Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dysphagia is more frequently observed in patients with neurologic diseases (stroke, bulbar or pseudo-bulbar syndrome, amyotrophic lateral sclerosis, cranial trauma). Furthermore, the presence of this pathology is obviously more frequently noted in the light of the increase in the length of the human life span. It has become evident that alternative feeding procedures such as the nasogastric tube or gastrostomy may bring about complications and deprive patients of the oral phase of deglutition which plays a leading role in stimulating digestive functions. The Authors report a systematic research on the rehabilitation aspects of neurogenous dysphagia. All the patients studied underwent a neurological examination and oropharyngeal functional evaluation using echo-videorecording of the oral phase of deglutition and fluoro-videorecording of the pharyngeal phase. The data obtained allowed for the selection of five patients considered suitable for the rehabilitation program. One of them had a multi-infarct encephalopathy, two a spastic hemiplegia f.b.c., a fourth a cerebellar syndrome and the last a sequela of meningioma removal of the ponto-cerebellar angle with peripheral paralysis of the right VII, IX, X, XI cranial nerves. This last patient also underwent a crico-pharyngeal myotomy. Therapy consisted in making the patient sensitive to swallowing movements and in training them to assume a compensatory posture as well as functional rehabilitation of the organs involved in deglutition. The first datum emerging from the study is the lack of etiological homogeneity found in the cases treated with evident variability in different deglutition organ impairment, even though there was the common denominator of the dysphagia symptom. With regard to the results obtained, there was a complete resolution in one patient, while in the other four there was such an improvement as to allow the patients a safe autonomous oral assumption of food. The positive results obtained are not only linked to the recovery of damaged organs, but also to the development of compensatory strategies such as the choice of appropriate food consistency and the assumption of postures which protect the respiratory tract from aspiration and favor crico-pharyngeal relaxation.
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PMID:[Rehabilitation of oro-pharyngeal dysphagia of neurogenic etiology using radiological examination: preliminary results]. 163 72

The reduction of working ability, because of disease, was considered in 1,053 subjects. 21 groups of maladies were found; the neurological disease and mental retardation (MR) caused various degrees of working inability in 416 subjects, i.e. in the 39.51% of the examined population; orthopaedic changes affected the 15.57% of the patients; psychic disorders determined some inability in 8.93% of the persons. The subjects unable to work receive, by Law, an economic help. This study was limited to neurological patients and to subjects mentally retarded. The working ability was reduced by 5 types of disturbances: neuromotor pathology, mental retardation, mental deterioration and dementia, epilepsy, other neurological diseases. The neuromotor pathology affected 163 subjects; the types of symptomatology: hemiplegia; it was found in 71 patients; 62 times it was the result of cerebrovascular disease; in 4 patients it was caused by a hypoxic-ischaemic pre-perinatal encephalopathy. 43 patients affected by cerebrovascular disease lost their personal autonomy, i.e. they could no longer do the activities of daily living (ADL); 7 patients lost their working ability; 12 subjects kept some ability to work. The hemiplegias which struck after 50 years of age were caused by cerebrovascular disease; paraplegia: 28 paraplegic patients have been seen; the aetiology was: poliomyelitis in 8 subjects; MS in 5 patients; ALS in 2 patients; in 13 patients the aetiology was unknown. 6 patients resulted unable to work; 8 persons kept some working ability; 14 patients lost the ability to do the ADL; tetraplegia, or double/bilateral hemiplegia, was found in 20 patients; the aetiology: poliomyelitis in 4 patients; pre-perinatal hypoxic ischaemic encephalopathy in 4 patients; 3 patients of MS; lesion of the cervical spinal cord because of breech delivery in 2 patients; the aetiology was not known in 7 persons. The ability to do the ADL was lost in 17 patients; 3 subjects kept some working ability. Double or bilateral hemiplegia (Little disease) was the model of neuromotor deficit subsequent natal encephalopathy (Infantile Cerebral Palsy, PCI); brachial plexus paralysis was only found from obstetrical (i.e. natal) origin; poliomyelitis and PKU resulted prevented as of 10 years. Mental Retardation (MR) was considered a borderline pathology between neurology and psychiatry; it included 162 subjects: in patients with severe MR a pre-perinatal hypoxic-ischaemic encephalopathy was found in 40.4% of the cases; in patients affected by moderate or light MR the same encephalopathy was found in the 11.3% of the subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Neurologic diseases, mental retardation and reduction in work capacity]. 293 89

The history of motor unit number estimation (MUNE) is given, together with brief descriptions of the various methods presently available. A small muscle of the hand contains about 100 motor units and greater numbers are found in larger muscles; beyond 60 years the numbers begin to decline. In ALS approximately half the motor units cease to function within 6 months of the involvement of the motoneuron pool, while in adult spinal muscular atrophy further loss may not occur over several years. The reduction in MUNE values in myotonic dystrophy remains an enigma, but even more curious are the losses and subsequent recoveries occasionally observed in hyperthyroidism and chronic renal failure; possibly, nontransmitting ("silent") synapses are involved. MUNE may also be used to study CNS problems such as hemiplegia and congenital brachial palsy. The availability of more powerful computers for EMG should lead to advances in MUNE.
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PMID:Motor unit estimation: anxieties and achievements. 771 21

There are several incurable diseases of motor neuron degeneration, including amyotrophic lateral sclerosis (ALS), primary lateral sclerosis, hereditary spastic hemiplegia, spinal muscular atrophy, and bulbospinal atrophy. Advances in gene transfer techniques coupled with new insights into molecular pathology have opened promising avenues for gene therapy aimed at halting disease progression. Nonviral preparations and recombinant adenoviruses, adeno-associated viruses, herpesviruses, and lentiviruses may ultimately transduce sufficient numbers of cerebral, brainstem, and spinal cord neurons for therapeutic applications. This could be accomplished by direct injection, transduction of lower motor neurons via retrograde transport after intramuscular injection, or cell-based therapies. Studies using transgenic mice expressing mutant superoxide dismutase 1 (SOD1), a model for one form of ALS, established that several proteins were neuroprotective, including calbindin, bcl-2, and growth factors. These same molecules promoted neuronal survival in other injury models, suggesting general applicability to all forms of ALS. Potentially correctable genetic lesions have also been identified for hereditary spastic hemiplegia, bulbospinal atrophy, and spinal muscular atrophy. Finally, it may be possible to repopulate lost corticospinal and lower motor neurons by transplanting stem cells or stimulating native progenitor populations. The challenge ahead is to translate these basic science breakthroughs into workable clinical practice.
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PMID:Gene therapy for amyotrophic lateral sclerosis and other motor neuron diseases. 1109 37

The authors provide an extensive review of new data related to the role of glutamate in CNS disorders, describing new aspects in glutamate and glutamatergic receptors-NMDA receptors, NR2B-selective antagonists, non-NMDA ionotropic glutamate receptors, N-acetylaspartylglutamate, and glutamate and glycine transporters. New findings in animal models and in human diseases-stroke, traumatic brain injury, Alzheimer's, Parkinson's and Huntington's diseases, tardive dyskinesia, ALS, olivopontcerebellar degeneration, AIDS, allergic encephalomyelitis, epilepsy, anxiety, depression, schizophrenia, liver disease, aminoglycoside antibiotic-induced hearing loss, hemiplegia, chronic pain and drug tolerance and abuse-are presented. Finally, the authors cite the progress achieved in the development of agents that interact with the glutamatergic system: NMDA channel blockers, competitive NMDA receptor antagonists, NR2B-selective antagonists, glutamate release inhibitors, glycineB antagonists, AMPA and kainate receptor antagonists, AMPA receptor-positive modulators and agents that act by modifying endogenous kynurenic acid metabolism.
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PMID:Glutamate in CNS disorders as a target for drug development: an update. 1561 69