Cause Of Coma Research Articles

Coma Due to Artery of Percheron Infarction: An Unusual Case Report

Ischemic stroke attributable to obstruction of the artery of Percheron (AOP), an infrequent anatomical arterial variant perfusing both medial thalami, can pose difficult diagnostic challenges. Obstruction or occlusion of the AOP results in bilateral paramedian thalamic infarction which is an unusual and rare vascular cause of coma. We present a 65-year-old male patient who came to the emergency department with altered sensorium for 10 days. The initial computed tomography (CT) brain was normal, followed by subsequent CT revealing an ill-defined hypodensity in the ventromedial aspect of the left thalamus and ventral aspect of the midbrain. T2/fluid-attenuated inversion recovery magnetic resonance imaging illustrated hyperintensity in the mesencephalon and bilateral paramedian thalami with restricted diffusion, suggesting an AOP infarct.

GFAP point-of-care measurement for prehospital diagnosis of intracranial hemorrhage in acute coma

BackgroundPrehospital triage and treatment of patients with acute coma is challenging for rescue services, as the underlying pathological conditions are highly heterogenous. Recently, glial fibrillary acidic protein (GFAP) has been identified as a biomarker of intracranial hemorrhage. The aim of this prospective study was to test whether prehospital GFAP measurements on a point-of-care device have the potential to rapidly differentiate intracranial hemorrhage from other causes of acute coma.MethodsThis study was conducted at the RKH Klinikum Ludwigsburg, a tertiary care hospital in the northern vicinity of Stuttgart, Germany. Patients who were admitted to the emergency department with the prehospital diagnosis of acute coma (Glasgow Coma Scale scores between 3 and 8) were enrolled prospectively. Blood samples were collected in the prehospital phase. Plasma GFAP measurements were performed on the i-STAT Alinity® (Abbott) device (duration of analysis 15 min) shortly after hospital admission.Results143 patients were enrolled (mean age 65 ± 20 years, 42.7% female). GFAP plasma concentrations were strongly elevated in patients with intracranial hemorrhage (n = 51) compared to all other coma etiologies (3352 pg/mL [IQR 613–10001] vs. 43 pg/mL [IQR 29–91.25], p < 0.001). When using an optimal cut-off value of 101 pg/mL, sensitivity for identifying intracranial hemorrhage was 94.1% (specificity 78.9%, positive predictive value 71.6%, negative predictive value 95.9%). In-hospital mortality risk was associated with prehospital GFAP values.ConclusionIncreased GFAP plasma concentrations in patients with acute coma identify intracranial hemorrhage with high diagnostic accuracy. Prehospital GFAP measurements on a point-of-care platform allow rapid stratification according to the underlying cause of coma by rescue services. This could have major impact on triage and management of these critically ill patients.Graphical

The arousal effect of An-Gong-Niu-Huang-Wan on alcoholic-induced coma rats: A research based on EEG

Ethnopharmacological relevanceAcute alcohol intoxication is one of the leading causes of coma. A well-regarded Chinese herbal formula, known as An-Gong-Niu-Huang-Wan (AGNHW), has garnered recognition for its efficacy in treating various brain disorders associated with impaired consciousness, including acute alcohol-induced coma. Despite its clinical effectiveness, the scientific community lacks comprehensive research on the mechanistic aspects of AGNHW’s impact on the electroencephalogram (EEG) patterns observed during alcohol-induced coma. Gaining a deeper understanding of AGNHW’s mechanism of action in relation to EEG characteristics would hold immense importance, serving as a solid foundation for further advancing its clinical therapeutic application. Aim of the studyThe study sought to investigate the impact of AGNHW on EEG activity and sleep EEG patterns in rats with alcoholic-induced coma. Materials and methodsA rat model of alcohol-induced coma was used to examine the effects of AGNHW on EEG patterns. Male Sprague-Dawley rats were intraperitoneally injected with 32% ethanol to induce a coma, followed by treatment with AGNHW. Wireless electrodes were implanted in the cortex of the rats to obtain EEG signals. Our analysis focused on evaluating alterations in the Rat Coma Scale (RCS), as well as assessing changes in the frequency and distribution of EEG patterns, sleep rhythms, and body temperature subsequent to AGNHW treatment. ResultsThe study found a significant increase in the δ-band power ratio, as well as a decrease in RCS scores and β-band power ratio after modeling. AGNHW treatment significantly reduced the δ-band power ratio and increased the β-band power ratio compared to naloxone, suggesting its superior arousal effects. The results also revealed a decrease in the time proportion of WAKE and REM EEG patterns after modeling, accompanied by a significant increase in the time proportion of NREM EEG patterns. Both naloxone and AGNHW effectively counteracted the disordered sleep EEG patterns. Additionally, AGNHW was more effective than naloxone in improving hypothermia caused by acute alcohol poisoning in rats. ConclusionOur study provides evidence for the arousal effects of AGNHW in alcohol-induced coma rats. It also suggests a potential role for AGNHW in regulating post-comatose sleep rhythm disorders.

Abstract 151: GFAP Measurements for Rapid Prehospital Identification of Intracranial Hemorrhage in Patients With Acute Coma

Background: Prehospital triage and treatment of patients with acute coma is challenging for rescue services, as the underlying pathogenetic conditions are highly heterogenous and difficult to assess. Glial fibrillary acidic protein (GFAP) has been recently identified as a biomarker of intracerebral hemorrhage. The aim of this study was to test the diagnostic value of a GFAP point-of-care(poc) device to rapidly differentiate intracranial hemorrhage from other causes of acute coma (including seizures, metabolic disorders, cardiovascular disorders, and intoxication) in the prehospital phase. Methods: Patients who were admitted to the emergency department due to acute coma (Glasgow Coma Scale scores between 3-8) were enrolled prospectively. Blood samples were collected already in the prehospital phase. Plasma GFAP measurements were performed on the i-STAT Alinity® (Abbott) device (duration of analysis 15 min). The primary endpoint was the final diagnosis at hospital discharge. Results: 95 patients were enrolled (mean age 64±20 years, 43% female). GFAP concentrations were strongly elevated in patients with a primary cerebral cause of coma compared to primary non-cerebral causes (p&lt;0.001). The GFAP concentrations (mean±SD in pg/mL) according to final diagnosis were as follows: intracerebral hemorrhage 4840±4500 (n=15), subarachnoid hemorrhage 4858±4662 (n=11), subdural or epidural hematoma 3462±4005 (n=4), ischemic stroke 992±2857 (n=12), seizure 45±21 (n=11), cardiovascular or metabolic disorder 258±888 (n=29), intoxication 30±2 (n=6), psychogenic stupor 29±0 (n=2); n=5 patients had missing diagnoses. GFAP values over 1000 pg/ml indicated a primary cerebral cause of coma with 100% certainty (hereof, 86% had intracranial hemorrhage). Conclusion: Increased GFAP plasma values in patients with acute coma identify a primary cerebral cause of coma (mostly intracranial hemorrhage) with very high diagnostic accuracy. Patients with primary non-cerebral causes of coma showed overall low GFAP concentrations. Prehospital GFAP measurements on a poc platform may allow rapid stratification according to the underlying cause of coma by rescue services. This could have major impact on triage and management of these critically ill patients.

Hypervitaminosis D induced hypercalcemia leading to coma: A case report

An elderly female presented with abdominal pain, vomiting and easy fatigability. Her sensorium gradually declined and became comatose. She was on Methotrexate, folic acid and prednisolone for her rheumatoid arthritis. The neurological examination and neuroimaging did not contribute in making the diagnosis. It is challenging to diagnose a metabolic cause of coma. Once diagnosis is established, the management becomes easier. On detailed investigation, she was found to have severe hypercalcemia with corrected serum calcium level being 18.2 mg%. Serum vitamin D level was also high, 150 ng/ml. On probing for detailed history, it was revealed that she had been taking a weekly dose of 60,000 IU of vitamin D for nearly 5 years. In recent times, association of various diseases has been reported with vitamin D deficiency. Vitamin D supplementation seems justified in this patient considering her age and the fact that she had rheumatoid arthritis; she was also taking corticosteroid. The recommended dose of vitamin D has been 400–800 IU/day. However, it is often prescribed at a dose of 60,000 IU/week, and sometimes patients self-medicate. There are no guidelines available for prescribing vitamin D at such a strength. Though safety of vitamin D has been established, vitamin D toxicity can occur sporadically with serious consequences. This was managed with intravenous fluids and diuretics. The patient also required subcutaneous calcitonin and low dose of corticosteroid, in addition to a session of haemodialysis for her hypercalcemia. The patient’s sensorium gradually improved as her calcium level returned to normalcy.

Bewusstseinsstörung auf der pädiatrischen Intensivstation: Ätiologie und Diagnostik – Englische Version

AbstractThis article provides an overview of the management of children with disorders of consciousness. Rapid diagnostics are necessary to identify treatable etiologies and minimize neurological sequelae. The differential diagnosis is extensive. Brief neurological findings include quantification of impaired consciousness using the Glasgow Coma Scale (GCS), testing of the eyes, motor function, and the presence of meningism. Laboratory tests include rapid exclusion of hypoglycemia and, if CNS infection is suspected, CSF examination. An emergency head CT is mandatory in cases of nonreactive unilateral or bilateral pupils before further diagnostic work-up is carried out. We recommend head MRI, especially if encephalitis, vasculitis, ischemic stroke, and sinus vein thrombosis are suspected. An EEG rarely provides clues to the cause of coma but it serves primarily as an objective measure of the severity of encephalopathy, the prognosis, and the effectiveness of therapy.

Malaria in Children: Updates on Management and Prevention.

Malaria in Children: Updates on Management and Prevention.

A Literature Review of Clinical Characteristics of Cerebral Malaria

Malaria is a disease transmitted by the bite of the female Anopheles mosquito and caused by protozoa of the genus Plasmodium. Malaria infection has several manifestations with cerebral malaria (CM) being the most severe neurological complication and a leading cause of malaria death. Cerebral malaria is characterized by a coma at least 1 hour after a seizure or a hypoglycemia, asexual forms of Plasmodium falciparum on peripheral blood smears, with the absence of any other causes of coma. This definition is quite vague in practice, thus making an accurate identification of clinical characteristics of cerebral malaria necessary in diagnosis to help reducing malaria deaths. This article is to summarize the medical literature to clarify the clinical characteristics of cerebral malaria.

Time-Frequency Analysis of Somatosensory Evoked High-Frequency (600 Hz) Oscillations as an Early Indicator of Arousal Recovery after Hypoxic-Ischemic Brain Injury.

Cardiac arrest (CA) remains the leading cause of coma, and early arousal recovery indicators are needed to allocate critical care resources properly. High-frequency oscillations (HFOs) of somatosensory evoked potentials (SSEPs) have been shown to indicate responsive wakefulness days following CA. Nonetheless, their potential in the acute recovery phase, where the injury is reversible, has not been tested. We hypothesize that time-frequency (TF) analysis of HFOs can determine arousal recovery in the acute recovery phase. To test our hypothesis, eleven adult male Wistar rats were subjected to asphyxial CA (five with 3-min mild and six with 7-min moderate to severe CA) and SSEPs were recorded for 60 min post-resuscitation. Arousal level was quantified by the neurological deficit scale (NDS) at 4 h. Our results demonstrated that continuous wavelet transform (CWT) of SSEPs localizes HFOs in the TF domain under baseline conditions. The energy dispersed immediately after injury and gradually recovered. We proposed a novel TF-domain measure of HFO: the total power in the normal time-frequency space (NTFS) of HFO. We found that the NTFS power significantly separated the favorable and unfavorable outcome groups. We conclude that the NTFS power of HFOs provides earlier and objective determination of arousal recovery after CA.

Neuroimmune Regulation in Sepsis-Associated Encephalopathy: The Interaction Between the Brain and Peripheral Immunity

Sepsis-associated encephalopathy (SAE), the most popular cause of coma in the intensive care unit (ICU), is the diffuse cerebral damage caused by the septic challenge. SAE is closely related to high mortality and extended cognitive impairment in patients in septic shock. At present, many studies have demonstrated that SAE might be mainly associated with blood–brain barrier damage, abnormal neurotransmitter secretion, oxidative stress, and neuroimmune dysfunction. Nevertheless, the precise mechanism which initiates SAE and contributes to the long-term cognitive impairment remains largely unknown. Recently, a growing body of evidence has indicated that there is close crosstalk between SAE and peripheral immunity. The excessive migration of peripheral immune cells to the brain, the activation of glia, and resulting dysfunction of the central immune system are the main causes of septic nerve damage. This study reviews the update on the pathogenesis of septic encephalopathy, focusing on the over-activation of immune cells in the central nervous system (CNS) and the “neurocentral–endocrine–immune” networks in the development of SAE, aiming to further understand the potential mechanism of SAE and provide new targets for diagnosis and management of septic complications.

Frequency of Nonconvulsive Seizures among Pediatric Systemic Cancer Patients with Acute Encephalopathy: Emergent Bedside EEG in Resource Constrained Communities

Purpose: To determine the incidence of nonconvulsive seizures (NCSz) among children with systemic cancer, who underwent unexplained acute severe encephalopathy (GCS≤8) during admission in ICUs and Neuro-ICUs.&#x0D; Study Design: Multicenter prospective observational study describing sub-clinical seizures and electroencephalographic (EEG) features of children (1-16 years) with acute unexplained encephalopathy who underwent emergent bedside EEG≥30min monitoring.&#x0D; Material and Methods: We conducted a prospective longitudinal observational study design and EEG assessment of 40 systemic cancer patients age ≤16years, consecutively diagnosed and admitted in intensive care units (ICUs) and neurointensive care units (Neuro-ICUs) of different cancer hospitals with unexplained acute impaired consciousness (GCS≤08) within ≤6hr of such deterioration. Bed-side EEG recordings of ≥30min were done according to the clinical scenario and the requirements of the treating neurologist/intensivist. Patients with brain tumor, brain metastasis, seizures or those with known cause of coma were excluded. Data surrounding clinical, electrographic, and treatment factors were collected Via a prospective systematic review of medical records and EEGs for correlation with diagnosis, change in the diagnosis and management.&#x0D; Results: Over a period of 2 years, 40 children, 22.5% 1-5yeras, 37.5% 6-10years, 40% 11-16years; boys 65% and girls 35%, who had systemic cancer with a median age of 9.8 years with unexplained acute deterioration of conscious level (GCS≤08). This cohort underwent bed-side EEG of ≥30 min, which was abnormal in 100% of the records. The main reasons for EEG requests were: 1) unexplained impaired consciousness 22(55%) and 2) reason one plus subtle convulsion 18(45%). The most common EEG abnormalities were invariant mixed theta-delta slowing (27.5%), followed by Low-amplitude delta pattern plus epileptiform discharges (20%) and there was electrographic evidence of EEG seizures in 17(42.5%) of the cohort. These electrographic seizures were present in 55.5% of 18 patients with subtle convulsions, whereas were documented only in 20% of the 22 patients without such movements. Electrographic seizures among patients with subtle convulsions responded to antiseizure drugs in 75% cases as compared 50% such response among patients without such convulsions.&#x0D; Conclusion: Emergent bed-side EEG record of ≥30 min is useful in systemic cancer patients admitted in NCUs and Neuro-ICUs with acutely impaired consciousness with or without abnormal body movements. Neurology consultation and EEG studies in these comatose patients provide useful diagnostic information.

Non-traumatic coma in young children in Benin: are viral and bacterial infections gaining ground on cerebral malaria?

BackgroundWhile malaria morbidity and mortality have declined since 2000, viral central nervous system infections appear to be an important, underestimated cause of coma in malaria-endemic Eastern Africa. We aimed to describe the etiology of non-traumatic comas in young children in Benin, as well as their management and early outcomes, and to identify factors associated with death.MethodsFrom March to November 2018, we enrolled all HIV-negative children aged between 2 and 6 years, with a Blantyre Coma Score ≤ 2, in this prospective observational study. Children were screened for malaria severity signs and assessed using a systematic diagnostic protocol, including blood cultures, malaria diagnostics, and cerebrospinal fluid analysis using multiplex PCR. To determine factors associated with death, univariate and multivariate analyses were performed.ResultsFrom 3244 admissions, 84 children were included: malaria was diagnosed in 78, eight of whom had a viral or bacterial co-infection. Six children had a non-malarial infection or no identified cause. The mortality rate was 29.8% (25/84), with 20 children dying in the first 24 h. Co-infected children appeared to have a poorer prognosis. Of the 76 children who consulted a healthcare professional before admission, only 5 were prescribed adequate antimalarial oral therapy. Predictors of early death were jaundice or increased bilirubin [odd ratio (OR)= 8.6; 95% confidential interval (CI): 2.03–36.1] and lactate > 5 mmol/L (OR = 5.1; 95% CI: 1.49–17.30). Antibiotic use before admission (OR = 0.1; 95% CI: 0.02–0.85) and vaccination against yellow fever (OR = 0.2, 95% CI: 0.05–0.79) protected against mortality.ConclusionsInfections were found in all children who died, and cerebral malaria was by far the most common cause of non-traumatic coma. Missed opportunities to receive early effective antimalarial treatment were common. Other central nervous system infections must be considered in their management. Some factors that proved to be protective against early death were unexpected.

Frequency of major causes of coma patients presented to emergency room of tertiary care hospitals with impaired conscious level, in Qassim region of Saudi Arabia.

Background: Disorders of consciousness including coma can be caused by a wide variety of etiologies affecting the central nervous system. Severity of coma may vary according to the causes of coma and patient’s characteristics. Objective: To determine frequency of major causes of coma patients presented to Emergency Department (ED) of tertiary care hospitals in Qassim region of Saudi Arabia. Methods: This retrospective audit study consisting of cases of coma, presented with impaired conscious level of any age and either gender admitted through ED of tertiary care hospitals in X region of Saudi Arabia over past 2 years. Patients with transient impairment of conscious level, pregnant women, referred cases of multiple organ failure and no clear etiological diagnosis on discharge were excluded from the study. After ethical approval, the data of the patients were collected retrospectively from the medical records on structured Proforma (Annexure-1). Results: Out of 422 patients of coma, 96 (22.7%) were observed with severely reduced GCS (≤8 score). About 2/3rd of patients had non-traumatic causes of coma (NTC) out of this cerebral infarction (16.4%) and metabolic brain dysfunction (15.6%) were the major causes in age group &gt;50 years. The most frequent single cause of altered mental status was traumatic brain injury (TBI) in 31% of cases with age group less the 40 years most affected 68%. Regarding the localization of coma, we observed; Diffuse brain dysfunction in 40% (n=169), Supra tentorial location in 44.8% (N=189) and infra tentorial localization in 15.2% (n=64) of cases, however the severe coma causes in older patients (&gt;60 years) were infratentorial stroke, CNS infection, brain metastasis and brain anoxia (p&lt;0.001). Conclusions: The leading cause of coma in our study in the age group less than 40 years was TBI about 68% of cases, but highly significant association of severe coma was found with older patients (&gt;60 years), infratentorial stroke, CNS infection, brain metastasis and brain anoxia.

Ocular changes as adiagnostic tool for malaria

According to the WHO Malaria Report 2019 a total of 229million people fall ill with malaria each year and two thirds of deaths involve children under 5years of age. To review the fundus changes in the context of malaria and the importance of ophthalmoscopy in the diagnosis. Summary of changes in cerebral malaria visible on fundus examination, possible underlying pathomechanisms and the value of ophthalmoscopy in practice. Retinal findings in malaria include white or gray staining of the retina (retinal whitening), color change of retinal vessels (orange or white staining), hemorrhages often with awhite center, such as Roth's spot and papilledema. The retinal changes in malaria are specific and may help to differentiate malaria from other causes of coma and fever. Smartphone-based fundus photography and artificial intelligence could support malaria diagnostics particularly in resource-poor regions.

Оказание скорой медицинской помощи пациентам в коматозном состоянии в г.Рязани в 2016–2020 гг.

The study objectives were to investigate the prevalence and to determine the most frequent causes of coma in patients in Ryazan; to determine the frequency of fatal outcomes at the stage of medical evacuation and the frequency of hospitalizations; to identify the features of emergency medical care in the prehospital period. Materials and methods. We analyzed statistical data on the number of witnesses who applied for emergency medical aid in cases of disturbance of consciousness in patients who were subsequently diagnosed as comatose patients; we revealed main causes and types of comatose states, number of fatal outcomes and frequency of hospitalizations in Ryazan. Materials of the study – cards of calls of ambulance crews in Ryazan in 2016-2020. Results of the study and their analysis. Analysis of statistical data for Ryazan in 2016-2020 showed a steady increase in the number of ambulance calls to patients in coma. In Ryazan, as in Russia as a whole, cerebral coma prevailed, with diabetic coma in second place and toxic coma – in third. In 2016-2020, the proportion of coma-related deaths was 2.7% in the prehospital period and had no upward trend. In 84% of cases patients were hospitalized in medical treatment organisations, patients with hypoglycemic coma sometimes refused hospitalization, there was no tendency in increase of the number of refusals. In the prehospital period, ambulance care for patients with coma was provided in accordance with the algorithms, average time to reach the call was 12.4 min, which corresponds to the respective norms for emergency calls for Ryazan.

Case report: \u201can unexpected origin of coma in a young adult\u201d

We report a peculiar case of acute non-traumatic coma due to neuromuscular hypoventilation syndrome caused by a non-traumatic spinal cord injury (NTSCI). A 21-year-old patient presented to the emergency room complaining of sudden onset weakness in his lower limbs and shortness of breath. While in the ER, he briefly became comatose and labs revealed an acute respiratory acidosis. Detailed neurologic examination ultimately revealed upper motor neuron signs and quadriplegia. He was ultimately diagnosed with a non-traumatic spinal cord injury, in particular, a cervical transverse myelitis which had caused acute diaphragmatic weakness. Although a very rare cause of coma, emergency medicine physicians need to be aware of transverse myelitis, a disorder that may result in rapidly progressive neurologic decline and is treated with immunomodulation.

Urgent considerations for assessment of coma in the emergency department

Not speaking, closed eyes, absent response to tactile, verbal or noxious stimuli are characteristic of comatose patients. Many causes of coma have been identified and reported in the literature. However, other causes might require extensive assessment and evaluation approaches. The attending physicians start with the baseline support of life for the affected patients, followed by rapid assessment and evaluation of the etiology and pathophysiology and adequate physical examination. In addition, it requires imaging and laboratory investigations whenever needed to determine the most appropriate management plan. In this literature review, we have conducted a brief discussion about the urgent considerations for the assessment of coma in the emergency department. Many causes can attribute to the development of coma. Therefore, adequate assessment and evaluation is a key component in the management of the affected patients in the emergency department. Moreover, the management approach might differ based on the underlying etiology. Nevertheless, caring for breathing, circulation, management of the airways, and stabilization are the main steps that should be done for each comatose patient. Physical examination is also critical in such situations, where imaging or conducting laboratory tests might not be suitable for some patients. Finally, the treatment plan should be directed based on the underlying etiology of coma.

The diagnostic value of the neurological examination in coma of unknown etiology

BackgroundIdentifying the cause of non-traumatic coma in the emergency department is challenging. The clinical neurological examination is the most readily available tool to detect focal neurological deficits as indicators for cerebral causes of coma. Previously proposed clinical pathways have granted the interpretation of clinical findings a pivotal role in the diagnostic work-up. We aimed to identify the actual diagnostic reliability of the neurological examination with regard to identifying acute brain damage.MethodsEight hundred and fifty-three patients with coma of unknown etiology (CUE) were examined neurologically in the emergency department following a predefined routine. Coma-explaining pathologies were identified retrospectively and grouped into primary brain pathology with proof of acute brain damage and other causes without proof of acute structural pathology. Sensitivity, specificity and percentage of correct predictions of different examination protocols were calculated using contingency tables and binary logistic regression models.ResultsThe full neurological examination was 74% sensitive and 60% specific to detect acute structural brain damage underlying CUE. Sensitivity and specificity were higher in non-sedated patients (87/61%) compared to sedated patients (64%/59%). A shortened four-item examination protocol focusing on pupils, gaze and pyramidal tract signs was only slightly less sensitive (67%) and more specific (65%).ConclusionsDue to limited diagnostic reliability of the physical examination, the absence of focal neurological signs in acutely comatose patients should not defer from a complete work-up including brain imaging. In an emergency, a concise neurological examination should thus serve as one part of a multimodal diagnostic approach to CUE.

Isolated basilar artery dissection following blunt trauma challenging the Glasgow coma score: A case report

Blunt cerebrovascular injury is a very rare complication of blunt trauma and a diagnostic challenge. A 14year old male fell 10m sustaining multi system trauma. The atypical Glasgow Coma Score was six with a fully preserved eye component. Initial whole-body CT scanning demonstrated multiple injuries but no obvious brain injury. Trauma management involved non-operative resuscitation and was successful, however profound coma occurred and brain stem reflexes disappeared on day two. Repeat brain CT scan demonstrated multiple cerebral and cerebellar ischemic lesions and no opacification of the vertebral or basilar arteries. Secondary analysis of the first CT scan demonstrated a small focal basilar artery dissection not initially reported. Our case report highlights an unusual cause of coma after traumatic brain injury where the clinical scenario mimics locked in syndrome. In such circumstances cerebrovascular injury, and in particular traumatic basilar artery dissection, must be actively excluded.

Brain Injury in Critical Illness and a Note on the Virus

Brain Injury in Critical Illness and a Note on the Virus