PubMed Health⌕ Search

Biomedical subjects

H Willison

Publications and source records attributed to H Willison.

6 recordsLinked to original sources
PubMed2001

Randomized controlled trial of intravenous immunoglobulin versus oral prednisolone in chronic inflammatory demyelinating polyradiculoneuropathy.

This multicenter, randomized, double-blind, crossover trial compared a six week course of oral prednisolone tapering from 60 mg to 10 mg daily with intravenous immunoglobulin (IVIg) 2.0 g/kg given over one to two days for treating chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Twenty-four of the thirty-two randomized patients completed both treatment periods. Both treatments produced significant improvements in the primary outcome measure, change in an 11-point disability scale two weeks after randomization. There was slightly, but not significantly, more improvement after IVIg than with prednisolone, the mean difference between the groups in change in disability grade being 0.16 (95% CI = -0.35 to 0.66). There were also slightly, but not significantly, greater improvements favoring IVIg in the secondary outcome measures: time to walk 10 meters after two weeks and improvement in disability grade after six weeks. Results may have been biased against IVIg by the eight patients who did not complete the second arm of the trial. A serious adverse event (psychosis) attributable to treatment occurred in one patient while on prednisolone and in none with IVIg.

Administration, Oral↗
PubMed2000

Long-term clinical and neurophysiological follow-up of patients with peripheral, neuropathy associated with benign monoclonal gammopathy.

The incidence of hematological malignancy in patients with monoclonal gammopathy of undetermined significance (MGUS) has been assessed as 17% to 25%. To ascertain whether this is true of neuropathy associated with MGUS, a long-term (5-42 years) retrospective clinical and neurophysiological follow-up was conducted in 50 cases (immunoglobulin M [IgM], n = 38; IgG, n = 11; IgA, n = 1). Only three patients developed hematological malignancy. Of 25 survivors with IgM paraproteinemia, 7 had myelin-associated glycoprotein antibodies with typical clinical features. Evoked distal muscle amplitudes were significantly smaller than for the other paraprotein classes. Preferential distal demyelination manifested by relative prolongation of distal motor latency was not apparent in the cases of long duration. Two patients with IgM antidisialosyl antibodies and cold agglutinating activity had a large fiber neuropathy with intermittent oculofacial involvement. Both responded to intravenous immunoglobulin. Findings in the remaining patients were varied. Recognition of IgM subgroups is important both for prognosis and possible response to treatment.

Adult↗
PubMed1995

Autoantibodies, neurotoxins and the nervous system.

Myasthenia gravis, the Lambert-Eaton myasthenic syndrome, and acquired neuromyotonia are three disorders of the neuromuscular junction or motor nerve that are caused by autoantibodies to ion channel proteins: acetylcholine receptors, voltage-gated calcium channels and voltage-gated potassium channels, respectively. The antibody titres can be measured using the relevant 125I-neurotoxins to label the extracted channels. Other disorders of the peripheral motor nerve are associated with antibodies to gangliosides. Sera with raised levels of anti-ganglioside antibodies have direct effects on the function of the distal motor nerve and motor nerve terminal. These conditions can be improved by therapies designed to reduce circulating antibodies. Antibodies that bind to neuronal surface antigens are proving to be of great clinical importance and interest in neurological disorders.

Autoantibodies↗
PubMed1994

Serum factor in Miller-Fisher variant of Guillain-Barré syndrome and neurotransmitter release.

Serum IgG autoantibodies to GQ1b ganglioside are associated with the acute phase of the Miller-Fisher syndrome (MFS). We investigated the effects of three anti-GQ1b-positive MFS sera in the mouse phrenic-nerve/diaphragm preparation. Miniature endplate potential frequencies increased eight-fold within 25 min, declined rapidly, and ceased altogether after 3 h, when nerve stimulation no longer evoked a response. One MFS convalescent serum (anti-GQ1b negative) and sera from healthy controls and from patients with other neurological diseases were without effect. Thus muscle weakness in MFS may be caused by a serum factor, likely to be GQ1b antibody, that leads to failure of acetylcholine release from motor nerve terminals.

Autoantibodies↗