Distal symmetric sensorimotor polyneuropathy

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. 

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. 

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. 

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). 

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