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)

Twenty-nine documented cases of cerebellar degeneration at the National Taiwan University Hospital during a 8-year period (1980 through 1987) were reviewed. They were classified as familial (N = 14) or sporadic (N = 15) to compare the clinical signs and symptoms between both groups. The familial cases had earlier onset, and gaze paresis was found only in this group. Patients younger than 30 years old were more often familial cases and had more frequent deep sensation involvement. Oculomotor abnormalities on electrooculographic (EOG) tracings of 21 patients were analysed. The defects included abnormal OKN (86%), jerky pursuit (76%), ocular dysmetria (57%), slow saccades (43%), abnormal VOR or VVOR (43%), and fixation instability (19%). Intravenous TRH therapy was used in 17 patients, and resulted in 8 (47%) subjectively and 6 (35%) objectively improved cases. The use of TRH therapy in cerebellar degeneration was discussed.
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PMID:Clinical manifestations and thyrotropin releasing hormone therapy in cerebellar degenerations. 184 43

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