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*

No abstract available.
Hematoma, Subdural, Acute*

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

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

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

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 nervous system toxicity is the most commonly recognized problem during treatment with carbamazepine (CBZ). The most common side effects of CBZ are drowsiness, incoordination, and vertigo. However, unusual conditions such as movement disorders, seizure aggravation, and encephalopathy have also been attributed to CBZ therapy. In case 1, cognitive dysfunction and exacerbation of preexisting gait disturbance were observed in a 63-year-old female who had frontal lobe epilepsy, schizencephaly, and lissencephaly treated with CBZ. The neurological symptoms were resolved 24 hours after the withdrawal of CBZ and induced with the reintroduction of CBZ. In case 2, myoclonic jerks occurred in a 37-year-old female when CBZ was readministered after a 4-day-withdrawal period of CBZ. The myoclonic jerks disappeared 12 days after CBZ was discontinued. In both cases, plasma CBZ levels were within the therapeutic range. We report two cases with encephalopathy and myoclonic jerks as unusual side effects of CBZ, with the plasma levels of CBZ being within the therapeutic range.
Adult ; Ataxia ; Carbamazepine ; Central Nervous System ; Epilepsy, Frontal Lobe ; Female ; Gait ; Humans ; Lissencephaly ; Malformations of Cortical Development ; Middle Aged ; Movement Disorders ; Myoclonus* ; Plasma ; Seizures ; Sleep Stages ; Vertigo

BACKGROUND AND PURPOSE: White-matter (WM) lesions are known to potentiate cognitive impairment in poststroke patients. The present study was designed to assess whether Ginkgo biloba extract (GB) and cilostazol, which were evaluated alone and in a combination formula (Renexin), can attenuate the WM lesions and cognitive decline caused by chronic hypoperfusion in the rat. METHODS: Animals were divided into five treatment groups: cilostazol (25 mg/kg/day), GB (20 mg/kg/day), Renexin (25 mg/kg/day cilostazol + 20 mg/kg/day GB), vehicle, and sham. The animals received the treatments orally 1 day after bilateral common carotid artery occlusion [two-vessel occlusion (2VO); except for the sham group, which underwent the surgery but the arteries were not occluded], and then the same dose every day for 21 days thereafter. Prior to sacrificing the rats, repetitive eight-arm radial maze testing was performed to examine their cognitive abilities. After drug administration and cognitive testing, brain tissues were isolated for Kluver-Barrera and terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick end-labeling (TUNEL) staining, immunohistochemical assessment of glial fibrillary acidic protein (GFAP) and CD11b (OX-42), and to assay free-radical scavenging activity. RESULTS: We found that the significant WM lesions induced by 2VO was ameliorated significantly by treatment with cilostazol, GB, and Renexin, in association with increased TUNEL-positive cells. In addition, chronic cerebral hypoperfusion caused a large increase in the degree of GFAP and OX-42 immunoreactivity and free-radical activity in the optic tract. These abnormalities were significantly reversed by the three drugs, but most prominently by Renexin, suggesting a markedly enhanced or supra-additive effect of cilostazol and GB when administered together. CONCLUSIONS: Significant attenuation of cytoarchitectural damage and apoptotic cell death was found with GB and cilostazol, but a markedly enhanced effect was seen for treatment with their combination in the WM of rat brains after bilateral occlusion of the common carotid arteries. We suggest that combination therapy with GB and cilostazol provides enhanced neuroprotective effects and induces subsequent cognitive improvement in patients with chronic ischemic conditions.
Animals ; Arteries ; Brain ; Carotid Artery, Common ; Cell Death ; Ginkgo biloba ; Glial Fibrillary Acidic Protein ; Humans ; Neuroprotective Agents ; Rats ; Salicylamides ; Tetrazoles ; Visual Pathways