Sensorimotor polyneuropathy

The neuromuscular complications of diabetes mellitus are most often neuropathic in origin, with distal sensorimotor polyneuropathies being the most common. In addition, ischemic infarction of skeletal muscle may occur due to occlusive vascular disease, with small and medium-sized arterioles particularly affected. This occurs in poorly-controlled diabetes and affects thigh, muscles in most cases. In acute stages, muscle biopsy findings are those of widespread muscle necrosis, edema, and phagocytic cell infiltration. Muscle regeneration may be incomplete and increased fibrous connective tissue may replace lost muscle tissue. 

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. 

OPIDN is defined as a delayed onset central and peripheral distal sensorimotor polyneuropathy caused by exposure to nerve agents (Brown and Brix, 1998), typically within 1 to 2 weeks, and less than 4 weeks, after exposure (Johnson, 1980). Symptoms attributable to effects on sensory (numbness, tingling, pain) and motor (fatigue, weakness, and paralysis) targets are present and display a typical axonal length-associated pattern (e.g. predominantly lower extremities, with upper extremities affected at higher agent exposure). No treatment exists, and recovery is slow and rarely complete. 

A 71-year-old woman, who had taken disopyramide 500 mg/day for 4 years, developed fatigue, paresthesia, pain, and cramps in her legs (8). She had proximal weakness in all four limbs and an unsteady gait. Electrophysiology showed a sensorimotor polyneuropathy, with reduced motor conduction velocity and muscle denervation. All antibodies were negative. The symptoms did not respond to prednisone but improved in the months after disopyramide withdrawal. 

The most commonly reported dose-limiting toxic effect of vinca alkaloids is a mixed sensorimotor polyneuropathy (35). Vincristine has been associated with highest incidence, followed by vindesine and vinblastine vinorelbine canses less neurotoxicity than the other congeners (2,5,8,36). The neurotoxic effects of vinca alkaloids are reversible (5). 

Albers J, Cavender G, Levine S, et al. 1982. Asymptomatic sensorimotor polyneuropathy in workers exposed to elemental mercury. Neurology 32 1168-1174. 

DG levels in diabetic patients [81], Furthermore, fidarestat, epalrestat and ranirestat [82] have been tested in patients with diabetic neuropathy, with improvement in nerve function. Ranirestat is currently being studied in a Phase 3 clinical trial in patients with diabetic sensorimotor polyneuropathy. 

Bril V, Buchanan RA. Long-term effects of ranire-stat (AS-3201) on peripheral nerve function in patients with diabetic sensorimotor polyneuropathy. Diabetes Care 2006 29 68-72. 

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. 

However, excess copper loss can occur when zinc is used to treat Wilson s disease [109 ]. Fatal copper deficiency also occurred in a 63-year-old man who had used excessive amounts of a zinc-based denture adhesive. He developed an anemia and a severe sensorimotor polyneuropathy the former responded to copper supplementation but the latter did not and he died of aspiration [110 ]. 

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. 

Nerve conductions showed a combined dyssch-warmian and dysneuronal sensorimotor polyneuropathy in the lower more than the upper limbs. EMC in the lower limbs distaUy showed slight-moderate recent denervation and slight established reinnervation. Quadriceps muscle biopsy showed slight-moderate recent denervation and reinnervation. 

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). 

Paraneoplastic neuropathies often occur in patients with carcinoma. Subacute sensory or sensorimotor axonal polyneuropathy, often with associated limbic encephalitis and cerebellar degeneration, is a common complication of small-cell lung cancer and other carcinomas, occasionally presenting even prior to diagnosis of the underlying neoplasm. Some patients with paraneoplastic neuropathy express anti-Hu antibodies, which recognize epitopes associated with the HuD neuronal RNA binding protein [37,38]. 

Diabetes mellitus is the most common cause of peripheral neuropathy in the United States. Approximately half of all diabetics demonstrate evidences of neuropathy. The usual clinical pattern is that of a slowly progressive, mixed sensorimotor and autonomic polyneuropathy. More acute, asymmetrical motor neuropathies are also seen, usually affecting the lumbosacral plexus, particularly in older persons with type 2 (non-insulin-dependent) diabetes mellitus. Patients with diabetes mellitus are also prone to develop isolated palsies of cranial nerve III or VII, and there is a high incidence of asymptomatic focal demyelin-ation in the distal median nerve. 

Acute intermittent porphyria is a dominantly inherited partial deficiency of porphobilinogen deaminase, and causes axonal polyneuropathy. Acute intermittent porphyria is caused by partial deficiency of porphobilinogen deaminase, an enzyme required for heme biosynthesis. Patients may present with acute abdominal pain, rapidly progressive sensorimotor axonal polyneuropathy or psychosis, and have elevated concentrations of the heme precursor 8-amino-levulinic acid in their urine. Symptoms may be precipitated by treatment with barbiturates or other drugs and are suppressed by treatment with hematin [59]. 

Nitrous oxide inactivates the enzyme methionine synthetase, and caution is urged in giving nitrous oxide to patients who may be deficient in vitamin B12. Low serum vitamin B12 concentrations have previously been reported in patients with sickle cell disease, but the reason for this is uncertain. Three cases of peripheral neuropathy have been reported in patients with sickle cell disease who received nitrous oxide (12-14). AU three had a history of frequent painful sickle crises, for which they received nitrous oxide for prolonged periods. Serum vitamin B12 concentrations were slightly reduced in two patients and very low in the third. The patients aU presented with difficulty in walking and paresthesia. Peripheral sensorimotor neuropathy was confirmed by nerve conduction studies. The patients all responded well to vitamin B12 injections and avoiding further exposure to nitrous oxide. Caution is therefore recommended when using nitrous oxide in patients with sickle cell disease or who are suspected of vitamin B12 deficiency. Two cases of polyneuropathy have also been reported after the use of nitrous oxide for 80 minutes and 3 hours in patients who were subsequently found to have pernicious anemia. They both responded well to hydroxocobalamin. 

Reports of neurological adverse effects after tetanus immunization have appeared (8). The most common reported complication is a polyneuropathy. In the majority of cases the onset occurred within 14 days of the last injection, and ranged in severity from a single nerve palsy to profound sensorimotor involvement of the nervous system, including cord and cortex. Recovery was usually complete (eight of 10 patients with onset at less than 14 days after injection) but three patients with onset at more than 14 days from injection had only partial recovery. 

Peripheral neuropathy Nerve entrapment syndrome Polyneuropathy Recurrent poly radiculopathy Peripheral neuropathy (sensorimotor and axonal) Nerve entrapment syndrome Homer syndrome, phrenic and vagal nerve palsies in large and extensive retrosternal goiters... 

Nervous system dysfunction beyond neuro-ophthafinolog-ical aspects is common in hypothyroidism. Electrophysiological abnormafities reported include sensorimotor axonal polyneuropathy, carpal tunnel syndrome and myopathy (Neeck et al.y 1990 Palumbo et ai, 2000 Duyff et ai, 2000). Sural nerve biopsies have previously showed reduction of myelinated fibers and degenerative changes in axons of all fiber classes with incomplete regeneration (Meier and Bischoff,... 

Polyneuropathy Rare Possible Sensorimotor, mostly axonal... 

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