Cases reported "Thalamic Diseases"

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1/40. 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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2/40. Thalamic degeneration with negative prion protein immunostaining.

    A 34-year-old woman presented with an insidious 5-year history of cognitive decline and apathy, associated with hypersomnia, ataxia, and dysarthria. magnetic resonance imaging of the brain showed cortical and subcortical atrophy. At autopsy we found abnormalities in the subcortical grey matter and brainstem, with a relatively preserved cerebral cortex. The thalami showed symmetrical neuronal loss and astrocytosis, particularly severe in the dorsal medial nucleus, followed by the lateral nuclei group. Prion protein immunostaining was negative, and there was no spongiform change. No mutations were detected in the prion protein gene.
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3/40. 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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4/40. Right medial thalamic lesion causes isolated retrograde amnesia.

    Pervasive retrograde amnesia without anterograde memory impairment has rarely been described as a consequence of circumscribed brain damage. We report this phenomenon in a 33 yr-old, right-handed man (JG) in association with the extension in the right thalamus of a previously small, bilateral thalamic lesion. JG presented with a dense amnesia for autobiographical material more than a few years old, with some sparing of recent memories. Furthermore, he was completely unable to recognise famous people or world events. Many other aspects of semantic knowledge were intact and there was no evidence of general intellectual impairment, executive dysfunction or loss of visual imagery. magnetic resonance imaging revealed an acute lesion in the right thalamus and two small, symmetrical, bilateral non-acute thalamic lesions. Follow-up neuropsychological assessment indicated a stable pattern of impaired retrograde and spared anterograde memory over 18 months and psychiatric assessments yielded no evidence of confabulation, malingering or other symptoms to suggest psychogenic amnesia. JG's profile indicates that the division of declarative memory into just two categories - episodic and semantic - is inadequate. Rather, his case adds to the growing body evidence to suggest that world knowledge pertaining to people and events is stored or accessed similarly to autobiographical information and differently from other types of more general factual knowledge. We hypothesize that the right mediodorsal thalamic nucleus and immediately surrounding regions comprise the central processing mechanism referred to by McClelland (Revue Neurologique, 150 (1994) 570) and Markowitsch (brain research review, 21 (1995) 117) as responsible for inducing and co-ordinating the recall of these sorts of cortically stored memory engrams.
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keywords = nucleus
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5/40. Auditory laterality and attentional deficits after thalamic haemorrhage.

    Thalamic lesions have been shown to produce severe cognitive deficits involving language and memory. A majority of the studies have reported cognitive deficits after lesions in the anterior and dorsomedial thalamic nuclei. We report five case studies of effects on language processing after postero-dorsal thalamic haemorrhages. Four of the patients had lesions on the right side, and one patient had a lesion on the left side. Effects on language processing were investigated with the dichotic listening test with consonant-vowel syllables. This test, in which conflicting auditory stimuli are presented simultaneously to the two ears, has been used to probe differences in language processing in the left and right hemispheres. The four patients with right-sided lesions reported almost none of the syllables presented to the left ear, and were unable to modify this massive right ear advantage by directing attention to the left or right ear. The patient with a left-sided lesion showed a weaker left ear advantage, and was able to modify his responses by shifting attention, to an extent similar to that of healthy reference individuals. When tested with monaural stimulus presentation, the scores of all patients rose to almost 100% correct for each ear. The pattern of effects with dichotic stimuli under different instructional conditions cannot be accounted for in purely structural terms, and indicates that lesions in the posterior part of the thalamus, including the pulvinar nucleus and medial geniculate body, produce deficits not only in processing of complex auditory stimuli but also in the allocation of attention to input from one ear or the other.
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6/40. Contributions of the left intralaminar and medial thalamic nuclei to memory. Comparisons and report of a case.

    A patient complained of memory disturbance after a small left thalamic infarction. Neuropsychological testing revealed her memory to be normal provided that she was allowed to rehearse or use semantic encoding strategies. When these strategies were prevented, her performance was impaired. Mapping of the lesion demonstrated involvement of the caudal intralaminar nuclei (centre median and parafascicular nuclei), and portions of the medial nuclei (medioventral [reuniens], centromedial, and the most inferior aspect of the mediodorsal nucleus). The majority of mediodorsal nucleus, the mammillary bodies, the mammillothalamic tract, and the anterior thalamic nuclei, were spared. A comparison among our patient's performances and those of alcoholic Korsakoff patients, patient NA, and amnestic patients with circumscribed diencephalic lesions suggests that there are two distinct behavioral and anatomic types of memory impairment associated with diencephalic lesions. The severe amnesia associated with damage to the mammillary bodies, midline nuclei, mammillothalamic tract, and/or dorsomedial nucleus of the thalamus (eg, Korsakoff and NA) is characterized by encoding deficits that never approximate normal performance. The memory disturbance associated with damage to the intralaminar and medial nuclei of the thalamus is milder and is characterized by severe distractibility.
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ranking = 0.6
keywords = nucleus
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7/40. 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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ranking = 0.2
keywords = nucleus
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8/40. Hypersexuality and dysexecutive syndrome after a thalamic infarct.

    Hypersexuality can result from insults to several neuroanatomical structures that regulate sexual behavior. A case is presented of an adult male with a thalamic infarct resulting in a paramedian thalamic syndrome, consisting of hypersomnolence, confabulatory anterograde amnesia (including reduplicative paramnesia), vertical gaze deficits, and hypophonic speech. A dysexecutive syndrome also manifested, consisting of social disinhibition, apathy, witzelsucht, motor inhibition deficits, and environmental dependence. Hypersexuality uncharacteristic of his premorbid behavior was evident in instances of exhibitionism, public masturbation, and verbal sexual obscenities. In contrast to the few previous reports of hypersexuality following thalamic infarct, this case neither involved mania nor hemichorea. The relevance of the mediodorsal thalamic nucleus in limbic and prefrontal circuits is discussed.
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ranking = 0.2
keywords = nucleus
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9/40. Central pain from cerebral abscess: thalamic syndrome in AIDS patients with toxoplasmosis.

    We describe two patients with acquired immunodeficiency syndrome (AIDS) who developed classic thalamic syndrome (TS) due to toxoplasma abscesses in the thalamic region. Treatment with amitriptyline provided substantial relief in both patients. Postmortem examination in one case revealed a lesion in the internal capsule and thalamic reticular nucleus. These observations indicate that (1) TS can result from an isolated lesion in the internal capsule and reticular nucleus of the thalamus, (2) cerebral abscess can cause classic TS, (3) central pain can be added to the many pain syndromes that afflict AIDS patients, and (4) an analgesic response to amitriptyline is possible in these patients.
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ranking = 0.4
keywords = nucleus
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10/40. Allodynia in the flank after thalamic stroke.

    Lesions responsible for thalamic pain are often thought to involve the ventral posteromedial nucleus and ventral posterolateral nucleus of the thalamus. We describe two patients with allodynia and hyperpathia in the contralateral flank caused by a small lesion in the posteroventral part of the thalamus. When considered with the literature, involvement of the ventral posteroinferior nucleus may be responsible for this unique post-stroke pain syndrome.
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ranking = 0.6
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