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)

Twenty-five children with acquired and congenital subglottic stenosis (SGS) were managed with the anterior cricoid split (ACS) operation at the authors' institution from September 1987 to January 1990. Ages ranged from 2.5 months to 5.5 years. Twenty-one (84%) of the children were extubated after 5 to 14 days of nasotracheal intubation and have remained stable after an average follow-up of 10 months. Atelectasis was a common postoperative problem, encountered in 12 (48%) of the patients. Other complications included a tracheocutaneous fistula, prolapse of soft tissue into the tracheal lumen via the cricoid incision, a subglottic granuloma, and 2 cases of prolonged lower extremity paresis following reversal of vecuronium. The results of this retrospective study indicate that the ACS is a valuable first-line procedure for the management of SGS in a variety of pediatric patients.
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PMID:Anterior cricoid split for subglottic stenosis: experience at the Children's Hospital of New Jersey. 151 65

A collection of symptoms and signs indistinguishable from ocular myasthenia can be caused by an intracranial mass. We illustrate this condition with the case of an adolescent girl with neurofibromatosis type 1 and a dorsal midbrain astrocytoma. At presentation, she had fatigable ptosis, upgaze paresis, and a positive "lid twitch" sign. Radiation therapy resulted in marked reduction of her signs, confirming that the muscle fatigue was central in origin. We discuss the possible mechanisms of this central fatigability.
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PMID:Midbrain myasthenia: fatigable ptosis, 'lid twitch' sign, and ophthalmoparesis from a dorsal midbrain glioma. 156 51

The topographic arrangement of the fascicular portion of the oculomotor nerve in the midbrain is not known. A patient with infarction involving the lateral portion of the fascicle had isolated monocular elevation paresis and ptosis, suggesting that the fibers destined to the elevators of the eye and eyelid course laterally in the fascicle.
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PMID:Monocular elevation weakness and ptosis: an oculomotor fascicular syndrome? 153 5

The entity of generalized livedo racemose and cerebrovascular bleeding disorders was introduced in 1965 by I. B. Sneddon describing 5 cases. it is not clear what role oral contraceptives and smoking play in the etiology of this syndrome. The case of a 44-year old multipara is described who had taken pills up to 1980 and smoked 5-10 cigarettes a day. In 1980 just before age 35 she suffered an apoplectic insult with hemisyndrome on the left side that she recovered from. An acute hypoglossal, and trigeminal paresis appeared on the left side. Computer tomogram showed a hypodense field in the area of both hemispheres of the brain. An audible mesosystolic click led to the diagnosis of suspecting cerebral embolism with mitral valve prolapse. Therapy was started with thrombocyte aggregation inhibitors. Although the prolapse could not be showed by echocardiography, the frontal mitral valve was slightly thickened. Another hospitalization in 1985 owing to a recurring attack of vertigo revealed higher blood pressure. She received betablocker treatment. In 1987 sudden weakness in the left arm and speech disorders ensued, and skin color alterations were manifest characteristic of generalized racemose livedo. Skin necrosis appeared on both toes. Sneddon syndrome was diagnosed, and full anticoagulation therapy was started with cumarin. The sensomotoric and speech symptoms receded only slightly. In 1988 a light cerebral insult occurred with the deterioration of the speech disorder. Laboratory finding showed immunoglobulin G (IgG) anticardiolipin antibodies (ACA) with 255 U/ml (normal range 0-10 U/ml), and normal IgM anticardiolipin antibodies with 8 U.ml (range of 0-10 U.ml). ACA has been detected in patients with lupus erythematosus and racemose livedo indicating the possible association of Sneddon syndrome with systemic lupus erythematosus.
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PMID:[Sneddon syndrome]. 187 23

Lesions of the oculomotor fascicles are localized clinically by associated neurologic deficits. We present two patients with bilateral ptosis, unilateral paresis of all other muscles innervated by the oculomotor nerve, and sparing of the contralateral superior rectus muscle--findings suggesting a lesion of the proximal oculomotor fascicles and the central caudal subnucleus. To our knowledge, these are the first such cases with radiologic confirmation of a lesion within the dorsal, paramedian midbrain.
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PMID:Unilateral oculomotor palsy and bilateral ptosis from paramedian midbrain infarction. 195 23

Oculomotor palsy secondary to a berry aneurysm is usually present with pupillary dilatation, followed by other signs of third cranial nerve dysfunction, including oculomotor paresis and ptosis. Partial paralysis of the nerve with pupil sparing has been observed, but ptosis as the sole sign of oculomotor paralysis has not previously been reported until now.
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PMID:Ptosis as the sole manifestation of compression of the oculomotor nerve by an aneurysm of the posterior communicating artery. 213 53

A 13-year-old boy, with no past medical history, was admitted after a car accident on October 29, 1989. On admission, he was alert. Physical examination revealed a bruise on the left frontal region, a fracture of right clavicula and right hemopneumothorax. He was treated with respirator due to dyspnea. On November 1, 1989, he was removed from respirator and expressed diplopia. Neurological examination showed bilateral ptosis, mild anisocoria, normal light reflex and horizontal gaze nystagmus in lateral gaze. Both eyes were deviated outward slightly in the primary position and showed inability to converge. The external ocular movements of both eyes were mildly limited in elevation and adduction. Ataxia was observed in bilateral upper extremities. Deep reflexes were normal and no pathological reflexes were observed. Brain CT scans showed no abnormality. On November 6, 1989, his ptosis and diplopia improved. On November 8, he was completely recovered. A magnetic resonance imaging on November 10 revealed no abnormality. We suggested that transient dysfunction of midbrain associated with head injury might cause transient bilateral primary oculomotor nerve paresis, nystagmus and ataxia.
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PMID:[A case of transient bilateral primary oculomotor nerve paresis associated with head injury]. 224 37

Botulinum toxin, a powerful pre-synaptic neurotoxin produced by Clostridium botulinum, interferes with the release of acetylcholine from nerve terminals. Since September 1985, we have been using this toxin to treat altogether 62 patients with benign facial spasms. Most of the patients had been on drugs or psychotherapy, 2 had received alcohol injections, 2 had undergone surgery of the orbicular branch, and 2 electrocoagulation of the facial nerve. In essential blepharospasm the duration of the beneficial effect after each treatment with botulinum toxin was about 3 1/2 months. In patients with hemifacial spasm the response was clearly longer, nearly 5 months in most cases. The treatment gave the best and longest-lasting relief of symptoms in patients suffering from disturbing myokymia. Response was poorest in patients suffering from facial spasms who simultaneously had a severe psychiatric disease. The most frequent side effect was mild or moderate ptosis (22.6%). Some patients complained of dry eyes and a few cases displayed facial nerve paresis. Side effects caused by botulinum toxin injections are transient but so also, unfortunately, is the beneficial effect on facial spasms.
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PMID:Long-term treatment of involuntary facial spasms using botulinum toxin. 239 12

Five patients with intracranial aneurysms had unilateral ptosis, limitation of supraduction, and normal pupillary reactivity. The most common aneurysm location for superior division paresis of the oculomotor nerve was the superior cerebellar-posterior cerebral artery junction, where aneurysms (3) of the basilar artery compressed and flattened the interpeduncular oculomotor nerve from below. A superior cerebellar artery aneurysm and brain stem infarction affected the intra-axial course of the oculomotor nerve producing superior division paresis. Only an aneurysm of the intracavernous carotid artery resulted in superior division paresis at the expected anatomic site of bifurcation of the oculomotor nerve into its superior and inferior divisions. Because the superior division supplies innervation exclusively to the superior rectus muscle and levator palpebrae, an aneurysm involving this branch does not affect the pupillo-constrictor fibers. Consequently, cerebral angiography should be considered in the initial evaluation of this ocular motor deficit.
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PMID:Intracranial aneurysms with superior division paresis of the oculomotor nerve. 277 54

Clinical signs in dogs with pseudorabies (Aujeszky's disease) were tabulated from 25 confirmed cases. The duration of disease was short, ranging from 6 to 96 hours. Eight dogs were euthanatized. Of those not euthanatized, 12 (71%) died within 24 hours of onset, 16 (94%) died within 48 hours, and only 1 (6%) lived longer than 48 hours (96 hours) after the onset of clinical signs. All of the dogs had ptyalism, 84% were restless, 84% were anorectic, 76% were atactic, and 64% wandered aimlessly. Sixty-four percent of the dogs had tachypnea, 60% had dyspnea, 56% vocalized, 52% were pruritic, 48% held their necks rigidly, 36% vomited, 36% had muscle spasms, 36% were aggressive, 28% had trismus, and 24% had dysphagia. Five of 25 dogs (20%) had abnormal pupillary light responses. Two of the 25 dogs circled and 2 walked backwards. Each of the following were detected once: blindness, ptosis, facial paresis, excessive lacrimation, head-tilt, head-pressing, signs of abdominal pain, and photophobia. All dogs had been exposed to swine, although in some instances the farmer was unaware pseudorabies existed in the herd or believed it was not in the herd on the basis of negative results on serologic testing.
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PMID:Clinical signs associated with pseudorabies in dogs. 277 5


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