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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 73-year-old right-handed man with ischemic infarction in the vascular territory of the right arteria cerebellaris superior is described. In the acute phase he presented with cerebellar and brainstem symptoms, followed within a few days by a paresis of the right arm and unexpected language disturbances of aphasic origin. The core features of the aphasic syndrome corresponded to a diagnosis of Luria's dynamic aphasia, complicated by expressive and receptive agrammatism. During one year follow-up the ataxia and paretic symptoms disappeared but the slightly ameliorated aphasic syndrome and the sensory disturbances in the left hemicorpus persisted. In the absence of any neuroradiological evidence for a structural lesion in the left frontal language areas, the hypothetical causative role of the right cerebellar lesion on the contralateral prefrontal aphasic symptomatology is advocated and supported by positive 99mTc-hexamethylpropyleneamine oxime single-photon emission-computed tomography findings, revealing a focal hypoperfusion in the clinically suspected areas. In our case, this phenomenon of so-called 'crossed cerebello-cerebral diaschisis', reflecting the distant functional impact of the right cerebellum on the contralateral prefrontal cortical areas, is for the first time associated with an aphasiologic substrate. The co-occurrence of a right cerebellar lesion and an aphasic syndrome forms the first clinical illustration of the pathophysiological hypothesis of a deactivation of prefrontal left hemisphere language functions due to the loss of excitatory impulses through cerebello-ponto-thalamo-cortical pathways.
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PMID:Cerebellar induced aphasia: case report of cerebellar induced prefrontal aphasic language phenomena supported by SPECT findings. 899 2

The influence of the cerebellum on cognitive functions (CF) is poorly known and understudied so far. Neurological, neuropsychological and neuroimaging non-randomized study was carried out in 25 patients (14 women, 11 men, mean age 51.8 +/- 18.0 years) with isolated cerebellum infarctions. Cognitive disturbances (CD) were detected in 22 (88%) patients. They included impairment of attention, planning, control, abstract reasoning, memory; speech (naming, fluency, agrammatism, dysprosodia), special visual, quasi-spatial and counting disorders that indicated dysfunction of the anterior and posterior associative areas of the brain cortex. The expression of CD was different: being clinically obvious in 6 patients (24%), they were found only by neuropsychological methods in 16 patients (64%). Clinically significant CD developed in the lesions of certain areas (posterior-lower- lateral and posterior-medial) of the cerebellum hemisphere related to the dominant brain hemisphere. The presence of these CD did not depend on infarctions size: in expressed CD it was smaller (mean 5.65 cm3) than in other cases (mean 12.8 cm3). Typical appearances of cerebellum infarction (ataxia, vertigo, vomiting) were observed in all the patients with clinically non-significant CD and only in 2 out of 6 with clinically significant CD. The study demonstrated a role of the cerebellum in CF modulation. The expression of CD in cerebellum infarctions depends on their localization. Topic localization of the cerebellum areas, controlling CD and movement, is different.
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PMID:[Cognitive disturbances in cerebellum infarctions]. 1555 17

The effects of the cerebellum on cognitive functions (CF) are poorly known and inadequately studied. Neurological, neuropsychological, and neuroimaging studies were performed on 25 non-random patients (14 female, 11 male, mean age 51.8 +/- 18.0 years) with isolated cerebellar infarcts. Cognitive impairments (CI) were seen in 22 patients (88%). These included impairments of attention, planning, control, abstract thought, memory, and speech disturbances (naming difficulties, irregularity of speech, agrammatism, dysprosodia), visuospatial and quasispatial disturbances, and counting impairments, demonstrating dysfunction of the anterior and posterior associative areas of the cortex. The extent of CI varied: 16 patients (64%) showed impairments only in neuropsychological tests, while six (24%) had clinically apparent impairments. Clinically significant CI developed in lesions of particular areas (posteroinferolateral and posteromedial/median) of the cerebellar cortex associated with the dominant hemisphere of the brain. The existence of clinically significant CI was independent of infarct size: infarcts were smaller (mean 5.65 cm3) in patients with marked impairments than in others (mean 12.8 cm3). The typical signs of cerebellar infarcts (ataxia, vertigo, vomiting) were seen in all patients with clinically insignificant and in only two of six patients with clinically significant CI. The present studies demonstrated the involvement of the cerebellum in the modulation of CF. The extent of CI in cerebellar infarcts depended on infarct location. The topical localizations of cerebellar zones controlling CF and movement are different.
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PMID:Cognitive impairments in cerebellar infarcts. 1613 55

Schmahmann's syndrome represents a novel clinical condition consisting of a constellation of cognitive and affective deficits following cerebellar disease. The complex was first described in 1998 as cerebellar cognitive affective syndrome (CCAS) on the basis of a careful neurological examination, detailed bedside mental state tests, neuropsychological investigations and anatomical neuroimaging of a group of 20 patients with focal cerebellar disorders. The syndrome was characterized by four clusters of symptoms including: (a) impairment of executive functions such as planning, set-shifting, verbal fluency, abstract reasoning and working memory, (b) impaired visuo-spatial cognition, (c) personality changes with blunting of affect or abnormal behaviour, and (d) language deficits including agrammatism, wordfinding disturbances, disruption of language dynamics and dysprosodia. This complex of neurocognitive and behavioural-affective symptoms was ascribed to a functional disruption of the reciprocal pathways that connect the cerebellum with the limbic circuitry and the prefrontal, temporal and parietal association cortices. With the introduction of Schmahmann's syndrome, clinical ataxiology has found its third cornerstone, the two others being the cerebellar motor syndrome (CMS) mainly delineated by the pioneer French and English neurologists of the 19(th) and early 20(th) century, and the vestibulo-cerebellar syndrome (VCS) consisting of ocular instability, deficits of oculomotor movements and ocular misalignment.
Cerebellum Ataxias 2015
PMID:Schmahmann's syndrome - identification of the third cornerstone of clinical ataxiology. 2633 Oct 45