Dopamine/BDNF loss underscores narcosis cognitive impairment in divers: a proof of concept in a dry condition.

PURPOSE: Divers can experience cognitive impairment due to inert gas narcosis (IGN) at depth. Brain-derived neurotrophic factor (BDNF) rules neuronal connectivity/metabolism to maintain cognitive function and protect tissues against oxidative stress (OxS). Dopamine and glutamate enhance BDNF bioavailability. Thus, we hypothesized that lower circulating BDNF levels (via lessened dopamine and/or glutamate release) underpin IGN in divers, while testing if BDNF loss is associated with increased OxS. METHODS: To mimic IGN, we administered a deep narcosis test via a dry dive test (DDT) at 48 msw in a multiplace hyperbaric chamber to six well-trained divers. We collected: (1) saliva samples before DDT (T0), 25 msw (descending, T1), 48 msw (depth, T2), 25 msw (ascending, T3), 10 min after decompression (T4) to dopamine and/or reactive oxygen species (ROS) levels; (2) blood and urine samples at T0 and T4 for OxS too. We administered cognitive tests at T0, T2, and re-evaluated the divers at T4. RESULTS: At 48 msw, all subjects experienced IGN, as revealed by the cognitive test failure. Dopamine and total antioxidant capacity (TAC) reached a nadir at T2 when ROS emission was maximal. At decompression (T4), a marked drop of BDNF/glutamate content was evidenced, coinciding with a persisting decline in dopamine and cognitive capacity. CONCLUSIONS: Divers encounter IGN at - 48 msw, exhibiting a marked loss in circulating dopamine levels, likely accounting for BDNF-dependent impairment of mental capacity and heightened OxS. The decline in dopamine and BDNF appears to persist at decompression; thus, boosting dopamine/BDNF signaling via pharmacological or other intervention types might attenuate IGN in deep dives.

Common Carotid Artery Occlusion in a Young Patient: Can Large-Vessel Stroke Be the Initial Clinical Manifestation of Coronavirus Disease 2019?

BACKGROUND: The occurrence of large-vessel occlusion in young patients with coronavirus disease 2019 (COVID-19) infection has been exceedingly rare. An extensive review of reported studies revealed a few reported cases. In the present report, we have described the clinical presentation, radiological findings, and outcome of large-vessel occlusion in a young patient with COVID-19 and reviewed the pertinent reported data on this condition. CASE DESCRIPTION: A 31-year-old woman was in her usual state of health until she had presented with a 3-day history of right-sided weakness, slurred speech, and decreased vision. The patient had been taken to several hospitals where she had been treated conservatively with analgesics and discharged. Shortly thereafter, her weakness had become progressive. She had become severely dysarthric and unresponsive. On arrival to the emergency department, her physical examination revealed that she was stuporous, with a Glasgow coma scale of 10 (eye response, 3; verbal response, 2; motor response, 5). The National Institutes of Health Stroke Scale score was 19 on presentation. Brain computed tomography and computed tomography venography revealed an occluded left internal carotid artery and left middle cerebral artery with subacute left middle cerebral artery territory infarction and midline shift. Computed tomography angiography revealed complete occlusion of the left common carotid artery. An emergent decompressive craniectomy was successfully performed. The patient was shifted to the intensive care unit. She was later found to be positive for COVID-19. CONCLUSIONS: Although rare, patients with COVID-19 can present with large-vessel occlusion. Prompt identification of COVID-19-related coagulopathy is essential to assess young patients with clinical manifestations of infarction.

Delayed Diagnosis of Postintubation Tracheal Stenosis due to the Coronavirus Disease 2019 Pandemic: A Case Report.

Tracheal stenosis is an uncommon but severe problem after long-term intubation. Here, we report a patient who came from a containment zone of coronavirus disease 2019 (COVID-19) and presented with complaints of breathlessness and cough. She was suspected to have an infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Later, she developed type 2 respiratory failure and carbon dioxide narcosis because of delay in diagnosis of severe, near-complete postintubation tracheal stenosis due to over suspicion of COVID-19 during the current pandemic.

Cerebellar Hippocampal and Basal Nuclei Transient Edema with Restricted diffusion (CHANTER) Syndrome.

BACKGROUND: Abnormal restricted diffusion on magnetic resonance imaging is often associated with ischemic stroke or anoxic injury, but other conditions can present similarly. We present six cases of an unusual but consistent pattern of restricted diffusion in bilateral hippocampi and cerebellar cortices. This pattern of injury is distinct from typical imaging findings in ischemic, anoxic, or toxic injury, suggesting it may represent an under-recognized clinicoradiographic syndrome. Despite initial presentation with stupor or coma in the context of obstructive hydrocephalus, patients may have acceptable outcomes if offered early intervention. METHODS: We identified an ad hoc series of patients at our two institutions between years 2014 and 2017 who presented to the neurocritical care unit with severe, otherwise unexplained cerebellar edema and retrospectively identified several commonalities in history, presentation, and imaging. RESULTS: Between two institutions, we identified six patients-ages 33-59 years, four male-with similar presentations of decreased level of consciousness in the context of intoxicant exposure, with acute cytotoxic edema of the cerebellar cortex, hippocampi, and aspects of the basal nuclei. All patients presented with severe cerebellar edema which led to obstructive hydrocephalus requiring aggressive medical and/or surgical management. The five patients who survived to discharge demonstrated variable degrees of physical and memory impairment on discharge and at follow-up. CONCLUSIONS: We present findings of a potentially novel syndrome involving a distinct pattern of cerebellar and hippocampal restricted diffusion, with imaging and clinical characteristics distinct from ischemic stroke, hypoxic injury, and known toxidromes and leukoencephalopathies. Given the potential for favorable outcome despite early obstructive hydrocephalus, early identification and treatment of this syndrome are critical.

Thalamic strokes that severely impair arousal extend into the brainstem.

In this study, we evaluate the role of the thalamus in the neural circuitry of arousal. Level of consciousness within the first 12 hours of a thalamic stroke is assessed with lesion symptom mapping. Impaired arousal correlates with lesions in the paramedian posterior thalamus near the centromedian and parafascicular nuclei, posterior hypothalamus, and midbrain tegmentum. All patients with severely impaired arousal (coma, stupor) had lesion extension into the midbrain and/or pontine tegmentum, whereas purely thalamic lesions did not severely impair arousal. These results are consistent with growing evidence that pathways most critical for human arousal lie outside the thalamus. Ann Neurol 2018;84:926-930.

Electro-Radiological Observations of Grade III/IV Hepatic Encephalopathy Patients with Seizures.

BACKGROUND: Neurological complications in liver failure are common. Often under-recognized neurological complications are seizures and status epilepticus. These may go unrecognized without continuous electroencephalography (CEEG). We highlight the observed electro-radiological changes in patients with grade III/IV hepatic encephalopathy (HE) found to have seizures and/or status epilepticus on CEEG and the associated neuroimaging. METHODS: This study was a retrospective review of patients with West Haven grade III/IV HE and seizures/status epilepticus on CEEG. RESULTS: Eleven patients were included. Alcohol was the most common cause of HE (54.5%). All patients were either stuporous/comatose. The most common CEEG pattern was diffuse slowing (100%) followed by generalized periodic discharges (GPDs; 36.4%) and lateralized periodic discharges (LPDs, 36.4%). The subtype of GPDs with triphasic morphology was only seen in 27.3%. All seizures and/or status epilepticus were without clinical signs. Magnetic resonance imaging (MRI) was available in six patients. Cortical hyperintensities on diffusion weighted imaging sequence were seen in all six patients. One patient had CEEG seizure concomitantly with the MRI. Seven patients died prior to discharge. CONCLUSION: Seizures or status epilepticus in the setting of HE were without clinical findings and could go unrecognized without CEEG. The finding of cortical hyperintensity on MRI should lead to further evaluation for unrecognized seizure or status epilepticus.

[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.

Relationship of time to presentation after onset of upper GI bleeding with patient characteristics and outcomes: a prospective study.

BACKGROUND AND AIMS: We performed a prospective multi-national study of patients presenting to the emergency department with upper GI bleeding (UGIB) and assessed the relationship of time to presentation after onset of UGIB symptoms with patient characteristics and outcomes. METHODS: Consecutive patients presenting with overt UGIB (red-blood emesis, coffee-ground emesis, and/or melena) from March 2014 to March 2015 at 6 hospitals were included. Multiple predefined patient characteristics and outcomes were collected. Rapid presentation was defined as ≤6 hours. RESULTS: Among 2944 patients, 1068 (36%) presented within 6 hours and 576 (20%) beyond 48 hours. Significant independent factors associated with presentation ≤6 hours versus >6 hours on logistic regression included melena (odds ratio [OR], 0.22; 95% CI, 0.18-0.28), hemoglobin ≤80 g/L (OR, 0.47; 95% CI, 0.36-0.61), altered mental status (OR, 2.06; 95% CI, 1.55-2.73), albumin ≤30 g/L (OR, 1.43; 95% CI, 1.14-1.78), and red-blood emesis (OR, 1.29; 95% CI, 1.06-1.59). Patients presenting ≤6 hours versus >6 hours required transfusion less often (286 [27%] vs 791 [42%]; difference, -15%; 95% CI, -19% to -12%) because of a smaller proportion with low hemoglobin levels, but were similar with regard to hemostatic intervention (189 [18%] vs 371 [20%]), 30-day mortality (80 [7%] vs 121 [6%]), and hospital days (5.0 ± 0.2 vs 5.0 ± 0.2). CONCLUSIONS: Patients with melena alone delay their presentation to the hospital. A delayed presentation is associated with a decreased hemoglobin level and increases the likelihood of transfusion. Other outcomes are similar with rapid versus delayed presentation. Time to presentation should not be used as an indicator for poor outcome. Patients with delayed presentation should be managed with the same degree of care as those with rapid presentation.

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.

Massive exacerbation of multiple sclerosis after withdrawal and early restart of treatment with natalizumab.

We present a 46-year-old woman with a relapse of multiple sclerosis (MS) that began 3 months after withdrawal from long-term treatment with natalizumab. Shortly after restart of a single dose of natalizumab she developed a fulminant MS rebound with stupor and tetraparesis. Cerebral MRI showed massive progression in the number of lesions and tumefactive lesions with ring gadolinium-enhancement. Stereotactic brain biopsy revealed acute demyelination and B-cell dominated inflammation. The patient improved during therapeutic plasma exchange. We speculate that early restart of natalizumab in the case of a relapse may worsen disease evolution possibly by modifying regulatory immune effector processes during an inflammatory rebound phase. A restart of natalizumab in MS patients suffering from a recent relapse or with signs of active inflammation should be considered with caution.

Morgagni hernia with respiratory failure aggravated by noninvasive positive pressure ventilation: a case report and overview of the literature.

An elderly woman diagnosed with multiple myeloma (MM) in 2007 had improved with chemotherapy. She had severe kyphosis and a diaphragmatic hernia (DH), but no respiratory symptoms. In 2011, because of thoracic deformity and emaciation, we advised her to continue the previously prescribed domiciliary noninvasive positive pressure ventilation (NPPV) therapy for chronic type II respiratory failure. However, she refused to continue NPPV. She was later admitted for deterioration in respiratory status and carbon dioxide (CO2) narcosis. We believed her low adherence to domiciliary NPPV caused CO2 narcosis; hence, we advised her to continue domiciliary NPPV and she complied. In May 2012, the now 79-year-old patient was admitted for acute exacerbation of chronic respiratory failure and CO2 narcosis. Chest imaging suggested that DH had caused a deterioration of her status. She underwent laparoscopic diaphragmatic hernia repair. Operative findings revealed a retrosternal hernia sac, and she was diagnosed as having a Morgagni hernia (MH). Her respiratory status subsequently improved. We hypothesize that NPPV increased intra-abdominal pressure, thereby worsening the MH and exacerbating respiratory failure. We believe that clinicians should be cautious when prescribing NPPV for MH patients.

Predictors of five days mortality in diabetic ketoacidosis patients: a prospective cohort study.

AIM: to determine the role of serum lactate and diabetic ketoacidosis (DKA) severity as predictors for five-days mortality in DKA patients. METHODS: a prospective cohort study was conducted in DKA patients admitted to emergency department (ED) at Cipto Mangunkusumo Hospital, Jakarta, Indonesia, during 2007-2008 periods. Predictors for 5 days mortality in DKA patients in this study including serum lactate and DKA severity (plasma glucose, arterial blood pH, serum bicarbonate, osmolality, anion gap, and alteration in sensorium) at admission. Cox's Proportional Hazard Regression Analysis was used to determine independent predictors for 5-days mortality among study population. RESULTS: sixty patients with diabetic ketoacidosis were enrolled in the study; in which 24 (40%) patients were died within 5 days after admission. In the multivariate analysis, the lactate level 4 mmol/L (HR, 3.09; 95% CI, 1.36-7.05) and altered in sensorium stuporous/comatose (HR, 3.38; 95% CI, 1.45-7.87) were identified as independent predictors for 5-days mortality in DKA adult patients. CONCLUSION: lactate level 4 mmol/L and altered in sensorium stuporous/comatose can be used to predict 5-days mortality in adult patients with DKA.

Wax on, wax off: a rare case of catatonia.

Catatonia was first described by a German psychiatrist, Karl Kahlbaum, in 1874. It is a behavioral syndrome marked by an inability to move normally, which can occur in the context of many underlying general medical and psychiatric disorders. A wide variety of neurologic, metabolic, drug-induced, and psychiatric causes of catatonia have been reported. We present a unique case of late onset catatonia in a 56-year-old man with no prior medical or psychiatric history initially presenting with stroke-like symptoms. The patient was awake and alert, with spontaneous eye opening, but completely nonverbal and not following any commands. Specifically, the patient demonstrated stupor, catalepsy, mutism, and negativism. After extensive emergency department testing, including negative computed tomography head, negative magnetic resonance imaging brain, negative electroencephalogram, and normal laboratory results, the patient was diagnosed with new-onset bipolar disorder with depressive features presenting as catatonia. Recognizing catatonia is important because it may be caused or exacerbated by treatment of the underlying disorder. Failure to institute treatment early in the course of catatonia is associated with a poor prognosis.

Supratentorial subdural hemorrhage of a previous head injury and cerebellar hemorrhage after cervical spinal surgery: a case report and review of the literature.

STUDY DESIGN: Case report. OBJECTIVE: To report a case of an acute supratentorial subdural hemorrhage (SDH) of a previous head injury site and cerebellar hemorrhage, after an incidental dural tear during spine surgery. SUMMARY OF BACKGROUND DATA: Intracranial hemorrhage, such as subdural, cerebellar, subarachnoid, and epidural hemorrhage after a dural tear during spinal surgery, is a rare and poorly recognized complication. Moreover, only 3 cases in patients with concurrent SDH and cerebellar hemorrhage have been described in the literature, and none of these reports demonstrated the bleeding point on the adhesion site of the dural at the regions of the previous head injury. METHODS: A case report and literature review are presented. RESULTS: A 46-year-old male underwent occipital cervical surgery for os odontoideum. Intraoperatively, a dural tear was noted and repaired, but he later developed postoperative disturbance of consciousness. A head computed tomographic scan revealed a supratentorial SDH and cerebellar hemorrhage. Evacuation of the supratentorial SDH was performed via craniotomy, and the bleeding point was revealed to be on the adhesion site of the dural where the patient had experienced a previous head injury. The patient made a full recovery. CONCLUSION: This report illustrates that cerebrospinal fluid leakage after a dural tear during spinal surgery may cause intracranial hemorrhage. A previous head trauma could be a risk factor for such hemorrhagic complications. Headache, nausea, and postoperative stupor after spinal surgery, especially after an accidental durotomy, should be considered possible indications of intracranial hemorrhage, and affected patients should be investigated with computed tomography or magnetic resonance imaging. LEVEL OF EVIDENCE: N/A.