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)

We randomly selected 26 patients with essential blepharospasm to receive either botulinum toxin or saline injection in their lower eyelids to evaluate the necessity of lower eyelid injection to relieve blepharospasm. As diplopia may occur from botulinum toxin injections for blepharospasm, most commonly from injection of the lower eyelid, and surgical relief of blepharospasm is often achieved by excision of only the upper eyelid protractors, omission of toxin from the lower eyelid seemed both desirable and possible. All patients received botulinum toxin in the upper eyelids, above the eyebrows, across the glabella, and near the lateral canthus. Thirteen of 15 patients who received saline in their lower eyelids had relief of spasm, with the same spasm-free interval as those who received toxin. We recommend avoiding injection of toxin in the medial two thirds of the lower eyelid in order to diminish the likelihood of diplopia from inferior oblique muscle paresis.
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PMID:The effect of omitting botulinum toxin from the lower eyelid in blepharospasm treatment. 339 68

The authors present their first results with the treatment of hemifacial spasm by controlled percutaneous thermocoagulation of the facial nerve. Seven patients have been treated to date with good immediate results on the movements, although a slight paresis of the homolateral facial musculature, aesthetically acceptable, persists after treatment. A long-term follow-up at more than 10 months was achieved in only 3 patients, who showed a complete regression of the spasm with partial disappearance of the facial hemiparesis.
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PMID:The treatment of hemifacial spasm with percutaneous radiofrequency thermocoagulation of the facial nerve. 347 76

Forty-eight patients were given serial injections of botulinum toxin in their eyelids for treatment of eyelid spasm during a two-year interval. Ninety-four percent obtained relief of spasm from botulinum toxin injection. The duration of the spasm-free interval as well as the incidence of ptosis and of diplopia was dose dependent. The marked increase in the incidence of these side effects with only a small increase in the duration of the spasm-free interval, when a dose of 25 units per lid was used, leads the authors to conclude that this dose is too high and should not be used. Since diplopia was most commonly caused by paresis of the inferior oblique muscle, and since blepharospasm usually can be controlled by excising the upper lid protractors, further studies are required to determine whether lower lid injection is necessary and, if it is found to be so, whether injecting only the lateral portion of the lid would be adequate.
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PMID:Treatment of facial spasm with botulinum toxin. An interim report. 376 37

Twenty-six patients with essential blepharospasm were treated with botulinum toxin by injection. The onset of protractor weakness in all patients ranged from one to five days following treatment. Maximal weakness developed within 12 days. There was a variable and gradual return of protractor strength over eight to 29 weeks in most patients and, with it, a return of spasm. Twenty-five patients received some degree of functional relief following initial injection. In most patients, however, the post-injection result could not be stabilized and repeat injections have been necessary to control recurrent spasms. There was one treatment failure. Three patients treated by injection following previous neurectomy and myectomy appeared to have a reduced requirement for subsequent injections. Complications included transient ptosis in six patients and mild exposure symptoms in four patients. Extraocular muscle paresis did not occur. There were no systemic side effects from the botulinum toxin injections.
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PMID:Botulinum toxin for the treatment of essential blepharospasm. 380 85

Irrigation of the subarachnoid space after aneurysmal subarachnoid hemorrhage (SAH) has been reported to alleviate subsequent arterial vasospasm. The authors have investigated the effect of lavage of the cerebrospinal fluid (CSF) space in the two-hemorrhage canine model of vasospasm. Twelve dogs had basilar cistern lavage with 120 cc of artificial CSF 24 hours after each of two SAH's, and 12 control dogs had two sequential SAH's without intervening lavage of clot. The amount of clot on the ventral brain stem was evaluated at sacrifice and was graded from 0 (no clot) to 4 (maximum clot) to assess the adequacy of clot removal. Dogs that had undergone lavage had a median grade of 1 (range Grade 0 to 2); control dogs had a median grade of 2 (range Grade 1 to 3.5, p less than 0.001. Wilcoxon rank sum test), indicating significant reduction of gross clot by lavage. The neurological findings were graded from 0 to 5, based on meningismus, ataxia, paresis, and cranial nerve deficits. No significant differences in neurological grade were found on any day between the two groups. Satisfactory angiograms were obtained before and 7 days after hemorrhage and were controlled for blood pressure and blood gases; these showed significant spasm in both groups. There was a mean reduction (+/- standard deviation) of 21.6% +/- 16.2% in basilar artery diameter in control dogs, compared to a 28.8% +/- 15.1% reduction in dogs with lavage (difference not significant, t-test). There was a strong, but insignificant, trend toward reduction of endothelial desquamation in the basilar and middle cerebral arteries in dogs with lavage compared to control animals (p = 0.06). Corrugation and tearing of the elastica, thickened intima, intimal fibroplasia, vacuolization of the endothelial or smooth-muscle cells, and presence of blood cells in the adventitia occurred similarly in both groups. It appears that cisternal lavage 24 hours after hemorrhage in this model has no effect on the angiographic, neurological, or most morphological sequelae of SAH, in spite of evidence for removal of clot as seen at sacrifice. Any postulated interaction of clot and vessel resulting in chronic vasospasm must occur before this time. Evaluation of the effect of much earlier lavage (for instance, 1 hour after hemorrhage) may elucidate the point at which vasospasm is instigated after SAH, and help in determining what factors cause vasospasm.
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PMID:Delayed CSF lavage for arteriographic and morphological vasospasm after experimental SAH. 405 8

Microvascular decompression has been widely used as a method for the treatment of hemifacial spasm and trigeminal neuralgia. We have experienced 30 such cases in the last 2 years; 25 of them were hemifacial spasm and 5 trigeminal neuralgia. Excellent results were obtained in 26 cases; the remaining two cases, both hemifacial spasm, were partially cured. Mild facial paresis appeared several days after the operation in 3 patients. In all the cases, the facial paresis recovered completely within several weeks. The cause of the facial paresis was not known. In 2 cases a slight hearing deficits were noticed after surgery, which has been gradually improving over several months. As this operation is functional surgery, operative complications must be avoided as much as possible. It has been our policy that we first try medical treatment and/or some kinds of nerve block and if no effects are obtained, we recommend the microvascular decompression. For microvascular decompression, suboccipital craniectomy is performed in lateral position. From the point of view of surgical technique, we stress several important points as follows: The head is elevated about 30 degrees, and it is kept approximately horizontal and should not be excessively rotated. Craniectomy is made as far laterally as the sigmoid sinus; its shape is elongated oval. Retraction of the cerebellum should not be done in the direction of the cranial nerves to avoid post-operative hearing deficit. Two tapered retractors are effectively used for cerebellar retraction. A third slim, tapered retractor is useful for holding an offending artery when exploring the root exit zone or placing a sponge for decompression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Posterior fossa microvascular decompression for hemifacial spasm and trigeminal neuralgia--some improvements on operative devices and technique]. 408 51

Recent reports indicate that malformations of arteries and veins in the posterior fossa are a common cause of facial spasm and trigeminal neuralgia. More rarely they may also cause facial nerve paresis and hearing loss. When vascular malformations are present, brainstem auditory evoked potentials (BAEPs) sometimes show abnormalities similar to those usually recorded in patients with tumours in the cerebellopontine angle. In three patients with facial spasm, one with trigeminal neuralgia and one with facial paresis pathologically delayed absolute latencies and/or interpeak latencies of BAEPs associated with vascular malformations were found. It is concluded that those BAEP abnormalities associated with tumours in the posterior fossa may also be caused by vascular malformations. BAEPs are valuable aids to the diagnosis of such malformations.
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PMID:Brainstem auditory evoked potential abnormalities in vascular malformations of the posterior fossa. 619 26

Methylaplysinopsin is a novel marine natural product that, after oral administration, prevented the effects of tetrabenazine in mice and rats. Methylaplysinopsin was a short-acting inhibitor of monoamine oxidase activity with greatest potency when serotonin was the substrate studied. The brain concentration of serotonin in the mouse was increased by methylaplysinopsin over the same time course as monoamine oxidase inhibition ex vivo. Methylaplysinopsin was also a weak inhibitor of the neuronal uptake of [3H]serotonin and a potentiator of the K+-induced release of [3H]serotonin from prelabeled synaptosomes. The predicted potentiation of serotonergic neurotransmission was supported by initial neurophysiological studies in an identified serotonergic pathway in the central nervous system of Aplysia. Two other studies on the pharmacology of marine natural products are reviewed. The majority of polyhalogenated monoterpenes isolated from red algae had central nervous system depressant properties. The exception is plocamadiene A, which caused, in mice, a reversible spastic paresis lasting up to 72 hours after oral administration. The severe muscle spasm was antagonized by diazepam. The final study discussed is the effect of a variety of marine natural products on the synthesis, neuronal uptake, and metabolism of GABA. Their selectivity is discussed with regard to the effects on metabolic respiration, and the correlation of neurochemical and neurophysiological effects on these marine substances.
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PMID:Methylaplysinopsin and other marine natural products affecting neurotransmission. 625 14

On the basis of histological and histochemical examinations of 100 postmortem observations of bacterial shock, 4 stages of disorders in the microcirculatory bed and in cell elements of organs in this complication are distinguished. The hemodynamic stage consists in redistribution of the blood flow, alternation of spasm and paresis, and vascular dystonia. In the stage of hemorheological disorders congestion is substituted by stasis, sludging of erythrocytes due to pachyemia. As a result of increased permeability of vessel walls, interstitial edema and early changes of parenchymatous cells of organs occur at the enzymatic level. The addition of DIBC syndrome leads to deeper ischemia of organs and formation of necroses, hemorrhages, acute ulcers. As a consequence, organ insufficiency (adrenal, renal, respiratory) develops.
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PMID:[Organ pathology of bacterial shock]. 667 Sep 42

Nine patients with radiological changes due to Strongyloides stercoralis (SS) are described. A wide variation in appearance exists ranging from mild edema of the duodenal and small bowel mucosa to grossly enlarged, prominent valvulae conniventes. Small bowel dilatation is significant, and in overwhelming infestation toxic dilatation with paresis results. Spasm, ulceration, and stricture are encountered in addition. The appearances usually improve and reverse with treatment. Ampullary involvement is responsible for reflux of barium into the pancreatic duct and biliary tree through a patulous sphincter. In 1 patient the colonic changes resembled ulcerative colitis.
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PMID:Radiological manifestations of Strongyloides stercoralis. 683 35


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