Sook Young Roh

Acute hepatic encephalopathy presenting as cortical laminar necrosis: Case report

We report on a 55-year-old man with alcoholic liver cirrhosis who presented with status epilepticus. Laboratory analysis showed markedly elevated blood ammonia. Brain magnetic resonance imaging (MRI) showed widespread cortical signal changes with restricted diffusion, involving both temporo-fronto-parietal cortex, while the perirolandic regions and occipital cortex were uniquely spared. A follow-up brain MRI demonstrated diffuse cortical atrophy with increased signals on T1-weighted images in both the basal ganglia and temporal lobe cortex, representing cortical laminar necrosis. We suggest that the brain lesions, in our case, represent a consequence of toxic effect of ammonia.

Ginkgotoxin Induced Seizure Caused by Vitamin B6 Deficiency

Although ginkgo is commonly used as an alternative treatment for memory loss, Alzheimer’s dementia and peripheral circulatory disturbances, it is also known to cause neuronal symptoms due to ginkgotoxin (4′-methoxypyridoxine or B6 antivitamin). We experienced a case of a 51-year-old female patient with generalized tonic clonic seizure and postictal confusion after eating large amounts of ginkgo nuts. Blood vitamin B6 level was decreased. After conservative treatment and pyridoxine medication, her mental symptoms were resolved completely and no seizures recurred.

Hot Cross Bun Sign Following Bilateral Pontine Infarction: A Case Report

The hot cross bun sign is characterized by cruciform T2 signal hyperintensity in the pons and has been reported to be a specific but not pathognomic for multiple system atrophy. It reflects degeneration of pontine neurons and transverse pontocerebellar fibers, regardless of the underlying pathogenic process. Here, we report a case of hot cross bun sign following bilateral pontine infarction due to Wallerian degeneration of the pontocerebellar fibers.

Asterixis in the leg induced by anterior cerebral artery infarction

Asterixis commonly occurs in a patient with metabolic encephalopathy, whereas focal brain lesions such as thalamus, cerebellum, or frontal area also cause focal or unilateral asterixis in the arms. We report a novel case of asterixis in the leg after unilateral anterior cerebral artery territory infarction. A 76-year-old man was admitted with sudden-onset mild right leg weakness and postural instability due to knee buckling. He was diagnosed with ischemic stroke in the left prefrontal area and cingulated gyrus by brain magnetic imaging. Needle electromyography of the right vastus lateralis muscle while standing showed intermittent periods of EMG silence, consistent with asterixis. There were no abnormal involuntary movements in the upper extremities. This case suggests that gait disturbance or postural instability after structural lesions in the prefrontal area may be directly related to asterixis in the leg, not in the arm associated with postural failure.

Cerebral Infarction Caused by Cerebral Venous Thrombosis Associated with Iron Deficiency Anemia

Cerebral venous thrombosis (CVT) is a rare condition and has a wide spectrum of symptoms, which makes it difficult to diagnose. CVT has been reported to be associated with various etiologies. However, there are few reported cases of CVT in association with iron deficiency anemia (IDA). Here we report a case of venous infarction caused by CVT associated with IDA. The patient had a good prognosis after iron supplementation and anticoagulation therapy. Since IDA can potentially cause CVT, treatment for IDA may be an important strategy to prevent cerebral infarction caused by CVT.

Valproic Acid-induced Hyperammonemic Encephalopathy Promoted by Levetiracetam

Encephalopathy resulting from the administration of levetiracetam (LEV) is a rare occurrence. We experienced a patient receiving LEV treated with valproic acid (VPA) for partial seizures with secondary generalization, following which she developed hyperammonemic encephalopathy and showed complete recovery after the drug was withdrawan. LEV is able to promote hyperammonemic encephalopathy when added to VPA.

A Case of Bilateral Medial Posterior Inferior Cerebellar Artery Infarction Associated with Subclavian Steal Syndrome

Subclavian Steal Syndrome (SSS) is the result of reversed ipsilateral vertebral arterial blood flow caused by proximal subclvian artery steno-occlusive disease. A 78-year-old man with a history of hypertension and smoking presented with sudden dizziness, nausea and vomiting; there was no history of recent trauma and arm claudication. Neurologic examination showed no abnormality except for ataxia of both arms. Diffusion Weighted Image (DWI) indicated acute bilateral medial Posterior Inferior Cerebellar Artery (PICA) infarction. Subsequent brain Magnetic Resonance Angiography (MRA) revealed chronic occlusion at the left proximal subclavian artery with decreased left vertebral artery flow and prominent left (PICA) from vertebral artery. Transcranial Doppler (TCD) ultrasonography showed reversal of flow within the left vertebral artery, and reactive hyperemic cuff test of the left arm showed aggravated reverse flow of left vertebral artery following release of blood pressure cuff inflation, which was suggestive of SSS. Although the etiologies of bilateral PICA infarction might be diverse, we experienced a case of acute bilateral medial PICA infarction, which were presumed as hemodynamic insufficiency due to SSS. *Corresponding author: Jeong Yeon Kim,Department of Neurology, Sanggye Paik Hospital, Inje University College of Medicine, Seoul, Korea, E-mail: jykimmd@paik.ac.kr Received Date: September 1, 2016 Accepted Date: November 6, 2016 Published Date: November 11, 2016 Citation: Kim, J.K., et al. A Case of Bilateral Medial Posterior Inferior Cerebellar Artery Infarction Associated with Subclavian Steal Syndrome. (2016) Int J Neuro Brain Dis 3(4): 13. Int J Neurol Brain Disord | Volume 3: Issue 4 www.ommegaonline.org

Atypical Manifestation of Multiple Cerebral Infarctions in Tuberculous Meningitis on Vessel Wall Imaging

Although the most cerebral infarcts in Tuberculous Meningitis (TBM) are due to vasculitis, the pathogenesis of vasculitis remains poorly understood and the imaging signs may be direct or indirect. We experienced a case of multiple cerebral infarctions in TBM showing segmental vessel wall thickening with enhancement of large vessels and concentric wall thickening with lumen narrowing leading to vessel compression on vessel wall imaging[1,2]. *Corresponding author: Jeong Yeon Kim, MD, PhD, Department of Neurology, Sanggye Paik Hospital, Inje University College of Medicine, 1342 Dongil-ro, Nowon-gu, Seoul, 07157, Korea, Tel:+82-2-950-1090; Fax:+82-2-950-1955; E-mail: jykimmd@paik.ac.kr Received Date: August 26, 2015 Accepted Date: December 03, 2015 Published Date: December 08, 2015 Citation: Kim, J.Y., et al. A typical Manifestation of Multiple Cerebral Infarctions in Tuberculous Meningitis on Vessel Wall Imaging (2016) Int J Neurol Brain Disord 3(1): 1-3. Int J Neurol Brain Disord | Volume 3: Issue 1 www.ommegaonline.org

Cerebral infarction caused by a tortuous subclavian artery: a case report.

Tortuous arteries are common clinical observation. Although mild tortuosity is asymptomatic, severe tortuosity can lead to ischemic attack in several organs. With advances in imaging technology, an increasing number of tortuous vessels have been detected. The purpose of this report is to describe a case of acute cerebral infarction due to tortuous subclavian artery and to review the literature.

Thrombocytopenia associated with levodopa treatment.

There were few cases of thrombocytopenia associated with levodopa. Herein, we report a patient with Parkinson’s disease, who suffered thrombocytopenia related to long-term use of levodopa.