Peripheral neuropathy

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Peripheral neuropathy

  1. 1. Peripher alNeuropathy
  2. 2. Peripher al Ner ve Myelin : Current cannot flow Axon : Not nerves left
  3. 3. Types of nerve fibers Diameter Conduction Function microns Velocity m/sA alpha 1-20 70-110 Motor, Proprioception beta 5-10 30-60 Touch gama 3-6 20-30 Fusimotor, spindles delta 2-5 20-30 Sharp painB <3 5-15 Autonomic, pregangl.C <1.3 0.5-2 Slow painNon myelinated
  4. 4. T he Peripher al Ner vousSystem  Motor: weakness, atrophy  Sensory loss  Large Fibers (position)  Small fiber (pain)  Reflex loss  Autonomic symptoms  (redness, dizziness, ED)
  5. 5. Definitions NeuropathyPathological process affecting a peripheral nerve/s MononeuropathyA single nerve affected Mononeuritis multiplexMultiple mononeuropathy or Multifocal neuropathy
  6. 6. PolyneuropathyDiffuse symmetrical disease usually beginning peripherally Acute/Chronic Static/Prog Relapsing/Recovering Motor Sensory Sensrimotor(Mixed) AutonomicDemyelinating AxonalRadiculopathy Nerve root disease
  7. 7. Mechanisms of damage Demyelination Myelin sheath disrupted GBS Post Diphtheric HSMN Axonal degeneration Axon damage Toxic neuropathies Wallerian degeneration Nerve section Compression Focal demyelination Entrapment-Carpel tunnel syndrome Infarction Arteritis Polyarteritis nodosa Churg-Strauss synd. DM Infiltration Infiltration Leprosy Sarcoidosis
  8. 8. Classification EXAMINATION FINDINGS  Purely Motor or Sensory or Sensorimotor?  Proximal or distal? Symmetric or asymmetric?  Multifocal, generalized, regional? Upper limbs, lower limbs, neck, trunk? TIMING  Acute or chronic?
  9. 9. ASSOCIATED FINDINGS Painful or painless? Hereditary or sporadic? ELECTRODIAGNOSIS Axonal or demyelinating? LABORATORYParaprotein present? Type? Antibody against nerve? CSF protein level? HISTOLOGY Inflammatory Cells
  10. 10. Epidemiology Prevalence  ~ 2.4%  ~ 8% in people older than 55 years DM is most common cause
  11. 11. Epidemiology Other common systemic causes  Metabolic disorders  Infectious agents  Vasculitis  Toxins  Drugs  Autoimmunity  Inherited
  12. 12. Diagnosis  Most important details to determine  Distribution  Duration  Course
  13. 13. Diagnosis  Clinical manifestations vary widely  Altered sensation  Pain  Muscle weakness or atrophy  Autonomic symptoms
  14. 14. Labor ator y Screening for“Treatable” Neuropathy? B12 Not truly length-dependent Diabetes This type of neuropathy generally a late finding ANA, chronic disease Screen for connective tissue screen diseases (late finding) TSH If positive, have you proven anything? ESR If onset is recent HIV Risk Factors Review medications Big question
  15. 15. Diagnosis  Electro diagnostic studies  Sensitive, specific, validated  Extension of neurologic exam  Nerve conduction studies (NCS)  Needle electromyography (EMG)
  16. 16. Diagnosis  Establish distribution  Mononeuropathy  Mononeuropathy multiplex  Polyneuropathy  Determine primary pathology  Demyelinating  Axonal
  17. 17. Mononeuropathy Focal lesion involving a single nerve Electro diagnostic studies indispensible  Localize site of injury  Determine severity of lesion
  18. 18. Mononeuropathy Causes  Entrapment  Carpal tunnel syndrome is most common  Foot drop  Focal compression  Trauma
  19. 19. MononeuropathyMultiplex Separate/noncontiguous involvement  Simultaneously  Serially Pattern  Random  Multifocal Frequently evolves quickly
  20. 20. MononeuropathyMultiplex Urgent assessment for vasculitis  Polyarteritis nodosa  Churg-Strauss disease  Connective tissue diseases  Rheumatoid arthritis  Sjogren’s syndrome
  21. 21. Polyneuropathy Most commonly distal symmetrical  Fiber effect is length-dependent  Toes and soles affected first  Associations  Systemic diseases  Metabolic disorders  Exogenous toxins
  22. 22. Polyneuropathy Diabetes is prototype  Chronic, sensory and motor  Commonest in developed world  Alcoholism is the second most common
  23. 23. Polyneuropathy Early symptoms  Sensory abnormalities  Numbness  Burning  Paresthesias  Dysesthesias  Distally predominant  Symmetrical
  24. 24. Polyneuropathy Evolution is centripetal  Symptoms spread up legs  Sensory loss  Dysesthesias  Ankles jerks are depressed  Patients have trouble walking on their heels  Foot plantar flexion remains strong
  25. 25. Polyneuropathy  Symptoms noticed in fingertips  Numbness  Dysesthesias Advanced picture is easily recognizable  Stocking-glove sensory loss  Distal muscle wasting and weakness  Absent tendon reflexes
  26. 26. Polyneuropathy Sub classification  Historical features are indispensible  Other medical conditions  Symptoms of systemic disease  Recent viral or other infectious diseases  Recent vaccinations  Institution of new medications
  27. 27. Polyneuropathy  Exposure to toxins  Alcohol  Heavy metals  Organic solvents  Family history  Duration and clinical course are helpful  Acute = days to weeks  Chronic = months to years
  28. 28. LaboratoryInvestigations  CBC  UREA  SUGAR  TFTs  B12  Methylmalonic acid  ESR  Homocysteine  CRP  Folate
  29. 29. Treatment General Subtype specific  Diabetes mellitus  Renal insufficiency  Hypothyroidism  Vitamin B12 deficiency  Systemic vasculitis
  30. 30. Treatment General  Pain  Antiepileptic drugs  Antidepressants  Tramadol
  31. 31. Treatment  Preventative and palliative  Weight reduction  Assiduous foot care  Good shoes  Ankle-foot orthoses as needed Several organizations provide support
  32. 32. Chronic Length DependentNeuropathy  Begins in toes or feet  Stocking distribution  Progresses rostrally  Tops and bottoms of feet  Weakness begins in ankles when sensation reaches calves Sometimes diagnosable, Never treatable?
  33. 33. Phenotype CIDP Small Differential
  34. 34. Phenotype-MADSAMNeur opathy Key DDx:  Brachial plexopathies  Vasculitis mononeuropathy multiplex  Compression neuropathies  HNPP (genetic testing)
  35. 35. Multifocal MotorNeur opathy (MMN) Almost always in hands and wrists Pattern of weakness is in the distribution of individual peripheral nerves  i.e. severe involvement in ulnar distribution sparing median Lack of atrophy in weak muscles No pathological reflexes
  36. 36. Uncertainty  Many cases are not easily definable because of multiplicity of patterns  Cases that are not clearly untreatable are possibly treatable

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