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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The best-known example of motor deficits after cortical lesions is contralateral paresis and spasticity after damage to the precentral motor strip. After recovery the residual motor functions can be used in a purposive and skillful manner. In patients with lesions of the supplementary motor area (SMA) and cingulate gyrus transient akinesia and mutism have been described. Lesions restricted to more lateral parts of the premotor field interfere with proximal muscle function and interlimb coordination, whereas distal motor activity and bimanual coordination are unimpaired. In contrast, hand function in patients with parietal lesions is severely disturbed. This dysfunction includes deficits such as ataxia, dysmetria and postural instability that are typically observed in deafferented patients. Severe disturbances of the purposive behaviour of the hand during exploratory finger movements and manipulation of objects are seen in patients with posterior parietal lesions. Observations in human patients are compatible with the hypothesis that lesions of the frontal agranular motor fields interfere with the control of postural and force control whereas parietal lesions are associated with motor programme disorders affecting the use of the hand or the eye as a sense organ or affecting more complex motor behaviour.
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PMID:Differential effects of cortical lesions in humans. 332 19

In a cross-sectional population study of Danish patients with AIDS 16 of 23 had clinical signs of neurological disease with muscle weakness or ataxia of the lower limbs as the dominant manifestation. Tibial and median nerve conduction was mildly slowed in a few patients and 15 had widening of cerebral ventricles at CT. However, all had prolonged latency of cortical evoked response following tibial nerve stimulation mainly due to slowing through the spinal cord. The prolongation of the latency of the evoked cortical responses was most pronounced in patients with lower limb ataxia and/or paresis. It is concluded that affection of the long tracts of the spinal cord are closely associated with the human immunodeficiency virus infection.
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PMID:Myelopathy in AIDS. A clinical and electrophysiological study of 23 Danish patients. 335 13

A Hansen type I cervical intervertebral disc prolapse was diagnosed in a 16-year-old American Saddler showing clinical signs of paresis and ataxia. An ante-mortem diagnosis was made by means of plain radiographs and a myelogram. The horse was euthanased and the diagnosis confirmed on a post-mortem examination.
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PMID:[Cervical intervertebral disk prolapse in a horse]. 336 56

A 61-year-old woman is presented with a bilateral total ophthalmoplegia as an initial ocular symptom, caused by a midbrain hematoma. She complained of acute headache, nausea, vomiting and bilateral closure of her eyelids. Examination on admission showed meningeal irritation; mild consciousness disturbance; bilateral total ophthalmoplegia; left hemiparesis; ataxia in all extremities, more marked to the left. Computed tomography demonstrated a small hematoma in the midbrain tegmentum. Angiography demonstrated midbrain arteriovenous malformation, and she was treated conservatively. Abduction of both eyes and adduction of the left eye appeared on the next day of the ictus, and after that, improved gradually. Left ptosis had improved since one week after the ictus. Light reflex of the left pupil had seen 5 days after the ictus. At the same time, the left pupil revealed an oval-shape. Right internal ophthalmoplegia continued to exist. One year later, the right eye deviated externally, and the left deviated inferio-medially. Abduction of both eyes was normal. Infraduction of both eyes was seen, but limited on the left. Upgaze paresis remained unchanged, and adduction of the right eye was absent. Adduction of the left eye showed almost full recovery. There was right complete ptosis, but left ptosis became indefinite. These ocular findings indicated typical right oculomotor paresis plus superior rectus paresis of the left eye, which suggested a destructive lesion in the right oculomotor nucleus. Also, her left extremities showed a hemiparesis as a pyramidal tract sign (Weber's syndrome) and an ataxia as a cerebellar sign (Claude's syndrome).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Midbrain arteriovenous malformation causing bilateral total ophthalmoplegia as an initial ocular symptom--a case report]. 337 Jan 70

Three patients with medial ventral cerebellar peduncular hemorrhages presented with a characteristic syndrome. This included (1) ipsilateral ataxia, (2) lower motor neuron type facial weakness, and (3) ipsilateral gaze paresis. The gaze paresis could not be overcome with a doll's head maneuver. The findings are explained by compression of the facial colliculus, with involvement of the sixth nerve nucleus and the middle cerebellar peduncle. Two patients were hypertensive; one was normotensive, and no etiology was identified with angiography. Of 40 patients with cerebellar hemorrhage seen at our institution, only those with medial cerebellar peduncular hematomas demonstrated this clinical triad, and we have not seen this clinical triad in other pathologic conditions. The diagnosis of a small medial cerebellar peduncular hemorrhage was established by CT. In two patients, repeat CT showed complete hematoma resolution. The patients shared a favorable prognosis.
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PMID:The clinical and computed tomographic features of cerebellar peduncular hemorrhage. 259 Feb 97

A retrospective study of 75 consecutive cases of spontaneous cerebellar haemorrhage was undertaken in order to evaluate the clinical features and natural history of this condition. A wide spectrum of clinical findings contributed to the poor clinical diagnostic accuracy of 23 per cent, with common misdiagnoses including brainstem stroke and vestibular or labyrinthine disturbance. Presentation with, or the later development of stupor or coma strongly correlated with poor outcome (severe disability or death; p = 0.002). The characteristics of conscious patients who remained stable were compared with those who subsequently deteriorated. The initial conscious state (alert, drowsy or confused), severity of symptoms and ataxia, and the size of haemorrhage on CT scan were not reliable prognostic indicators. However, the presence of bilateral gaze paresis, anarthria (present in eight cases), limb weakness, a systolic blood pressure above 200 mmHg and moderate hydrocephalus significantly correlated with a poor outcome. The presence of these signs warrants consideration of urgent surgical intervention at the time of diagnosis. Since no clinical or radiological findings excluded the possibility of further deterioration, careful monitoring in an intensive care unit is necessary within the first 48 h in those conscious patients who are likely to remain stable. Guidelines for making the clinical diagnosis and for selecting those patients who will require transfer to adequately equipped centres are suggested.
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PMID:Cerebellar haemorrhage--diagnosis and treatment: a study of 75 consecutive cases. 344 85

Two horse farms, on which there was a high incidence of proven and suspected equine degenerative myeloencephalopathy (EDM), were studied. Symmetric ataxia and paresis, along with laryngeal adductor, cervicofacial, local cervical, and cutaneous trunci hyporeflexia, characterized the syndrome. Serum vitamin E concentration reflected a deficient state in affected and unaffected horses on both farms when compared with selected reference groups and with published values. A high incidence of the disease was evident in offspring of two particular sires on one farm. Vitamin E supplementation resulted in correction of the deficient state in most horses and was associated with a drastic reduction in the incidence of EDM on one farm from 40% to less than 10% the year following vitamin E supplementation. In addition, during the last year, the severity of signs in the few cases was dramatically reduced. This information substantiates the hypothesis that EDM is a vitamin E-responsive disorder of Equidae with a possible familial predisposition.
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PMID:Equine degenerative myeloencephalopathy: a vitamin E deficiency that may be familial. 350 20

Stated are the values of the basic microelements in fallow deer in the region of Northeast Bulgaria as established through biogeochemical analysis. In unfavourable years metabolism is disturbed resulting in lowering the defense mechanism of the body. A number of bacterial species, and, more specifically, Escherichia coli increase their virulence and cause gastrointestinal disorders and diseases. Copper, selenium, and arsenic deficiency lead to endemic ataxia with characteristic clinical symptoms--the so-called spring diarrhea and endemic paresis. The Microsal Nesse polymicroelement preparation has been tested to prevent diseases as applied to the drinking water and to the forest and fruit silage. It contributes to strengthening the resistance of fallow deer, lowering the chronic diseases of the lungs, stomach, and intestines as well as to improving the shooting trophies.
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PMID:[Diseases of the fallow deer in northeastern Bulgaria and their prevention]. 354 70

Modulation of acute monensin toxicosis in swine was evaluated in 2 studies. In study 1, 56 weanling male pigs were allotted to 14 groups of 4 each. Pigs in 7 groups were given tiamulin in the drinking water (to supply 7.7 mg/kg of body weight/day) for 3 days before and for 2 days after monensin administration. Monensin was given as a single oral dose (at 0, 7.5, 15, 25, 50, 75, or 100 mg/kg) to pigs in groups with or without tiamulin exposure. Prominent acute clinical signs of monensin toxicosis (hypermetria, hind limb ataxia, paresis, knuckling of hind limbs, and recumbency) developed by 2 to 6 hours after dosing in pigs given 15 or 25 mg of monensin/kg with tiamulin exposure, but not in pigs given the 15 or 25 mg of monensin/kg without tiamulin exposure. Also, the extent of monensin-induced skeletal muscle damage at 4 days after monensin dosing was enhanced in pigs given 7.5, 15, or 25 mg of monensin/kg and exposed to tiamulin. In study 2, 48 weanling male pigs were allotted to 8 groups of 6 each. Four groups of pigs were given 20 mg of monensin/kg orally, and 4 groups were given 100 mg of monensin/kg orally. For each monensin dose, a group was treated 24 hours before monensin administration with (i) selenium (Se)-vitamin E preparation, 0.25 mg of Se and 68 IU of d-alpha-tocopheryl acetate (vitamin E)/kg, IM; (ii) vitamin E only, 68 IU of d-alpha-tocopheryl acetate/kg; (iii) Se only, 0.25 mg of Se/kg; or (iv) vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and/or vitamin E. 367 64

A clinicopathological study of a neurologic disease in Rottweiler dogs was conducted. Clinical data were available on 16 dogs, 11 of which were examined pathologically. All dogs had a history of progressive gait abnormalities, which had commenced insidiously at an age varying from 1.5 to 3.5 years. In most dogs the fore limbs were affected prior to the hind limbs. At neurologic examination ataxia of all 4 limbs was seen, in some instances accompanied by an apparent paresis. Proprioceptive positioning was delayed whereas spinal reflexes were often hyperactive. Plain and contrast radiographs of the spine did not reveal any compressive lesions in 5 dogs examined. Cerebrospinal fluid analysis in 4 dogs was normal. Electrodiagnostic testing in 3 dogs revealed no abnormalities. At pathologic examination demyelinating lesions were found in the central nervous system. These were largely confined to the cervical spinal cord and brain stem and had a rather characteristic more or less symmetric distribution. Pedigree data suggested that the disease is transmitted genetically.
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PMID:Progressive ataxia due to central demyelination in Rottweiler dogs. 372 41


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