Symptomatic Unilateral Carotid Artery Disease: An Uncommon but Reversible Cause of Corticobasal Syndrome.

INTRODUCTION: Symptomatic carotid artery disease (CAD) represents an uncommon but treatable cause of corticobasal syndrome. CASE REPORT: We present the clinical details and successful management of a previously healthy 77-year-old patient who presented with 1-year cognitive dysfunction, alien limb syndrome, limb kinetic apraxia, and ipsilateral cortical sensory deficit, fulfilling the criteria of the diagnosis of probable corticobasal syndrome. Imaging modalities, including magnetic resonance imaging and time-of-flight magnetic resonance angiography, revealed acute external borderzone infarcts of the right hemisphere due to symptomatic CAD causing near occlusion of the vessel. The patient underwent a right carotid endarterectomy, leading to a marked improvement in mobility and neuropsychological evaluation. CONCLUSION: This case highlights the importance of swift diagnosis of symptomatic CAD in patients with corticobasal syndrome. Moreover, it emphasizes the efficacy of carotid endarterectomy in achieving symptom improvement in such cases.

Challenges in diagnosis and management of cerebral venous thrombosis as underlying cause of lobar intracerebral hemorrhage.

OBJECTIVES: Cerebral venous thrombosis is an uncommon, yet life-threatening condition, affecting mainly young and middle-aged individuals. Moreover, it represents an underrecognised etiology of lobar intracerebral hemorrhage (ICH). The clinical course of CVT is variable in the first days after diagnosis and medical complications including pulmonary embolism (PE) may result in early neurological deterioration and death if left untreated. MATERIALS AND METHODS: Case report. RESULTS: We describe a 46-year-old man with acute left hemiparesis and dysarthria in the context of lobar ICH due to underlying CVT of Trolard vein. Diagnosis was delayed because of misinterpretation of the initial neuroimaging study. Subsequently, the patient rapidly deteriorated and developed submassive PE and left iliofemoral venous thrombosis in the setting of previously undiagnosed hereditary thrombophilia (heterozygous prothrombin gene mutation G2021A). Emergent aspiration thrombectomy was performed resulting in the successful management of PE. A follow-up MRI study confirmed the thrombosed Trolard vein, thus establishing the CVT diagnosis. Anticoagulation treatment was immediately escalated to enoxaparine therapeutic dose resulting in clinical improvement of neurological deficits. CONCLUSIONS: Delayed diagnosis of cerebral venous thrombosis with underlying causes of lobar ICH may result in dire complications. Swift initiation of anticoagulants is paramount even in patients with lobar intracerebral hemorrhage as the initial manifestation of cerebral venous thrombosis.

The Role of Vitamin B6 in Peripheral Neuropathy: A Systematic Review.

INTRODUCTION: Vitamin B6 is a water-soluble vitamin that is naturally present in many foods and is accessible in many dietary supplements. The three natural forms are pyridoxine, pyridoxal, and pyridoxamine. Both vitamin B6 deficiency and high B6 intake have been described as risk factors for developing peripheral neuropathy (PN). The aim of this systematic review is to characterize and comprehensively describe B6-related PN. METHOD: A systematic, computer-based search was conducted using the PubMed database. Twenty articles were included in this review. RESULTS: Higher vitamin B6 levels, which usually occur following the taking of nutritional supplements, may lead to the development of a predominantly, if not exclusively, sensory neuropathy of the axonal type. After pyridoxine discontinuation, such patients subjectively report improved symptoms. However, although low vitamin B6 levels can be seen in patients suffering from peripheral neuropathy of various etiologies, there is no firm evidence that low B6 levels have a direct causal relationship with PN. Many studies suggest subjective improvement of neuropathy symptoms in patients suffering from PN of various etiologies after receiving B6 supplementation; however, no data about B6 administration as a monotherapy exist, only as part of a combination treatment, usually with other vitamins. Therefore, the potential therapeutic role of B6 cannot be confirmed to date. Supplementation with vitamin B6, even as part of a nutritional multivitamin supplement, has not been proven harmful at permitted daily doses in patients who already suffer from PN. CONCLUSION: Current scientific evidence supports a neurotoxic role of B6 at high levels. Although some studies suggest that low B6 is also a potential risk factor, further studies in this area are needed.