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Query: UMLS:C0003635 (apraxia)
 2,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatosensory and motor functions of both hands were examined in 10 patients with unilateral parietal cortex lesions as revealed by computerized tomography. Tests of elementary somatosensory functions comprised surface sensibility, vibration, and position sense. For evaluation of complex somatosensory functions, the recognition of surface textures and object forms was tested. Motor performance was examined by measuring force and position control as well as manipulative and explorative motor behaviour. All patients showed varying degrees of sensory disturbance. Although the patients had no or minor paresis, they all had motor deficits concerning force control, fine movements, and manipulation with the hand contralateral to the lesion. Patients with more posteriorly located parietal lesions revealed predominantly severe disturbances of complex sensibility, precision grip, manipulation, and explorative finger movements. The characteristic and consistent feature of the disturbed motor behaviour was the loss of the purposive nature of the motor acts which were no longer adequate for the tasks (tactile apraxia). Paresis or ataxia could not account for this deficits.
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PMID:Role of the parietal cortex for sensorimotor transformation. Evidence from clinical observations. 275 92

Ten right-handed patients suffering from visuospatial impairment were examined. The impairment was ascertained by a test requiring visual organization (picture completion). The patients did not suffer from other neuropsychological disorders (e.g., aphasia, dementia). Furthermore, psychiatric symptoms and defective oculomotion (gaze paresis, ocular paresis) were controlled. CT scan data revealed that in 4 patients the impairment was associated with lesions of the posterior right hemisphere. All lesions involved the central optic pathways and were accompanied by visual field defects. On the other hand, 6 patients turned out as suffering from damage of the cerebellum or brainstem. The available electronystagmographical data revealed impaired visual fixation, an oculomotor defect characterizing gaze apraxia, the diagnostic marker of Balint's syndrome.
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PMID:Visuospatial disorders and related lesions of the brain. 277 81

Binswanger, in his 1894 dissertation on the differential diagnosis of general paresis of the insane, described a slowly progressive dementia associated with macroscopic loss of white matter. In recent years interest in Binswanger's disease was rekindled with CT demonstration of extensive white matter low densities in some patients. To define the clinical spectrum, we reviewed 22 consecutive cases in which the CT appearances suggested a diagnosis of Binswanger's disease. Two patients had focal neurological deficits at presentation, but recent anoxic or hypoglycaemic insults could not be excluded as the cause of the CT abnormalities. The 20 remaining patients were demented and showed variable combinations of corticobulbar dysfunction and gait dyspraxia. The duration of symptoms ranged from a few months to several years. Sixty per cent of this group gave a history of discrete stroke events and focal cortical and/or lacunar infarcts were a frequent CT finding. Binswanger's disease is probably due to chronic or acute-on-chronic white matter ischaemia. The association with lacunar and cortical infarctions suggests that a combination of large and small vessel disease produces diffuse ischaemia maximal in white matter watershed zones. Binswanger's disease is clinically differentiated from multi-infarct dementia by its time course.
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PMID:Subcortical arteriosclerotic encephalopathy: Binswanger's disease. 366 81

Moderate unilateral weakness of shoulder and hip muscles and limb-kinetic apraxia were observed in 11 patients with frontal lobe lesions on the side opposite to the neurological deficits. On the CT scans, the posterior border of the lesions lay anterior to the precentral gyrus, thus involving the premotor cortex but not the primary motor cortex. In 9 cases, the lesions were caused by a brain infarct, in 2 cases by a tumour. In 1 patient the lesion was purely subcortical. Whereas the paresis affected all hip muscles, in the shoulder mainly those movements associated with abduction and elevation of the arm were disturbed. The EMG showed considerable delays for the preactivation of proximal arm muscles during rapid arm movements, thus interfering with the normal proximal-distal sequencing of muscle action. Limb-kinetic apraxia only became apparent during tasks requiring certain coordinations between both arms or legs. Bimanual interaction was normal. Two patients with proximal hemiparesis and small lesions in the precentral gyrus which have been examined for comparison showed no limb-kinetic apraxia and different distributions of the paretic shoulder girdle muscles. In view of the long-standing controversies as to the functional role of the premotor cortex and the question of specific deficits after lesions of this area, the relevant literature is reviewed.
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PMID:Lesions of premotor cortex in man. 392 94

Ideational apraxia is a rare behavioural disturbance observed in patients with a lesion in the posterior part of the hemisphere dominant for language. The main feature is an impairment in carrying out sequences of actions requiring the use of various objects in the correct order necessary to achieve an intended purpose. The syndrome cannot be explained as being due to paresis, aphasia, impaired visual recognition, mental deterioration or a combination of these disorders. It must be considered as a higher order motor disturbance. Perservation plays an important role but can not explain the syndrome. Evidence is presented to suggest that ideational apraxia is a disturbance in the conceptual organization of actions. Lines of future research are indicated.
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PMID:Ideational apraxia. 619 68

A case of mutism due to left hemisphere infarction is described. Recovery revealed mild motor dysphasia. Review of the literature showed that the case resembles aphemia but is unique by virtue of its duration, and the absence of associated apraxia and paresis.
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PMID:Mutism following left hemisphere infarction. 621 Mar 46

The present study compares the phonatory ability of a patient with a deep-reaching left-sided lesion in the region of the cortical face area with that of two squirrel monkeys in which the patient's lesion has been reduplicated bilaterally. The lesion involved Broca's area, the inferior pre- and postcentral cortex, rolandic operculum, inferior parietal cortex insula, claustrum, parts of the putamen and white matter underlying the inferior frontoparietal and insular cortex. While the squirrel monkey did not show any phonatory deficits, the patient became aphonic for more than 10 weeks following the insult. After that period, phonation recovered steadily to a slightly breathy but monotonous voice with a somewhat reduced singing capacity. During the aphonic period, there was a bilateral complete paresis of the vocal folds. Both, patient and monkey, showed a paresis of the lower facial and tongue muscles which was accompanied by dysarthria and buccolingual apraxia in the patient and feeding difficulties in the monkey. The discrepancy between human aphonia and intact monkey phonation, on the one hand, and intact phonation and defective orofacial behaviour in the monkey, on the other, is explained by the anatomical fact that there is a direct cortical projection to the nucleus ambiguus in man but not in monkey, whereas the facial and hypoglossal nuclei receive direct cortical projections in man and monkey. The lack of direct cortical control of the laryngeal motoneurones in the monkey is paralleled by a lack of volitional control of fine vocal fold movements.
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PMID:The effects of deep-reaching lesions in the cortical face area on phonation. A combined case report and experimental monkey study. 718 29

A 48-year-old female developed apraxia, followed by aphasia and dementia. Clinical examination also showed an alien member sign, supranuclear gaze paresis, myoclonus and rigidity on the right arm. The examination of the frontal lobe biopsy showed typical lesions of Alzheimer's disease as the only neuropathological abnormality. The association of this clinical syndrome with Alzheimer's pathology is unusual.
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PMID:[Alien limb behavior associated with Alzheimer's disease]. 780 54

Apraxia is an impairment of voluntary movements not caused by paresis, sensory deficits or aphasia. It appears mainly after left-hemispheric parietal or callosal lesions. Our patient had a temporary apraxia that could be correlated with the development of the perifocal area around a left parietooccipital cerebral bleeding. These neuropsychological disorders belonged to the development and the disappearance of the perifocal area as seen via several MRI.
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PMID:[Neuropsychological analysis of transitory partial performance disorders. A video and MRI supported study]. 782 28

In 25 patients with subacute sclerosing panencephalitis in various phases of the disease CT and NMR imaging of the brain were done at the same times and the findings were related to clinical symptomatology. NMR imaging, in contrast to CT imaging, demonstrated even very small brain changes in the initial stage. The inflammatory-demyelinizing process begins in SSPE as a rule in the white matter of the occipital lobes, and only later in appears in the vicinity of the anterior horns of the lateral ventricles. Spreading of subcortical changes in the occipital lobes and their later penetration into the parietal lobes causes the development of ideatory apraxia frequent in these cases, and involvement of the cortex of the occipital lobes leads to visual agnosia. The paresis of extremities in later stages not always are correlated with greater intensity of changes in the contralateral cerebral with greater intensity of changes in the contralateral cerebral hemisphere. Hydrocephalus developing after longer duration of the disease is an expression of postinflammatory brain atrophy and not of disturbances in cerebrospinal fluid absorption.
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PMID:[Changes in NMR and CT images in SSPE]. 806 44


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