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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurologically impaired infants have immature, damaged, or abnormally developed nervous systems that may cause abnormalities of sucking and swallowing, among other problems. Sucking abnormalities usually present as absence of the sucking response, weakness or incoordination of sucking and swallowing, or some combination of these problems. More investigation of the responses of these infants to various stimuli and training techniques is greatly needed. Although training neurologically impaired infants to breastfeed may present a challenge to even the most experienced neonatal nurse, physician, or therapist, most infants improve and can learn to suckle at the breast. If a mother has intended to nurse her infant, she should be encouraged to do so, even when the infant has abnormalities of sucking, except in the rare and most severely affected infants who remain dependent on gavage or gastrostomy feedings. Various techniques of stimulating, positioning, and progressive weaning to the breast can be helpful in teaching mother and infant to breastfeed. Encouraging support should be provided by all professionals involved with the mother and infant, as well as by a team experienced in helping with such problems. Most importantly, mother and staff must be patient, because the rewards for both the infant and mother are worth the effort.
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PMID:Sucking disorders in neurologically impaired infants: assessment and facilitation of breastfeeding. 354 10

Diaphragmatic dysfunction is an important entity, as it can cause severe dyspnea, ventilation-perfusion abnormalities, and ventilatory failure. The most frequent and important dysfunctions are diaphragmatic weakness, incoordination between the diaphragm and other respiratory muscles, fatigue, and paralysis. Methods for the diagnosis of dysfunction are reviewed and specific dysfunctions are briefly discussed with methods for their evaluation.
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PMID:Diagnosis of diaphragmatic dysfunction. 356 93

Approximately 250 sheep were poisoned and died from ingesting death camas (Zygadenus paniculatus) within a 2-day period on a foothill range in southeastern Idaho. Sixty to 70% of the poisoned sheep were 80-90 lb lambs and the rest were mature ewes. Poisonings were confirmed by field investigation, microhistological analysis of plant fragments from rumen contents of dead sheep, clinical signs, gross and microscopic analysis of tissues, and by experimentally feeding death camas collected on the poisoning site to 3 ewes at the Poisonous Plant Research Laboratory at Logan, UT. Clinical signs and gross and microscopic analysis of tissues were similar in ewes from the field investigation to those in ewes experimentally fed death camas. Ataxia, muscular weakness, trembling, incoordination, discharge of frothy saliva from the mouth and nose, vomition, dyspnea, collapse and death were the most common clinical signs. Gross changes included severe pulmonary congestion and subcutaneous hemorrhage. Microscopic lesions were those of severe pulmonary congestion.
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PMID:Death camas poisoning in sheep: a case report. 382 76

Observations on patients with frontal lesions including the premotor cortex but not the primary motor cortex as shown by CT scans have shown a slight or moderate weakness of the contralateral shoulder or hip muscles which remained as a permanent deficit. The second deficit was an incoordination between movements requiring temporal adjustment between proximal muscle activities of both sides (limb-kinetic apraxia). From the clinical examination there was no evidence for deficient sensory guidance of movement. Visual control of hand and finger movements was normal as long as the arm could be supported during the tasks. In contrast, gross abnormalities of visually guided reaching (visuomotor ataxia) or somesthetic movement control (tactile apraxia) are seen after parieto-occipital lesions. On the basis of clinical observations it is therefore more likely that sensory-motor integration and transformation already takes place at the posterior lobes, where corresponding disturbances are pronounced but are absent after frontal lobe lesions.
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PMID:Clinical aspects of premotor function. 391 45

A 36 year old woman was admitted to the hospital in November 1983 because of her inability to walk. For 3 months prior to admission, she took oral contraceptives (OCs) as a treatment for amenorrhea. 2 months prior to admission, she had general malaise, anorexia, and unsteady gait. 1 month before her admission, tingling and numbness began in the fingertips and spread up to the forearms, a tight feeling around the waist developed, and walking became ataxic. On admission to the hospital, she was thin and pale with greying hair. Her mind was clear and there were no abnormalities of the cranial nerves. Her extremities were hypotonic but not wasted. Slight muscle weakness of the hands and feet was noted. There was myokymia in both legs. Deep tendon reflexes of the extremities were absent. The plantar responses were extensor and lack of coordination in the extremities was noted. There was a definite glove and stocking type of hypesthesia to pinprick and cotton wool. Vibration sense was decreased below T11 and lost in both legs. There was a marked loss of position sense to passive movement in the legs and some impairment in the hands. Laboratory examination revealed mild magaloblastic anemia, elevated LDH, borderline low concentration of vitamin B12 in the serum, increased excretion of methylmalonate in the urine, achylia, positive antiparietal cell antibody and positive anti-intrinsic factor antibody. Cyanocobalamin absorption by the Schilling test was 5.6% after intrinsic factor, 11.3%. The diagnosis of pernicious anemia was made. Upper gastrointestinal studies showed typical carcinoid tumors of the stomach. Cerebrospinal fluid was normal. Peripheral nerve conduction studies demonstrated normal or slightly decreased motor conduction velocities and absent sensory action potential. Sural nerve biopsy was performed. Myelinated fibers were moderately decreased in number to 5554/mm squared and pronounced loss of large myelinated fibers was demonstrated in fiber histogram. Teased method of the single fiber showed mainly axonal degeneration. Anemia and neurologic function improved rapidly with parenteral hydroxocobalamin therapy and 1 month after treatment commenced, she was able to walk without assistance. The clinical significance of peripheral nerve involvement of subacute combined degeneration of the spinal cord was discussed, as the peripheral nerve affection is only poorly understood in contrast to the myelopathy. This was followed by discussion of the possible effect of the OCs and gastric carcinoid to neurological manifestation of pernicious anemia. (author's modified)
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PMID:[Subacute combined degeneration of spinal cord. Significance of peripheral nerve involvement]. 401 64

Following the ingestion of an alleged aphrodisiac known as "yo-yo," a 16-year-old girl experienced an acute dissociative reaction accompanied by weakness, paresthesias, and incoordination. Subsequent symptoms included anxiety, headache, nausea, palpitations, and chest pain. Hypertension, tachycardia, tachypnea, diaphoresis, pallor, tremors, and an erythematous rash were noted on physical examination. Serum epinephrine and norepinephrine levels were found to be elevated. Symptoms resolved spontaneously but lasted approximately 36 hours. The ingested substance was identified as yohimbine. The pharmacology of yohimbine and the treatment of yohimbine poisoning are discussed.
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PMID:Yohimbine: a new street drug. 403 64

Clinically normal Nubian goats were given the antiprotozoal drug imidocarb at single intramuscular doses of 6, 12, 18 and 24 mg/kg, and the various clinical, biochemical and pathological manifestations were recorded. At a dose of 6 mg/kg the drug produced no change in any of the parameters studied. At higher doses, the drug produced dose dependent changes which included increased heart and respiratory rates, increased defaecation, urination, depression, incoordination of movement, weakness of the hindlegs, recumbency, and finally death. Just prior to death, there was a significant decrease in the number of erythrocytes, and in packed cell volume, and haemoglobin concentration. In plasma there was an increase in the activity of aspartate transaminase, urea and creatinine concentrations and inhibition of cholinesterase activity. The main histopathological changes were associated with hepatic and renal damage. Three goats were pre-treated with atropine sulphate (1 mg/animal) and after one hour given imidocarb intramuscularly at a dose of 12 mg/kg. The changes were similar but much less severe when compared with those in animals given imidocarb alone at the same dose.
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PMID:Some effects of imidocarb in goats. 408 55

Five Rottweiler dogs were examined because of progressive ataxia of thoracic and pelvic limbs of several months' to 4 years' duration. Hypermetria, especially of the thoracic limbs, and head incoordination and tremors were obvious features in the 3 older dogs. None of the dogs had evidence of weakness or loss of conscious proprioception. An electroencephalogram in 1 severely affected dog was normal. Electromyograms in 2 severely affected dogs were normal except for some positive sharp waves and fibrillation potentials in the interosseus muscles of all 4 feet. Cerebrospinal fluid evaluations of 2 severely affected dogs were normal. A reduced number of sensory nerve endings, compared with age-matched controls, was seen on histologic examination of a conjunctival biopsy specimen in 1 severely affected dog. An antemortem diagnosis of neuroaxonal dystrophy was suspected from the signalment, history, and neurologic examination findings. The diagnosis was confirmed on the basis of microscopic findings in 3 dogs necropsied.
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PMID:Neuroaxonal dystrophy of Rottweiler dogs. 669 79

Two patients in whom polyneuropathy was associated with hypothyroidism have been studied clinically and electrophysiologically. Sural nerve biopsy was performed on both patients and the nerve studied by light and electron microscopy. Both patients had symptoms of paraesthesiae and muscle pain and there was distal weakness, sensory impairment and incoordination in both upper and lower limbs. Gait was impaired and tendon reflexes were depressed. Electrophysiological studies demonstrated moderate slowing of motor conduction velocity and absent sensory potentials. Microscopic studies of the sural nerves revealed a loss of myelinated fibers of all diameters but particularly those of large diameter. On teased fibre examination, the predominant abnormality was axonal degeneration and electron microscopy showed degenerating fibres, prominent cluster formations, abnormalities of mitochondria and prominent glycogen deposits within Schwann cells. Quantitative study of unmyelinated fibres indicated a relative increase in fibres of small diameter. It is concluded that the polyneuropathy associated with hypothyroidism is due largely to axonal degeneration.
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PMID:Hypothyroid polyneuropathy. Clinical, electrophysiological and nerve biopsy findings in two cases. 706 43

The authors report a case of Charcot-Marie-Tooth disease that mimicked Friedreich's ataxia and featured impaired tendon reflexes in the limbs, incoordination mimicking cerebellar disease in the extremities, extensor plantar responses on both sides, bilateral foot deformity, imparied position sense in the toes, absent vibratory sense in the distal parts of the legs and minimal distal weakness with wasting. Motor conduction velocity in the upper limbs was substantially reduced. Other cases similar in nature reported in the literature resemble spino-cerebellar degeneration in general, and Friedreich's ataxia, in particular. It is emphasized that the natural history, EMG, motor conduction velocity studies and examination of other affected members of the family permit the correct diagnosis to be made in such cases. It is also emphasized that patients similar to the one reported here may also resemble, and should be differentiated from, cases of familial dorsal column ataxia (Biemond type). Stress is put upon the fact that when Charcot-Marie-Tooth disease mimicks spino-cerebellar degeneration, substantial slowing of motor conduction in the upper limbs is generally sufficient to establish the diagnosis. The relation between Friedreich's ataxia an Charcot-Marie-Tooth disease is reviewed and it is concluded that these two disorders are distinct clinical and pathological entities.
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PMID:A case of Charcot-Marie-Tooth disease mimicking Friedreich's ataxia: is there any association between friedreich's ataxia and Charcot-Marie-Tooth disease? 710 97


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