Symmetrical polyneuropathy

Saudek, C. D., Werns, S., Reidenberg, M. M. Phenytoin in the treatment of diabetic symmetrical polyneuropathy, Clin. Pharmacol. Ther. 1977, 22, 196-199. 

Another patient developed a symmetric polyneuropathy with flaccid paraplegia while her ciclosporin serum concentrations were about twice normal (27). Electromyography showed features of axonal degeneration in the peripheral nerves and neurological symptoms improved on ciclosporin dosage reduction. 

Terrovitis IV, Nanas SN, Rombos AK, Tolls G, Nanas JN. Reversible symmetric polyneuropathy with paraplegia after heart transplantation. Transplantation 1998 65(10) 1394-5. 

A prediction of this hypothesis is that a decline in circulating IGFs may predispose to symmetrical polyneuropathy in disease states. This underlies the specific interrelated theory that decline in circulating IGFs is pathogenic for diabetic neuropathy (Ishii,... 

The large-fibre neuropathy may involve both sensory and motor nerves. Large fibres facilitate motor function, vibration sense, position sense and cold thermal perception. Most patients with a distal symmetric polyneuropathy have a mbced variety of neuropathy with involvement of both large and small-fibre damages. Above symptoms are characterized by having a glove and stocking distribution. 

Neurological involvement is noted in 50% to 78% of patients (26,27). Mononeuritis multiplex is the most frequent ( 70% patients with peripheral neuropathy) at CSS onset whereas symmetrical polyneuropathy can be seen in up to 30% of patients (26,27). Central nervous system (CNS) involvement (cranial nerves palsies, cerebral hemorrhage or infarction, convulsions, coma, and psychiatric features) is rarely seen (16). 

The earliest reports of neurological complications of AIDS described distal symmetrical, painful sensory neuropathy occurring in HIV patients (Snider et al. 1983). Dysimmune inflammatory polyneuropathy was subsequently recognized as a complication of AIDS (Lipkin et al. 1985). Progressive polyneuropathy associated with cytomegalovirus (CMV) infection was documented as the first truly opportunistic infection of the peripheral nerve (Eidelberg et al. 1986). 

DIES-associated neuropathy has a variety of chnical presentations, including painful symmetric or asymmetric sensorimotor neuropathy, distal sensory neuropathy, mononeuritis multiplex, and demyelinating polyneuropathy (Gherardi et al. 1998). Cranial neuropathy without evidence of a more generahzed neuropathy may occur, typically as a facial nerve palsy in association with parotidomegaly (Itescu et al. 1990 Brew 2003). The neuropathy develops subacutely over days to weeks. In some cases, muscle weakness may be a result of an inflammatory myositis (Kazi et al. 1996). 

As might be predicted from these similarities between PNS and CNS, many disease entities can affect both these tissues. It should be noted, however, that the clinical expression of such diseases is variable and is sometimes restricted to the PNS. For example, patients with thiamine deficiency may display symmetrical distal sensorimotor polyneuropathy without accompanying CNS degeneration. Untreated infection with human immunodeficiency virus (HIV) may cause early polyneuropathy, with dementia appearing months or years later. Similarly, patients with sulfatidase deficiency or adrenoleukodystrophy may present initially with polyneuropathy, while their CNS dysfunction remains clinically undetectable. 

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... 

Adrenoleukodystrophy is an X-linked dysmyelinative disorder caused by mutations in the ABCD1 gene, which encodes the peroxisomal integral membrane ALD protein, a member of the ATP binding cassette transporter family. These mutations result in impaired clearance of plasma very-long-chain fatty acids. Affected males may present with symmetrical distal axonal polyneuropathy, adrenocortical insufficiency or CNS demyelination, while occasional heterozygous women demonstrate deficits suggestive of multiple sclerosis [56]. Manipulation of dietary fatty acid intake has some minimal therapeutic effect, while bone marrow transplantation has diminished deficits in a few patients. (See in Ch. 41.)... 

The prevalence of diabetic neuropathy rises from 7.5% at the time of diagnosis to 50% after 25 years and seems to be directly related to the duration of diabetes. The commonest type is a symmetric sensory and autonomic polyneuropathy. Once symptomatic autonomic neuropathy is present the prognosis for survival is substantially diminished. The clinically silent phase of diabetic nephropathy in Type-II diabetes may last 5-10 years. It is characterized by rising urinary albumin excretion caused by a capillary lesion in the glomerulus. Microalbuminuria varies and can be found in 15-60% of all Type-II diabetics it is defined by an excretion rate between... 

In diabetic patients, the incidence of clinically manifested deficits in peripheral nervous system function increases with duration of disease and is approx 50% after 25 yr of disease. The resulting diabetic neuropathies comprise a group of distinct disorders that can affect both somatic and autonomic nerves, the most common of which is symmetric sensory polyneuropathy. Clinical signs of overt human diabetic neuropathy include decreases in nerve conduction velocity and action potential amplitude and in resistance to ischemic conduction failure. These abnormalities may be accompanied by sensory deficits and, in some cases, severe pain. In diabetes of long standing, morphological deterioration is evident, and both nerve fiber loss and segmental demyelination may occur. 

Distal symmetric sensorimotor polyneuropathy is the most common form of diabetic neuropathy. Small fibre neuropathies involving unmyelinated C and A5 fibres are involved in symptoms like pain, which is burning and superficial and associated with allodynia, hypoalgesia and defective warm thermal sensation. Patients can experience dys-, para, hypo- or hyperaesthesia, tingling, pins and needles or electric-shock-like sensations. 

A female adult heart transplant recipient developed reversible progressive symmetrical demyelinating sensorimotor polyneuropathy in the distal muscles of the legs while taking tacrolimus [142 ]. The condition immediately resolved after withdrawal of tacrolimus. 

Nemni R, Galassi G, Cohen M, et al. Symmetric sarcoid polyneuropathy analysis of sural nerve biopsy. Neurology 1981 31 1217 1223. 

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