Neurofibromatosis is a heterogenous hereditary disease with autosomal dominant transmission divided into two distinct types on the basis of genetic and clinical characteristics. Cervical vessels are rarely involved in neurofibromatosis type 1 (von Recklinghausen's disease). In the present paper, we report a 32-year-old female patient of neurofibromatosis type 1 with spinal arteriovenous malformation (AVM). She suffered from posterior neck pain and paresthesia on her right 3rd, 4th, and 5th fingers for a half a year. MRI showed ectasia of the right dural sac and signal void tortuous tubular structures at the cervical level. The right vertebral artery fed this cervical AVM in angiography.
Adult ; Angiography ; Arteriovenous Malformations* ; Dilatation, Pathologic ; Female ; Fingers ; Genetic Diseases, Inborn ; Humans ; Magnetic Resonance Imaging ; Neck Pain ; Neurofibromatoses* ; Neurofibromatosis 1* ; Paresthesia ; Vertebral Artery

No abstract available.
Hematoma, Subdural, Acute*

Cerebral aspergillosis is a rare condition that affects primarily the immunocompromised host. Most of cerebral aspergillosis is developed by hematogenous dissemination from extracranial foci, but aspergillosis of sino-nasal origin rarely affects the CNS. In case 1, wel symptom of tumor recurrence was unilateral numbness of the chin. A 65-year-old male was admitted because of paresthesia around the left chin and left lower lip. Neurologic examination revealed hypesthesia on the left side of chin, lower lip and buccal mucous mem-brane. Bone scan (Tc-99m MDP) showed focal hot uptakes on the left mandible and left first rib. Brain CT with bone window setting showed a focal osteolytic lesion in the bone marrow of the left mandibular canal without destruction of bone cortex. Both coronal T1 weighted image and axial T2 weighted image showed focal low signal intensities on the left ramus. The pathophysiologic mechanism could be understood by identification of the pathologic focus.
Aged ; Aspergillosis* ; Bone Marrow ; Brain ; Chin ; Humans ; Hypesthesia ; Immunocompromised Host ; Lip ; Male ; Mandible ; Neurologic Examination ; Paresthesia ; Recurrence ; Ribs

BACKGROUND & OBJECTIVES: MNDA antagonists such as ketamine and MK-801 in experimental status epilepticus model were reported to have the effect of neuroprotection. It may be postulated that one of the mechanisms of neuronal damage is a calcium influx related to excitatory neurotransmmition. So we investigated the effects of various voltage gated calcium channel blockers on epileptogenic and neuroprotection in the hippocampus of lithium-pilocarpine induced status epilepticus animal mode]. Methods ; Each Sprague-Dawley rat (N=47) was injected intraperitoneally with lithium 3mEq/kg and pilocarpine 30 mg/kg to produce the satus epilepticus. The effects of pre-(15 minute before the injection of pilocarpine) and post-administration(15 minutes after the onset of seizure) of various voltage gated calcium channel (VGCC) blockers[nimodipine (NMDP), flunarizine (FRZ), verapamil(VPM), and diltiazem(DTZ) -20mg/kg I.p.] were tested by conting survived neurons on the hippocampus in lithim-pilocarpine induced status epilepticus rat model. RESULTS: Pre- & post- administration of each VGCC blocker protected the neurola damage in CA1 and CA3 area of the hippocampus (CA1 6.0+1.87 and CA3 2.6+0.89 in seizure control group, 43.2+/-4,32, and 28.0+4.47 in the NMDP, 44.8+/-7.46 and 29.0+4.30 in post-NMDP, 43.0+0.74 and 29.6+4.78 in pre-FRZ, 45.4+/-6.88 and 23.6+/-5.68 in post-FRZ, 37.2+/-5.85 and 18.4+5.68 in pre-VPM, 38.8+4.92 and 16.6+4.39 in post-VPM, 38.8+6.14 and 17.2+3.70 in pre-DTZ, and 39.6+8.26 and 15.6+5.41 in post-DTZ). The latencies from pilocarpine injection to the seizure onset behavioral alteration ictal electroencephalographic discharges during status epileptics were not changed despite pre- and post-adminstration of each VGCC blocker. These result indicate that VGCC blockers do not have a direct effect on epileptogenesis but have some relationship with neuroprotection. CONCLUSION: It was concluded that the neuroprotecting effect of VGCC blocker in the neuronal damage due to status epileptics appears to be produced by blocking the intracellular calcium influx through the VGCC, blochers might be helpful to reduce neuronal damage in human with status epilepticus.
Animals ; Calcium Channel Blockers* ; Calcium Channels* ; Calcium* ; Dizocilpine Maleate ; Flunarizine ; Hippocampus* ; Humans ; Ketamine ; Lithium ; Models, Animal* ; Neurons ; Pilocarpine ; Rats* ; Rats, Sprague-Dawley ; Seizures ; Status Epilepticus*

BACKGROUND & OBJECTIVES: MNDA antagonists such as ketamine and MK-801 in experimental status epilepticus model were reported to have the effect of neuroprotection. It may be postulated that one of the mechanisms of neuronal damage is a calcium influx related to excitatory neurotransmmition. So we investigated the effects of various voltage gated calcium channel blockers on epileptogenic and neuroprotection in the hippocampus of lithium-pilocarpine induced status epilepticus animal mode]. Methods ; Each Sprague-Dawley rat (N=47) was injected intraperitoneally with lithium 3mEq/kg and pilocarpine 30 mg/kg to produce the satus epilepticus. The effects of pre-(15 minute before the injection of pilocarpine) and post-administration(15 minutes after the onset of seizure) of various voltage gated calcium channel (VGCC) blockers[nimodipine (NMDP), flunarizine (FRZ), verapamil(VPM), and diltiazem(DTZ) -20mg/kg I.p.] were tested by conting survived neurons on the hippocampus in lithim-pilocarpine induced status epilepticus rat model. RESULTS: Pre- & post- administration of each VGCC blocker protected the neurola damage in CA1 and CA3 area of the hippocampus (CA1 6.0+1.87 and CA3 2.6+0.89 in seizure control group, 43.2+/-4,32, and 28.0+4.47 in the NMDP, 44.8+/-7.46 and 29.0+4.30 in post-NMDP, 43.0+0.74 and 29.6+4.78 in pre-FRZ, 45.4+/-6.88 and 23.6+/-5.68 in post-FRZ, 37.2+/-5.85 and 18.4+5.68 in pre-VPM, 38.8+4.92 and 16.6+4.39 in post-VPM, 38.8+6.14 and 17.2+3.70 in pre-DTZ, and 39.6+8.26 and 15.6+5.41 in post-DTZ). The latencies from pilocarpine injection to the seizure onset behavioral alteration ictal electroencephalographic discharges during status epileptics were not changed despite pre- and post-adminstration of each VGCC blocker. These result indicate that VGCC blockers do not have a direct effect on epileptogenesis but have some relationship with neuroprotection. CONCLUSION: It was concluded that the neuroprotecting effect of VGCC blocker in the neuronal damage due to status epileptics appears to be produced by blocking the intracellular calcium influx through the VGCC, blochers might be helpful to reduce neuronal damage in human with status epilepticus.
Animals ; Calcium Channel Blockers* ; Calcium Channels* ; Calcium* ; Dizocilpine Maleate ; Flunarizine ; Hippocampus* ; Humans ; Ketamine ; Lithium ; Models, Animal* ; Neurons ; Pilocarpine ; Rats* ; Rats, Sprague-Dawley ; Seizures ; Status Epilepticus*

Diaschisis is classically defined as a sudden inhibition of function, produced by an acute focal disturbance in a remote area which is anatomically connected through fiber tracts. Transhemispheric diaschisis can underlie some diffuse symptoms of acute supratentorial stroke such as agitation, confusion, and coma. We experienced a patient with right middle cerebral artery infarction, presenting a quadriparesis and hypoesthesia at sensory level. This case suggests the diaschisis exacerbate the initial focal deficit such as weakness and sensory loss.
Coma ; Dihydroergotamine ; Humans ; Hypesthesia ; Infarction, Middle Cerebral Artery* ; Quadriplegia* ; Stroke

Central hypoventilation syndrome (CHS) can be caused by any lesions to the medullary respiratory centers, cerebral cortex, corticospinal pathways, and their connections. We report 5 patients with central hypoventilation syndrome and analyzed 26 patients who experienced central hypoventilation syndrome during sleep and waking states. We compared initial clinical symptoms and signs, maximal neurologic deficits, brain MRI and pathologic findings, and associated autonomic dysfunctions. The patients with respiratory failure during waking states showed quadriplegia, a rapidly progressing respiratory failure. The patients who had automatic respiratory failure showed mild hemiparesis, bulbar dysfunction, dysautonomia, and subacute to chronic recurrent respiratory failures. These results support the concept of two separate respiratory systems: a voluntary system and an automatic system. The respiratory management of these patients with central hypoventilation syndrome should be considered critical to their survival.
Brain ; Cerebral Cortex ; Humans ; Hypoventilation* ; Magnetic Resonance Imaging ; Neurologic Manifestations ; Paresis ; Primary Dysautonomias ; Pyramidal Tracts ; Quadriplegia ; Respiratory Center ; Respiratory Insufficiency ; Respiratory System

BBACKGROUND & OBJECTIVE: Borderzone(BZ) infarcts located between two main arterial territories can be classified into several subtypes. Anterior and posterior BZ and internal junctional infarcts. We performed this study to describe the different clinical features between each subtypes. Method : Thirty-five (29 men, 6 women) acute stroke patients whose brain imaging (CT/MRI) showed BZ infarcts were included in this study. BZ infarcts were classified into three types : anterior and posterior BZ and internal junctional infarct. And we tried to describe different clinical features such as mode of onset, positive neurologic findings, and neuroanatomical correlation with clinical manifestations. Result : All BZ infarcts were 51. Anterior 9(18%), posterior 23(45%); and internal junctional 19 (37%). Most common type were posterior BZ and internal junctional infarct alone (11 each). Twenty-eight (80%) patients presented the symptoms correlated with BZ infarct. Asymptomatic patients whose symptom was not correlated with BZ infarct were 7(20%). Clinicoradiologic classification in symptomatic group were reclassified into P'(posterior BZ) in 16 (57%) ; I'(internal junctional BZ) in 8(29%), N(not classified) in 4. None was included to A'(anterior BZ). We could not find any different clinical features according to each subtype but only the group P' characteristically showed transient loss of consciousness, Gerstman syndrome, hemianopsia, and limb shaking. Conclusion : Most frequently involved areas were posterior BZ and internal junctional infarct alone. In follow-up of combined anterior and posterior BZ infarct, posterior almost always preceded anterior. The patients with symptoms correlated with radiological localization of BZ infarct is 80%. Fifty percent of them had acute onset. In pure internal junctional infarct, 45 % showed symptoms not correlated with radiological localization. None had the anterior BZ symptomatology.
Classification ; Extremities ; Follow-Up Studies ; Hemianopsia ; Humans ; Infarction* ; Male ; Neuroimaging ; Neurologic Manifestations ; Stroke ; Unconsciousness

The present report discusses four cases of chronic renal failure, which developed symptoms of parkinsonism in response to levosulpiride. The temporal relationship between levosulpiride discontinuation and the disappearance of parkinsonism suggests a causal link. In addition, decreased striatal dopamine transporter bindings assessed by [I-123] IPT SPECT were observed in two patients suggesting that a dopamine blocking agent causes the dysfunction of nigrostriatal dopaminergic neurons and that such injury may be involved in the pathogenesis of drug-induced parkinsonism.
Dopamine ; Dopamine Plasma Membrane Transport Proteins ; Dopaminergic Neurons ; Humans ; Kidney Failure, Chronic ; Parkinsonian Disorders ; Tomography, Emission-Computed, Single-Photon

BACKGROUND: EGCG(epigallocatechin gallate), a major green tea extract, is a potent free radical scavenger which has been shown to reduce free radical-induced lipid peroxidation. The purpose of this study was to examine whether EGCG reduces focal ischemia/reperfusion-induced brain injury in rats. METHODS: Male Wistar rats were anesthetized with ketamine and xylazine and subjected to 120 min of temporary middle cerebral artery occlusion by an intraluminal nylon suture coated with poly-L-lysine. The drug (EGCG, n=8) or vehicle (normal saline, n=8) was administered iv.(as a 50 mg/kg bolus) immediately after the onset of middle cerebral artery occlusion. Neurologic status was evaluated 2 hours after occlusion and 24 hours after. Twenty-four hours after ischemia, the brain was perfusion-fixated and the infarct volume was determined. RESULTS: EGCG significantly improved the neurological status at 24 hours after middle cerebral artery occlusion.(p<0.05), and reduced total infarct volumes (p<0.01). CONCLUSIONS: These results demonstrate the neuroprotective effect of EGCG in a rat model of transient focal cerebral ischemia.
Animals ; Brain ; Brain Injuries ; Brain Ischemia ; Humans ; Infarction, Middle Cerebral Artery* ; Ischemia* ; Ketamine ; Lipid Peroxidation ; Male ; Middle Cerebral Artery* ; Models, Animal ; Neuroprotective Agents ; Nylons ; Rats ; Rats, Wistar ; Reperfusion Injury* ; Sutures ; Tea* ; Xylazine