Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Outcomes in self-care following rehabilitation in 226 patients were correlated with 11 stroke syndromes, reflecting several pathophysiologic disturbances subsequent to either infarction or hemorrhage in cerebral or vertebro-basilar vessels. Self-care was scored on a 20-point scale for bed movements, transfers, feeding, dressing, personal hygiene, and bathing. Interjudge error among therapists did not exceed 2.5%. Mean score in left cerebral infarction without aphasia was used as a referent value. Scores in left cerebral infarction with aphasia and right parietal lobe syndrome with and without spatial agnosia were similar to the referent. Brain stem dysfunction with spasticity and right cerebral infarction with paresis and spatial agnosia fell below the referent value (Pless than 0.05). Higher levels were achieved in the syndromes of left and right anterior cerebral artery territories, brain stem dysfunction with ataxia, and left parietal lobe syndrome with comprehension aphasia, although t-values were not significant. Length of stay among the 11 groups was fairly uniform except for the group with brain stem dysfunction with spasticity and the group with left hemiplegia with spatial agnosia. These groups indicated rather severe disabilities. Aside from neurologic dysfunction the range of scores was influenced by associated cardiopulmonary involvement.
 ...
PMID:Neurophysiologic syndromes in stroke as predictors of outcome. 68 54

Visuomotor ataxia causes difficulty in the prehension of objects under visual control which can occur without paralysis of ocular fixation and spatial agnosia. This can involve the total visual field or the right or left half-fields, and can affect both hands or one only. 1) Unilateral visuomotor ataxia is localized to the two right or left homonymous half-fields and can affect both hands or one only. It is direct when the ataxic hand is on the same side as the affected visual half-field, and crossed when the ataxic hand is contralateral to the affected visual half-field. 2) Bilateral visuomotor ataxia involves the total visual field. Each hand may be ataxic only for the contralateral visual field with a crossed bilateral visuomotor ataxia, or in the homolateral field with a direct bilateral visuomotor ataxia. The anatomical and clinical observations reported imply the existence of visuomotor connections, both direct and crossed, the latter crossing the median line through the corpus callosum.
 ...
PMID:[Difficulty in manual prehension under visual control (author's transl)]. 71 97

Visuomotor ataxia is a disorder of movement performed under visual control. It can occur in the absence of disturbance of ocular fixation and in the absence of spatial agnosia. This disorder may extend over the whole visual field or it may be localized to one visual half-field, right or left. It may involve both hands or one hand only, so that visuomotor ataxia may be divided into: (1) Unilateral visuomotor ataxia, localized to a single field. In this case it may affect both hands or a single hand. It is direct when the hand is ataxic in the ipsilateral visual field and it is crossed when the hand is ataxic in the contralateral visual field; (2) Bilateral visuomotor ataxia, involving the whole visual field. Each hand may be ataxic only in the contralateral visual field, that is, bilateral crossed visuomotor ataxia; or in the ipsilateral field when it is called bilateral direct visuomotor ataxia. The observed clinical variations which are described here imply the existence of both direct and crossed visuomotor connections, the latter probably crossing the corpus callosum in the splenium.
 ...
PMID:Visuomotor ataxia. 88 89

The underlying mechanism of visual agnosia and optic aphasia has not been fully elucidated, although a number of hypotheses have been proposed. Besides, the difference between these two conditions has been a matter of debate. We report here the result of neuropsychological evaluation in a case of associative visual agnosia evolving to optic aphasia. A 64-year-old right-handed patient was found to be disoriented and confused after undergoing the operation of gastrectomy. CT scan revealed a large infarction in the territory of left posterior cerebral artery. Since 3 weeks after onset, neuropsychological investigations were carried out during 5 months. He was alert and co-operative. Right homonymous hemianopia with macular sparing was noted, but his visual acuity was normal. There was neither a global deterioration of intellectual capacities nor aphasia. Most striking finding was his difficulty in identifying common objects and colours along with a profound alexia. Prosopagnosia was absent. Visual naming both for objects and line drawings was severely impaired. He was unable to describe or demonstrate the use of the objects which could not be named. Pointing to objects named by the examiner was also severely impaired. Although tactile naming was also impaired, both of auditory naming for environmental sounds and naming objects in response to verbal descriptions were preserved. While he was not able to copy the objects skillfully, matching of identical objects and matching objects to line drawings were normal. Clumsiness of coping was thought to be due to his constructional apraxia and visuomotor ataxia. Therefore, his deficit in visual domain was considered to be associative visual agnosia.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Visual agnosia evolving to optic aphasia--a case study]. 130 17

Alexia without agraphia is readily recognized in its pure (without other neurologic findings) but rare form. However, this deficit is more common when associated with other behavioral disturbances that result from trauma or cerebral infarction to the posterior cerebral hemispheres. Two cases presented with alexia without agraphia following infarction within the posterior cerebral artery territory. Because of initial confusion and disorientation the patients were diagnosed as demented and unsuitable for rehabilitation. Both subjects had a visual field deficit and color agnosia. Prosopagnosia, simultanagnosia, and ataxia of visual-motor control were also present. The second case was unusual because of pure word blindness associated with a right occipital lobe lesion. Only a few such cases have been reported in the literature worldwide. This paper demonstrates that careful delineation of cognitive deficits permits greater understanding of functional disorders with improved rehabilitation outcome.
 ...
PMID:Alexia without agraphia and associated disorders: importance of recognition in the rehabilitation setting. 356 19

The case reported here is that of a woman, without any significant pathological antecedent. At age 54, she developed signs of thalamic dementia and died 5 years later. The prominent symptoms were massive anterograde amnesia, apathia, apragmatism, ataxia and a frontal syndrome. She never showed aphasia, apraxia, agnosia or disorders of ocular motility. The C. T. Scan showed lacunar low densities in the mesencephalon and both thalami, mainly on the left side, as well as hydrocephalus caused by a stenosis of the aqueduct as shown by other neuroradiological procedures. The neuropathological examination showed space-occupying lacunae, bulging in the third ventricle, squeezing the aqueduct and protruding into the fourth ventricle. These lacunae were situated in the territory of the paramedian mesencephalo-thalamic arterial pedicle. They were perivascular spaces distensions, probably caused by disorder of the permeability of the arterial wall. This hypothesis is supported by the presence of severe lesions of segmental necrotizing angeitis on a paramedian mesencephalic artery. The etiology of this angeitis is unknown. As far as we know, such neuropathological lesions have never been reported previously. Therefore the pathology and etiopathogeny of cerebral lacunae should be reconsidered.
 ...
PMID:[Thalamic dementia. Expansive lacunae of the thalamo-paramedian mesencephalic area. Hydrocephalus caused by stenosis of the aqueduct of Sylvius]. 613 53

We presented a rare care who had right frontal lobe infarction, with left side pseudoataxia, and the mechanism, causing pseudoataxia, was considered. The patient, a 51 year-old, righ-handed male, was admitted on August 9, 1980, complaining of left-side pseudoataxia. About p.m. 7:00, July 29, 1980, he suddenly noticed numbness of the left foot, and he found himself difficulty in standing in the next morning. He had a mild paresis and tactile-tactile of the left side including the face, which was rapidly improved. However, there was pseudoataxia of the left extremities, which had not been improved. On physical examination, dysarthria, aphasia, finger agnosia, difficulty in right left orientation or muscle weakness was not recognized, and there was no sensory disturbance except for slight impairment of stereognosis, two point discrimination and vibratory sense. Demonstrable impairment of tactiletactile from was observed in the left hand. Notable dysmetria, terminal tremor and dysdiadochokinesia were seen in the left limbs, which were remarkably worsened with eyes closed. However, tapping and line-drawing tests were normal. Babinski-Weil's test disclosed typical compass gait. There was marked swaying in Romberg position. Tandem gait was impossible with a tendency to decline the left. Deep reflexies were normal except for mildly hyperactive radial reflex in the left. Carotid and vertebral angiographies revealed neither evidence of vascular occlusion nor displacement of vessels CT scan demonstrated a low density area, which included the right inferior and middle frontal gyri, the head of the right caudate nucleus and a part of anterior crus of right internal capsule. There was enlargement of anterior horn of the right lateral ventricle. Caloric test, electronystagmography, eye tracking test or optokinetic nystagmus test disclosed no abnormalities. Vibration induced falling, which is the postural reaction to muscle vibration during standing (Ekuland, G., 1972), was not recognized when the left Achiles' tendon was stimulated. Pseudoataxia of this patient differed from the typical cerebellar or vestibular ataxia. From a review of the literatures concerning frontal pseudoataxia, almost all cases had no distinct cerebellar signs, and showed positive Romberg's sign. The impairment of tactile-tactile form and postural reaction to vibratory stimulation to the left leg, appeared in this case, could be hardly explained by the lesion of parietal lobe or deconnection syndrome. Sensory perception of parietal lobe and pyramidal motor system were thought to be almost normal in this case. Therefore, these findings should be due to impairment of integration center between sensory and motor systems. The pseudoataxia in frontal lesion seems to occur as the results of involvement of this center, in which caudate nucleus maybe has important role, but not as the results of disturbances in the front-ponto-cerebellar or front vestibular pathway.
 ...
PMID:[Frontal pseudoataxia, discussion on its mechanism (author's transl)]. 732 87

Interest in progressive focal cerebral syndromes associated with classical degenerative diseases has increased in recent years. Descriptions of posterior cortical atrophy with progressive visual agnosia are relatively rare. We present 5 patients (2 women) ranging in age between 57 and 72 years old. In all cases symptoms began and progressed with no known etiology. All cases were sporadic. The main clinical signs are difficulty in recognizing objects, colors, persons or places; topographical disorientation and visual memory alterations; alexia, simultagnosia, loss of ocular fixing and optic ataxia. Some patients presented other disturbances of praxis or memory and 2 progressed to global dementia. Language function was preserved and behavioral disturbances did not develop. The amplitude of the P100 visual evoked potential was low but latency was normal in 4 patients and prolonged in 1. Brain images showed atrophy and hypoperfusion in the parieto-occipital area. The neuropathology status of these patients is unknown.
 ...
PMID:[Posterior cortical atrophy with progressive visual agnosia]. 775 9

A 28-year-old man had a asymptomatic meningioma in right parasagittal parietal lobe. At surgery, the parietal lobe remarkably swelled before completion of total removal of the tumor, although any suggestive factor causing brain swelling was not found intraoperatively. CT scan was examined immediately after surgery and only revealed a small hematoma in the tumor bed without any additional lesion in thalamus or basal ganglia. It was inexperienced post-operative complication that involuntary hemiballistic movement of left limbs appeared immediately after recovery from general anesthesia, although the post-operative complications of right parietal lobe syndromes, such as left hemi-anesthesia, hemi-agnosia, hemiparesis and hemi-ataxia were predictable. The hemiballistic movement persisted for 2 days postoperatively and the other complications completely recovered in the next 3 months. MRI, taken at post-operative 14th day, did not detect any abnormal lesion in well-known responsible areas for hemiballismus such as subthalamus, thalamus and basal ganglia. We suppose that the parietal lobe, especially Broadmann's area 7 may be one of the responsible areas for provoking hemiballistic involuntary movement.
 ...
PMID:[Hemi-ballistic involuntary movement manifested as an parietal lobe syndrome]. 837 99

A 66-year-old woman presented with a rapidly progressive dementia initially characterized by an auditory agnosia. She experienced a rapid progression of her aphasia and developed ataxia and myoclonus. An initial neurological evaluation suggested a left parieto-temporal lesion, however, neuroimaging did not reveal any. An MRI of her brain demonstrated highly focal T2 hyperintensities in her basal ganglia. The patient was diagnosed with Creutzfeldt-Jacob Disease (CJD) on the basis of the presence of two proteins in the CSF that are highly sensitive and specific for CJD. Pathological examination confirmed the diagnosis. The differential diagnosis and utility of MRI in patients with CJD is discussed.
 ...
PMID:A 66-year-old woman with a rapidly progressing dementia and basal ganglia involvement. 923 37


1 2 3 4 5 Next >>