
Abstract Since the inception of the Neurocritical Care Society (NCS), neurocritical care has evolved into a rapidly expanding discipline. Within the intensive care field, neurocritical ill patients represent a highly vulnerable population compared with non-neurocritical patients, with substantial ethical complexity, facing barriers to equitable care that are pronounced in low- and middle-income countries (LMICs).
Objective This article evaluates whether early serum thyroxine (T4) concentrations predict neurological and psychological outcomes following moderate-to-severe traumatic brain injury (TBI). Materials and Methods This prospective cohort enrolled 56 adults (44 men) with moderate (Glasgow Coma Scale [GCS] 9-12; n = 19) or severe (GCS <= 8; n = 37) TBI at a tertiary trauma center. Total T4 and free T4 (fT4) were measured within 10 days of injury, then at 6 and 12 months. Neurological outcome was assessed using Glasgow Outcome Scale-Extended (GOSE); depression and anxiety were evaluated with Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 (GAD-7) at 1 year. Multivariable logistic regression examined independent associations between baseline T4 and unfavorable outcome (GOSE <= 4), as well as clinically significant depressive (PHQ-9 >= 10) or anxiety (GAD-7 >= 10) symptoms. Results Median baseline fT4 was significantly lower in severe versus moderate TBI (0.77 vs. 0.89 ng/dL, p = 0.021) and correlated positively with admission GCS ( rho = 0.34, p = 0.010). Unfavorable neurological outcome at 6 months occurred in 26/54 evaluable patients (48%). After adjusting for age, sex, admission GCS, and cranial computed tomography score, each 0.1 ng/dL decrease in baseline fT4 increased odds of unfavorable outcome by 28% (adjusted odds ratio [OR] 1.28; 95% confidence interval 1.07 - 1.55; p = 0.007). At 1 year, 18/50 (36%) and 15/50 (30%) screened positive for depression and anxiety, respectively. Lower early fT4 independently predicted both depressive (adjusted OR 1.35 per 0.1 ng/dL decrease; p = 0.004) and anxiety symptoms (adjusted OR 1.29; p = 0.017). Serial measurements demonstrated spontaneous T4 normalization in most survivors by 6 months. Conclusion Early reduction in serum fT4 frequently occurs after moderate-to-severe TBI and independently predicts functional recovery and subsequent affective morbidity. Routine fT4 measurement during the acute phase may enhance prognostication and identify patients requiring endocrine and psychological surveillance.
Minor traumatic brain injury in infancy leading to fatal hemispheric cerebral infarction is a rare entity. We present the case of an 8-month-old child who developed a right-sided hemispheric infarction following trivial trauma, consistent with an acute ischemic stroke involving the territories of the right anterior, middle, and posterior cerebral arteries. The patient was initially managed conservatively, and surgical intervention was planned after resuscitation improved the Glasgow Coma Scale (GCS) score from 3/15 to 5/15. A right-sided decompressive hemicraniectomy was subsequently performed. The patient was discharged with a GCS of 11/15 on postoperative day 17. This case highlights the resilience and potential for recovery in pediatric patients with timely and appropriate intervention, despite severe radiological and clinical findings.
Objective In previous studies, it has been proposed that white fiber connections result in disconnection syndromes in animals and humans, leading to higher-level neurological deficits even when cortical areas remain intact. These conclusions were applied to delineate a surgical approach for neurosurgeons. Materials and Methods Ten previously frozen and formalin-fixed cadaveric human brains were included in the study. The Klingler's method of fiber dissection was adopted where the cerebral hemispheres were prepared by numerous cycles of freezing and thawing. The chief tools used to carry white fiber dissection were wooden spatula and fiber bundles were studied by the naked eye as well as using the operating microscope. Using gyrus-based approach, the fiber tracts that came across during dissection were acknowledged. Results In this study, we have defined a lateral approach to dissecting white fiber tracts of the brain with the help of modified Klingler's technique. The dissection of white fiber bundles was done through gyrus. The fiber bundle course as well as its functional corelationship were observed. Conclusion The knowledge of the anatomy of white fiber bundles is crucial during planning surgical trajectory, which further help to reduce the risk of postoperative complications. The three-dimensional anatomy of white fiber tracts relevant to lateral approach presented will aid in planning neurosurgery. The course of white fiber bundles and the relationships with adjacent bundles is decisive to optimize the quality of resection and functional outcome.
Traumatic carotid artery injury is a rare yet potentially fatal complication of head and neck trauma. Often masked by primary brain injury, it may remain undiagnosed until the onset of devastating neurological consequences. We present two contrasting cases of traumatic brain injury with carotid artery injury—one where the injury was missed initially, leading to malignant infarction and death, and another where timely detection resulted in a favorable outcome. These cases underscore the importance of heightened clinical suspicion and standardized screening for carotid artery injury in specific trauma patterns, especially in patients presenting with high-risk mechanisms or unexplained neurological deterioration.
Neurogenic shock is thus defined as autonomic failure, leading to hypotension, bradycardia, and metabolic vasodilation. The primary pathology lies in the cessation of the sympathetic outflow following the spinal or brain stem injury insult. Thus, an understanding of the neuroanatomic substrate of neurogenic shock's pathophysiology is a prerequisite for a successful approach to diagnosis and therapy. Therefore, this narrative review will comprehensively discuss the neuroanatomic structures involved in the pathology of neurogenic shock, emphasizing their functional significance in the context of the impairment consequences.
Stunned myocardium syndrome (SMS) is a reversible myocardial dysfunction occurring after ischemia and reperfusion, commonly described in cardiac contexts but underrecognized in traumatic brain injury (TBI). We present a case of severe TBI complicated by SMS after cardiac arrest, underscoring the importance of early recognition and multidisciplinary management.