Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A questionnaire study on sexual problems occurring with multiple sclerosis (MS) was carried out with 217 patients who had previously participated in the University of Washington Multiple Sclerosis Project. More than one-half of the participating subjects were ambulatory without aids and nearly 75% did not use a wheelchair. Sexual dysfunction was reported by 56% of the women and 75% of the men. Among the women, the most commonly occurring sexual symptoms (in decreasing order of frequency) were fatigue, decreased sensation, decreased libido, decreased frequency or loss of orgasm and difficulty with arousal. Men reported the most common problem was erectile dysfunction, followed by decreased sensation, fatigue, decreased libido, and orgasmic dysfunction. Although loss of mobility, weakness and depression are not significantly associated with sexual dysfunction, spasticity and bladder dysfunction appear to be associated. However, even where these symptoms were absent, sexual dysfunction was perceived in at least 50% of the cases. The data indicate that sexual dysfunction can be anticipated in at least 50% of the women and about 75% of the men affected by MS, regardless of mobility level. It is most likely to occur in patients with spasticity and bladder dysfunction.
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PMID:Sexual dysfunction in multiple sclerosis. 670 86

The authors reviewed the clinical findings, radiological evaluation, and operative therapy of 39 patients with syringomyelia. Syringoperitoneal (SP) shunting was used in 15 patients and other procedures were used in 24 patients. Follow-up periods ranged from 1 1/2 to 12 years. During the period of this study, metrizamide myelography in conjunction with early and delayed computerized tomography scanning replaced all other diagnostic procedures in patients with syringomyelia. Preoperative accuracy for the two procedures was 87%. The most common symptoms were weakness (79%), sensory loss (67%), pain (38%), and leg stiffness (28%). Surgery was most effective in stabilizing or alleviating pain (100%), sensory loss (81%), and weakness (74%); spasticity, headache, and bowel or bladder dysfunction were less likely to be reversed. Approximately 80% of patients with idiopathic and posttraumatic syringomyelia and 70% of those with arachnoiditis improved or stabilized. Better results were obtained in patients with less severe neurological deficits, suggesting the need for early operative intervention. A higher percentage of patients had neurological improvement with SP shunting than with any other procedure, especially when SP shunting was the first operation performed. Patients treated with SP shunts also had the highest complication rate, most often shunt malfunction. These results indicate that SP shunting is effective in reversing or arresting neurological deterioration in patients with syringomyelia.
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PMID:Surgical treatment of syringomyelia. Favorable results with syringoperitoneal shunting. 674 90

A double-blind trial with two parallel groups was carried out to compare the antispastic effect and tolerability of a new muscle relaxant, tizanidine (DS 103-282), with those of baclofen in the treatment of spasticity due to multiple sclerosis. Twenty-one hospitalized patients with stable spasticity participated in the 6-week trial. Eleven received tizanidine and 10 baclofen in gradually increasing daily doses. The optimal daily dose of tizanidine was between 8 and 36 mg and that of baclofen between 10 and 80 mg. Overall spastic state, spasms and clonus were similarly improved with both medications. In contrast, muscle strength, bladder function and the activities of daily living were more improved on tizanidine than on baclofen. Tiredness was the most frequent side-effect on tizanidine and muscle weakness on baclofen. The laboratory tests did not show any pathological changes with either medication. According to these results, tizanidine provides a new therapeutic alternative in the treatment of spasticity.
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PMID:A double-blind comparative trial of new muscle relaxant, tizanidine (DS 103-282), and baclofen in the treatment of chronic spasticity in multiple sclerosis. 701 49

A 12-year-old girl had chronic nonspherocytic hemolytic anemia due to triosephosphate isomerase deficiency. Developmental and motor delay and muscular weakness were followed by cerebellar dysfunction and finally spasticity with hyperreflexia. Abnormal histopathological findings were hyaline cell bodies and axonal "spheroids" in the hypothalamus and cerebellar cortex, severe neuronal loss in the dentate and olivary nuclei, and partial loss of cerebellar Purkinje's and granular layer cells (olivocerebellar atrophy).
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PMID:Triosephosphate isomerase deficiency. A case report with neuropathological findings. 711 3

In 25 patients with spasticity, pharmacokinetics and effects of dantrolene sodium were investigated after prolonged administration. A beneficial effect occurred in seven patients. The results were better on 100 mg daily than on a higher daily dose. An increase of the daily dose from 200 to 400 mg was not associated with higher blood levels. Many side effects were noted such as: anorexia, nausea, drowsiness, depression and muscle weakness. From this study we conclude that dantrolene sodium is a muscle relaxant with a weak to moderate effect in patients with spasticity; the effect at doses higher than 200 mg daily is probably poor.
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PMID:The effect of dantrolene sodium in relation to blood levels in spastic patients after prolonged administration. 724 Nov 61

In 22 families with the "pure" form of hereditary spastic paraplegia inheritance was autosomal dominant in 19 and autosomal recessive in three. Examination of intrafamilial correlation of age of onset in the dominant cases suggested that the disorder is genetically heterogeneous. Two forms of dominant hereditary spastic paraplegia were identified: one with an age of onset mostly below 35 years (type I), and the other onset usually over 35 years (type II). In the type I cases, delay in walking was not infrequent and spasticity of the lower limbs was more marked than weakness. The disorder was very slowly progressive and was extremely variable in terms of severity. Sixteen per cent of the patients aged over 20 years were asymptomatic but clinically affected. In the type II group muscle weakness, urinary symptoms and sensory loss were more marked. This form of the disease evolved more rapidly. In the three families demonstrating autosomal recessive inheritance the clinical features were very similar to those of the dominant cases. Biological fitness of patients from both the dominant groups was not impaired and no definite evidence of new mutation was observed. A cumulative frequency curve of age of onset in the type I group was constructed with suggested that an asymptomatic child of an affected parent has a 20% chance of developing the disease at the age of 25 years; the risk is probably even less if the child is clinically normal.
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PMID:Hereditary "pure" spastic paraplegia: a clinical and genetic study of 22 families. 731 Apr 5

In two groups of patients posterior tibial nerve (PTN) and sural nerve (SN) somatosensory evoked potentials (SEPs) were compared to each other and related to classified neurological signs. Group A consisted of 7 patients with hereditary spastic paraparesis (HSP) and 8 with primary lateral sclerosis (PLS), with solely or primarily motor deficits. Group B consisted of 12 patients with different spinal cord diseases causing variable mixed sensory and motor impairments. Normal values were derived from 39 controls. A clear trend towards more frequently prolonged PTN SEP than SN SEP latencies was found in both groups and appears to make PTN SEPs more useful for clinical application than SN SEPs. No significant differences were found in SEP abnormalities when the two patient groups were compared to each other. No relationships were found between SEP abnormalities and spasticity, weakness or any single sensory modality, making the two SEPs questionable as a quantitative test for neurological deficits in our patients.
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PMID:Posterior tibial and sural nerve somatosensory evoked potentials: a study in spastic paraparesis and spinal cord lesions. 750 31

Sixteen patients with lathyrism, age ranging between 18 and 55 years and duration of illness between 2 and 25 years, underwent H reflex studies with the aim of studying motor neurone excitability. The patients had marked spasticity (Ashworth score ranging between 2 and 5) and mild to moderate leg weakness. Knee and ankle reflexes were exaggerated in all and the plantar response was extensor in 14 patients. The H reflex abnormalities included increased HM ratio indicating increased motoneurone excitability, significant lack of vibratory inhibition indicating altered transmission in the premotoneuronal portion of the H reflex pathway, and lack of reciprocal inhibition (P < 0.01). These H reflex abnormalities were not related to spasticity, weakness, clonus or plantar response. The H reflex recovery curve in 6 patients revealed increased excitability throughout the recovery curve. The secondary facilitation started and peaked slightly earlier than normal, and the late depression was not marked indicating change in excitability of motoneurones or of interneurones.
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PMID:H reflex studies in neurolathyrism. 752 Dec 88

Over recent years botulinum toxin type A has emerged as a safe and effective treatment for a number of previously refractory conditions associated with excessive muscle activity. The list of indications is expanding, but at present it is generally considered to be the treatment of choice for focal dystonias such as blepharospasm, torticollis, laryngeal dystonia, and oromandibular dystonia, as well as hemifacial spasm, strabismus, and some forms of limb spasticity. Carefully targeted intramuscular injections of a small amount of the toxin block the release of acetylcholine at the neuromuscular junction, producing a chemical denervation, with the aim of reducing excessive muscle activity without producing significant functional weakness. In some situations electrophysiological assessment and localisation of the muscles for injection is necessary. Treatment is symptomatic, with effects lasting 3 to 4 months and most patients requiring up to 4 injections per year to maintain the beneficial effect. Appropriate use of the toxin requires both an understanding of the physiological action of the potential muscles involved in each situation, together with a knowledge of the likely dose necessary to reduce muscle activity to the required level. Botulinum toxin represents a major advance in the management of these conditions, many of which responded poorly to previously available forms of therapy.
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PMID:Botulinum toxin in clinical practice. 753 96

We administered local botulinum toxin injections on the leg adductors of 12 patients with spastic paraparesis (9 patients with HAM, 2 patients with spinal spastic paraparesis, 1 patient with an identified degenerative disease). Two of them were wheelchair-bound and the other patients could walk with or without help. The patients were assessed by the time to walk 10 m and the spasticity score which was derived from the degree of muscle tone and spasm frequency of leg adductors. After the initial injection, 7 of the 12 patients improved spasticity scores and 8 of the 10 patients could walk 10 m within a shorter time. The time to walk 10 m was markedly shortened in moderate cases. However, one patient complained of leg weakness and the time to walk 10 m was prolonged. Five of the 12 patients received injections 3 to 7 times, and were followed up for a mean of 16.2 months. In 4 of the 5 patients, repeated injections could maintain the improvement of spasticity score and time to walk 10 m. However, injection was discontinued in one patient because of leg weakness. The other side effects were pain and swelling at the injected site and dysarthria. However, these side effects were slight and transient and did not require treatment. No other systemic side effects were observed. In conclusion, the beneficial effects of botulinum injections to spastic paraparesis were (1) improvement of objective symptoms in mild cases, (2) improvement of ADL in moderate cases, and (3) improvement of objective symptoms and ease of nursing care in severe cases. Furthermore, we confirmed the long-term efficacy and safety of botulinum toxin.
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PMID:[Treatment of spastic paraparesis with botulinum toxin with reference to beneficial effects, disease severity and long-term treatment]. 761 46


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