Guillain-Barre syndrome polyneuropathy

Acute inflammatoiy demyelinating polyneuropathy is a common cause of reversible paralysis. Acute inflammatory demyelinating polyneuropathy (AIDP), the classic form of the Guillain-Barre syndrome, often begins a week or two after recovery from cytomegalovirus, Epstein-Barr virus or Mycoplasma infection. Patients present with rapidly advancing symmetrical weakness, loss of deep tendon reflexes, often with distal numbness, and limb or back pain. Cerebrospinal fluid (CSF) protein concentration is elevated, but in most cases there is little or no increase in number of inflammatory cells in the CSF. This albumino-cytologic dissociation contrasts with the elevation of both... 

Pathological conditions in which capsaicin itself is not sufficiently active, but more potent vanilloids are expected to be of greater therapeutic value. For example diabetic neuropathy (Ross and Varipapa, 1989), postherpetic neuralgia (Watson et al., 1988 Bernstein et al., 1989), chronic distal painful polyneuropathy (Low et al., 1995), post-mastectomy pain syndrome (Watson et al., 1989), Guillain-Barre syndrome (Morgenlander et al., 1990), reflex sympathetic dystrophy (Cheshire and Snyder, 1990), vulvar vestibulitis (Friedrich, 1988). 

Acute autoimmune demyelinating polyneuropathies such as Guillain-Barre syndrome and chronic polyneuropathies may involve some glycolipid antigens, as described later. 

Takigawa T, Yasuda H, Terada M, Haneda M, Kashiwagi A Saito T, Saida T, Kitasato H, Kikkawa R (2000) The sera from GMl gan-glioside antibody positive patients with Guillain-Barre syndrome or chronic inflammatory demyelinating polyneuropathy blocks Na+ currents in rat single myehnated nerve fibers. Intern Med 39 123-127. 

Preparations for intravenous administration are mainly used in patients with general immune deficiency states (primary or secondary) or diseases like idiopathic thrombo-cjhopenic purpura (ITP) and autoimmune diseases (5,6). Neurological disorders (for example Guillain-Barre syndrome and chronic demyelinating polyneuropathy) have been treated with intravenous immunoglobulin (7-9). 

Adverse effects of flu immunization on the nervous system range from polyneuropathy to meningoencephahtis and Guillain-Barre syndrome (32). 

Penicillamine, both L-penicillamine and the racemic mixture, strongly inhibit pyridoxal-dependent enzymes, cause pyridoxine deficiency in animal experiments, and are neurotoxic. Although this effect is much weaker with D-penicillamine, a few case reports have shown that D-penicillamine can also occasionally cause a polyneuropathy, as either a toxic or an allergic reaction (69-72). Rarely, an optic neuropathy (73) or a polyradiculoneuropathy (Guillain-Barre syndrome) (74,75) can occur. 

Isolated case reports of Guillain-Barre syndrome after HDC vaccine have been published (SED-11, 684) (SEDA-15, 356) (3). Polyneuropathy and oculomotor nerve impairment have been reported after Russian cell-culture vaccine (SEDA-12, 284). 

Isolated reports of adverse effects have included abscess formation (SEDA-11, 288) dermatomyositis, neuralgic amyotrophy, polyradiculoneuritis with paresis of the urinary bladder and bowel (SEDA-9, 283) asymmetrical polyneuropathy, demyelinating polyneuropathy, and Guillain-Barre syndrome (SEDA-14, 281) and subcutaneous nodules. Polyvinylpyrrolidone thesaurismosis, revealed by inflammatory manifestations after tetanus booster injection, has also been reported (SEDA-10,288). 

FIGURE 20.61 Locations of T lymphocytes among sural nerve biopsy specimens from 13 cases of chronic inflammatory demyelinat-ing polyneuropathy (CIDP) and 22 cases of Guillain-Barre syndrome (CBS). Percentages positive are as reported in Schmidt B, Toyka KV, Keifer R, et al. Inflammatory infiltrates in sural nerve biopsies in Guillain-Barre syndrome and chronic inflammatory demyelinating neuropathy. Muscle Nerve. 1996 19 474-487. 

Neuropathy in human immunodeficiency virus infection has many causes. Multiple mechanisms cause neuropathy in patients with HIV. An immune-mediated, Guillain-Barre-like syndrome (see below) may occur at the time of HIV seroconversion. Later in the course of infection, patients may present with mononeuropathy multiplex, sometimes as a consequence of vasculitis associated with coinfection with hepatitis C. Distal sensory-autonomic axonal polyneuropathy may develop in patients with more advanced HIV, either as a consequence of high titers of HIV itself or of the neurotoxicity of antiretroviral drugs [18,19],... 

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