Persistent Hiccup Treated by Levetiracetam

No abstract available.

Inhibitory Effect of Apocynin on Proteasome Inhibition-Induced Apoptosis in Differentiated PC12 Cells

BACKGROUND: The dysfunction of the proteasome system has been implicated in neuronal degeneration. Apocynin, a specific inhibitor for nicotinamide adenine dinucleotide phosphate oxidase, has anti-inflammatory and anti-oxidant effects. However, the effect of apocynin on the neuronal cell death induced by proteasome inhibition has not been studied. METHODS: Using differentiated PC12 cells, in the respect of cell death process the suppressive effect of apocynin on the proteasome inhibition-mediated apoptosis was examined. RESULTS: The proteasome inhibitors MG132 and MG115 induced a decrease in Bid and Bcl-2 protein levels, an increase in Bax and p53 levels, mitochondrial depolarization, efflux of cytochrome c into cytosol and increase in caspases (-8, -9 and -3) activities. Treatment with apocynin attenuated the proteasome inhibitor-induced changes in the apoptosis-related protein levels, formation of reactive oxygen species, glutathione (GSH) depletion and cell death. CONCLUSIONS: Apocynin may attenuate the proteasome inhibitor-mediated apoptosis in differentiated PC12 cells by inhibiting the activation of the mitochondria-mediated pathway and the caspase-8- and Bid-dependent pathways. The preventive effect of apocynin appears to be attributed to inhibition of the production of reactive oxygen species and the depletion of cellular GSH contents.

Inhibitory Effect of Rotundarpene on Parkinsonian Neurotoxin 1-Methyl-4-Phenylpyridinium-Induced Apoptotic Cell Death

BACKGROUND: The extract and hemiterpene glycosides of Ilex Rotunda Thunb exert antioxidant and anti-inflammatory effects. The effect of rotundarpene on apoptosis in neuronal cells caused by the 1-methyl-4-phenylpyridinium (MPP⁺) has not been reported previously. METHODS: Using differentiated PC12 cells and human neuroblastoma SH-SY5Y cells, we investigated the effect of rotundarpene on MPP⁺-caused apoptosis in relation to the cell death process. RESULTS: MPP⁺-induced cell death was identified using the MTT and neutral red uptake tests. Apoptosis was induced by eliciting decreases in the cytosolic levels of Bid and Bcl-2 proteins, increases in the cytosolic levels of Bax and p53, disruption of the mitochondrial transmembrane potential, and the release of cytochrome c and the activation of caspase-8, -9, and -3 in differentiated PC12 cells and SH-SY5Y cells. Treatment with rotundarpene reduced the MPP⁺-induced changes in the levels of apoptosis-regulated proteins, formation of reactive oxygen species, depletion and oxidation of glutathione, and cell death in both PC12 and SH-SY5Y cells. CONCLUSIONS: Rotundarpene may reduce MPP⁺-induced apoptosis in neuronal cells by suppressing the activation of the mitochondria-mediated pathway and the caspase-8 and Bid pathways. Rotundarpene appears to act by inhibiting the production of reactive oxygen species and by the depletion and oxidation of glutathione.

A Recurrent Ischemic Stroke Stabilization after Using Non-Vitamin K Antagonist Oral Anticoagulant (NOAC)

Current stroke guidelines recommend the administration of non-vitamin-K-antagonist oral anticoagulant (NOAC) for the prevention of cardioembolic stroke induced by nonvalvular atrial fibrillation. We report a patient who suffered from recurrent posterior circulation strokes-occurring eight times in 4 months-even under adequate antiplatelet medication. Changing the medication from antiplatelet agents to NOAC stopped the stroke recurrence. We suggest that NOAC has a role in the prevention of recurrent stroke of undetermined etiology in the posterior circulation.

Cervicogenic Headache due to Seronegative Rheumatoid Arthritis

No abstract available.

Hypertensive Encephalopathy with Atypical Imaging Findings

No abstract available.

Hyperintense Cerebrospinal Fluid on Fluid Attenuation Inverse Recover Image Caused by Left Internal Carotid Arterty Stenosis

No abstract available.

Spinocerebellar Ataxia Type 2 with Only Clinical Feature of Memory Impairment: Case Report

Spinocerebellar ataxia (SCA) is one of a group of genetic disorders characterized by slowly progressive incoordination of gait and often associated with poor coordination of hands, speech, and eye movements. There are more than 35 different types of spinocerebellar ataxias, each caused by a different genetic mutation. Spinocerebellar ataxia type 2 (SCA2) is a subtype of type I autosomal dominant cerebellar ataxia (ADCA type I) characterized by truncal ataxia, dysarthria, slowed saccades and less commonly ophthalmoparesis and chorea. The age at onset varies from 3 to 79 years (mean 33). Usually, the first symptom of the disease is the gait ataxia, followed by the cerebellar dysarthria. Of late, other clinical manifestations of SCA2 are the cognitive dysfunctions, which include frontal executive impairment, verbal short-term memory deficits as well as reduction of attention and concentration. We report a 56-year old woman identified as spinocerebellar ataxia type 2 (SCA2) with only clinical feature of memory impairment.

Inhibitory Effect of 3,4,5-Tricaffeoylquinic Acid on Parkinsonian Toxin 1-Methyl-4-phenylpyridinium-induced Apoptosis

BACKGROUND: 1-Methyl-4-phenylpyridinium (MPP+) causes a neuronal cell injury that is similar to the findings observed in Parkinson's disease. Caffeoylquinic acid derivatives have demonstrated anti-oxidant and anti-inflammatory effects. Nevertheless, the effect of 3,4,5-tricaffeoylquinic acid (3,4,5-triCQA) on the neuronal cell death due to exposure of parkinsonian toxin MPP+ remains unclear. METHODS: Using differentiated PC12 cells, the preventive effect of 3,4,5-triCQA on the MPP+-induced cell death in relation to apoptotic process was examined. RESULTS: MPP+ induced a decrease in Bid, Bcl-2 and survivin protein levels, increase in Bax levels, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), cleavage of PARP-1, and an increase in the tumor suppressor p53 levels. 3,4,5-Tricaffeoylquinic acid attenuated the MPP+-induced changes in the apoptosis-related protein levels, formation of reactive oxygen species, depletion of GSH, nuclear damage and cell death. 3,4,5-Tricaffeoylquinic acid attenuated another parkinsonian neurotoxin rotenone-induced cell death. CONCLUSIONS: 3,4,5-Tricaffeoylquinic acid may attenuate the MPP+-induced apoptosis in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect seems to be ascribed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.

Inhibitory Effect of Flavonoid Luteolin on 6-Hydroxydopamine Cytotoxicity via Suppression of Apoptosis-Related Protein Activation

BACKGROUND: Flavonoid luteolin has been shown to exhibit cell protective effect. However, it is still uncertain whether the effect of luteolin on cellular toxicity of the parkinsonian toxin 6-hydroxydopamine is mediated by apoptosis-related protein activation. METHODS: In differentiated PC12 cells exposed to 6-hydroxydopamine in combination with luteolin, we observed the apoptosis-related protein activation, nuclear damage, formation of reactive oxygen species and cell death. RESULTS: 6-Hydroxydopamine caused apoptosis by inducing a decrease in Bid, Bcl-2, Bcl-xL and survivin levels, increase in Bax levels, cytochrome c release and activation of caspases. Treatment with luteolin reduced changes in the apoptosis-related protein levels, formation of reactive oxygen species, nuclear damage and cell death. CONCLUSIONS: Luteolin may reduce the 6-hydroxydopamine-induced apoptosis in differentiated PC12 cells by suppressing the activation of the caspase-8- and Bid-dependent pathways and the mitochondria-mediated apoptotic pathway, leading to caspase activation. The preventive effect of luteolin may be associated with its inhibitory effect on the production of reactive oxygen species. Luteolin may attenuate the oxidative stress and mitochondrial dysfunction-induced neuronal cell death take place in Parkinson's disease.

A Case of Prosopometamorphopsia Restricted to the Nose and Mouth with Right Medial Temporooccipital Lobe Infarction that Included the Fusiform Face Area

BACKGROUND: Metamorphopsia includes a broad spectrum of visual perceptual distortions, such as alteration of perceived object size or, rarely, altered perception of faces, termed prosopometamorphopsia. CASE REPORT: This report describes a patient who complained of metamorphopsia restricted to the center of the face, particularly the lower part of the face (nose and mouth), following infarction of the right medial temporooccipital lobe that included the fusiform face area. CONCLUSIONS: The fusiform face area is commonly believed to be a face-selective cortical region dedicated to the visual analysis of face stimuli. We speculate that any injury to this brain area could bring about prosopometamorphopsia involving whole or unilateral face perception, or very rarely, as in our case, distortion restricted to the central area of the face. Furthermore, there could be topographical correspondences between facial structures and the fusiform face area.

Carotid Cavernous Fistula Mimicking Internal Carotid Artery Aneurysm

No abstract available.

A Case of Familial Creutzfeldt-Jacob Disease (V180I) Initially Presenting with Depression

Creutzfeldt-Jakob disease (CJD) is a degenerative neurological disorder that is incurable and invariably fatal. It is characterized by rapidly progressive dementia presenting with memory loss, personality changes and hallucinations. The symptoms of CJD are caused by progressive death of neurons in the central nervous system, which is associated with build-up of the abnormal prion proteins forming amyloids. In human, CJD can be acquired genetically through a mutation of the gene encoding for the prion protein (PRNP). This occurs in only 5-10% of all CJD cases. We report a 64-year old woman with CJD carrying a V180I mutation that features late onset, rapid progression, no periodic sharp wave complexes on electroencephalography, and cortical signal change and edema in bilateral frontotemporoparietal lobes and basal ganglia on MRI.

Ocular Neuromyotonia in a Patient with Orbital Metastasis

No abstract available.

Neurosyphilis Mimicking Temporal Arteritis

No abstract available.

Effect of Extracellular Signal-Regulated Kinase Inhibition on Oxysterol 7-Ketocholesterol-Induced Apoptosis

BACKGROUND: Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The extracellular-signal-regulated kinase (ERK) signaling pathway plays a crucial role in almost all cell functions, including proliferation, differentiation, survival, and death. However, the effect of ERK inhibition on oxysterol-induced apoptosis remains uncertain. METHODS: This study assessed the effect of ERK inhibition on the apoptotic effect of 7-ketocholesterol. RESULTS: Treatment with 7-ketocholesterol increased phosphorylated-ERK1/2 levels in differentiated PC12 cells, while the total amount of ERK was not altered. 7-Ketocholesterol decreased Bid and Bcl-2 levels, increased Bax and p53 levels, and promoted cytochrome c release, which elicits the activation of caspases (-8, -9, and -3), nuclear damage, and cell death. ERK and farnesyltransferase inhibitors inhibited the 7-ketocholesterol-induced phosphorylation of ERK1/2, activation of apoptosis-related proteins, and cell death in PC12 cells. CONCLUSIONS: The ERK and farnesyltransferase inhibitors, which did not exhibit toxicity, may inhibit the 7-ketocholesterol toxicity on differentiated PC12 cells by suppressing the activation of the caspase-8-dependent pathway as well as activation of the mitochondria-mediated cell-death pathway, leading to the activation of caspases. The inhibition of ERK may confer a beneficial protective effect against the neuronal cell injury induced by cholesterol oxidation products.

Diffusion Tensor Imaging Findings in Two Cases of Internal Capsular Genu Infarction

Internal capsular genu infarcts infrequently cause cognitive impairment and behavioral changes, and little is known about the underlying mechanism. Using diffusion-tensor imaging (DTI) and the fractional anisotropy (FA) index in the region of interest (ROI) and ipsilesional frontal cortex, we evaluated two patients with internal capsular genu infarction who presented with frontal dysfunction and cognitive impairment. The reported findings help to elucidate the mechanism underlying cognitive deterioration in internal capsular genu infarction.

Role of Casein Kinase 2 in Parkinsonian Toxin 1-Methyl-4-phenylpyridinium-induced Cell Death

BACKGROUND: Protein casein kinase 2 is involved in signal transduction, cell growth, and apoptosis. However, it has not been elucidated whether parkinsonian toxin 1-methyl-4-phenylpyridinium (MPP+)-induced neuronal cell death is mediated by a casein-kinase-2-mediated pathway. METHODS: We monitored apoptosis-related protein activation, changes in the level of casein kinase 2, nuclear damage, and apoptosis in differentiated PC12 cells exposed to MPP+ in combination with casein kinase 2 inhibitor. RESULTS: Casein kinase 2 inhibitors [4,5,6,7-tetrabromobenzotriazole (TBB), 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole, and apigenin] reduced MPP+- and rotenone-induced cell death in differentiated PC12 cells. TBB inhibited the MPP+-induced activation of apoptosis-related proteins (decreases in Bid and Bcl-2 levels, increase in Bax levels, cytochrome c release, and caspase-3 activation), increase in casein kinase 2 levels, and nuclear damage. CONCLUSIONS: Administering casein kinase 2 inhibitor TBB at concentrations that do not induce toxic effects may reduce MPP+-induced cell death in differentiated PC12 cells by suppressing the apoptosis-related protein activation that leads to cytochrome c release and subsequent activation of caspase-3. The results suggest that MPP+-induced cell death process is mediated by a casein kinase 2 pathway.

Temporary Spontaneous Remission in Primary CNS Lymphoma

Spontaneous remission in untreated primary central nervous system lymphoma is rare. A 66-year-old man was admitted with dizziness and gait disturbance. Initial fluid-attenuated inversion-recovery images revealed hyperintensities in the upper brainstem, left temporal lobe, and right occipital lobe. The patient's symptoms and lesions disappeared spontaneously after 1 month. However, he was readmitted after 4 months with right hemiparesis. Magnetic resonance imaging revealed a homogenous enhanced lesion in the left basal ganglia with a vasogenic pattern. This disease warranted biopsy, which revealed large B-cell lymphoma.

Prostaglandin E2 Attenuates 7-Ketocholesterol Toxicity by Suppressing Changes in Mitochondria-Associated Cell Death Process

BACKGROUND: It has been shown that defects in mitochondrial function are involved in the induction of neuronal cell injury. Prostanoids such as prostaglandin E2 (PGE2) are thought to play an important role in inflammation and neurologic disorders. However, the effect of PGE2 on cholesterol-oxidation-product-induced neuronal cell injury remains uncertain. METHODS: The effect of PGE2 on toxicity of 7-ketocholesterol (7-KCS) was assessed in PC12 cells that were differentiated following treatment with nerve growth factor. The mitochondria-mediated apoptotic process was evaluated by examining the inhibitory effect of PGE2 on 7-KCS-induced toxicity. RESULTS: 7-KCS induced BID cleavage, increased the production of proapoptotic Bax protein, decreased antiapoptotic Bcl-2, increased p53, and promoted cytochrome c release in the cytosolic fraction, which subsequently elicited the activation of caspase-3, DNA fragmentation, and cell death. Treatment with PGE2 inhibited this 7-KCS-induced apoptotic process and cell death. CONCLUSIONS: The results show that PGE2 inhibits 7-KCS-induced toxicity in differentiated PC12 cells by suppressing the mitochondria-mediated apoptotic process. PGE2 may protect against cholesterol-oxidation-product-induced neuronal cell injury.