Carbon monoxide poisoning causes hypoxic brain damage with various neurological complications. Cerebral hemorrhagic infarction has rarely been reported as a complication of carbon monoxide poisoning. The author experienced a patient who developed cerebral infarction in the striatocapsular area extending to the corona radiata after carbon monoxide poisoning, which was followed by hemorrhagic transformation associated with neurological deterioration.
Carbon Monoxide Poisoning* ; Carbon Monoxide* ; Carbon* ; Cerebral Infarction* ; Hemorrhage ; Humans ; Hypoxia, Brain ; Infarction

A 79-year-old woman experienced the sudden onset of cognitive impairment that interfered with her activities of daily living. A neurological examination revealed no focal neurological deficits. Brain magnetic resonance imaging showed an acute infarction in the left anterior corona radiata, and neuropsychological tests revealed attention deficit, verbal memory impairment, and frontal executive dysfunction. This case suggests that a focal infarction affecting the anterior portion of the corona radiata can cause a strategic infarct dementia that predominantly manifests as frontal lobe dysfunction.
Activities of Daily Living ; Aged ; Brain ; Cognition Disorders ; Dementia* ; Dementia, Vascular ; Female ; Frontal Lobe ; Humans ; Infarction* ; Magnetic Resonance Imaging ; Memory ; Neurologic Examination ; Neuropsychological Tests

BACKGROUND: Involuntary movement is a rare symptom of stroke. The pathophysiologic mechanism is poorly understood. METHODS: We retrospectively evaluated the medical records of 1547 stroke patients who have been admitted to the Seoul National University Hospital from March, 1988 to March, 1997. RESULTS: We found 18 patients with involuntary movements. Dystonia was observed in 10 patients, ballism or chorea in 8 patients and tremor in 5 patients. Anatomical structures responsible for dystonia were thalamus, lenticular nucleus, caudate nucleus and midbrain. Ballism-chorea was associated with lesions of subthalamic nucleus, thalamus, and lenticular nucleus. Tremor was associtated with lesions of thalamus, lenticular nucleus and midbrain. Ballism-chorea was present in the onset of stroke in 6 cases, 2 months after stroke in 1 case, and 21 months after in 1 case. But only 1 case of dystonia was present in the onset of stroke, 2 cases within 7 days, 5 cases in one week to one month, and 2 cases after one month. The involuntary movements subsided in 5 cases of hemiballism-chorea and in 3 cases of dystonia In most of the improved cases, the symptoms subsided in a month. CONCLUSIONS: Basal ganglia and thalamus were the main areas involved where lesions associated with involuntary movements were reported. The nature of involuntary movements was variable. However, lesions in subthalamic nucleus resulted only in ballism-chorea. The presence of only ballism chorea, but not any other involuntary movements, due to subthalamic nucleus lesions indicates that an indirect pathway may play a role in the pathogenesis of ballism-chorea. The latency between the onset of stroke and involuntary movements was longer in dystonia than ballism-chorea. The course of ballism-chorea was generally better than dystona.
Basal Ganglia ; Caudate Nucleus ; Chorea ; Corpus Striatum ; Dyskinesias* ; Dystonia ; Humans ; Medical Records ; Mesencephalon ; Retrospective Studies ; Seoul ; Stroke* ; Subthalamic Nucleus ; Thalamus ; Tremor

No abstract available.
Blinking ; Infarction ; Trigeminal Nerve Diseases

No abstract available.
Extremities* ; Sarcoma*

Oromandibular dystonia (OMD) is a focal dystonia that is characterized by repetitive or sustained spasms of the masticatory, facial, or lingual muscles. The etiology is idiopathic in most cases. A patient presenting with OMD associated with diabetic hyperglycemia is reported herein. A 74-year-old woman with a history of diabetes developed OMD. Brain MRI revealed a high signal intensity in the bilateral putamen on T1-weighted imaging. Nonketotic hyperglycemia was detected. The OMD gradually subsided with normalization of the hyperglycemia and medication with haloperidol over 10 days.
Aged ; Basal Ganglia ; Brain ; Dystonia* ; Dystonic Disorders ; Female ; Haloperidol ; Humans ; Hyperglycemia* ; Magnetic Resonance Imaging ; Muscles ; Putamen ; Spasm

BACKGROUND: Patients with lacunar infarction often show neurological deterioration during the acute period of stroke. The aim of this study was to identify the predictors for early neurological deterioration (END) in patients with lacunar infarction using clinical variables and the findings of diffusion-weighted imaging (DWI). METHODS: This study involved 104 consecutive patients with acute lacunar infarction in the lenticulostriate artery territory who were admitted within 24 hours after onset between January 2010 and October 2014. END was defined as a decrease of > or =1 point in the National Institutes of Health Stroke Scale (NIHSS) motor score or > or =2 points in the total NIHSS score during the first 7 days after stroke onset. Clinical characteristics including initial NIHSS score, vascular risk factors, laboratory parameters, and DWI findings including the size, location, and shape of the lacunar infarction were evaluated to identify predictors for END. RESULTS: END occurred in 25 (24%) patients with lacunar infarction. The initial NIHSS score (odds ratio, 1.47; p=0.01), number of infarct slices (odds ratio, 1.95; p<0.01), and infarction with an irregular shape (odds ratio, 2.87; p=0.048) were independently associated with END in multivariable logistic regression analysis. In receiver operating characteristic curve analysis, the best threshold for predicting END was an NIHSS score of 4 points (sensitivity, 72%; specificity, 68%) and an infarct slice number of 3 (sensitivity, 84%; specificity, 62%). CONCLUSIONS: This study suggests that the initial NIHSS score, number of infarct slices, and an irregular lesion shape are independent predictors for END.
Arteries ; Humans ; Infarction ; Logistic Models ; National Institutes of Health (U.S.) ; Risk Factors ; ROC Curve ; Sensitivity and Specificity ; Stroke ; Stroke, Lacunar*

Selective gray-matter involvement has been recognized in global cerebral ischemia, but is not readily acknowledged to occur in focal ischemic stroke. The author reports two patients with acute infarcts that selectively affected the gray matter of the basal ganglia among the striatocapsular areas, but spared the white matter of the internal capsule. The clinical manifestation was transient ischemic attack in both patients. The observations indicate that selective gray-matter injury can occur following focal ischemia under a certain condition of transient ischemic attack.
Basal Ganglia ; Brain Ischemia ; Humans ; Infarction ; Internal Capsule ; Ischemia ; Ischemic Attack, Transient ; Stroke

Posterior reversible encephalopathy syndrome (PRES) is characterized by neurotoxic symptoms and neuroimaging finding of reversible cerebral edema in association with various conditions including hypertension, eclampsia, and autoimmune diseases. The author experienced a 47-year-old woman with systemic lupus erythematosus and systemic sclerosis overlap syndrome who developed PRES. The patient presented with alteration of consciousness in association with hypertension and increased autoimmune activity. Magnetic resonance imaging revealed vasogenic edema in the bilateral cerebral cortex, subcortical white matter, basal ganglia, brainstem, and cerebellum.
Autoimmune Diseases ; Basal Ganglia ; Brain Edema ; Brain Stem ; Cerebellum ; Cerebral Cortex ; Consciousness ; Eclampsia ; Edema ; Female ; Humans ; Hypertension ; Lupus Erythematosus, Systemic ; Magnetic Resonance Imaging ; Middle Aged ; Neuroimaging ; Posterior Leukoencephalopathy Syndrome ; Pregnancy ; Scleroderma, Systemic ; White Matter