Cases reported "Thalamic Diseases"

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1/17. Simultaneous bilateral thalamic hemorrhage: case report.

    A 60-year-old man presented with an extremely rare case of simultaneous hypertensive bilateral thalamic hemorrhage manifesting as left hemiparesis with headache followed by deterioration in consciousness and tetraparesis. CT scan confirmed the bilateral thalamic hemorrhages 17 hours after onset. magnetic resonance imaging showed the bilateral thalamic lesions had similar signal intensities, consistent with the simultaneous onset, and had no evidence of hemorrhagic reason. Conservative treatment achieved some neurological improvement, but he died of pneumonia six months after onset. The prognosis of a patient with bilateral hemorrhages is worse than would be indicated by the size of the hemorrhages.
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2/17. Acute bilateral thalamic necrosis in a child with mycoplasma pneumoniae.

    A previously neurodevelopmentally intact 5-year-old male was admitted to hospital with a right lower lobe pneumonia with pleural effusion, subsequently confirmed to be a mycoplasma pneumoniae infection. On the seventh day of the illness he had a prolonged generalized tonic or tonic-clonic convulsion, requiring intubation and ventilation. He was slow to regain consciousness (child's Glasgow coma Score 7-10 over 6 days) and brain imaging with CT and then MRI demonstrated bilateral thalamic lesions with oedema and central haemorrhage suggestive of acute bilateral thalamic necrosis, without striatal or white-matter involvement. He was treated with a 2-week course of erythromycin, and as an autoimmune process was considered possible, 5 days of intravenous methylprednisolone (20 mg/kg/day) followed by a 4-week oral prednisolone taper. He made a slow recovery over the next few weeks with almost complete neurological recovery by 2 months but with significant dysarthria, drooling, and a mild left hemiparesis. At 9 months, significant dystonia continued to affect his speech and, together with tremor, his upper-limb fine motor function bilaterally. His gait, personality, and higher cognitive functions appeared to have recovered fully. Although acute striatal necrosis, acute disseminated encephalomyelitis, and encephalitis have been reported with mycoplasma pneumoniae and a similar picture of acute bilateral thalamic necrosis with influenza-A ('acute necrotizing encephalopathy'), this is the first reported case of mycoplasma pneumoniae-associated isolated acute bilateral thalamic necrosis.
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3/17. Paramedian thalamopeduncular infarction: clinical syndromes and magnetic resonance imaging.

    We prospectively examined 11 patients with magnetic resonance imaging-documented infarction in the paramedian thalamopeduncular region, which is supplied by the superior mesencephalic and posterior thalamosubthalamic arteries. Variations in the size and rostral-caudal extent of infarction correlated with the following three clinical patterns: (1) With unilateral paramedian mesencephalic infarction, an ipsilateral third nerve paresis was accompanied by mild contralateral hemiparesis or hemiataxia. Contralateral ptosis and impaired upgaze were observed in two patients; one of them showed additional damage to the posterior commissure. (2) With bilateral infarction in the thalamopeduncular junction, involving the mesencephalic reticular formation, supranuclear vertical gaze defects were accompanied by impaired consciousness or memory, and mild aphasia in some patients. Persistent amnesia was observed only when the dominant anterior nucleus or mamillothalamic tract was damaged. (3) With larger thalamopeduncular infarcts, partial or complete third nerve paresis was combined with supranuclear gaze disturbance and delayed contralateral tremor. An unusual gaze disorder, a variant of the vertical "one-and-a-half syndrome," occurred with a small strategically placed lesion at the thalamopeduncular junction, best explained by selective damage to supranuclear pathways or partial nuclear involvement. The primary cause of these infarctions was embolism to the basilar apex or local atheroma at the origin of the posterior cerebral artery.
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4/17. Increased regional cerebral blood flow in the contralateral thalamus after successful motor cortex stimulation in a patient with poststroke pain.

    The mechanisms underlying poststroke pain have not been clearly identified. Although motor cortex stimulation (MCS) sometimes reduces poststroke pain successfully, the exact mechanism is not yet known. For further investigation of the neural pathways involved in the processing of poststroke pain and in pain reduction by MCS, the authors used positron emission tomography (PET) scanning to determine significant changes in regional cerebral blood flow (rCBF). This 58-year-old right-handed man suffered from right-sided poststroke pain for which he underwent implantation of a stimulation electrode in the right motor cortex. After 30 minutes of stimulation, his pain was remarkably reduced (visual analog scale scores decreased 8 to 1) and he felt warmth in his left arm. The rCBF was studied using PET scanning with 15O-labeled water when the patient was in the following states: before MCS (painful condition, no stimulation) and after successful MCS (painless condition, no stimulation). The images were analyzed using statistical parametric mapping software. State-dependent differences in global blood flow were covaried using analysis of covariance. Comparisons of the patient's rCBF in the painful condition with that in the painless condition revealed significant rCBF increases in the left rectus gyrus (BA11), left superior frontal lobe (BA9), left anterior cingulate gyms (BA32), and the left thalamus (p < 0.05, corrected). On the other hand, there were significant decreases in rCBF in the right superior temporal gyrus (BA22, p < 0.01, corrected) and the left middle occipital gyrus (BA19, p < 0.05, corrected). The efficacy of MCS was mainly related to increased synaptic activity in the thalamus, whereas the activations in the rectus gyrus, anterior cingulate gyrus, and superior frontal cortex as well as the inactivation of the superior temporal lobe may be related to emotional processes. This is the first report in which the contralateral thalamus was significantly activated and pain relief was achieved using MCS.
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5/17. Dissociated unilateral convergence paralysis in a patient with thalamotectal haemorrhage.

    A 47 year old male was admitted in a comatose state. CT scan showed a haemorrhage in the right pulvinar thalamus descending into the right part of the lamina quadrigemina. He presented with anisocoria, prompt bilateral pupillary light reaction, and unilateral convergence paralysis contralateral to the lesion in combination with upward gaze palsy. During an observation period of two months, the convergence reaction returned to normal. MRI showed a lacunar lesion ventral to superior right colliculus. angiography revealed an arteriovenous malformation (right posterior cerebral artery--sinus rectus) as the possible cause of the haemorrhage.
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6/17. A syndrome of bilateral hemorrhage of the thalamus and myocarditis with fatal course.

    We report the case of a 41-year-old patient with bilateral hemorrhage of the thalamus, leading to death. Post-mortem examination showed acute myocarditis. Neuropathological study showed perivascular infiltrates in affected thalamic regions. Laboratory investigation failed to find any causal agent. We hypothesize an infective agent, affecting the heart and thalamus, as the cause of this syndrome. Diaschisis due to the strategic anatomical position of the thalamus may have been responsible for coma state and death.
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7/17. Capsular and thalamic infarction caused by tentorial herniation subsequent to head trauma.

    Five patients (4 male and 1 female) were observed to have capsular and thalamic infarction ascribed to descending transtentorial herniation (DTH) caused by head injury. A lucid interval immediately after the trauma and the presence of an epidural hematoma (EDH) characterized all five cases. At the time of hospitalization consciousness was seriously impaired and signs of cerebral herniation were apparent. Two to four days after the trauma, low attenuation in the computed tomography (CT) images pinpointed intracerebral damage in the anterolateral part of the thalamus and in the internal capsule on the same side as that of the EDH in three patients, and in the other two patients bilateral thalamic and capsular damage was noted. The low attenuation implicated the perforating arteries, that is the anterior thalamoperforating and anterior choroidal arteries, suggesting infarcted regions caused by occlusion of these arteries. Findings in the present study suggest that arterial occlusion in closed head injury may result from DTH. Moreover, infarction may be attributed to the delayed effects of injury.
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8/17. aphonia due to paramedian thalamo-subthalamic infarction. Remarks on two cases.

    We describe two patients in whom CT brain scans imaged paramedian thalamo-subthalamic infarcts in the territory of the thalamo-mesencephalic arteries. Such infarcts give rise to a complex syndrome marked by disturbances of consciousness and of eye movement and neuropsychological disorders, including attentional, memory and, more rarely, language deficits. A loss of voice volume may accompany aphasic disturbances but is exceedingly rare in isolation. In the cases described the aphonia, total but transient, was the only language disorder. The physiopathological mechanisms involved in aphonia are complex and controversial.
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9/17. The syndrome of unilateral tuberothalamic artery territory infarction.

    The study of 3 personal cases and 5 published cases of unilateral infarct limited to the territory of the tuberothalamic artery suggests that this syndrome should be differentiated from the other thalamic syndromes. The onset is usually sudden, with moderate contralateral weakness. Sensory changes may be present but remain mild. The patients are apathetic, show perseveration and may be disoriented. In left-sided infarcts, transcortical aphasia, verbal and visual memory impairment and sometimes acalculia are found. In right-sided infarcts, hemispatial neglect, visual memory impairment and disturbed visuospatial processing are common. A decreased level of consciousness, disturbed ocular movements, severe motor weakness and delayed abnormal movements do not occur. Involvement of the ventral lateral and dorsomedial nucleus with sparing of the intralaminar nuclei, posterolateral formation and upper midbrain may explain this picture. The fact that the tuberothalamic artery arises from the posterior communicating artery, which often receives its supply from the carotid system, further justifies considering unilateral tuberothalamic infarcts as a syndrome.
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10/17. language and memory disturbances from mesencephalothalamic infarcts. A clinical and computed tomography study.

    Three right-handed subjects presented impairment of consciousness, paralysis of vertical gaze, aphasia and memory disturbances. Computed tomography scans showed low-density lesions in the paramedian areas of the left thalamus. Neuropsychological examination revealed a fluent aphasia in one patient and a nonfluent in two; all had paraphasias and perseveration. comprehension, repetition and writing were normal. In the literature on so-called thalamic aphasia only a few cases are reported with involvement of the paramedian nuclear complex.
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