Diabetic Peripheral Neuropathies A clinical and electro physiologic understanding

1. Diabetic Peripheral Neuropathies A clinical and electro physiologic understanding

2. Diabetic Neuropathy General: Prevalence – 30 to 50% DiabCare Asia Statistics – 37% Diabetic State is the trigger Uncontrolled diabetes – worsens over time Good control of diabetes - not the guarantee for – cure, arrest, reversal

3. Diabetic Peripheral Neuropathy - 1 Major divisions • Symmetric Sensorimotor Diabetic polyneuropathy • Lumbosacral plexus neuropathy • Truncal racdiculopathies • Diabetic mononeuropathies Invariably associated with some autonomic nervous system involvement and / or cranial neuropathies

4. Diabetic Peripheral Neuropathy - 2 • Incidence of neuropathic symptoms many times more and more sites are involved than in non diabetic persons • Autonomic neuropathy has diabetes as almost the sole major cause, other than ageing or smoking

5. Diabetic Peripheral Neuropathy - 3 • Sensory symptoms and signs distally, numbness or paresthesia • Ascends from toes • Glove and Stocking anesthesia - a phenomenon dependent on fiber length

6. Diabetic Peripheral Neuropathy - 4 • Generally or eventually symmetric, • Initially, not infrequently, asymmetric, often confined to single nerves • Tear drop abdominal thoracic anesthesia, somewhat unusual presentation, not rare

7. Diabetic Peripheral Neuropathy - 5 More severe cases – • Paresthesia tingling and numbness, • Dysesthesia, ??? • Deep, aching, severe night pains • Paroxysmal jabbing pain • Pain – small fiber neuropathy

8. Diabetic Peripheral Neuropathy - 6 More severe cases – • Pain & temp loss with intact vibration and position sense; the reflexes and power may be normal – suggests A delta or thin, unmyelinated fiber involvement sparing large fibers of somatic sensation

9. Diabetic Peripheral Neuropathy - 7 Dominantly Large fiber Sensory and motor involvement Sensory Neuropathy – Symptoms, positive or negative, Loss of light touch, pain, pressure, Post columns get involved vibration perception, joint position sensation is lost Diabetic pseudotabes occurs Large fibers intact - NCV – nearly normal

10. Diabetic Peripheral Neuropathy - 8 Dominantly Large fiber involvement – Sensory and motor involvement Muscle weakness Intrinsic foot muscle - extensors and flexors of toes, weakness, atrophy and foot drop, foot deformities due to motor neuropathy

11. Diabetic Peripheral Neuropathy - 9 • Once established, stays • Exacerbates with other illnesses, • Neuropathic joints suggestive of autonomic neuropathy, usually accompanied by dense sensory neuropathy and other tissue changes, as well as altered joint structure • Painless foot ulcers suggestive of severe sensory neuropathy

12. Diabetic Peripheral Neuropathy - 10 • Severe painful neuropathy causes depression • Diabetic neuropathic cachexias • Severe exacerbations of burning pains, allodynia ie excessive pain sensation to non noxious stimuli with sensory deficits, anoxexia, weight loss, depression • Generally recovers

13. Hyperglycemic Neuropathy • Widespread parasthesias in newly diagnosed cases, after recovery from ketosis • Improve rapidly with control, could have a different pathophysiologic basis than the one with long term complications

14. Proximal Motor Neuropathy - 1 • Peaks in 6th decade in type 2 • Diabetes mild • Control not good • Acute / sub acute pain • Pelvic girdle weakness and atrophy, illiopsoas and quadriceps, hip adductor gluteni, namstrings • Knees buckle, stairs difficult

15. Proximal Motor Neuropathy - 2 • Sensory symptoms present. • Commonly – paresthesias, deep aches, ↑ at night, not relieved by rest, SLR neg. • Unilateral, may become bilateral • Reflexes Lower Limbs + • Recovery usual and nearly full • Takes 6 – 18 months • Reassurance necessary

16. Thoracic Radiculopathy: - 1 • Middle aged mild diabetics • Acute herpes like deep ache • Multiple segment, single, bilateral, or unilateral • Paresthesia, cutaneous hyper sensitivity • Severe cases show paraspinal and abdominal muscle weakness

17. Thoracic Radiculopathy: 2 • Imagings normal • Waste of money • Recovers with a few months to an year • Left sided pains disturbing as cardiac • Pains could be as such disturbing • Electromyography shows – Acute denervation, insertional hyperactivity and fibrillation potentials

18. Diabetic Mononeuropathy: 3 Also called Diabetic Mononeuropathy Multiplex Probably closure of vasa nervorum the cause • Focal necrotic pathological changes Or entrapment mononeuroathy, supposedly more common in daibetes, e. g, carpal tunnel Trauma to superficial nerves Distal polyneuropathies can be super imposed on Mononeuropathy multiplex

19. Understanding Electromyography And Nerve Conduction Velocity

20. EMG and NCV - 1 • Uses surface and needle electrodes, calculated electrical current is delivered to the sensory and motor nerves, • Creates action potentials in sensory and motor nerves that are measurable • The amplitude of these potentials is measured by using microprocessor based technology

21. EMG and NCV - 2 • The current generated by action potentials also carries impulses with velocities that are measurable • Specific changes in sensory or motor nerves or primary muscle changes can be detected thereby localizing diagnosis

22. Electrophysiology Diagnosis - 1 EMG and NCV measure only the large myelinated, fast conducting fibers • Conduction velocities are indicative of the integrity or otherwise of the individual functioning or malfunctioning nerve fiber • Amplitude is indicative of the fiber number that is present and functioning,

23. Electrophysiology Diagnosis - 2 Conduction velocity of a fiber depends on fiber size, state of myelination, nodal and internodal length and axonal resistance Synchronous velocities indicate healthy fibers Asynchronous – malfunctioning or unhealthy fibers

24. Electrophysiology Diagnosis - 3 Reduction in axon number results in reduced amplitude of action potentials EMG measures cumulative amplitude arising from all the functioning or firing axons Number is reduced due to • Dead or dying axons - Dying ones cause fibrillations, fasciculations

25. Pathology of Peripheral Nerves • Metabolic hypothesis: • ↑ Sorbitol, ↓ myoinositol, ↓ ATP and 1, 3, 4 PIs • Nonenzymatic glycation of proteins • Abnormal flow along the nerve fibers of proteins • Ischemic insult due to vasa nervorum closure • Nerve hypoxia, oxidant stress • Necrotising or simple vasculitis, angiitis

26. Management of Diabetic Peripheral Neuropathy: 1 • Hyperglycemia, (I.V. Insulin) • Aldose reductase inhibitors • Orlestatin, sorbinil • Moderate to good improvement with sorbinil, on EMG, NCV also • Hypersensitivity with sorbinil

27. Management of Painful Diabetic Polyneuropathy: 2 • Analgesic, normoglycemia • Phenytoin, carbomazepine – Indians feel beeter. West not enthusiastic • Amitryptiline 150 mg a day – hyperesthesia helped as also depression • Gabapentin useful, costly, high doses