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 painful shoulder in the paralysed stroke patient, is a great problem in the field of physical medicine. Certain pathological changes are taking place in the patients with extensive paralysis in the upper limb. These changes are: (1) lesions or rupture of the rotatorcuff, (2) displacement of caput humeri in a caudal direction, (3) neuropathy of plexus brachialis with peripheral paresis. Careless handling of the patients' arm and the passive pull of the heavy, paralytic arm are claimed to be the main cause for these lesions. Correct handling of the patient and support of the shoulder is necessary to prevent these injuries from taking place. The different arm-slings used for this purpose, are not good enough. The article describes an orthosis which supports the shoulder joint and reposition caput humeri (if this has been luxated). It also gives the patient a better balance by straightening the trunk and letting the arm hang extended and slightly abducted along the side of the body. The orthosis is only tested in a few patients. Further development and testing on several patients are now being planned.
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PMID:Upper extremity orthoses for stroke patients. 745 Sep 56

Treatment with N-methyl-D-aspartate (NMDA) receptor antagonists, such as ketamine (KET) or phencyclidine (PCP), can trigger apoptotic neurodegeneration in neonatal rodents; however, little is known about the behavioral alterations resulting from such treatment. Here, rats were sc treated with saline; 10 mg/kg PCP on postnatal days (PNDs) 7, 9, and 11; 20 mg/kg KET (six injections every 2 h on PND 7); or a regimen of ketamine and 250 mg/kg L-carnitine (KLC) both administered on PND 7 with additional 250 mg/kg doses of L-carnitine given on PNDs 8-11. Postinjection, the home cage behavior of each pup was categorized on PNDs 7-11. Slant board and forelimb hang behaviors were examined on PNDs 8-11 and 12-16, respectively. The initial KET or KLC injections on PND 7 elevated abnormal home cage activity (i.e., paresis and paddling); however, KLC pup behavior returned to normal by the fourth injection, indicating the protective effects of L-carnitine against NMDA antagonist toxicity. PCP treatment caused substantial abnormal home cage activity on each injection day (PNDs 7, 9, and 11). Latencies to turn on the slant board were significantly longer on PND 8 for KET- and PCP-treated pups and PND 10 for PCP-treated pups. On PND 12, the forelimb hang time of PCP-treated pups was significantly shorter. Body weight was decreased on PNDs 8-18 in PCP-treated pups and PNDs 8-10 in KET-treated pups. These data indicate that developmental NMDA antagonist treatment causes short-term behavioral alterations which appear related to motor coordination and may be cerebellar in nature. Furthermore, single PCP injections appear more potent at altering behavior than multiple injections of KET.
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PMID:Neonatal PCP is more potent than ketamine at modifying preweaning behaviors of Sprague-Dawley rats. 1866 23