Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The maximum force of voluntary muscle contraction was registered under isometric conditions in nine patients with recessive myotonia congenita. The recordings were made on the upper arm. Five patients with severe myotonia had a transient weakness after muscle rest. Electromyographic registrations with wire electrodes showed that the myotonic muscle fiber discharges disappeared during the transient weakness. Medication improving myotonic stiffness also improved the weakness. The cause of transient weakness seems to be similar to that of myotonic stiffness. It is known that an increasing depolarization of the myotonic muscle fiber membrane leads to the myotonic discharges and myotonic stiffness. In severe myotonia the progressing depolarization could cause a loss of excitability of the muscle fiber membrane and thereby a transient paresis of a more or less large number of muscle fibers.
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PMID:Transient muscular weakness in severe recessive myotonia congenita. Improvement of isometric muscle force by drugs relieving myotomic stiffness. 8 Dec 74

Four patients without symptoms of episodic hyperkalemic weakness from two families with paramyotonia congenita (Eulenburg) are described. 1. Maximum voluntary muscle contraction of the upper and lower arm was studied under isometric conditions at different temperatures. If the temperature was lowered stepwise, distinct paresis occured at 32--31 degrees C which increased with the amount of muscular effort. The upper arm muscles, however, developed weakness gradually after cooling. 2. During cooling of the resting muscle, the EMG showed dense spontaneous activity of the fibrillary type, which decreased again at about 30 degrees C. It can be assumed that in paramyotonia congenita cooling produces muscle cell membrane depolarization which at a critical level causes the firing of action potentials and finally muscular paresis. 3. Increasing muscular stiffness can be interpreted as abnormally slow muscular relaxation after isometric contraction. In the forearm muscles the time to 3/4 relaxation after cooling was about six times normal, in the upper arm muscles only two times normal. As an additional parameter the mechanical resistance to passive stretching of a muscle has been studied. This passive muscular tension increased simultaneously with the onset of weakness. 4. The close relation between weakness and stiffness suggest that both symptoms are caused by the same basic defect which is probably located in the sarcolemma. It is suggested that a defect of the sodium channel causes a cooling-dependent increase in sodium conductance. Raised intracellular sodium causes in the first place membrane depolarization, and in the second place depression of calcium reuptake through competition by sodium for calcium binding sites. This would explain muscle stiffness and delayed relaxation as well.
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PMID:Influence of temperature on isometric contraction and passive muscular tension in paramyotonia congenita (Eulenburg). 9 68

Abducens nerve paresis may be of nuclear, of peripheral distal neurogenic origine, or is simulated by a myogenic weakness of abduction. Polygraphic emg analysis of the oculoauricularphenomenon (oap) permits a differentiation. In the emg, the oap proved to be a physiologic and constant automatic and always bilateral interaction between the hemolateral abducens nerve and both Nn. faciales with corresponding and obligatory coinnervation of the Mm. retroauricularis of the external ear. In case of medullary, nuclear or internuclear lesions, the oap is disturbed, instable, diminished or abolished, whereas in distal neurogenic or myogenic paresis, even in complete paralysis the oap is bilaterally well preserved.
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PMID:[Electromyographic differential diagnosis in cases of abducens nerve paresis with nuclear or distal neurogenic sive myogenic origine (author's transl)]. 11 67

The effects of dantrolene sodium, an anti-spasticity drug with a site of action within the muscle fibres, were studied in 19 patients with spastic paresis. Oral doses were successively increased from 100 mg/day to a maximal tolerated level or up to 800 mg/day. Trial periods were 8-13 weeks. The responses of stretch reflexes to local cooling over the spastic muscles were used to differentiate alpha and gamma spasticity. In the knee extensor and flexor muscle groups, cryo-negative alpha-spasticity was seen in 25 and cryo-positive gamma-spasticity in 4 muscle groups. Ankle clonus was cryo-positive in 14 of 15 cases. Resistance to passive knee joint movements, ankle clonus and isometric or isokinetic muscle strength was determined quantitatively. The gait was recorded by intermittent-light photography and the muscle activation patterns in gait were studied in recordings of the average EMG from limb muscles. Functional disability and spasms were assessed from clinical examinations and interviews. Passive resistance at slow (6%/sec) and fast (30 degrees/sec) knee joint movements decreased by 32% in the extensor muscles (p = 0.005 resp. 0.001) and by 23-26% in the flexor muscles (not significant). Reduced passive resistance was observed in 16 of the muscles with alpha-spasticity and in all 4 of the muscle groups with gamma-spasticity. Clonus was diminished or abolished in 14 of 15 patients with this sign. Maximal isometric or isokinetic muscle strength was unaltered in the majority of the patients. In a few the strength was increased, in some it was decreased. The averaged EMG activity during walking as studied in 10 patients were increased in 35 of the 57 muscle groups examined. In some muscle groups, exaggerated activity attributable to spastic reflexes was reduced. Motor disability was decreased significantly in 10 patients. It was not significantly changed in 5 and deteriorated in 4 patients. Drowsiness and subjective muscle weakness were the most frequent side-effects. SGOT and SGPT were increased in 3 cases.
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PMID:Action of dantrolene sodium in spasticity with low dependence on fusimotor drive. 13 20

In the differential diagnosis of intermittent claudication some rare myopathies have to be considered. The most frequent is phosphorylase deficiency (McArdle's disease). Exercise-induced muscular pain, weakness, contractures and occasionally myoglobinuria are the most prominent clinical signs. Serum creatine phosphokinase, aldolase and lactic dehydrogenase may be elevated after exertion. In the ischemic forearm test there is no rise of serum lactic acid. The enzyme deficiency can be demonstrated by histochemical and biochemical examination of a muscle specimen. Further, but more infrequent, enzymatic disturbances of glycolysis are phosphofructokinase deficiency and phosphohexoisomerase inhibitor, which also yield an abnormal ischemic forearm test and must be demonstrated histochemically and biochemically. Apart from muscular signs, myopathy with lactic acidosis is associated with palpitation, dyspnea and exhaustion, and a disproportionate rise in serum lactic acid level after exertion. Histochemically and electronmicroscopically demonstrable fat accumulation in the muscle can be a sign of a disturbance in lipid metabolism. This type of exercise-induced myopathy has been reported only in a few cases with carnitine-pylmityltransferase deficiency, which has to be demonstrated biochemically. Muscular contractures also exercise-induced but painless and reversible within seconds may be due to deficient uptake of sarcoplasmic calcium in the tubular system. Dyskalemic paralysis causes painless paresis within minutes of hours after exertion, which disappears within hours to a few days. Myopathy with tubular aggregates can be differentiated from other exercise-induced myopathies by morphology. Myotonia combined with painful contractures characterizes myopathia myotonica.
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PMID:[Exercise-induced muscular weakness, myalgia and contractures. I. A clinical review]. 13 80

The risk of facial nerve paresis after parotidectomy is thought to be within acceptable limits, although it is difficult to find published data regarding the specific magnitude of this risk. This study reviews the subject and reports postoperative facial function in 100 consecutive patients who had parotidectomies at the Henry Ford Hospital during a 9-year period. Permanent weakness of a major branch was identified in 2 of 77 patients having lateral lobectomy for parotid disease. Both patients demonstrated marginal mandibular paresis after surgery for adenolymphoma. No weakness was noted in 16 patients undergoing total parotidectomy. No unanticipated nerve disability was noted in 4 patients having partial nerve sacrifice in extended procedures; 3 patients had complete sacrifice of the nerve.
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PMID:Facial nerve function in 100 consecutive parotidectomies. 22 63

Reciprocal reflex connections were studied in capsular hemiplegia and spastic paresis with spinal cord lesions, using Lloyd's technique. Effects of conditioning stimulation of the tibial or peroneal nerve on the H reflex in the antagonists were examined. Stimulus intensity was controlled with reference to the threshold of the M wave. Weaker stimulation than this threshold was regarded as stimulation of group I afferents. It aroused no subjection sensation in intact subjects. Early and strong inhibition, comparable to Ia inhibition in the cat (Lloyd 1946), was observed from weak stimulation of the tibial nerve on the pre-tibial (flexor) H reflex, but not from the peroneal nerve on the triceps surae (extensor) H reflex in capsular hemiplegia. Alcohol block of extensor motor points resulted in reduction of spasticity without further paralysis in the blocked muscle and a remarkable increase in strength of the antagonist pre-tibial muscles. These results suggest that an extensor spasticity withe flexor weakness, which is common in capsular hemiplegia, may be due to an imbalance of reflex activities via Ia muscle afferents, and that a part of flexor weakness can be restored by "disinhibition' by reduction of Ia inflow from extensor muscles. Ia inhibition was also observed in one third of cases with spinal cord lesions at rest. It returned to normal after recovery from spastic paresis by radical therapy in some cases.
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PMID:Reciprocal Ia inhibition in spastic paralysis in man. 28 52

In the course of multiple episodes of thiamine deficiency in the rhesus monkey, the triad of anorexia, apathy, and hind limb weakness is the earliest clinical manifestation. In later episodes, nystagmus, abducens paresis, midline ataxia, dysmetria, and congestive heart failure are also seen. With the exception of dysmetria, the neurologic signs promptly respond to thiamine administration. Pair-fed controls showed no clinical signs. Neither peripheral neuropathy nor edema was observed. Thiamine-deficiency in the experimental animals was confirmed by blood transketolase assays.
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PMID:Clinical manifestations of chronic thiamine deficiency in rhesus monkey. 40 80

Ten football players seen from 1973 through 1977 at the University of Wisconsin Hospitals were found to have clinical and electrodiagnostic evidence of injury to the upper trunk of the brachial plexus. Each had upper limb paresis following one or more blows to the head or shoulders. The development of persistent weakness often was preceded by burning paresthesias in the upper limb. Our experience suggests that the syndrome of burning paresthesias and subsequent arm weakness frequently is secondary to stretching of the brachial plexus.
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PMID:Upper trunk brachial plexopathy in football players. 43 Jun 86

Of 15 patients with monocular limitation of elevation, six had no deviation in primary gaze while the remaining nine had hypotropia of the involved eye. Twelve of 15 patients had restriction to upgaze on forced duction testing. Eleven of these 12 had normal upward saccadic velocity, which suggested normal elevator function. Four patients had reduced saccadic velocity, which indicated true elevator weakness. Superior rectus muscle paresis alone could account for limited elevation and would reduce upward saccadic speed. Patients with a diagnosis of "double elevator palsy" only infrequently (about one quarter of cases) have palsy of an elevator muscle and may have only a single elevator palsy. The identification of a true elevator weakness is most important in planning management.
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PMID:Double elevator palsy. 44 25


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