Cases reported "Thalamic Diseases"

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1/8. A combined pattern of movement disorders resulting from posterolateral thalamic lesions of a vascular nature: a syndrome with clinico-radiologic correlation.

    We report a series of seven patients in whom a combined pattern of complex movement disorders restricted to one upper extremity emerged as a result of posterolateral thalamic lesions of vascular origin. This disorder was mainly characterized by choreiform and dystonic movements associated with variable, rhythmic, alternating movements of low frequency (myorhythmia). All cases showed, on computed tomography scan and/or magnetic resonance imaging, focal lesions involving the posterolateral quadrant of the thalamus. review of similar cases reported with identical clinico-radiologic features allows us to conclude that it is possible to establish an accurate anatomoclinical correlation based on the clinical phenomenology, even before imaging studies are performed, in these cases. The opposite is not entirely possible, however, because lesions in the same quadrant of the thalamus are often associated with different patterns of abnormal movements or present without abnormal movements.
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2/8. Disappearance of haemorrhagic stroke-induced thalamic (central) pain following a further (contralateral ischaemic) stroke.

    We report the case of a patient who, following a right thalamic haemorrhage, developed thalamic syndrome characterised by burning pain and hyperalgesia in the left side of the body. Three years later, following a further (contralateral ischaemic) stroke, she reported the complete disappearance of the pain and hyperalgesia. To our knowledge, this is the first described case of disappearance of thalamic syndrome following a second stroke, different in nature from and contralateral to the first. Various hypotheses, based on the nervous tracts and nuclei involved in pain processing, may be advanced to explain this occurrence.
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3/8. Thalamic astasia: inability to stand after unilateral thalamic lesions.

    Inability to stand in the absence of motor weakness or marked sensory loss is usually considered to reflect midline cerebellar disease. However, the 15 patients reported here had astasia related to unilateral thalamic lesions, documented by autopsy and computed tomography in 2 patients and by computed tomography in 13. The lesions, including infarction (6), hemorrhage (7), and tumor (2), involved primarily the superoposterolateral portion of the thalamus, but spared the rubral region. Alert, with normal or near-normal strength on isometric muscle testing and a variable degree of sensory loss, the patients could not stand and 7 of them could not sit up unassisted. They fell backwards or toward the side contralateral to the lesion. They appeared to have a deficit of overlearned motor activity of an axial and postural nature. In the vascular cases, the deficit improved in a few days or weeks. However, these patients had a tendency to sustain falls during the rehabilitation period.
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4/8. The neuropsychology of paramedian thalamic infarction.

    A longitudinal study of three patients with CT-scan documented paramedian thalamic infarctions (bilateral, primarily right, unilateral left) is reported and the neuropsychology of human paramedian thalamic infarction is reviewed. The neuropsychological deficits following these selected lesions, the nature of the clinical memory disorder, and the neuroanatomy of memory are discussed. The significance of cortical/subcortical relationship in explaining observed behavioral changes is emphasized. brain damage with maximum involvement in the dorsomedial nuclei and mamillothalamic tracts appears to cause primarily a memory disorder and frontal-limbic behavioral changes, the severity and profile of deficits depending on lesion extent and location. Both anterograde and remote memory loss may be present. Asymmetry in memory at the level of the thalamus was observed, following the left-verbal, right-nonverbal dichotomy.
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5/8. Computed tomography and MR imaging of thalamic neuroepithelial cysts.

    Neuroepithelial cysts of the CNS are rare. Two cases of noncolloid neuroepithelial cysts of the thalamus are reported. Computed tomography and magnetic resonance imaging aided in ascertaining the nature of these cysts.
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6/8. Unilateral germinomas involving the basal ganglia and thalamus.

    Clinical characteristics of six cases of germinoma involving a unilateral basal ganglion and thalamus are summarized. The incidence was estimated as 10% of all intracranial germinomas. The average age at the onset was 10.5 years. The sex incidence showed a male dominance. The clinical course was slowly progressive, and the average duration between onset and diagnosis was 2 years 5 months. Common symptoms and signs were hemiparesis in all cases, fever of unknown origin and eye symptoms in most, mental deterioration and psychiatric signs in three, and convulsions, pubertas praecox, and diabetes insipidus in two. Signs of increased intracranial pressure were found in only two cases in the later state of the disease. early diagnosis is difficult because of nonspecific symptomatology and slow progression. Carotid angiography and pneumoencephalography showed abnormal findings compatible with basal ganglia and thalamic tumors, but not specific to germinoma. Ipsilateral cortical atrophy and ventricular dilatation might be significant findings. Radioisotope scanning was useful. Computerized tomography scans were the best method of detecting the location and nature of this tumor, and repeat scans showed response to radiation therapy.
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7/8. Paramedian thalamic infarction following blunt head injury--case report.

    A 19-year-old male was admitted following a blow to the face. Computed tomographic (CT) scans 1 hour after injury revealed low-density areas in the bilateral thalami and midbrain, which were enhanced postcontrast except for the core 3 hours later. CT scans 2 days after injury revealed that the size of the low-density areas had increased. CT scans and magnetic resonance images 3 weeks after injury disclosed only small infarcted lesions in the bilateral thalami, the right side of the midbrain, and the left internal capsule. These findings suggest that the injury initially caused thrombus on the basilar arterial wall, leading to occlusion of the perforators, but almost all affected perforators were recanalized. Bilateral thalamic infarction resulting from head injury is unusual, as is the transient nature of the infarction in this case.
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8/8. Selective dorsolateral frontal lobe dysfunction associated with diencephalic amnesia.

    We report three cases with unilateral thalamic ischemic lesions that resulted in lasting material-specific memory impairments and concomitant selective frontal lobe-related cognitive deficits. In two cases the lesions were limited to the left thalamus, and in the third the right thalamus was involved. These deficits were associated with ipsilateral diencephalic, striatal, and dorsolateral prefrontal hypoperfusion. The damage implicated the ventral anterior nucleus, the mamillothalamic tract, and the rostroventral internal medullary lamina. These findings suggest that medial thalamic damage involving the ventral and rostral sector of the dorsal thalamus will concurrently affect functionally and neurally distinct limbodiencephalic pathways and diencephalic connections with the frontal cortex. A review of the neuropsychological and neuroimaging findings from previously reported cases with vascular lesions of the thalamus further supports this contention. The presence of frontal lobe-related cognitive deficits, though not obligatorily related to the memory problems, may contribute to some aspects of the memory deficits and affect the nature of the memory disorder observed in some cases with diencephalic amnesia.
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