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

This series involves 29 patients treated for chronic pain (9 patients) or severe spasticity (20 patients). The surgical technique used was the microsurgical D.R.E.Z.-tomy technique as described by Sindou. In the first group, three patients had malignant pain, while the six others had deafferation pain. In the second group, spasticity involved the upper limb in 13 patients and the lower limbs in 7 patients. Out of 20 patients, one-third suffered from cerebral palsy. In the first group, results one year after surgery were excellent or good in 7 out of the 9 patients. In the group treated for spasticity, a significant decrease in spastic disorders was observed in 16 of the 20 patients over a 1 to 4 year follow-up period. There was also an improvement of voluntary movements in 11 patients and a decrease in pain in 15 patients belonging to this group. A number of complications were noted: cerebrospinal fluid leakage in two cases, painful anesthesia in the C5 to T1 territory in one case, transient paresis of the upper limb in six cases. One patient died as a result of an expansive pneumatocele (3.4% of cases).
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PMID:[Surgery of the radiculo-spinal cord junction in the treatment of chronic pain and incapacitating spasticity. Report of a series of 29 patients]. 226 43

The torque during isokinetic knee extensions and flexions was determined in repeated tests at 3 speeds of angular rotation in 25 patients with pareses considered to be hysterical after relevant examinations and follow-up. The torque records were combined with surface EMG from the quadriceps and the hamstring muscles in some patients. Besides the weakness, 3 signs were observed that are not usually seen in patients with pareses due to verified peripheral or central lesions. These signs were: Enlarged variability of torque in repeated tests of the same movement (larger than 20% of maximum torque in 22 patients). Higher torque in fast movements than in slow movements (8 patients). Force production in knee flexion less than that expected from the weight of leg and lever arm due to restraining activation of the quadriceps muscle (12 patients). The restraint was present although there was no spasticity. The signs reflect inconsistent and contradictory motor performance that is not compatible with a genuine paresis. Thus, they aid the identification of weakness of functional origin.
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PMID:Isokinetic measurements of muscle strength in hysterical paresis. 241 88

Recovery from rabies was studied in an experimental model. Young adult mice were inoculated in a hindlimb footpad with street rabies virus (fox salivary gland isolate). In a group of 62 mice, 97% developed clinical rabies with paresis of the extremities and spasticity, and 37% recovered with neurological sequelae. There was an acute inflammatory reaction in the brainstem and grey matter of the spinal cord, and degeneration of myelinated axons in the white matter of the cord and in the dorsal roots. Rabies virus antigen was found in the central nervous system of all mice examined between day 5 and 13, and also in trigeminal and dorsal root ganglia. Surviving mice had neutralizing antibodies in serum and brain tissue, and 90% survived an intracerebral challenge with the CVS strain of fixed rabies virus. Spontaneous recovery from rabies encephalomyelitis was demonstrated with evidence of viral replication and pathological changes in the central nervous system.
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PMID:Spontaneous recovery from the encephalomyelitis in mice caused by street rabies virus. 258 21

Is characterized by several various signs. One of these, spasticity, involves a velocity dependent increase in muscle stiffness during stretch and by hyperactive tendon jerks. When intense, spasticity impedes residual strength in antagonistic muscles and interferes with attempts to move, especially if complicated by clonus and/or spasms. Assessment of spasticity is multifactorial and implies clinical as well as instrumental methods. The pathophysiological mechanisms responsive for the hyperexcitability of the myotatic reflex can be studied by methods of clinical neurophysiology. It appears that there are various factors involved at the spinal level, involving reduction in both pre- and post-synaptic inhibitions. Although spasticity is not responsible for the major part of the disability imposed by upper motor neurone syndrome, it should be reduced. The therapeutic methods are medical, surgical or from physical medicine. In many cases, the results have been validated by blind studies. As paresis is the most disabling effect, it would be worthwhile to develop drugs able to reduce spasticity and increase muscle strength at the same time. Recent trials suggest than TRH-T may be effective in this regard.
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PMID:[Pyramidal syndrome: its physiopathology and treatment]. 269 2

Analysis of the neurologic symptomatology in 22 patients with Niemann-Pick disease type C revealed 3 phenotypes: (1) an early-onset, rapidly progressive form associated with severe hepatic dysfunction and psychomotor delay during infancy and later with supranuclear vertical gaze paresis, ataxia, marked spasticity, and dementia; (2) a delayed-onset, slowly progressive form heralded by the appearance, usually in early childhood, of mild intellectual impairment, supranuclear vertical gaze paresis, and ataxia, and later associated with dementia and, variably, seizures and extrapyramidal deficits; (3) a late-onset slowly progressive form distinguished from the 2nd pattern by later age of onset (adolescence or adulthood) and a much slower rate of progression. The existence of the 1st and 2nd phenotypes within the same sibship suggests that they are variant expressions of the same clinicopathologic disorder. Niemann-Pick disease type C should be considered not only in infants and children who present with organomegaly and a progressive neurodegenerative course, but also in adolescents and adults who have insidiously progressive neurologic dysfunction and only slight organomegaly. Associated with the disease is a marked deficiency in the ability of cultured fibroblasts to esterify exogenously supplied cholesterol. Assay of this deficiency is particularly useful for confirming the diagnosis in patients with atypical presentation.
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PMID:Clinical spectrum of Niemann-Pick disease type C. 276 97

A survey of the literature of neurological manifestations associated with the acquired immune deficiency syndrome (AIDS) shows a broad disease spectrum affecting approximately one third of the patients in large hospital series. The complications include focal cerebral lesions caused by abscesses, lymphomas, leucoencephalopathy or infarcts as well as encephalitis, meningitis and myelitis. Most opportunistic infections of the central nervous system presumably are caused by toxoplasma gondii, cytomegalovirus and cryptococcus neoformans. One tenth of all patients have neurological disease as their initial symptom of AIDS. The diagnosis should always be considered in patients at risk and in males with an unusual neurological history or with a peculiar CT scan of the brain. Besides the opportunistic complications of AIDS, LAV/HTLV-III itself probably attacks the nervous system and gives rise to concomitant lesions of the long tracts of the spinal cord with ataxia, paresis and spasticity and to subacute encephalopathy and peripheral nerve abnormalities as well.
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PMID:Neurological complications and concomitants of AIDS. 303 38

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

The term spasticity is used to describe many relatively unrelated syndromes and, because they share few common pathophysiologic mechanisms, it is not possible to define the physiology or pharmacology of spasticity. In patients with spastic paresis, it is the latter negative symptom (rather than the spasticity) that accounts for almost all the functional disability. Clinical neurophysiologic techniques are useful for categorization of patients with clinically identical syndromes into subgroups which respond to different therapies. Fusimotor or spindle primary afferent hyperactivity have not been demonstrated in spastic patients; reduction in central inhibitory mechanisms probably accounts for spastic hyper-reflexia. Increased passive muscle stiffness may also be clinically significant. Therapies for spasticity include elimination of causative or enhancing factors, frequent muscle stretching, surgical approaches and chemotherapy. The latter includes dantrolene (which weakens muscles), baclofen (particularly useful for reduction of flexor spasms and flexor dystonia in patients with spinal lesions) and diazepam.
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PMID:Physiologic and pharmacologic approaches to spasticity. 332 74

Sixteen patients suffering from spasticity due to multiple sclerosis were treated with baclofen and tizanidine in a partially blind cross-over study. No significant difference in efficacy was found. The most striking difference was seen in the side-effects: baclofen frequently caused more or less severe muscle weakness and even falling during walking and standing. Treatment with tizanidine produced an apparent improvement of mobility in some patients suffering from moderate or marked paresis associated with a marked spasticity of their legs. Isometric muscle strength did not show any significant changes during either treatment. The different impact of baclofen and tizanidine on mobility and weight support seems to be related to their different site of action in spasticity.
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PMID:Tizanidine versus baclofen in the treatment of spasticity in multiple sclerosis patients. 337 47

The relationship between the interruption of the human pyramidal tract and its attendant clinical manifestations has been a matter of concern to neurologists and neurosurgeons for over a century. We presently report three cases of unilateral pyramidal tract ischemic lesions within the cerebral hemispheres who presented with a contralateral pure spastic hemiplegia syndrome. In none could we find any disturbance in the somatosensitive evoked potentials of the four limbs. The review of some cases on record since the time of Charcot and Erb has made it clear that the pyramidal syndrome is a valid clinical concept which should be qualified according to the particular animal species one is referring to. In man, it manifests itself by paresis, hyperactive muscular reflexes, spasticity and Babinski sign. Based on this evidence we propose the idea of a "differential control" exerted by the pyramidal tract upon the segmental neuronal pool as its key mode of normal functioning.
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PMID:[Pure spastic hemiplegia of pyramidal origin]. 340 87


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