in our differential diagnoses in patients with altered mental status.

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.

Pervasive refusal syndrome. Three German cases provide further illustration.

Pervasive refusal syndrome (PRS) has been proposed as a new diagnostic entity among child and adolescent psychiatric disorders. It is characterized by a cluster of life-threatening symptoms including refusal of hood intake, decreased or complete lack of mobilization, and lack of communication as well as retreat from normal life activities. Active refusal to accept help as well as neglect of personal care have been core features of PRS in the limited number of cases reported in the last decade. There have, however; been cases with predominantly passive resistance, indicating the possibility that there may be a continuum from active refusal to passive resistance within PRS. Postulating this continuum allows for the integration of "depressive devitalization" -- a refusal syndrome mainly characterized by passive resistance -- into the concept of PRS. Here, three case vignettes of adolescent patients with PRS are presented. The patients' symptomatology can be allocated on this continuum of PRS. PRS and dissociative disorders are compared in greater detail and contrasted within this discussion of differential diagnoses at the poles of such a continuum. PRS is a useful diagnosis for cases involving symptoms of predominating refusal and retreat which cannot satisfactorily be classified by existing diagnostic categories, and which can mostly clearly be separated from dissociative disorder.

[Dissociation (conversion) - malingering - antisocial personality disorder: differential diagnostic reflection on the basis of a case study]. / Dissoziation (Konversion) - Simulation - Dissozialität: Differentialdiagnostische Überlegungen anhand eines Fallbeispiels.

In this case report we refer to the big challenge of making a diagnosis in a deliberate malingering in the field of mental disorders. We specifically describe the difficulty regarding the differentiation between a conversion disorder and malingering of a serial delinquent. For such a person avoiding criminal persecution is one of the most frequent reason to deceitfully simulate a mental illness. In this field, symptoms of conversion disorders exceed the average; furthermore, a great number of organic-neurological illnesses may appear to be very similar to a conversion disorder or in many cases a neurological disorder can actually be detected in the course of a somatic examination. A further obstacle for the differential diagnosis can be seen in the difficulty to discern it from factitious disorders. However, it is quite possible to discern the deliberate malingering of a mental disorder from a conversion disorder by means of the diligent diagnosis of a competent and experienced doctor/assessor who specialises.

Seizures and stupor during intravenous mannose therapy in a patient with CDG syndrome type 1b (MPI-CDG).

MPI-CDG (formally called CDG 1b), caused by phosphomannose isomerase (MPI) deficiency, leads to hypoglycaemia, protein losing enteropathy, hepatopathy, and thrombotic events, whereas neurologic development remains unaffected. Dietary supplementation of mannose can reverse clinical symptoms by entering the N-glycosylation pathway downstream of MPI. When oral intake of mannose in patients with MPI-CDG is not possible, e.g. due to surgery, mannose has to be given intravenously. We report a patient with MPI-CDG on intravenous mannose therapy that showed severe depression of consciousness and seizures without apparent cause. EEG and cranial MRI findings were compatible with metabolic coma whereas extended laboratory examinations including repeated blood glucose measurements were normal. Importantly, an intravenous bolus of glucose immediately led to clinical recovery and EEG improvement. Mannose did not interfere with glucose measurement in our assay. We suggest that in patients with MPI-CDG, intravenous mannose infusion can lead to intracellular ATP deprivation due to several mechanisms: (1) in MPI deficiency, mannose 6-P cannot be isomerised to fructose 6-P and therefore is unavailable for glycolysis; (2) animal data has shown that accumulating intracellular mannose 6-P inhibits glycolysis; and (3) elevated intracellular mannose 6-P may induce an ATP wasting cycle of dephosphorylation and rephosphorylation ("honey bee effect"). The mannose-induced metabolic inhibition may be overcome by high-dose glucose treatment. We caution that, in patients with MPI-CDG, life-threatening central nervous system disturbances may occur with intravenous mannose treatment. These may be due to intracellular energy failure. Clinical symptoms of energy deficiency should be treated early and aggressively with intravenous glucose regardless of blood glucose levels.

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.

Decreased Glasgow Coma Scale score does not mandate endotracheal intubation in the emergency department.

BACKGROUND: Decreased consciousness is a common reason for presentation to the emergency department (ED) and admission to acute hospital beds. In trauma, a Glasgow Coma Scale score (GCS) of 8 or less indicates a need for endotracheal intubation. Some advocate a similar approach for other causes of decreased consciousness, however, the loss of airway reflexes and risk of aspiration cannot be reliably predicted using the GCS alone. STUDY OBJECTIVE: A survey of all poisoned patients with a decreased GCS who were admitted to an ED short-stay ward staffed by experienced emergency physicians, to establish the incidence of clinically significant aspiration or other morbidities and endotracheal intubation. METHODS: A prospective, observational study was conducted of all patients admitted to the ED short-stay ward with a decreased level of consciousness (GCS < 15). RESULTS: The study included 73 patients with decreased consciousness as a result of drug or alcohol intoxication. The GCS ranged from 3 to 14, and 12 patients had a GCS of 8 or less. No patient with a GCS of 8 or less aspirated or required intubation. There was one patient who required intubation; this patient had a GCS of 12 on admission to the ward. CONCLUSIONS: This study suggests that it can be safe to observe poisoned patients with decreased consciousness, even if they have a GCS of 8 or less, in the ED.

[Suicide case of carbon dioxide poisoning using dry ice].

We had a suicide case suspected to result in death from carbon dioxide poisoning by dry ice in the car. A clay cooking stove with charcoal was in the car, but the charcoal had no burning sign. CO hemoglobin saturation degree of the suicide victim's blood was 0%. Moreover, there were signs that 50 kg of dry ice was brought in the car. To clarify the cause of death, reproducibility testing was carried out by using a car under the same conditions. CO2 concentration in it increased to 22% and O2 concentration decreased to 16% within 20 minutes. From these observations, his death was considered to be caused by hypoxia and CO2 narcosis. CO2 in the suicide victim's blood was higher than those in the blood of healthy persons, and the same range was visible in the blood of fire victims. These data might support above supposition concerned with the cause of death. Blood analysis will be helpful in clearing the cause of death by CO2 poisoning.

[Coma: etiology, diagnosis, and treatment]. / Koma: priezastys, diagnostika, gydymas.

SUMMARY: Coma is the disorder of consciousness because of the damage to diffused bilateral cerebral hemisphere cortex or reticular activating system. Coma can be caused by neurogenic (head brain injury), metabolic (endogenic), and toxic (exogenic) factors. To determine the cause of metabolic and toxic coma, laboratory tests are performed; in case of neurogenic coma, the neurologic examination is essential, when five systems are evaluated: the level of consciousness (according to Glasgow Coma Scale or Full Outline of Unresponsiveness Scale), photoreaction of pupils and ophthalmoscopic examination, oculomotoric, motoric, and cardiopulmonary systems. For the treatment of coma, adequate oxygenation and correction of blood circulation disorders are important. The treatment of metabolic coma is guided by special schemes; antidotes often are needed in the treatment of toxic coma, and surgery helps if traumatic brain injury is present. The prognosis and outcomes of the comatose patient depend on the age and comorbid diseases of the patient, the underlying cause of coma, timely medical help and its quality, and intensive treatment and care of the patient in coma.

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.