Prochlorperazine-induced neuroleptic malignant syndrome.

Neuroleptic malignant syndrome (NMS) is a rare yet severe condition typically associated with antipsychotic medications. Here, we present a case of NMS induced by prochlorperazine in a 76-year-old male with multiple comorbidities, aiming to delineate its clinical manifestation, diagnostic complexities, and treatment approaches. Our methodology involved a thorough documentation of the patient's medical history, initial symptoms, physical examination findings, laboratory results, diagnostic processes, and subsequent therapeutic interventions. The patient exhibited classic NMS symptoms, including fever, altered mental status, autonomic dysregulation, and generalized rigidity, consistent with diagnostic criteria. Notably, laboratory investigations failed to reveal the typical abnormalities often seen in NMS cases, highlighting the diverse presentation of this syndrome. Management strategies primarily focused on benzodiazepines and amantadine, leading to a gradual improvement in symptoms and eventual resolution of NMS. This underscores the critical role of early recognition and appropriate pharmacotherapy in managing prochlorperazine-induced NMS, even at standard dosage levels. The absence of characteristic laboratory findings in NMS poses challenges in diagnosis, necessitating a comprehensive clinical assessment for accurate identification. Moreover, this case emphasizes the need for further research to better understand the pathophysiology of prochlorperazine-induced NMS and optimize treatment protocols. In conclusion, our case report sheds light on the complexities surrounding NMS induced by prochlorperazine, emphasizing the importance of vigilant monitoring and tailored therapeutic strategies in mitigating its potentially life-threatening consequences.

Basilar Artery Fenestration Versus Hypoglycemia-Induced Vertebrobasilar Insufficiency: A Case Report.

PURPOSE: Vertebrobasilar insufficiency (VBI) is a common transient neurological condition related to posterior circulation hemodynamic insufficiency. However, it is rarely seen as an initial presentation in basilar artery (BA) fenestration or hypoglycemia. We present this case to further clarify the association between BA fenestration and hypoglycemia-induced VBI, as well as the difficulty in diagnosis, especially in acute clinical settings. CASE REPORT: Herein, we report a case with BA fenestration, in which the patient suffered from transient episodes of focal neurological deficits, including dysarthria, focal limbs weakness, and ataxia with subsequent total recovery. Apart from hypoglycemia, no other abnormal laboratory surveys were found. This concurrent finding of hypoglycemia with transient focal neurological deficit poses a difficulty in differentiating between hypoglycemia-induced VBI and true acute ischemic stroke in the clinical setting. Subsequent brain imaging studies revealed no evidence of acute infarction and no evidence of atherosclerosis changes in vessels but BA fenestration was observed. We prescribed antiplatelets for the prevention of future strokes. However, currently, no consensus exists regarding the prevention of cerebral ischemia with BA fenestration. CONCLUSION: BA fenestration-induced VBI and hypoglycemia-induced VBI are rarely reported and their mechanisms of action remain uncertain and controversial. However, BA fenestration-induced VBI may pose a risk for future cerebral ischemic events and warrants further investigations.