Cases reported "Brain Infarction"

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1/14. 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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keywords = nucleus
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2/14. An unusual concomitant tremor and myoclonus after a contralateral infarct at thalamus and subthalamic nucleus.

    A 72-year-old woman experienced a sudden onset of spontaneous tremor and myoclonus of right extremities that completely subsided 24 hours after onset. neuroimaging study revealed an infarct at the left ventral portion of thalamus and subthalamic nucleus. Concomitant dyskinetic movement disorders after stroke are extremely rare and the mechanism is herein discussed.
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ranking = 711.80384693136
keywords = thalamic nucleus, nucleus
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3/14. An unusual homonymous visual field defect.

    A 75-year-old man suddenly became aware of an inferior right homonymous visual field defect. Although static perimetry suggested a lesion of the left lateral geniculate nucleus, kinetic perimetry indicated that the presumed homonymous horizontal sectoranopia noted on static perimetry was actually an incomplete homonymous hemianopia with incomplete sparing of the temporal crescent. The location of the lesion was subsequently confirmed by magnetic resonance imaging. This case shows the value of kinetic perimetry in assessing homonymous visual field defects.
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ranking = 0.33333333333333
keywords = nucleus
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4/14. A clustering of unfavourable common genetic mutations in stroke cases.

    OBJECTIVES: The aetiological role of common genetic mutations was analysed in a subgroup of stroke patients. MATERIAL AND methods: A total of 406 patients were examined because of ischaemic stroke. After a detailed clinical scrutiny, 5 were found who did not exhibit any of the classical clinical risk factors. In this clinically homogeneous subgroup of stroke patients, the prothrombin A20210G, hong kong, Cambridge and methylenetetrahydrofolate reductase C677T (MTHFR C677T) mutations, angiotensin-converting enzyme polymorphism (ACE polymorphism) and apolipoprotein E (APO E) genotype were examined. RESULTS: In all 5 patients, the same type of clustering of three mutations was manifested. A heterozygous Leiden V mutation was observed in all 5 subjects, while a heterozygous MTHFR C677T mutation and an I/D genotype for ACE polymorphism were detected in 4 of them, and a homozygous D/D genotype and a homozygous MTHFR C677T mutation in 1. This type of clustering of the mutations was not observed in the remaining 401 stroke patients. CONCLUSION: These results suggest that the Leiden mutation might possibly be an aetiological factor for stroke in a rare subgroup of patients who do not display any of the classical risk factors. The roles of ACE D polymorphism and the MTHFR C677T mutation in stroke, should also be taken into consideration in this subgroup of stroke patients. These unfavourable genetic factors might be aetiological factors if they are clustered together in a stroke patient not presenting any of the standard clinical risk factors.
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keywords = group
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5/14. 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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keywords = nucleus
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6/14. 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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keywords = nucleus
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7/14. Severe ADC decreases do not predict irreversible tissue damage in humans.

    BACKGROUND AND PURPOSE: A mismatch between diffusion- and perfusion-weighted MRI is thought to define tissue at risk of infarction. This concept is based on the assumption that diffusion slowing of and decreases in the apparent diffusion coefficient (ADC) serve as indicator of tissue proceeding to infarction. We tested this hypothesis. methods: MRI (diffusion weighted, perfusion weighted, MRA, T2 weighted) was performed in 15 patients with acute stroke within 2.9 /-0.8 hours (mean /-SD) of onset and on days 1 and 7. After intraindividual realignment of the ADC maps, the development of ADC range volumes and ADC values was determined. RESULTS: An increase (354%, group A1) in the total ADC-based lesion volume below a threshold of < 80% occurred in 4 patients on day 1, persisting on day 7 with a pronounced increase of ADC range volumes with low ADC values. An increase in total ADC-based lesion volume (201%, group A2) followed by a secondary drop to day 7 was found in 7 patients. A significant reduction in total ADC-based lesion volume (14%, group B) was found in 4 patients. ADC-based lesion volume increase was associated with persistent vessel occlusion in group A, whereas recanalization in group B resulted in ADC volume decrease. ADC normalization was observed independently from the degree of the initial ADC decrease on days 1 and 7 in group B. CONCLUSIONS: In line with results from animal experiments, ADC decreases do not reliably indicate tissue infarction Even severely decreased ADC values may normalize in human stroke, and it seems likely that ADC normalization depends on the duration and severity of ischemia rather than the absolute value.
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ranking = 0.00032050556117051
keywords = group
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8/14. Isolated superior rectus palsy due to contralateral midbrain infarction.

    BACKGROUND: Isolated superior rectus palsy due to a contralateral midbrain lesion has not been reported. CASE DESCRIPTION: A 71-year-old woman suddenly developed diplopia. Examination showed that she had isolated superior rectus paresis. magnetic resonance imaging showed a tiny infarct at the area of the oculomotor nucleus on the contralateral side. CONCLUSION: Isolated superior rectus palsy may be caused by a contralateral midbrain lesion that selectively involves crossing superior rectus nerve fibers.
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ranking = 0.33333333333333
keywords = nucleus
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9/14. Thalamic thermo-algesic transmission: ventral posterior (VP) complex versus VMpo in the light of a thalamic infarct with central pain.

    The respective roles of the ventral posterior complex (VP) and of the more recently described VMpo (posterior part of the ventral medial nucleus) as thalamic relays for pain and temperature pathways have recently been the subject of controversy. Data we obtained in one patient after a limited left thalamic infarct bring some new insights into this debate. This patient presented sudden right-sided hypesthesia for both lemniscal (touch, vibration, joint position) and spinothalamic (pain and temperature) modalities. He subsequently developed right-sided central pain with allodynia. projection of 3D magnetic resonance images onto a human thalamic atlas revealed a lesion involving the anterior two thirds of the ventral posterior lateral nucleus (VPL) and, to a lesser extent, the ventral posterior medial (VPM) and inferior (VPI) nuclei. Conversely, the lesion did not extend posterior and ventral enough to concern the putative location of the spinothalamic-afferented nucleus VMpo. Neurophysiological studies showed a marked reduction (67%) of cortical responses depending on dorsal column-lemniscal transmission, while spinothalamic-specific, CO2-laser induced cortical responses were only moderately attenuated (33%). Our results show that the VP is definitely involved in thermo-algesic transmission in man, and that its selective lesion can lead to central pain. However, results also suggest that much of the spino-thalamo-cortical volley elicited by painful heat stimuli does not transit through VP, supporting the hypothesis that a non-VP locus lying more posteriorly in the human thalamus is important for thermo-algesic transmission.
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ranking = 1
keywords = nucleus
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10/14. Ondine's curse in a patient with unilateral medullary and bilateral cerebellar infarctions.

    Central sleep apnea (CSA), also known as Ondine's curse (OC), is a phenomenon characterized by episodes of repeated apnea during sleep due to disorders of the central nervous system. We report a patient with CSA/OC due to right dorsolateral medullary and bilateral cerebellar infarctions that occurred in the clinical setting of right vertebral artery stenosis. polysomnography (PSG) showed repeated episodes of absence of nasal cannula flow accompanying cessation of thoracic and abdominal respiratory movements and a decline in blood oxygen saturation. The duration of apnea was as long as 12 seconds. Brain magnetic resonance (MR) images showed acute infarctions involving the right dorsolateral medulla, bilateral cerebellar vermis and paramedian cerebellar hemispheres. MR angiography showed nonvisualization of the right vertebral artery. Transcranial Doppler sonography showed a high resistance flow profile in the right vertebral artery and normal flow patterns in the basilar artery and left vertebral artery. These findings suggest that the medullary and bilateral cerebellar infarcts were caused by stenosis/pseudo-occlusion of the right vertebral artery. Reduced respiratory afferent inputs to the dorsal respiratory group of medullary neurons, the nucleus tractus solitarius and reduced "automatic" components of the respiratory drive may play a role in the development of CSA/OC.
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ranking = 0.33338675092686
keywords = nucleus, group
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