Diabetic Sensory Neuropathy

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Chronic peripheral sensorimotor neuropathy / Distal symmetrical neuropathy / diabetic polyneuropathy:
Most common type – usually given the generic term ‘diabetic neuropathy’. First affects most distal parts of the longest nerves. Clinically affects up to 50% of those with diabetes after 25 years, but reported prevalence’s vary from 5% to 100%, depending of the sensitivity of the testing (eg sensitive electrophysiological tests vs. clinical symptoms). There is a long asymptomatic latency period before clinically apparent.

Clinical features:
Predominantly sensory and symmetrical; first present in most distal aspects of the legs; spreads in a ‘stocking and glove’ distribution; pain – may be unremitting, sharp, stabbing or burning; muscular cramps in bed; skin tenderness (hyperaesthesia); paraesthesia (“walking on stones”) – pain usually worse at night and ‘numbness’ (loss of sensation); useful early sign is decreased vibration sensation; other clinical signs are impaired proprioception sense, absent ankle jerks, reduction/loss of touch, pain and temperature sense. Can affect hands in severe cases. Sometimes first presentation may be a foot ulcer.
Toes are commonly believed to claw due to denervation of intrinsic muscle, but muscle strength is usually normal initially.

Most important permissive factor for diabetic foot complications – LOPS – ‘loss of protective sensation’.

Small fibre neuropathy:
May be a distinct type of neuropathy; neuropathic pain (burning, deep, aching) is predominant with vibration and proprioception still intact;

Aetiology/pathogenesis:
Possible aetiologic mechanisms include any or a combination of the following possible mechanisms:
• hyperglycaemia – both the DCCT and UKPDS demonstrated the role that good glucose control had on progress; poorly understood how hyperglycaemia may damage nerve
• abnormality in vasa nervosum  local ischaemia  poor nerve conduction
• Polyol pathway – glucose is converted to sorbitol via aldose reductase during hyperglycaemic states  increased activity of the polyol pathway  accumulation of sorbitol
• Increased levels of sorbitol  depletion of myoinositol – hyperglycaemia inhibits the neural uptake of myoinositol
• oxidative stress – hyperglycaemia  increase in free radicals  this oxidative stress may impair nerve function
• Advanced glycation end products  increase glycation of neural proteins  may play a role in demyelination
• abnormality in fatty acid metabolism – in diabetes that conversion of linoleic acid to gamma-linoleic acid (GLA) is impaired  affects nerve due to ischaemic changes (as further product of GLA is a vasodilator) or due to altered prostaglandin metabolism. The use of oral evening primrose oil (high in gamma linolenic acid) showed improvement in some nerve conduction tests
• antibodies to neural tissue has been demonstrated in those with diabetes – role is not known in aetiology

Pathologically – distal axon loss; reduce myelinated fibre density; focal areas of demyelination

Risk factors – older age, longer duration of diabetes, HLA-DR3/4, taller (longer nerves more susceptible), hyperglycaemia, hypertension, dyslipidaemia, smoking, alcohol abuse

Diabetic sensorimotor neuropathy is a diagnosis of exclusion: ie need to rule out other causes such as alcoholic neuropathy.

Treatment:
Many of risk factors are modifiable. Patient education (prevention of injury due to LOPS).
Intensive/optimal glucose control delays onset (DCCT & UKPDS); analgesia; aldose reductase inhibitors (have shown some improvement in nerve function, especially in animal studies); aminoguandine (inhibits AGE formation; improve nerve function in experimental models); gamma-linoleic acid (?); local applications of capsaicin and Opsite® dressings may help painful cases; tricyclics (first line treatment for painful neuropathy); anticonvulsants for more severe pain; nerve growth factor showed early promise, but recent trials not effective .

Related Topics:
Ipswich Touch Test

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