The most common type of neuropathy in diabetes mellitus is:
Ans. A. Distal symmetric polyneuropathy. (Ref. H - 17th / pg. 2289; 2653; Table 379-4)The most common type of neuropathy in diabetes mellitus is Distal symmetric polyneuropathy. .Harrison's 17th / pg. 2289"In DM, Subclinical neuropathy is much more common than clinical neuropathy. Distal symmetrical polyneuropathy is the most common type of neuropathy in DM, followed by carpal tunnel syndrome, other mononeuropathies, and autonomic neuropathy."Harrison's 17th / pg. 2653 "By far the most common form of diabetic neuropathy is a length-dependent diabetic sensorimotor polyneuropathy (DSPN)."Diabetic sensorimotor polyneuropathy (DSPN)# Proposed criteria for the diagnosis of DSPN are two or more of the following:- symptoms or signs of neuropathy,- abnormal EDx studies, quantitative sensation test abnormalities,- heart rate decrease with deep breathing or Valsalva maneuver.# The diagnosis of DSPN is usually straightforward, although other contributors to the neuropathy should be excluded, including nutritional (vitamins B1 and B12 and folate deficiencies), toxic (alcohol, vitamin B6 toxicity), immune- mediated (paraprotein), and inherited causes. An alternative diagnosis should be sought in patients with rapidly progressive or asymmetric weakness, a family history of neuropathy, exposure to toxins, or prior malignancy. A glucose tolerance test is indicated in all patients presenting with neuropathy. EDx studies show mixed findings of axonal loss and demyelination in a length-dependent pattern. Nerve biopsy and lumbar puncture are not necessary unless alternative diagnoses are being considered.# Various hypotheses have been invoked to account for DSPN. Increased neuronal concentrations of glucose induce the conversion of glucose to sorbitol by aldose reductase using NADPH as a coenzyme. Sorbitol decreases levels of myo-inositol and phosphoinositides, leading to a decrease in diacylglycerol, protein kinase C, and Na+, K+, ATPase activity.# Rx consists of strict glucose control, which prevents the neuropathy from worsening; established neuropathy does not usually reverse. Aldose reductase inhibitors to treat and prevent diabetic neuropathy have been studied in >30 trials. Although controlled trials of the aldose reductase inhibitors sorbinol and tolrestat were found to improve electrophysiologic or morphometric markers of DSPN, any clinically meaningful improvement in pain or sensation has been inconsistent. Rx with recombinant nerve growth factor was ineffective. Alpha lipoic acid (thioctic acid), an antioxidant, has been shown to improve experimental diabetic neuropathy, and a meta-analysis of clinical trials suggested that the Rx (600 mg/ d IV for 3 weeks) is safe and improves symptoms and signs of neuropathy. Pancreatic transplantation can halt progression of DSPN but is a realistic therapy only for patients who have renal failure and are undergoing combined kidney and pancreas transplantation.# Glycemic control is essential for the prevention of diabetic autonomic neuropathy. Once neuropathy is established, few effective Rxs exist.Classification of Neuropathy by Histopathology DemyelinatingAxonalNeuronalPatternProximal = distalDistal > proximal; length- dependentNon-length-dependent; UE, LE, faceOnsetAcute/subacuteSlow evolutionRapidSymptomsParesthesia and weaknessDysesthesias and distal weaknessParesthesias, gait ataxiaSensory signsVibration and proprioception > pain and temperaturePain and temperature affected > vibration and proprioceptionVibration and proprioception > pain and temperatureMotorDistal and proximal weaknessDistal weaknessProprioceptive weaknessDTRsAreflexiaDistal areflexiaAreflexiaNCSVelocity affected > amplitudeAmplitudes affected > velocitySensory amplitudes affected; radial > suralNerve biopsyDemyelination and remyelinationAxonal degeneration and regenerationAxonal degeneration but no regenerationPrognosisRapid recoverySlow recoveryPoor recoveryCausesGBS, diphtheria, CIDP, DM, MMNToxic, metabolic, HIV, CMT2, DMSjogren's, cisplatin, pyridoxineNote: Although there is evidence of immune activation in CIDP, the precise mechanisms of pathogenesis are unknown.Biopsy typically reveals little inflammation and "onion-bulb" changes (imbricated layers of attenuated Schwann cell processes surrounding an axon) that result from recurrent demyelination and remyelination. The response to therapy suggests that CIDP is immune-mediated; CIDP responds to glucocorticoids, whereas GBS does not.Classification of Neuropathy by Fiber TypeSmall-fiber sensory (painful neuropathies and dissociated sensory loss)# Hereditary sensory neuropathies (early)# Lepromatous leprosy# Diabetic (includes glucose intolerance) small-fiber neuropathy# Amyloidosis# Analphalipoproteinemia (Tangier disease)# Fabry's disease (pain predominates)# Dysautonomia (Riley-Day syndrome)# HIV and antiretroviral therapy neuropathyLarge-fiber sensory (ataxic-neuropathies)# Sjogren's syndrome# Vitamin B12 neuropathy (from dorsal column involvement)# Cisplatin neuropathy# Pyridoxine toxicity# Friedreich's ataxiaSmall- and large-fiber: Global sensory loss# Carcinomatous sensory neuropathy# Hereditary sensory neuropathies (recessive and dominant)# Diabetic sensory neuropathy# Vacor intoxication# Xanthomatous neuropathy of primary biliary cirrhosis (tabes dorsalis)Motor-predominant neuropathies# Immune neuropathies: acute (Guillain-BarrA(c) syndrome); relapsing# Heritable motor-sensory neuropathies# Acute intermittent porphyria# Diphtheritic neuropathy# Lead neuropathy# Brachial neuritis# Diabetic lumbosacralplexus neuropathy (diabetic amyotrophy)Autonomic# Acute: Acute pandysautonomic neuropathy, botulism, porphyria, GBS, vacore, amiodarone, vincristine# Chronic: Amyloid, diabetes, SjAUgren's, HSAN 1 and III (Riley-Day), Chagas, paraneoplastic
Distal symmetric polyneuropathy
Painful mononeuropathy
Autonomic neuropathy
Cranial neuropathy
Endocrinology