Neurological complications due to beta-propiolactone (BPL)-inactivated antirabies vaccination

Swamy, H. S.; Shankar, S. K.; Chandra, P. Sarat; Aroor, Suresh Rao; Krishna, Amresh; Perumal, V.G.Kalia

doi:10.1016/0022-510x(84)90113-8

Cited by 34 publications

(11 citation statements)

References 8 publications

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“…Sensitization to MBP occurs in patients developing neurological complications after inoculation with rabies vaccine containing sheep brain (Hemachudha et al 1987a) and could thus account for the PNS involvement seen in such cases (Appelbaum et al 1953;Swamy et al 1984;Hemachudha et al 1987b). As sensitization to MBP also occurs in post-infectious encephalomyelitis (Lisak et al 1974;Johnson et al 1984), PNS involvement would also be expected and could possibly account for many of the neurological signs in this disease.…”

Section: Discussionmentioning

confidence: 99%

The pathophysiology of myelin basic protein-induced acute experimental allergic encephalomyelitis in the Lewis rat

Pender

1988

Journal of the Neurological Sciences

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Histological and electrophysiological studies were performed on Lewis rats with acute experimental allergic encephalomyelitis (EAE) induced by inoculation with guinea-pig myelin basic protein (MBP) and Freund's adjuvant. The histological studies showed demyelination in the lumbar, sacral and coccygeal dorsal and ventral spinal roots and to a lesser extent in the spinal cord, including the dorsal root entry and ventral root exit zones. The electrophysiological studies demonstrated reduced conduction velocities between the lumbar ventral roots and sciatic nerve. Conduction block was demonstrated at the ventral root exit zone of the lumbar spinal cord but was less severe than in rats with whole spinal cord-induced acute EAE. Recordings of the M wave and H reflex elicited in a hindfoot muscle by sciatic nerve stimulation showed a normal M wave, indicating normal peripheral nerve motor conduction, but a markedly reduced H reflex. The reduction in the H reflex is accounted for by demyelination-induced nerve conduction block in the dorsal and ventral spinal roots, intramedullary ventral roots and at the dorsal root entry and ventral root exit zones of the spinal cord. Demyelination and nerve conduction abnormalities were well established in the relevant lumbar segments on the day of onset of hindlimb weakness. It is concluded that demyelination in the lumbar ventral roots and to a lesser extent in the lumbar spinal cord, including the ventral root exit zone, is an important cause of hindlimb weakness in myelin basic protein-induced acute EAE in the Lewis rat.

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Section: Discussionmentioning

confidence: 99%

The pathophysiology of myelin basic protein-induced acute experimental allergic encephalomyelitis in the Lewis rat

Pender

1988

Journal of the Neurological Sciences

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“…a radiculopathy has been shown in 82% cases with ADEM [1,10,13]. ADEM may evolve over the course of up to 3 months [7].…”

Section: Discussionmentioning

confidence: 99%

An unusual Guillain-Barré Syndrome mimic: a case of Spinal ADEM and review of the literature

Roshanisefat¹,

Henderson²

2016

Clin Case Rep Rev

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“…Introduction of the non-neural human diploid cell vaccine has virtually eliminated neuroparalytic complications of rabies vaccinations. [6][7][8][9][10][11] When smallpox vaccination was a part of a universal immunisation programme, encephalomyelitis followed one in 4000 vaccinations. Currently, postimmunisation encephalomyelitis is most commonly associated with measles, mumps, and rubella vaccinations.…”

Section: Epidemiologymentioning

confidence: 99%

Acute disseminated encephalomyelitis

Garg

2003

Postgraduate Medical Journal

206

161

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Acute disseminated encephalomyelitis (ADEM) is an acute demyelinating disorder of the central nervous system, and is characterised by multifocal white matter involvement. Diffuse neurological signs along with multifocal lesions in brain and spinal cord characterise the disease. Possibly, a T cell mediated autoimmune response to myelin basic protein, triggered by an infection or vaccination, underlies its pathogenesis. ADEM is a monophasic illness with favourable long term prognosis. The differentiation of ADEM from a first attack of multiple sclerosis has prognostic and therapeutic implications; this distinction is often difficult. Most patients with ADEM improve with methylprednisolone. If that fails immunoglobulins, plasmapheresis, or cytotoxic drugs can be given. Recent literature suggests that a significant proportion of patients with ADEM will later develop multiple sclerosis; however, follow up experience from developing countries does not support this view.

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Neurological complications due to beta-propiolactone (BPL)-inactivated antirabies vaccination

Cited by 34 publications

References 8 publications

The pathophysiology of myelin basic protein-induced acute experimental allergic encephalomyelitis in the Lewis rat

The pathophysiology of myelin basic protein-induced acute experimental allergic encephalomyelitis in the Lewis rat

An unusual Guillain-Barré Syndrome mimic: a case of Spinal ADEM and review of the literature

Acute disseminated encephalomyelitis

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