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IN THE NAME OF GOD

Diabetic Neuropathy (DN) is a common complication of diabetes affecting peripheral nerves with various symptoms such as pain, sensory loss, and autonomic dysfunction. Learn about classification, pathogenesis, tests like EMG and NCV, and treatment options for DN.

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IN THE NAME OF GOD

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  1. IN THE NAME OF GOD

  2. DIABETIC NEUROPATHY 5% per years retinopathy-nephropathy-neuropathy IDDM- NIDDM vulnerable to DN leading cause of peripheralneuropathy

  3. frequency of D N 7-80% risk of developing symptomatic D N 5years:4-10% 25years:15% 66% have objective D N IDDM 15%--- NIDDM 13% symptomatic age& D M correlate with abnormal vibration test

  4. higher percentage in those with low serum insulin concentration risk factors with increased foot sensation :poor glycemic control-height-age-alcohol EMG&NCV demonstrate subclinical abnormalities in most patients with IDDM after5-10years D N

  5. CLASSIFICATION : symmetric focal clinical features distal symmetrical P N most common DN 75% of all DN sensory loss & autonomic symptoms correlate with severity most patients have minor motor sign

  6. stocking&glove distribution begin in the toes in more advanced cases anterior chest & abdomen are affected dyeing back process large fiber-------small fiber

  7. LARGE FIBER D N painless paresthesias(toe&feet) impairment of vibration&position DTR-ataxia sensory loss DIABETIC POLYRADICULONEUROPATHY onset distal symmetric then proximal segment L S roots-thoracic—cervical E M G –low grade active denervation(thoracic)

  8. trigeminal blink reflex is spared DIABETIC POLYRADICULOPATHY normal S N C V —root level is affected(EMG&clinical) NIDDM&IDDM are associated with CIDP ------response to IVIG SMALL FIBER D N deep pain burning-aching-shooting allodynia –temperature & pain are impaired—preservation of deep sense & DTR—autonomic

  9. HYPERGLYCEMIC D N can occur before the onset of D M IGT OGTT--------small fiber be undergo GTT DN painful P N (unknown cause)should TREATMENT INDUCED NEUROPATHY lasts for weeks

  10. DIABETIC NEROPATHIC CACHEXIA acute painful D N—depression-insomnia-weightloss -impotence M>F ACRODYSTROPHIC NEUROPATHY sensory loss-foot ulcer distal joint destruction CHRONIC FOOT ULCER---trauma ischemia infection

  11. NEUROPATHIC ARTHROPATHY(CHARCOTJOINT) -----foot ulcer-autonomic impairment D D syphilis DIABETIC PSEUDOTABES :lancinating pain-loss of joint sensation abnormal pupil EMG&NCV ARE HELPFULIN CONFIRMING NCV – H reflex & amplitude of sural nerve

  12. active denervation potential DIABETIC AUTONOMIC NEUROPATHY usually correlate with severity of somatic neuropathy subclinical-sever(heart-GI-GU ) OH-resting tachycardia- H R unresponsive to respiration-------hallmark of autonomic D N OH— failure of sympathic&cardiac compensatory is impaired

  13. D D---hypovolemia-medication VAGAL DENERVATION-----tachycardia in rest –silent MI GI motility abnormality-fecal incontinence-delayed gastric emptying(nausea)-diarrhea-bacterial overgrowth-colonic atony(constipation)-bladder atony impotence sudomotor abnormalities

  14. distal anhidrosis gustatory sweating pupillary abnormalities ASYMMETRIC PROXIMAL NEUROPATHY(DIABETIC AMYOTROPHY) Bruns Garland syndrome weakness of pelvifemural muscles age>50years NIDDM—unrelated to duration of DM

  15. sever pain in lower back&hip&tigh weakness— DTR-opposite leg affect minor paresthesias-weight loss >50% steady progression-pain receds spontaneously-recovery up to 24 months 66% overlap with distal DN EMG: low amplitude-fibs- IMAGING: R/O other causes SURAL NERVE BIOPSY (ischemia)

  16. TRUNCAL NEUROPATHY T4-T12 roots involved pain in chest & abdomen- bulging of abdominal wall-older patients NIDDM-allodynia-abrupt onset D D:H Z-mass lesions Recovery :several months E M G :active denervation focal anhidrosis

  17. LIMB MONONEUROPATHY mecanisms:1-infarction 2-entrapment infarction: abrupt onset-acute axonal degeneration-slow recovery median-ulnar-proneal(most common) Entrapment :insidious onset-focal conduction block- MULTIPLE MONONRUROPATHIES abrupt onset-proximal nerve-

  18. nerve infarction due to occlusion of vasnervorum D D :systemic vasculitis CRANIAL MONO NEUROPATHIES third nerve palsy is most common pupillary sparing 4th-sixth&seventh are affected acute ischemic damage Recovery : after 3-5 months

  19. INCREASED INCIDENCE OF ENTRAPMENT NEUROPATHY D M is found in 8-12%patients with CTS—25%DM patients have electrodiagnostic CTS—8%symptomatic risk of CTS---women 2/2 men 2/5 times reason ? ischemia or hypoxia entrapment----- possibility of DM

  20. LABORATORY FINDINGS ; confirmation of DM :random BS>200mg FBS>126mg/dl 2HPP>200mg/dl IGT---- BS=140-200 FBS=110-126 mg/dl EMG&NCV abnormalities S>M D>P leg>hand PATHOLOGY: small vessel occlusion—immune mediate—loss of myelinated fibers—axonal degeneration

  21. painless distal D N----large fiber painful distal D N-----small fiber PATHOGENESIS OF D N: nerve blood flow- endoneurial vascular resistance– myoinositol-activate polyol pathway------aldosereductase)-accumulation of sorbitol & fructose - autooxidation -endoneurial hypoxia : impairment of axonal transport & reduce nerve NA-K ATP ase activity----- axonal atrophy

  22. TREATMENT optimal glucose control insulin pump----at 5 years reduce 64% pancreas transplantation prevents of DN myoinositol ? alberstatin ? lipoic acid----improved sensory symptoms(and also C peptide) VEGF----- nerve blood flow

  23. IV methyl prednisolone—IVIG SYMPTOMATIC O H: 6-10 inches head elevated—drinking two cups of cofee—eating more frequent small meals—daily fluid intake & salt ingestion(10-20gr/d)-elastic body stocking-fludrocortisone(/1-/6mg/d)-midodrin Fluoxetin-dDAVP-octreotide NSAIDs(ibuprofen)-phenylpropanolamine-metoclopramide-tetracycline or erythromycin-clonidin

  24. G U COMPLICATIONS-----urologist frequent voiding-manual abdominal compression-intermittent cathaterization—betanechol-sildenafil-proper skin care

  25. Management of neuropathic pain 30-50% reduction of pain ASA-acetaminophen-NSAIDs TCA block of serotonin &NE reuptake amitriptyline(10-25mg)-desiprmine nortriptyline SSRI are less effective

  26. Venlafaxine has fewer side effect than TCA 150-225 mg/day Doxepin Duloxetine 60-120 mg/day moderate effect Bupropion 300 mg/day 30%reduced pain Anticonvulsants: Carbamazepine 1000-1600mg/day Oxcarbazepine1200mg/d

  27. Gbapentin300mg/d--------900-3600mg/d Pregabalin150-600mg/d Topiramatehas minor effect Lamotrigine200-400mg/d moderate relief Mexiletine(oral analog of lidocaine) ? Tramadol 200-400mg/d Dextromethorphan high dose---partial relief ataxia-sedation

  28. Narcotic analgesics should be limited-oxycodon Alpha lipoic acid 600 mg/d TENS 15-30 min/d 4 weeks Acetyl L carnitin100mg tds Topical agents: capsaicin cream o.o25 or o.o75 patches containing 5% lidocain

  29. STROKE & DM Increased risk of CVD 2-4 folds mortality & morbidity Macrovascular involvement is leading cause of death due to DM DM atherosclerosis-cardiac embolism

  30. Retinopathy & autonomic neuropathy increased risk of ischemic stroke High insulin level in DM is associated with risk of athersclerosis and cerebrovascular small vessel disease DM abnormalities of platelet-rheological- coagulation-fibrinolytic may play a role in the pathogenesis of stroke

  31. HCT-fibrinogen-factor 5&7-platlet aggregation& adhesion-release of beta thromboglobulin--- RBC deformability and fibrinolytic activity

  32. SLEEP DISORDER IN DM Particulary autonomic DN causes OSA&CSA CSA fragmentation of sleep EDS

  33. Hypoglycemic Encephalopathy This condition is now relatively infrequent but is an impor­ tant cause of confusion, convulsions, stupor, and coma;

  34. Hyperglycemia Seizures and focal signs such as a hemiparesis, a hemisensory defect, choreoathetosis, or a homonymous visual field defect are more common than in any other metabolic encephalopathy and may erroneously suggest the possibility of a stroke.

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