Cases reported "Brain Infarction"

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1/82. 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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2/82. A follow-up study of cognitive impairment due to inferior capsular genu infarction.

    Abulia, memory loss, other cognitive deficits, and behavioral changes consistent with dementia can follow an inferior capsular genu infarction, but only little is known about the time course of these disturbances. The present study describes the long-term outcome of cognitive defects in four patients with inferior capsular genu infarction who underwent a neuropsychological examination within 3 and 12 months of onset. Three patients had infarcts in the inferior genu of the left internal capsule and had similar symptoms in the acute phase: disorientation, memory loss, language impairment, and behavioral changes. The patient with right-side infarct showed memory impairment and behavioral changes. Three patients had deficits in one or more cognitive domains on the first assessment, but none was demented. By the second evaluation all subjects had improved. In two patients there were a moderate memory defect persisted and a language disturbance. Improvement in these disturbances during long-time follow-up demonstrates that there are alternative pathways that reestablish the functional connections damaged by the strategically located capsular genu infarct. Inferior capsular genu infarction is not a cause of persisting "strategic infarct dementia."
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3/82. osteomyelitis, lateral sinus thrombosis, and temporal lobe infarction caused by infection of a percutaneous cochlear implant.

    OBJECTIVE: cochlear implantation has become a routine operation in the last 10 years. The most common soft tissue complications with transcutaneous cochlear implants include infection or necrosis of the flap and extrusion of the implant and device failure. The most common complication reported with percutaneous devices include minor skin irritations at the pedestal site, retraction of skin from the pedestal site, and loosening of screws that retain the pedestal. We describe one case of lateral sinus thrombosis and secondary temporal lobe infarction caused by infection of a screw anchoring the percutaneous pedestal of an Ineraid implant. STUDY DESIGN: Case report. SETTING: Tertiary referral center. CONCLUSIONS: Intracranial complications of a percutaneous bone-anchored pedestal may occur with little prodrome. Computed tomography (CT) scan of the pedestal and bone anchoring screws may be indicated if local evidence of infection persists.
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4/82. myxoma on anterior mitral leaflet presenting with symptoms of cerebellar artery infarction.

    This report describes a patient who had dizziness and loss of balance. During routine investigation, a mass located on the anterior mitral valve leaflet was detected on transthoracic echocardiography. The patient underwent surgery for a mass located on the mitral valve, and histopathologic examination determined the mass was a myxoma.
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5/82. Unilateral thalamic infarction and vertical gaze palsy: cause or coincidence?

    Although vertical gaze palsy (VGP) is commonly associated with lesions of the rostral mesencephalon, there is some evidence that VGP may also be caused by a unilateral thalamic lesion. The case of a 68-year-old man with persistent upward gaze palsy after a unilateral thalamic infarction, demonstrated on computed tomography and magnetic resonance imaging scans, is presented. Subsequent high-resolution magnetic resonance scanning, however, showed involvement of the rostral mesencephalon as well. The authors suggest that in previous patients with VGP ascribed to a unilateral thalamic infarction, a coexisting mesencephalic involvement may have been missed because of inappropriate imaging techniques. Strong evidence of unilateral thalamic infarction as a cause of VGP is still lacking.
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6/82. Bilateral ptosis with pupil sparing because of a discrete midbrain lesion: magnetic resonance imaging evidence of topographic arrangement within the oculomotor nerve.

    The topographic arrangement within the midbrain oculomotor nerve is not adequately elucidated in humans. Two patients with a partial oculomotor palsy because of a localized infarction or hematoma were treated. Both patients had bilateral ptosis, impaired adduction, and supraduction. One patient had impaired infraduction and pupillary involvement on one side. Results of computed tomography and magnetic resonance imaging revealed discrete lesions at the dorsal midbrain tegmentum that spared the rostral midbrain. The authors' cases elucidate that pupillary components take the most rostral course. This report provides indirect magnetic resonance imaging evidence to prove the course of pupillary fibers. Based on the different neuro-ophthalmologic findings in the authors' cases (sparing or affecting pupillary component and infraduction), the nerves of the inferior rectus and inferior oblique for infraduction pass more rostrally than those of medial rectus, superior rectus, and levator palpebrae. The nuclear and fascicular arrangement within the midbrain oculomotor nerve is speculated to be pupillary, extraocular, and eyelid elevation in the rostro-caudal order, based on the neuro-ophthalmologic impairment and magnetic resonance imaging findings in the authors' patients and in previous animal experiments. Knowing the fascicular and nuclear arrangement within the midbrain in detail will offer diagnostic clues for differentiation of causes for partial oculomotor palsy.
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7/82. Apraxic agraphia due to thalamic infarction.

    The authors report a patient of pure apraxic agraphia with normal praxis due to left thalamic infarction. 15O-gas-PET showed reduced oxygen metabolism in the left thalamus and the left dorsolateral premotor area, while MRI and 11C-fulumazenil-PET showed no remarkable lesions in the frontal cortex. The patient's word imaging remained normal. The authors hypothesize that thalamic destruction causes pure apraxic agraphia by exerting a remote effect on left dorsolateral premotor area and blocking somewhere between graphemic area and motor programming.
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8/82. Postanoxic parkinsonism: clinical, radiologic, and pathologic correlation.

    The authors report a 72-year-old patient who presented with parkinsonism after hypoxic-ischemic insult. T1-weighted MRI revealed high signal intensity lesions in the basal ganglia. Pathologic study of the brain disclosed multiple foci of old infarcts with gliosis and lipid-laden and hemosiderin-laden macrophages, indicating a previous minor hemorrhage after infarction. This observation provided pathologic correlation with the patient's clinical symptoms and MRI.
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9/82. Isolated inferior rectus palsy as a result of paramedian thalamopeduncular infarction.

    The authors present the cases of two patients with isolated inferior rectus muscle paresis presumed to be caused by paramedian thalamopeduncular infarction that involved supranuclear descending pathways, just before the inferior rectus subnucleus in one patient, and just before subnucleus or fascicular fibers in the other patient. Both patients had no other associated neurologic dysfunction. The lesions that cause isolated inferior rectus palsy in these patients are documented by magnetic resonance findings. Although vascular ischemic lesions as the cause of isolated inferior rectus palsy were reported previously, to the authors' knowledge, it has not been demonstrated radiologically.
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10/82. 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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