Cases reported "Brain Infarction"

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1/15. Natural course of combined limb and palatal tremor caused by cerebellar-brain stem infarction.

    After infarction of the left superior cerebellar peduncle and dentate nucleus, a patient developed tremor of the left upper limb beginning on the twelfth day followed by palatal tremor appearing 10 months after infarction. Surface electromyogram revealed a difference in the frequency of the tremor in the upper limb and soft palate. When the palatal tremor appeared, brain magnetic resonance T2-weighted images revealed high signal intensity of the contralateral, right inferior olivary nucleus. Subsequently, when the amplitude of palatal tremor became less severe, the high olivary signal intensity subsided whereas the hypertrophy of the nucleus remained. This patient provides useful information on the pathogenesis of skeletal and palatal tremor with brain stem or cerebellar lesions based on the differences in the onset and frequency of tremors and morphologic changes in the inferior olive.
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2/15. Involuntary masturbation as a manifestation of stroke-related alien hand syndrome.

    alien hand syndrome is a perplexing and uncommon clinical diagnosis. We report an unusual manifestation of alien hand syndrome in a 73-yr-old man with a right anterior cerebral artery infarct affecting the right medial frontal cortex and the anterior portion of the corpus callosum. We conclude that alien hand syndrome should be considered in patients who present with a feeling of alienation of one or both upper limbs accompanied by complex purposeful involuntary movement.
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3/15. Thalamic tremor: correlations with three-dimensional magnetic resonance imaging data and pathophysiological mechanisms.

    tremor associated with a single focal thalamic lesion has rarely been reported. Furthermore, the exact localization of the lesions is difficult to determine because of the imprecision of "conventional" radiology (computed tomography scan and/or "standard" magnetic resonance imaging). The aim of this study was to identify which thalamic structures are involved in tremor associated with a single focal thalamic lesion. We selected two patients who presented with unilateral postural and kinetic tremor of the upper limb related to a localized thalamic infarction. Three-dimensional T1-weighted magnetic resonance imaging sequence (MP-rage sequence) was used to determine the precise topography of the lesions by stereotactic analysis using the atlas of Hassler. The lesions were located within the pulvinar, the sensory nuclei, the mediodorsal nucleus, and the ventral lateral posterior nucleus (according to the classification of Hirai and Jones), the latter including the ventral intermediate nucleus (Vim according to the classification of Hassler). However, the Vim was spared. The subthalamic area, which can induce tremor, was not involved. After having compared the topography of the lesions with the clinical findings, we suggest that thalamic tremors may result from the interruption of the cerebellar outflow tract to the Vim within the thalamus.
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4/15. Symptomatic palatal myoclonus: an unusual cause of respiratory difficulty.

    A 67-year-old man presented with dysphagia and difficulty breathing. physical examination revealed palatal myoclonus. In this patient, the respiratory difficulty was caused by the fragmentation of breathing. Electromyographic examination of the cricothyroid muscle demonstrated rhythmic myoclonic jerks. magnetic resonance imaging (MRI) yielded a pontine midline and right sided tegmental infarct. The patient responded to sodium valproate.
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5/15. Neuronal activity in the globus pallidus in chorea caused by striatal lacunar infarction.

    pallidotomy was performed in a patient with hemichorea caused by lacunar infarction in the striatum. chorea in the lower limb was reduced after a neurosurgical lesion in the medial portion of the sensorimotor territory of the internal segment of the globus pallidus, and chorea in the upper limb disappeared after an additional lesion in the lateral portion of that same area. Intraoperative neuronal recording revealed that mean firing rates were low, and that firing was irregular in the globus pallidus compared with off-state parkinsonian patients. These results suggest that chorea with striatal infarction is driven by phasic neuronal activity with a low firing rate in the globus pallidus and that the neural pathway of chorea has a functional somatotopical organization in the globus pallidus.
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6/15. Patent foramen ovale complicated by paradoxical embolism and brain infarct in a patient with advanced ovarian cancer.

    BACKGROUND: Recent investigations of patients with cerebral and peripheral arterial emboli of unknown cause suggest that paradoxical embolism through a patent foramen ovale might be responsible for more arterial embolic events than previously realized. CASE: A 60-year-old woman with advanced ovarian cancer presented with sudden onset of expressive aphasia and right upper hemiplegia postoperatively. A patent foramen ovale diagnosed by echocardiography with contrast combined with the presence of thrombosis in her right femoral vein leads us to speculate that her stroke was secondary to a paradoxical embolism. CONCLUSION: Paradoxical embolism should be considered in the differential diagnosis of ovarian cancer patients with embolic stroke and it may be appropriate to include a cardiac echo as part of the diagnostic evaluation.
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7/15. Thalamic venous infarction as a cause of subacute dementia.

    The clinical picture of deep cerebral vein thromboses (DCVT) usually is acute, combining vigilance disorders, headaches, and focal neurologic deficit. The authors describe a patient who presented with isolated subacute dementia as the sole manifestation of DCVT. In the setting of subacute cognitive deficit, the diagnosis of DCVT must be considered when neuroimaging shows bilateral thalamic changes. Enhanced venous MR angiography is the noninvasive method of choice to ascertain the diagnosis.
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keywords = headache
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8/15. Bathing headache: a variant of idiopathic thunderclap headache.

    Bathing headache is rarely described in literature. We report four middle-aged Taiwanese women who developed severe throbbing headache with maximum intensity of onset during bathing. Diffuse cerebral vasospasm was demonstrated in one of them. All their headaches resolved spontaneously (n = 1) or after nimodipine treatment (n = 3). Except for one patient with vasospasm in whom reversible posterior leukoencephalopathy and an asymptomatic cerebellar infarction developed, the others recovered without any complications. The clinical profile of bathing headache points to idiopathic thunderclap headache. It may not be as benign as previously reported. nimodipine might be effective in treatment of this special headache syndrome.
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9/15. Cerebellar infarction in adolescent males associated with acute marijuana use.

    OBJECTIVE: To demonstrate the clinical characteristics, radiologic findings, and neuropathological features of tetrahydrocannabinol-related posterior fossa ischemic stroke in adolescent patients. DESIGN: A retrospective case and chart review of 3 cases encountered at a tertiary care institution over a span of 5 years. SETTING: Inpatient and intensive care hospitalization units managing children and adolescents. SUBJECTS: male adolescent patients with ischemic cerebellar stroke after use of marijuana. DIAGNOSTIC INVESTIGATIONS: Computed tomography brain scans (3 subjects), magnetic resonance imaging brain study (1 subject), cerebral arteriography (1 subject), cerebellar biopsy (1 subject), and necropsy (2 subjects). RESULTS: Three adolescent males had similar presentations of headache, fluctuating level of consciousness or lethargy, visual disturbance, and variable ataxia after self-administration of marijuana. They developed primary cerebellar infarctions within days after the exposure that could not be attributed to supratentorial herniation syndromes and only minimally involved brainstem structures. CONCLUSIONS: Episodic marijuana use may represent a risk factor for stroke in childhood, particularly in the posterior circulation. Early recognition of the cerebellar stroke syndrome may allow prompt neurosurgical intervention, reducing morbidity.
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10/15. Clinical features of postoperative cerebral venous infarction.

    There is a potential risk of sacrificing the cortical vein during neurosurgical operations, particularly in the interhemispheric or subtemporal approach. An impaired cortical vein might cause cerebral venous circulatory disturbances (CVCDs) resulting in venous infarction. In this article, we have reviewed the management and results of eight cases with symptomatic postoperative venous infarction.We have encountered eight cases with symptomatic postoperative venous infarction (0.3%) during the past 5 years. The series is composed of 3 males and 5 females, with ages that ranged from 43 to 76 years (mean age of 58.1 years), and consisted of five brain tumors, one cavernoma, one dural AVF, and one trigeminal neuralgia. Initial symptoms occurred intra-operatively in two, on 0 day after the operation in one, 1 day in three, 3 days in one, and 4 days in one case. The symptoms were intra-operative brain edema in two cases, disorientation in one, cerebellar signs in one, hemiparesis in one, aphasia in two, and headache in one case. Two cases required surgical intervention. The results were a good outcome in 6 and a fair outcome in 2 cases.In conclusion, there are two types of postoperative venous infarction; severe onset (severe type) and gradual onset (mild type). The former needs immediate treatment from the intra-operative period onward, and the prevention of the ongoing venous thrombosis is essential in the latter.
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