The Glasgow Coma Scale: 50-year anniversary.

In 1974, Sir Graham Teasdale and Bryan Jennett wrote the "Assessment of coma and impaired consciousness, A practical scale," which has become one of the most influential papers in the history of traumatic brain injury, with more than 10,000 citations as of January 2024. Today, it is one of the most widely used tools in emergency departments, providing a reliable general overview of the patient's consciousness status.

Cerebral Venous Thrombosis Presenting as Simultaneous Intracerebral Hemorrhage.

A 37-year-old pregnant woman presented to the emergency department with central facial palsy, ipsilateral right hemiparesis, and seizures. Brain Computed Tomogram (CT) showed intracerebral hemorrhage (ICH) and bilateral frontal edema. Magnetic resonance imaging (MRI) revealed multifocal hemorrhages consistent with a diagnosis of multiple simultaneous ICH (MSICH) (Figure 1). We suspected cerebral venous thrombosis (CVT) and performed a MR angiogram confirming this diagnosis (Figure 2). Upon admission, the patient was treated with low-molecular-weight heparin and transitioned to direct oral anticoagulation at discharge. Non traumatic MSICH is a rare imaging finding with high mortality, usually arterial in origin (1). However, since treatment options vary, cerebral venous thrombosis should always be considered in the differential diagnosis, especially in young female patients with known risk factors, such as pregnancy and puerperium (2-4). MRI modalities (Echo-GRE) are valuable tools in identifying ICH when CT is inconclusive (5).

Stroke in Tuberculous Meningitis.

A 17-year-old male presented with a 20-day history of vomiting, abdominal pain, weight loss, headache and fever progressing to dysarthria, somnolence, urinary incontinence, slurred speech, weakness, and inability to walk. Neurological examination revealed diminished visual acuity and diplopia. A head computed tomography (CT) showed acute hydrocephalus (Figure 1). Cerebrospinal fluid (CSF) analysis revealed pleocytosis (lymphocyte predominant), hypoglycorrhachia (8 mg/dL), and hyperproteinorrachia (156 mg/dL). The brain magnetic resonance imaging (MRI) revealed leptomeningitis, basal ganglia infarcts and basal meningeal enhancement highly suggestive of tuberculous meningitis (TBM) (Figure 2). We calculated a positive Thwaites score (-5) for TBM. The patient responded well to antituberculous treatment and dexamethasone. At 2 year follow-up the patient remains symptom-free. Stroke is a frequent complication of TBM and might contribute to long-term disability. Brain imaging findings, such as basal meningeal enhancement and basal exudates, hydrocephalus, and infarctions (TBM triad) are useful tools to rapidly identify probable TBM(3,4). Brain infarcts in TBM are located mostly in the arterial territory of distal branching arterires(5). Other less frequent imaging findings are tuberculomas and vasospasm. Key message: Hydrocephalus, basal meningeal enhancement, and basal ganglia infarcts should raise suspicion of tuberculosis, especially in endemic regions.

Expanding Diagnostic Workup for hypertensive Intracerebral hemorrhage: a retrospective LATAM cerebrovascular registry comparison.

Background: The leading cause of spontaneous intracerebral hemorrhage (ICH) is hypertensive arteriolopathy. In addition to age and hypertension history, patients usually present other comorbidities that potentially increase morbimortality. Ancillary studies other than non-contrast computerized tomography (NCCT) may help clarify the diagnosis and increase the detection of potentially modifiable vascular risk factors. Unfortunately, their use is not routinely performed. Objective: The study aimed to determine the frequency of ancillary studies performed in patients with hypertensive ICH. Methods: We performed a retrospective analysis of three Latin American cerebrovascular registries from academic medical centers, analyzing the results with descriptive statistics focusing on diagnosis and short-term outcomes. Results: We analyzed a total of 1,324 patients (mean age 64 years). Hypertension and obesity were the most prevalent risk factors. Only 14% underwent MRI, 10.3% extracranial ultrasonography, and 6.7% echocardiography. Among the three registries, the Latin America Stroke Registry performed more ancillary studies. Most of the patients presented a poor clinical outcome and in-hospital death. Conclusions: The use of ancillary studies in the diagnostic workup of ICH was poor in the three registries, and mortality was high. The lack of ancillary studies performed may negatively impact outcomes.

Vascular cognitive impairment and dementia: a narrative review.

Vascular cognitive impairment (VCI) is the second most common cause of cognitive impairment after Alzheimer's disease. The VCI spectrum involves a decline in cognition attributable to vascular pathologies (e.g., large infarcts or hemorrhages, microinfarcts, microbleeds, lacunar infarcts, white matter hyperintensities, and perivascular space dilation). Pathophysiological mechanisms include direct tissue injury, small vessel disease, inflammaging (inflammation + aging), atrophy, and altered neurotransmission. VCI is diagnosed using distinct clinical and radiological criteria. It may lead to long-term disability and reduced quality of life. An essential factor for reducing cognitive impairment incidence is preventing stroke by managing traditional and non-traditional cerebrovascular risk factors. This article reviews the spectrum of VCI, epidemiology, risk factors, pathophysiology, diagnosis, available treatment, and preventive strategies.

O comprometimento cognitivo vascular (CCV) é a segunda causa mais comum de comprometimento cognitivo depois da doença de Alzheimer. O espectro do CCV envolve um declínio na cognição atribuível a patologias vasculares (por exemplo, grandes infartos ou hemorragias, microinfartos, micro-hemorragias, infartos lacunares, hiperintensidades da substância branca e dilatação do espaço perivascular). Os mecanismos fisiopatológicos incluem lesão tecidual direta, doença de pequenos vasos, inflammaging (inflamação+envelhecimento), atrofia e neurotransmissão alterada. O CCV é diagnosticado usando critérios clínicos e radiológicos distintos. Pode levar à incapacidade a longo prazo e à redução da qualidade de vida. Um fator essencial para reduzir a incidência de comprometimento cognitivo é prevenir o acidente vascular cerebral através do manejo dos fatores de risco cerebrovasculares tradicionais e não tradicionais. Este artigo revisa o espectro do CCV, epidemiologia, fatores de risco, fisiopatologia, diagnóstico, tratamento disponível e estratégias preventivas.