Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with cervical spinal cord injury can gain useful hand function from a good rehabilitation programme and non-operative hand care. Effective prehension can usually be achieved by proper positioning, exercises, and splinting but when grasp is poor, tendon transfers are very effective in furthering the goal of independence. These patients have been reviewed extensively and classified into groups according to remaining neurological function. Group I patients have weak elbow flexion and weak shoulder function or less. No tendon transfers were done. Group II patients have shoulder control, elbow flexion and weak wrist extensors. Some of these patients can be improved by transferring the brachioradialis to the radial wrist extensor. Group III patients have the above and good to normal brachioradialis and two radial wrist extensors. Transferring the brachioradialis to restore opposition and the extensor carpi radialis longus to the flexor digitorum profundi provides strong and effective prehension. Group IV patients have the above plus pronator teres and flexor carpi radialis which can be used for transfer. Opposition and finger flexion can be restored by a variety of transfers. In groups III and IV tendon transfers were done only when automatic grasp was poor or absent. If finger grasp was good and thumb function ineffective only opponens transfers were done in order to achieve key pinch. Group V patients have all muscles functioning but with varying degrees of intrinsic weakness. Opponens transfer is useful for these patients. Indications and contraindications to surgery are given. All the patients have improved function and strength following their tendon transfers. No patient has regretted having had surgery.
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PMID:Tendon transfers to improve grasp in patients with cervical spinal cord injury. 113 25

A 57-year-old woman presented with a slowly progressive gait disturbance in 1992 (53 years of age). Over the next year, she gradually began to talk less, but her speech itself became more rapid than before. He speech was frequently too fast even for family members to understand. In 1997, she was admitted to our hospital. On admission, the patient was disoriented but able to follow simple verbal commands, to name things, and to write simple words. Neither apraxia, aphasia, hemispatial neglect, nor a corpus callosum disconnection syndrome was observed. There was no muscle weakness or atrophy. She showed a positive Babinski sign with mild spasticity in the legs and Gegenhalten, but no rigidity. Her speech was monotonous and abnormally fast (cluttering-like speech). Her speech became faster and faster toward the end of sentences, skipping several syllables or even words. She was unable to speak slowly and clearly, even when efforts were made to pace her speech to the speed set by the examiner. She was able to stand only with a wide base of support and body flexion. When standing, she was unable to place one foot directly beside the other; as she tried to have one foot near the other, the former repelled the latter. She had great difficulties in taking her first step forward, and showed rapid freezing of gait even when she managed to succeed in starting. She was able to imitate walking or bicycling with her legs unloaded, indicating that her gait disturbance was a kind of apraxia of gait. Her intelligence was somehow difficult to assess because of her peculiar speech disturbance. However, her family members had noticed her memory disturbance and personality change (offensiveness) since 3 to 4 years before the admission. Moreover, she was defective not only on Hasegawa Damentia Scale-Revised but also on Raven's Colored Progressive Matrices which estimates non-verbal intelligence. It was also noted that she was inattentive and lazy in thinking on questionnaires. Thus we considered that she was at least mildly demented and the type of dementia was of frontal pathology. Laboratory data were all normal except for the head MRI, which demonstrated prominent and thinness of the corpus callosum from the anterior part of the body to splenium without any other brain lesions that could cause the thinness secondarily. Our case resembles two cases reported by Sunohara et al in 1985, together comprising a unique clinical feature. Although Sunohara et al did not refer to the thinness of the corpus callosum in their cases, the clinical profiles in our case and theirs raise the possibility that they form a new disease entity. A further study in a large number of similar cases, including autopsies will provide a conclusion.
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PMID:[A case report of dementia with cluttering-like speech disorder and apraxia of gait]. 1042 42