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)

A necrotizing skeletal myopathy of rear limbs was diagnosed in 17 flocks of commercial turkeys. The mean mortality attributed to the myopathy was 2.29% (range = 0.13-9.7%) over a mean period of 9.6 days (range = 6-14 days). The mean age of the birds at the time of onset was 7.4 weeks (range = 4-10.5 weeks). Clinically, birds experienced an episode of watery droppings and high-pitched crying, followed by rear-limb paresis or paralysis. Creatine kinase and aspartate aminotransferase were markedly elevated in birds with the myopathy. Grossly, a few birds had pale streaking in the muscles of the thighs and legs. Histologically, acute and subacute degeneration was present in myofibers of the legs, abdomen, thighs, back, and tail. The subacute lesion was characterized by marked sarcolemmal cell proliferation. Feed analyses ruled out selenium deficiency and the presence of mycotoxins as etiologies. Monensin was present in approved usage or only slightly elevated levels. A known potentiating antibiotic was being used concurrently with monensin in only one flock.
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PMID:A syndrome in commercial turkeys in California and Oregon characterized by a rear-limb necrotizing skeletal myopathy. 148 64

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

In a family with two sets of dizygotic twins, three, possibly all four, siblings were affected by the same disorder. The parents were unrelated and the illness seemed limited to one generation. Onset was in the early to mid-20s with tics and choreiform movements, dysarthria, and dysphagia. Two twins had epilepsy. There was a marked dyscoordination of bulbar musculature reminiscent of pseudobulbar paresis. Involuntary movements were prominent during the first years, but then disappeared and were replaced by an akinetic-rigid parkinsonian appearance in the late stage. The intellect remained largely intact. Tendon reflexes were reduced. Varying degrees of peripheral nerve changes were seen. Two patients died after 22-24 years from causes indirectly related to the main illness. Marked degenerative changes were found in the caudate nucleus and putamen. Acanthocytes in significant numbers could not be detected in peripheral blood. Lipoproteinelectrophoresis was normal. Creatine kinase levels were moderately raised in one patient, normal in the others. Although certain clinical resemblances exist with neuroacanthocytosis, the exact nosologic status of the disorder has not been determined.
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PMID:Progressive pseudobulbar paresis, early choreiform movements, and later rigidity: appearance in two sets of dizygotic twins in the same family. 961 54