Cases reported "Cerebral Infarction"

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1/31. Adverse effect of dopamine agonist therapy in a patient with motor-intentional neglect.

    Studies in animals and humans report dopamine agonists can improve neglect. Because dopamine deficit reduces intention to act, it has been suspected the dopamine agonist bromocriptine would improve deficient hemispatial intention. Thus, the effect of bromocriptine on line bisection was examined in a patient with neglect and failure of the action-intention system. The 58-year-old patient had left-sided neglect from a right cerebral infarction involving both cortical and subcortical (striatal) structures. It was determined that neglect on a line bisection task was attributable to a motor-intentional bias by testing under congruous and incongruous video monitoring. Testing sessions were held before starting bromocriptine, on 20 mg/d, and after stopping bromocriptine. The patient's ipsilesional bias increased on bromocriptine, and improved when bromocriptine was stopped. bromocriptine may worsen neglect if putamenal receptors are damaged. dopamine agonists may activate the normal hemisphere, increasing an intentional bias. Clinicians using dopaminergic pharmacotherapy should assess patients for this possible adverse effect.
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2/31. Down's syndrome with mucosa-associated lymphoid tissue, thyroid lymphoma and cerebral infarction.

    Primary lymphoma of the thyroid gland is rare. The histopathology of most low-grade thyroid lymphomas is of a mucosa-associated lymphoid tissue (MALT) type. A typical feature of this type of lymphoma is a close lymphocyte-epithelium interaction. It tends to appear in patients with a history of autoimmune disease or chronic inflammatory disorders. A clinical picture of hypothyroidism may be present. hyperthyroidism associated with thyroid lymphoma is also rare. Thyroid lymphoma could be misdiagnosed as lymphocytic thyroiditis or small cell anaplastic carcinoma. It is rarely reported in patients with Down's syndrome. In this report, we describe a Down's syndrome patient with MALT thyroid lymphoma and cerebral infarction. The patient, a 42-year-old man, presented with chest discomfort and bilateral leg weakness of one week's duration. physical examination of his neck showed a right-sided mass lesion. neurologic examination revealed decreased muscle power and hyperreflexia in both lower legs. Babinski's sign was present bilaterally. Endocrinologic studies showed subclinical hypothyroidism. A thoracolumbar radiograph showed disc space narrowing. Thyroid sonography revealed a hypoechoic mass lesion in the right lobe of the thyroid gland. Fine needle aspiration cytology of the neck mass demonstrated a large amount of lymphocyte infiltration. An I131 thyroid scan and 24-hour uptake revealed the possibility of thyroid malignancy at the upper poles of both thyroid lobes. Computerized tomography of the brain revealed a lacunar infarct in the posterior aspect of the left putamen. magnetic resonance imaging of the lumbar spine revealed a healed L4 compression fracture with L4-5 retrolithesis. The patient later underwent a right total thyroidectomy. The pathologic finding showed MALT lymphoma. The patient received steroid suppression therapy, and after nine months of treatment and follow-up, he developed clinical hypothyroidism. Neither local tumor recurrence nor distant metastasis was found.
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3/31. Unusual CT and MRI appearance of carbon monoxide poisoning.

    Unilateral low attenuation areas within the right putamen, globus pallidus and thalamus were observed on CT in a patient after exposure to carbon monoxide. A transient bilateral appearance was found on subsequent CT examinations. Hemorrhagic infarction of the right putamen, and ischemic lesions in both thalami were visualized on MRI 2 weeks later.
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4/31. Hemiballism with hyperglycemia and striatal T1-MRI hyperintensity: an autopsy report.

    We report on an autopsy findings of a 92-year-old male with hemiballism-hemichorea associated with hyperglycemia and striatal hyperintensity on T1-weighed magnetic resonance imaging (MRI), a recently described clinicoradiological syndrome. Histologically, the putamen contralateral to the hemiballism consisted of multiple foci of recent infarcts associated with reactive astrocytic and interneuronal response. Substrate responsible for the MRI signal changes is still inconclusive. copyright movement Disorder Society.
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5/31. A case of micrographia after subcortical infarction: possible involvement of frontal lobe function.

    Most reports of micrographia associated with focal brain lesions have related this finding to damage in the left basal ganglia. Here we describe the case of a 68-year-old man presenting with reversible micrographia accompanied by hypophonia in the absence of extrapyramidal signs after cerebral infarction in the left subcortical region. At the time of the patient's admission, diffusion-weighted magnetic resonance imaging sequence showed the lesion to principally involve the corona radiata, with some involvement of the putamen. Neurologically, mild right-sided brachiofacial hemiparesis and grasp reflexes - a frontal lobe sign - were observed. As his micrographia and hypophonia improved, the patient's grasp reflexes improved in parallel. In addition, recovery of regional cerebral blood flow in the left frontal lobe was confirmed by single photon emission computed tomography (technetium-99 m HMPAO). The present case suggests the possibility that the function of frontal-subcortical circuit might also be involved in the production and improvement of micrographia and that micrographia and hypophonia may share a common pathophysiology.
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6/31. Lacunar infarctions due to cholesterol emboli.

    BACKGROUND AND PURPOSE: hypertension is commonly considered the major cause of lacunar infarctions. However, in some cases, it has been suggested that lacunes could be caused by cerebral emboli from cardiac or carotid sources. cholesterol cerebral emboli have been rarely reported as a cause of lacunes. CASE DESCRIPTION: We describe a 79-year-old patient with a progressive multi-infarct dementia who developed transient motor aphasia and paresis of the right arm. Computed tomography showed lacunar infarcts in the right caudate nucleus, left thalamus, and left putamen, as well as an old right frontal infarction. Neuropathological examination demonstrated no prominent vascular hyalinosis, but did show multiple cholesterol emboli occluding small arteries around lacunar infarcts and leptomeningeal arteries near cortical infarcts. The cholesterol material presumably originated in the extended atheromatous changes along the aortic arch. CONCLUSIONS: Our report confirms that lacunes can be caused by cholesterol emboli in some patients. Small cerebral emboli should not be overlooked as a cause of lacunes.
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7/31. Delayed oculogyric crises associated with striatocapsular infarction.

    Oculogyric crises are dystonic, usually upward, conjugate eye deviations. We describe an 11-year-old girl who developed oculogyric crises 3 1/2 years after infarction of the right caudate, putamen, and internal capsule. Her abnormal eye movements responded to anticholinergic agents. This is the first reported association between oculogyric crises and striatocapsular infarction.
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8/31. Emotional facial paresis with striatocapsular infarction.

    Emotional facial paresis (EFP) refers to hemifacial paresis of emotionally evoked or spontaneous smiling or weeping with preserved volitional movements of the face. The anatomical location for this phenomenon has been controversial. We report a 15-year-old boy with EFP. Follow-up MRI demonstrated infarction limited to the head of the caudate, putamen and anterior limb of the internal capsule on the contralateral side. This case lends support for selective damage at a striatal or capsular site in the production of EFP.
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9/31. aphasia associated with verified subcortical lesions: three case reports.

    aphasia classically has been described as an acquired impairment of language behavior subsequent to cortical brain injury to the dominant hemisphere. Traditionally, lesions in the internal capsule have been described as resulting in pure motor deficits, which may be accompanied by dysarthria without aphasia. Only recently has the literature suggested that lesions in the putamen and internal capsule may result in aphasia. We describe three clinical cases in which aphasia resulted from left subcortical lesions. The lesions were demonstrated using computed tomographic (CT) scan; language deficits were measured objectively using the Porch Index of Communicative Ability (pica). Two of the three patients experienced excellent recovery of language skills, suggesting that subcortical lesions may have a more favorable prognosis in recovery from aphasia than do cortical lesions. The encouraging recovery may be related to fiber pathway disruption rather than cortical destruction.
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10/31. Spontaneous hemiballism and disappearance of parksinsonism following contralateral lenticular lacunar infarct.

    Hemiballism was observed in a 77-year-old woman with Parksinson disease after a contralateral lenticular infarct without apparent involvement of the subthalamic nucleus. Parkinsonian signs ipsilateral to the hemiballism remained abolished despite subsequent nearly complete recovery from the hyperkinesias. It is argued that clinical events were due to a single ischemic lesion of the putamen-pallidum complex.
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