Lateral medullary syndrome is famous for its unique symptom complex such as crossed sensory change or Homer syndrome, and thus hardly can be misdiagnosed. Though this syndrome has been reported to be able to accompany ipsilateral motor weakness, the sensory change of extremities is known to be almost always contralateral to the lesion. We recently experienced one case presented with weakness and dysmetria on the right associated with ipsilateral sensory change. But few days later, he showed additional neurologic signs compatible with right lateral medullary syndrome. Brain MRI showed rostro-caudally elongated lesion extending from right lateral medulla to the upper cervical cord. Here we suggest the probable neuroanatomical substrate for this symptom and clinico-radiologic relationship with previous literature.
Brain ; Cerebellar Ataxia ; Extremities ; Lateral Medullary Syndrome* ; Magnetic Resonance Imaging ; Neurologic Manifestations ; Stroke*

It has been known that the hypothermia have protective effect on neuronal survival after ischemic damage. We performed this study to evaluate the effect of the small changes in postischemic body temperature on the histopathological change of hippocampus in the transient global cerebral ischemia model. Mongolian gerbils were subjected to this study. Nine animal subgroups were investigated, including naive gerbils who underwent sham operation or carotid artery occlusion with postischemic rectal temperature maintained at 32.5, 34.5, 36.5 and 38.5C respectively. Carotid occlusion was maintained for 10 minutes and then reperfusion started. During ischemia, body temperature was maintained 36.5degrees C in all animals. For one hour after ischemia, body temperature was maintained constant at 36.5degrees C in the normothermia group, 38.5 degrees C in the hyperthemia group, 34.5 degrees C in mild hypothermia group, and 32.5 degrees C in moderate hypothermia group respectively. Seven days after the operation, the surviving animals were decapitated and perfusion fixated. After preparing coronal brain slices, viable neurons in hippocampal region were counted using cresyl violet staining. There were significant differences in the hippocampal neuronal survival in normothermia and hyperthermia groups compared with shamoperated group(P<0,01), and neuronal damages in mild and moderate hyperthemia groups were not significantly different from sham operated. Survival rate at postischemic 7th day was also significantly lower in hyperthermia group. We could confirm the protective effect of hypothermia on ischemic neuronal damage by histopathological study. Also hyperthemia was observed to aggravate neuronal death, Careful control of body temperature might have clinical effect in ischemic stroke.
Animals* ; Body Temperature ; Brain ; Brain Ischemia ; Carotid Arteries ; Fever ; Gerbillinae ; Hippocampus ; Hypothermia ; Ischemia* ; Models, Animal* ; Neurons* ; Perfusion ; Reperfusion ; Stroke ; Survival Rate ; Viola

Vascular dementia (VaD) is a dementia syndrome resulting from brain dysfunction produced by cerebrovascular disease. It is one of the most common causes of in the elderly, along with Alzhedimer's disease. Identification of VaD is particularly importent since its course may be modifiable through controlling risk factors. Hypxic-ischemic injury is responsible for most of VaD, and leukoencephalopathy and lacunes;some have traditional cortical infarctions. Clinical course of VaD is variale and not all the cases exhibit a classic stepwise progression. The clinical manifestations of VaD is include focal neurologic signs, extrapyramidal dysfunction, and incontinence. Neurobehaviaral abnormalities most often resemble those of subcortical dementia, but some patients manifest cortical dysfunction syndromes (aphasia, agnosia, apraxia). Personality changes and depression are common. A variety of pathological alterations associated with VaD include arterial territory infarctions, laminar necrosis, granular atrophy, sclerosis, lacunes, and subcortical leukoencephalopathy. Diagnosis of VaD depends on meeting following three criteria;1) dementia, 2) clinical and neuroimaging evidence of cerbrovascular disease, and 3) a compelling temporal relationship between the cognitive changes and the vascular insults. Treatment of VaD includes prevention of further vascular injury, control of neuropsychiatric disturbances, and application of appropriate rehabilitative strategies.
Aged ; Agnosia ; Atrophy ; Brain ; Classification* ; Dementia ; Dementia, Vascular* ; Depression ; Diagnosis ; Humans ; Infarction ; Leukoencephalopathies ; Necrosis ; Neuroimaging ; Neurologic Manifestations ; Risk Factors ; Sclerosis ; Vascular System Injuries

A 38-year-old woman, affected by chronic myeloid leukemia, received a BMT from his HLA identical brother. A mild acute graft-versus-host disease (GVHD) developed during the first month after the BMT. A typical clinical and electrophysiological feature of myasthenia gravis (MG) developed 3 months after the BMT requiring medication with pyridostigmine and steroids. Laboratory findings including acetylcholine receptor antibody and other autoantibodies were negative. MG is a well-characterized autoimmune disease which, on rare occasions, is also diagnosed as chronic GVHD after BMT. We report a first case of MG during an acute GVHD period. Since the patient had a myasthenic symptom during an acute GVHD period and no evidence of antibody mediated autoimmunity, this is likely to be an immune complication of acute GVHD. (J Korean Neurol Assoc 19(1):60~61, 2001
Acetylcholine ; Adult ; Autoantibodies ; Autoimmune Diseases ; Autoimmunity ; Bone Marrow Transplantation* ; Bone Marrow* ; Female ; Graft vs Host Disease ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Myasthenia Gravis* ; Pyridostigmine Bromide ; Siblings ; Steroids

BACKGROUND: The neuropsychiatric derangements in dementing patients are common and troublesome in their managements. The purpose of this study is to compare the behavioral changes in patients with subcortical vascular dementia (SVaD) and to those in patients with Alzheimer's disease (AD) by using the Korean version of the neuropsychiatric inventory (K-NPI). METHODS: The K-NPI was administrated to the close caregivers of 19 patients with AD (who met the criteria of the NINCDS-ADRDA for probable AD) and 14 patients with SvaD (who met the criteria of the NINDS-AIREN criteria for probable or possible VaD). Groups were matched for age, education and dementia severity. We evaluated the prevalence, the composite score (frequency X severity) of each behavioral domain in K-NPI between two groups. RESULTS: The most common behavioral disturbances were anxiety (63%) in AD and apathy/indifference (93%) in SVaD. Patients with SVaD had significantly greater total K-NPI scores than patients with AD and exhibited apathy/indifference, agitation/aggression and anxiety more frequently. Composite score of apathy/indifference over 4.7 point discriminates between AD and SVaD with accuracy of 75.8%. CONCLUSIONS: The K-NPI provides behavioral profiles that differentiate patients with SVaD from patients with AD. Patients with SVaD are more behaviorally disturbed. Clinicians need to pay more attention to the behavioral disturbances when managing the patients with SVaD.
Alzheimer Disease* ; Anxiety ; Caregivers ; Dementia ; Dementia, Vascular* ; Education ; Humans ; Prevalence

The ptosis secondary to cerebral hemispheric lesion (cerebral ptosis) is unusual and has not been well documented. Although the precise anatomical localization and clinical course of cerebral ptosis were not clear, there have been a few clinical and electrophysiologlcal reports that right hemisphere had its functional asymmetry or dominancy in the cortical control of eyelid movement. We present 4 patients of cerebral ptosis with acute onset of cerebral infarction in right middle cerebral artery territory. All of them are right-handed and presented acute onset of left hemiparesis and bilateral ptosis, but have no signs of involvement of oculomotor or sympathetic nerve pathway. In conclusion, the blepharoptosis could be caused by hemispheric lesion per se and be a sign of right hemispheric lesion rather than that of left one.
Blepharoptosis ; Cerebral Infarction ; Eyelids ; Humans ; Middle Cerebral Artery ; Paresis

Gelastic Seizure(Ictal laughter) is frequently associated with hypothalamic hamartoma that is congenital tumor composed of heterotrophic and hyperplastic tissue located in the hypothalamus near the interpeduncular cistern, tuber cinereum, and mamillary body. The seizure usually begins in infancy or childhood and may be accompanied with precocious puberty and cognitive decline. A 14 year-old boy visited to our hospital because of paroxysmal frequent involuntary laughing regardless of emotional change. Brain MRI showed nonenhancing hypothalamic mass that had isointensity with gray matter on T1W1 and hyperintensity on T2Wl. So it was suspected that he had a gelastic seizure accompanied with hypothalamic hamartoma.
Adolescent ; Brain ; Hamartoma* ; Humans ; Hypothalamus ; Magnetic Resonance Imaging ; Male ; Mamillary Bodies ; Puberty, Precocious ; Seizures* ; Tuber Cinereum

Meningeal irritation signs sometimes develop after myelography due to bacterial infection by contamination during the procedure or chemical irritiation by contrast media itself. CSF profiles of chemical meningitis often mimick those of bacterial meningitis, sometimes causing difficulty in differentiation, but in that case clinical course soon reverse in short time without any complication. Postmyelography chemical meningitis by metrizamide (AmipaqueR) has been well described but iohexol (OmnipaqueR) has rarely been reported to cause chemical meningitis. We experienced a patient of chemical meningitis by iohexol and here descibe the case.
Bacterial Infections ; Contrast Media ; Humans ; Iohexol ; Meningitis* ; Meningitis, Bacterial ; Metrizamide ; Myelography*

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

It is well known that the status epilepticus induced by the administration of pilocarpine to lithium-pretreated rats is a role model to study for the cholinergic system in epileptogenesis and the pathogenesis of status epilepticus. Although the researches for the expression of the c-fos proto-oncogene in seizure models have been studied, the exact role of the c-fos expression is still uncertain. To evaluate the characteristics of lithium-pilocarpine seizure model, we designed this study by following three steps; (1) the analysis of clinical manifestations by video, and electroencephalogram through implanted cortical electrodes during the course of status epilepticus induced by intraperitoneal administration of lithium chloride (5 mEq/kg) followed by pilocarpine(50 mg/kg) in Sprague-Dawley rats, (2) Fos expression and the time course of Fos appearance by the immunocytochemistry, (3) Neuropathologic change by cresyl violet stain. The presentation of clinical manifestations were cholinergic symptoms and signs, stereotyped behaviour, motor seizures, and status epilepticus in order. Electroencephalographic findings showed five patterns : (I) discrete seizure with interictal slowing; (ii) merging seizures with waxing and waning ictal discharges; (iii) continuous ictal discharges; (iv) continuous ictal discharges with flat periods; and (v) periodic epileptiform discharges on a flat background. The neuroanatomical sites of Fos expression were the taenia recta, anterior olfactory nucleus, olfactory tubercle, piriform cortex, entorhinal cortex, amygdala, septum, accumbens, caudate-putamen, hippocampus, dentate gyrus, thalamus, and cerebral neocortex. The Fos immunostaining appeared first in the taenia tecta, anterior olfactory nucleus, olfactory tubercle, and piriform cortex at 1 hour after pilocarpine injection, and was maximal in the most areas of cerebral cortex and limbic area between 4 and S hours. The thalamus and the caudate-putamen became stained after 4 hours. In the hippocampal formation, firstly, the Fos was stained maximally in the dentate gyrus at 3 hours followed by in the CA1, CA2, and CA3 regions. The Fos was disappeared in the dentate gyrus and CA2 region of hippocampus within 18 hours, but became stained sustainly in the CA3 and CA1 regions of hippocampus at 24 hours. Llght microscopic findings revealed widespread brain damage. The neuropathological changes were found within the anterior olfactory nucleus, piriform cortex, entorhinal cortex, thalamus, hippocampal formation, amygdaloid complex, lateral septum, neocortex and substantia nigra. There were only swollen and edematous change of neurons at 1 hour, but severely shrunken and darkened neuronal degeneration and neuronal loss at 72 hours. The neuronal degeneration and loss in hippocampal formation appeared severe in the CA1 and hilum, moderate in CA2, and mild in CA3 and dentate gyrus. In conclusion, it was suggested that cholinergic system (muscarinic receptor) played an important role in the induction of the seizure because Fos was expressed in the brain areas containing muscarinc receptor and the lithium-pilocarpine seizure was a good model to study for the status epilepticus.
Amygdala ; Animals ; Brain ; Cerebral Cortex ; Dentate Gyrus ; Electrodes ; Electroencephalography* ; Entorhinal Cortex ; Genes, fos ; Hippocampus ; Immunohistochemistry ; Lithium Chloride ; Neocortex ; Neurons ; Olfactory Pathways ; Pilocarpine ; Rats ; Rats, Sprague-Dawley ; Seizures* ; Status Epilepticus ; Substantia Nigra ; Taenia ; Thalamus ; Viola