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)

Four patients had a characteristic motor paresis that was dramatically improved by sympathetic block. The cause of this paresis could not be determined by the usual neurological examinations. It was similar to reflex sympathetic dystrophy in that the patients experienced severe pain, swelling, coldness, and muscle atrophy in the affected limbs or other parts of the body in the course of their illness. However, the motor paresis could precede the pain or develop after the pain had disappeared. Even in the absence of pain, the motor paresis was exacerbated by sympathetic stimulation using epinephrine, norepinephrine (nor-adrenalin), or isoproterenol hydrochloride (Proternol) loading and was improved by regional intravenous infusion of reserpine or by sympathetic ganglion block. Loading with pilocarpine, atropine sulfate (Bosmin), and edrophonium chloride (Antirex) did not influence the paresis. This motor paresis is thought to be due to abnormally increased sympathetic tone and may be considered a motor form of reflex sympathetic dystrophy. However, motor paresis closely related to sympathetic dysfunction is quite a new condition that we call "sympathetic motor paresis." This is important clinically because a long-standing effect can be expected from permanent sympathetic ganglion block with dehydrated ethanol.
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PMID:Motor paresis improved by sympathetic block. A motor form of reflex sympathetic dystrophy? 273 Mar 81

Tuberculous osteomyelitis of the temporal bone is a rare and dangerous entity that should be included in the differential diagnoses of infectious processes of the base of skull. A 21-year-old man presented with petrous apicitis, extradural and retromandibular abscesses, and paresis of the facial nerve. Immediate middle fossa craniotomy and drainage of the extradural abscess, in combination with a mastoidectomy, incision and drainage of the facial abscess, and antimicrobial therapy for gram-positive cocci, failed to check the destructive nature of the infection. The patient subsequently developed labyrinthitis, sensorineural hearing loss, and meningitis. Intraoperative biopsy specimens confirmed the presence of tuberculoid granulomas, and the infectious process responded to triple-drug therapy. Tuberculosis of the temporal bone should not always be considered an indolent infection. The management of tuberculous infection of the temporal bone is outlined.
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PMID:Tuberculous petrous apicitis. 400 40

On the morning after taking alcohol in large amounts together with intranasal heroin, a 25-year-old man experienced pain, swelling and blistering in both arms together with right brachial plexus paresis. Creatine kinase (1930 U/l), acute phase proteins and IgE (238 IU/ml) were elevated. The pain was largely relieved by guanethidine block (given once only), and the swelling and blisters responded to methylprednisolone (80 mg daily for 7 days, then gradually reduced). Function returned in the lower division of the brachial plexus within ten days, but the upper division was still paretic 2.5 months later. After injecting heroin intravenously, a 27-year-old man woke up next morning with fever (39 degrees C) and proximal flaccid paralysis of the right arm. In addition to leucocytosis (25,600/microliters), creatine kinase was raised to 28,890 U/l and pANCA to a titre of 1:50 (antineutrophil cytoplasm antibody, perinuclear fluorescence pattern). The cerebrospinal fluid showed increases in cell count (15/microliters) and protein (73 mg/dl). Acute renal failure supervened after two days but was successfully treated. The paresis was still present at four months, though improved. A 21-year-old woman developed an upper brachial plexus lesion after attempting suicide with intravenous heroin accompanied by flunitrazepam (20 mg by mouth) and a bottle of whisky. She had raised levels of C-reactive protein (12 mg/dl) and IgM (4.0 milligrams). The paresis cleared up within six weeks without specific therapy. In view of the immunological abnormalities it seems possible that the immune system was involved in the pathogenesis of the plexus lesions and the rhabdomyolysis.
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PMID:[Brachial plexus lesions and rhabdomyolysis following heroin abuse. Indications for an immunological cause]. 782 62

A 21 year old man with a five month history of facial paresis, diplopia, and gait disturbance diagnosed with a brain stem tumor at another institution was evaluated. Computed tomography, magnetic resonance imaging, clinical and laboratory evaluations suggested a pontine astrocytoma, and the mass was excised. Pathological diagnosis was a tuberculoma confirmed by postoperative positive Mantoux testing. CT and MRI appearances of tuberculomas have been described, but can not differentiate them completely from other tumors such as astrocytomas. Because the incidence of tuberculomas has increased in recent years and they may mimic exophytic tumors of pons, it is important to include pontine tuberculoma in the differential diagnosis of pontine tumors.
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PMID:A pontine tuberculoma mimicking an exophytic brain stem tumor. 812 91

A 21-year-old male presented with sudden onset of right-sided third nerve paresis. Angiogram showed a fenestrated posterior communication artery on the right side and no other vascular anomalies. There was no other lesion that could suggest a cause for the third nerve weakness. Fenestration of the posterior communicating artery has not been reported till date. The case is discussed and the literature on the subject is reviewed.
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PMID:Fenestration of the posterior communicating artery. 1286 25

A 21-year-old patient with ankylosing spondylitis under treatment with the TNF-alpha inhibitor infliximab developed a multifocal, demyelinating axonal neuropathy affecting several peripheral nerves simultaneously (mononeuritis multiplex). This represents an additional rare peripheral nervous system side effect of infliximab therapy. The underlying cause is unknown. Intravenous immunoglobulin therapy (0.4 g/kg per day for five days) led to a complete regression of muscle paresis and sensory defects in this case.
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PMID:[Mononeuritis multiplex under the TNF-alpha inhibitor infliximab]. 2132 39