Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The olivopontocerebellar atrophies (OPCA) can be divided into five disease entities. One of these, dominant OPCA with dementia and extrapyramidal signs, is better defined by the family we studied. Five persons in three generations were affected by progressive ataxia, tremor, rigidity and mental deterioration, beginning in their twenties and thirties. Neurologic examination showed mental deterioration, high-pitched dysarthric voice, gaze paresis, rigidity and coarse tremor. This disease differs from other dominant and recessive OPCAs clinically because of the prominent mental deterioration and extrapyramidal signs, and pathologically because of cortical, lentiform and substantia nigra neuronal loss.
 ...
PMID:Dominant olivopontocerebellar atrophy with dementia and extrapyramidal signs: report of a family through three generations. 517 58

Mammalian exposure to toxic levels of the trialkyltin compounds, triethyltin (TET) and trimethyltin, results in pathological manifestations largely restricted to the nervous system. The remarkable features of TET toxicity are cerebral edema and muscular weakness. Rats exposed orally to TET (10-30mg TET Br/l of drinking water) progress through an increasingly compromised state beginning with mild ataxia and hindlimb weakness after one week, spastic paresis of the hindlimbs by two weeks; and hindlimb paraplegia and sensory changes by 3 weeks. Histopathological studies of chronic TET-exposed rats report minimal ultrastructural damage to distal peripheral nerves, myelin, and muscle. Chromatolytic reactions are observed in some alpha motor neurons; intramyelinic vacuolization in the ventral roots and horn is substantial by 3 weeks. Myelin vacuolization and degeneration are observed to a lesser extent in the dorsal roots of the spinal cord. Wet weights and myofiber diameters of EDL and soleus muscles are reduced during chronic TET intoxication, but no histopathology is evident using light microscopy. Conduction of compound action potentials in vivo along distal sensory fibers, ventral roots and distal motor fibers (in sciatic n.) is normal in 3 week TET rats as compared to control; however, nerve conduction velocity is decreased in the segment of the H-reflex arc involving the dorsal roots. Earlier studies by Stoner and coworkers led to suggestions that the neuromuscular junction may be preferentially affected by TET and could contribute, in part, to the symptoms of muscular weakness. In support of this hypothesis preliminary studies from our laboratory and others indicate that neurotransmission is functionally depressed at the myoneural junction following chronic TET treatment in vivo or when applied in vitro to isolated muscle preparations. Stimulated, but not unstimulated, release of acetylcholine from the vascular perfused rat phrenic nerve-hemidiaphragm preparation is decreased by TET especially at higher stimulation rates (20 Hz). In vitro administration of TET Br (10(-6)M) results in an irreversible decrease in the amplitude of evoked endplate potentials; chronic in vivo exposure to TET causes a decrease in the resting membrane potential of soleus muscle (in situ recordings) and provokes a peculiar post-stimulus (200Hz bursts) elevation of spontaneous miniature endplate potentials in isolated cut diaphragm preparations.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Neuromuscular function and organotin compounds. 609 43

Behavioral, polygraphic, biochemical and histological aspects of thiamine deficiency in rats induced by thiamine-deficient food and pyrithiamine treatment (40 mg/kg daily for 4 days) are described. Behavioral alterations were essentially characterized by ataxia, pilo-erection and paresis. Polygraphic data indicated an increase in slow-wave sleep (SWS) of 33% and decreases in paradoxical sleep (PS) and wakefulness (W), respectively, of 69% and 27%. These effects were reversed by complete food and thiamine administration, the reversal including an overshoot in PS. Biochemical assays, performed when the polygraphic data indicated a large effect, demonstrated a significant increase in serotonin (5-HT) and 5-hydroxyindolacetic-acid (5-HIAA). These effects were particularly evident in the raphe system and the locus coeruleus. Histological data from the raphe dorsalis displayed a notable increase in yellow fluorescence in pyrithiamine-treated animals over controls. We conclude from these experiments that a deficiency in thiamine affects the serotonergic system and that the subsequent effects on sleep are a consequence of this serotonergic change.
 ...
PMID:Sleep and indolamine alterations induced by thiamine deficiency. 618 42

Degenerative myelopathy was diagnosed in a 6-year-old cat that had progressive ataxia, posterior paresis, and loss of conscious proprioception over a period of 8 months. Corticosteroid therapy did not alleviate clinical signs, and the cat was euthanatized. Microscopic examination of the spinal cord revealed diffuse degeneration of myelin attended by marked astrocytosis. The degenerative changes were most marked in the thoracolumbar segment. The cause of the degenerative lesions was not apparent.
 ...
PMID:Degenerative myelopathy in a cat. 624 72

An outbreak of paresis occurred on a small isolated stud farm in July 1980. Of the 42 horses on the stud, infection was confined to a group of nine in-foal mares and their foals and eight other horses which were either housed together at night or grazed adjacent pastures. Eight mares and two geldings developed ataxia or paresis and one mare died. Equid herpesvirus 1 was isolated from 17 animals and serological studies confirmed that 24 of 26 animals sampled had experienced infection.
 ...
PMID:An outbreak of paresis in mares and geldings associated with equid herpesvirus 1. 628 Mar 66

Twelve Lewis rats were inoculated with a guinea pig spinal cord tissue preparation. They developed experimental allergic encephalomyelitis (EAE) after 12-14 days, manifested by weight loss, tail flaccidity, ataxia, hind limb paresis and incontinence. The CNS lesions are produced in this animal model on the basis of inflammatory demyelination, which provides a useful model for multiple sclerosis. Concomitantly with EAE, all animals developed vestibular hyperreactivity (VH) of otolith and canal reflexes. In surviving animals these reflexes renormalized after full clinical recovery. The major effect on the canal response was an increased duration of postrotatory nystagmus caused by an increase in time constant. These findings are similar in part to those previously reported in patients with multiple sclerosis.
 ...
PMID:Physiological abnormalities in experimental allergic encephalomyelitis (EAE). I. Vestibular hyperreactivity (VH) in rats with EAE. 633 52

12 Lewis rats were inoculated with a guinea pig spinal cord tissue preparation. They developed experimental allergic encephalomyelitis (EAE) after 12-14 days manifested by weight loss, tail flaccidity, ataxia, hind limb paresis or paralysis and urinary incontinence. Concomitantly with EAE, all animals developed vestibular hyperreactivity (VH) of canal and otolith reflexes. Other signs of brain-stem dysfunction were also observed: abducens paralysis, facial weakness, tachypnoe and mydriasis with defective pupillary light reflex. The vestibular and other abnormalities subsided with some delay after recovery from clinical EAE, whilst histological abnormalities were still present in the CNS.
 ...
PMID:Physiological abnormalities in experimental allergic encephalomyelitis (EAE): II. Correlation between clinical signs and vestibular hyperreactivity and other signs of brain-stem dysfunction in rats with EAE. 633 24

Seven affected individuals from three generations in a kindred having over 250 members were identified as having possible, probable, or definite Creutzfeldt-Jakob disease. Spongiform encephalopathy was found at postmortem examination in two cases. Detailed inpatient neurological examinations were performed on four of the subjects, three of whom were first observed with supranuclear gaze paralysis, gait ataxia, and rapidly progressive dementia. Supranuclear gaze paresis can be seen as an early feature of Creutzfeldt-Jakob disease, although it has been regarded as a late sign. In this, the largest reported kindred of Creutzfeldt-Jakob disease, most of the affected patients were farmers. Possible modes of infection are discussed.
 ...
PMID:Supranuclear gaze palsy in familial Creutzfeldt-Jakob disease. 635 15

When a patient with a peripheral monocular paresis is forced to look with the paretic eye, head movements induce the sensation of an unstable visual world. The patient behaves as if he had acute bilateral labyrinthine lesions. These symptoms are due to the lack of compensatory ocular movement and the patients complain that the visual objects move in the direction opposite to the head. The patients develop ataxia, nausea, vomiting and past pointing. The symptoms, however, are transient and consistently disappear after approximately 48 hours. The central adaptation to looking and seeing with the paralysed eye is associated with a plastic change of the VOR. This plastic adaptation is probably induced by the large retinal slip produced by the lack of compensatory movement of the eye and can be studied in the normally mobile eye in the dark. The psychophysical adaptation is probably generated by an efferent copy or corollary discharge of the vestibular system to the visual system that cancels the retinal error.
 ...
PMID:Looking with a paralysed eye: adaptive plasticity of the vestibulo-ocular reflex. 647 Jul 22

A 61 year-old man with severe hypertension present with a crural paresis and ipsilateral ataxia. CT scan showed a low density area suggestive of a lacuna in the posterior limb of the internal capsule.
 ...
PMID:[Crural hemiparesis with ipsilateral ataxia]. 649 11


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>