Peripheral Neuropathy an overview


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Peripheral Neuropathy an overview; description of clinical manifestations of a wide array of peripheral neuropathies.

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Peripheral Neuropathy an overview

  1. 1. Margarita Correa MD, FAAPMR Physical Medicine and Rehabilitation Physical Medicine Institute Clermont, FL
  2. 2. Anatomy <ul><li>The peripheral nerves include: </li></ul><ul><ul><li>cranial nerves (with the exception of the second) </li></ul></ul><ul><ul><li>spinal nerve roots </li></ul></ul><ul><ul><li>dorsal root ganglia </li></ul></ul><ul><ul><li>peripheral nerve trunks and their terminal branches </li></ul></ul><ul><ul><li>peripheral autonomic nervous system </li></ul></ul>
  3. 3. Anatomy <ul><li>Nerves are composed of different types of axons: </li></ul><ul><ul><li>Large, myelinated axons include motor axons and the sensory axons responsible for vibration sense, proprioception and light touch </li></ul></ul><ul><ul><li>Small myelinated axons are composed of autonomic fibers and sensory axons and are responsible for light touch, pain and temperature </li></ul></ul><ul><ul><li>Small, unmyelinated axons are also sensory and subserve pain and temperature </li></ul></ul>
  4. 4. History <ul><li>Symptoms </li></ul><ul><ul><li>Numbness, tingling (feeling of pins and needles) of hands and/or feet </li></ul></ul><ul><ul><li>Burning pain of hands and/or feet </li></ul></ul><ul><ul><li>Numbness around mouth </li></ul></ul><ul><ul><li>Loss of sensation to touch </li></ul></ul><ul><ul><li>Loss of positional sense </li></ul></ul><ul><ul><li>Weakness and leg cramping </li></ul></ul><ul><ul><li>Difficulty picking things up or buttoning clothes </li></ul></ul><ul><ul><li>Constipation </li></ul></ul>
  5. 5. Physical Examination <ul><li>A cranial nerve examination can provide evidence of mononeuropathies or proximal involvement </li></ul><ul><li>A fundoscopic examination may show abnormalities such as optic pallor, which can be present in leukodystrophies and vitamin B 12 deficiency </li></ul><ul><li>Direct strength testing of muscles innervated by cranial nerves V, VII, IX/X, XI and XII is important, as mild bilateral weakness can be missed by observation only </li></ul>
  6. 6. Physical Examination <ul><li>The motor examination includes a search for fasciculations or loss of muscle bulk (atrophy) </li></ul><ul><li>Muscle tone is normal or reduced </li></ul><ul><li>The pattern of weakness helps narrow the diagnosis: symmetric or asymmetric, distal or proximal, and confined to a particular nerve, plexus or root level </li></ul>
  7. 7. Physical Examination <ul><li>In a patient with a distal symmetric sensorimotor neuropathy, the sensory examination shows reduced sensitivity to light touch, pinprick and temperature in a stocking-and-glove distribution </li></ul><ul><li>Vibration and position sense are reduced in the distal legs prior to involvement of the arms </li></ul><ul><li>In patients with severe loss of position sense, there may be athetoid movement of the fingers or arms when the eyes are closed (pseudoathetosis) or a Romberg sign </li></ul><ul><li>Patients with mononeuritis multiplex may have sensory loss in specific nerve distributions </li></ul>
  8. 8. Physical Examination <ul><li>Deep tendon reflexes are reduced or absent </li></ul><ul><li>A bilateral foot drop may result in a steppage gait in which the patient must lift the knees very high in order to clear the toes </li></ul><ul><li>Proximal weakness results in an inability to squat or to rise unassisted from a chair </li></ul><ul><li>Severe, longstanding neuropathy can result in trophic changes including kyphoscoliosis, pes cavus, loss of hair in affected areas or ulceration </li></ul>
  9. 9. Physical Examination <ul><li>Affected autonomic fibers: orthostatic hypotension without a compensatory rise in heart rate </li></ul><ul><li>Respiratory rate and vital capacity should be evaluated in Guillain-Barré syndrome to assess for respiratory compromise </li></ul><ul><li>The presence of lymphadenopathy, hepatomegaly or splenomegaly, and skin lesions may provide evidence of systemic disease </li></ul><ul><li>Pale transverse bands in the nail beds, parallel to the lunula (Mees' lines) suggest arsenic poisoning </li></ul>
  10. 10. Laboratories <ul><li>The most common presentation is distal symmetric sensorimotor neuropathy, i.e. diabetes mellitus </li></ul><ul><li>Initial evaluation should include: </li></ul><ul><ul><li>fasting serum glucose (FBS) </li></ul></ul><ul><ul><li>glycosylated hemoglobin (A1C) </li></ul></ul><ul><ul><li>blood urea nitrogen (BUN) </li></ul></ul><ul><ul><li>creatinine (Cr) </li></ul></ul><ul><ul><li>complete blood cell count (CBC) </li></ul></ul><ul><ul><li>erythrocyte sedimentation rate (ESR) </li></ul></ul><ul><ul><li>urinalysis </li></ul></ul><ul><ul><li>vitamin B 12, folate </li></ul></ul><ul><ul><li>TSH levels </li></ul></ul>
  11. 11. Autoantibodies to Peripheral Nerves Antigens <ul><li>Anti-Asialo-GM1 ganglioside neuropathy </li></ul><ul><li>Anti-GD1a ganglioside neuropathy </li></ul><ul><li>Anti-GD1b ganglioside neuropathy </li></ul><ul><li>Anti-GM1 ganglioside neuropathy </li></ul><ul><li>Anti-GM2 ganglioside neuropathy </li></ul><ul><li>Anti-GQ1b ganglioside neuropathy </li></ul><ul><li>Anti-MAG/SGPG neuropathy </li></ul><ul><li>Anti-sulfatide neuropathy </li></ul><ul><li>Asialo GM1 antibody </li></ul><ul><li>GD1a antibody </li></ul><ul><li>GD1b antibody </li></ul><ul><li>GM1 antibody </li></ul><ul><li>GM2 antibody </li></ul><ul><li>GQ1b antibody </li></ul><ul><li>MAG/SGPG antibody </li></ul><ul><li>Sulfatide antibody </li></ul>
  12. 12. Rheumatologic, Autoimmune, and Vasculitic Disease <ul><li>Disease </li></ul><ul><li>Laboratories </li></ul><ul><li>Polyarteritis </li></ul><ul><li>SLE </li></ul><ul><li>Rheumatoid arthritis </li></ul><ul><li>Wegener’s granulomatosis </li></ul><ul><li>Sjögren’s syndrome </li></ul><ul><li>Celiac disease </li></ul><ul><li>Cryoglobulins, immune complexes, CH50, hepatitis B and C serology, parvovirus serology, HIV-1 serology </li></ul><ul><li>ANA, dsDNA antibodies </li></ul><ul><li>Cyclic citrullinated peptide antibody, rheumatoid factor </li></ul><ul><li>Anti-neutrophil cytoplasmic antibody (ANCA) </li></ul><ul><li>SS-A/Ro antibody, SS-B/La antibody </li></ul><ul><li>Gliadin, transglutaminase, and endomysial antibodies </li></ul>
  13. 13. Paraneoplastic Disease <ul><li>Neoplasm </li></ul><ul><li>Laboratory </li></ul><ul><li>Lung cancer </li></ul><ul><li>Monoclonal gammopathy </li></ul><ul><li>Myeloma </li></ul><ul><li>Macroglobulinemia </li></ul><ul><li>Chronic lymphocytic leukemia </li></ul><ul><li>Hu antibodies </li></ul><ul><li>Immunoglobulin profile, IFE, serum & urine </li></ul><ul><li>Immunoglobulin profile, IFE, serum & urine, VEGF level </li></ul><ul><li>Immunoglobulin profile, IFE, serum & urine </li></ul><ul><li>Immunoglobulin profile, IFE, serum & urine </li></ul><ul><li>IFE = immunofixation electrophoresis </li></ul><ul><li>VEGF = vascular endothelial growth factor </li></ul>
  14. 14. <ul><li>Primary Amyloidosis </li></ul><ul><li>Heavy Metal Toxicity: </li></ul><ul><li>Lead, Arsenic, Mercury </li></ul><ul><li>Laboratory </li></ul><ul><li>Immunoglobulin profile, IFE, serum & urine </li></ul><ul><li>Kappa/lambda light chains, free with ratio, serum </li></ul><ul><li>Lichen Amyloidosis </li></ul><ul><li>Laboratory </li></ul><ul><li>Urine heavy metals </li></ul><ul><li>Lead Intoxication </li></ul>
  15. 15. Nutritional Diseases <ul><li>Vitamin Deficiency </li></ul><ul><li>Laboratories </li></ul><ul><li>Vitamin B 12 deficiency </li></ul><ul><li>Vitamin B 6 deficiency </li></ul><ul><li>Vitamin B 6 toxicity </li></ul><ul><li>Vitamin B 1 deficiency </li></ul><ul><li>Vitamin E deficiency </li></ul><ul><li>Folate deficiency </li></ul><ul><li>CBC, serum B 12 </li></ul><ul><li>Serum B 6 </li></ul><ul><li>Serum B 6 </li></ul><ul><li>Serum B 1 </li></ul><ul><li>Serum vitamin E </li></ul><ul><li>Serum folate </li></ul>
  16. 16. Infectious and Inflammatory Disease <ul><li>Infectious Agent </li></ul><ul><li>Laboratories </li></ul><ul><li>AIDS </li></ul><ul><li>Lyme disease </li></ul><ul><li>Herpes zoster </li></ul><ul><li>Cytomegalovirus </li></ul><ul><li>Hepatitis B </li></ul><ul><li>Hepatitis C </li></ul><ul><li>Parvovirus </li></ul><ul><li>Sarcoidosis </li></ul><ul><li>HIV-1 antibody </li></ul><ul><li>Borrelia burgdorferi antibodies (total, IgG, IgM) </li></ul><ul><li>Varicella zoster antigen and antibodies (IgG, IgM) </li></ul><ul><li>CMV antigen and antibodies (IgG, IgM) </li></ul><ul><li>HBs antigen, HBc antibodies (IgG, IgM) </li></ul><ul><li>Hepatitis C antibody </li></ul><ul><li>Parvovirus antibody </li></ul><ul><li>Angiotensin converting enzyme </li></ul>
  17. 17. Diagnosis <ul><li>Autonomic studies include determination of: </li></ul><ul><ul><li>heart rate variation with respiration </li></ul></ul><ul><ul><li>heart rate response and blood pressure to standing/tilting </li></ul></ul><ul><ul><li>blood pressure response to sustained hand grip </li></ul></ul><ul><ul><li>measure of sympathetic skin response </li></ul></ul>
  18. 18. Diagnosis <ul><li>The cerebrospinal fluid (CSF) is useful in evaluation of myelinopathies and polyradiculopathies </li></ul><ul><ul><li>An elevated total protein level with less than 5 white blood cells (albuminocytologic dissociation) is present in acquired inflammatory neuropathy (e.g., Guillain-Barré syndrome, CIDP) </li></ul></ul><ul><ul><li>Cytology (lymphoma) </li></ul></ul><ul><ul><li>Special studies such as: </li></ul></ul><ul><ul><ul><li>Lyme polymerase chain reaction </li></ul></ul></ul><ul><ul><ul><li>Cytomegalovirus branched chain DNA (polyradiculopathy or mononeuritis multiplex in AIDS) </li></ul></ul></ul>
  19. 19. Diagnosis <ul><li>Nerve biopsy is only helpful in very specific cases to diagnose vasculitis, leprosy, amyloid neuropathy, leukodystrophies, sarcoidosis and, occasionally, CIDP </li></ul><ul><li>The sural nerve is the one most commonly selected for biopsy </li></ul>
  20. 20. EMG & NCS <ul><li>EMG and nerve conduction studies are often the most useful initial laboratory studies in the evaluation of patients with peripheral neuropathy </li></ul>
  21. 21. Electrodiagnosis <ul><li>Sensory NCS: sural, superficial peroneal, median, ulnar (at least in one side), if abnormal study on the contralateral side </li></ul><ul><li>Motor NCS: peroneal and tibial nerve, median and ulnar (at least in one side), if abnormal study on the contralateral side, *F-waves/H-reflexes </li></ul><ul><li>Cranial nerves: if affected, perform direct facial nerve stimulation, blink reflex, spinal accessory </li></ul><ul><li>Needle EMG: one upper and lower limb muscle, distal & proximal including paraspinal regions, document on the contralateral side in the more affected muscles </li></ul>
  22. 22. Classification <ul><li>Hereditary </li></ul><ul><li>Acquired </li></ul><ul><li>Focal </li></ul><ul><li>Idiopathic </li></ul>
  23. 23. Facts <ul><li>Diabetes and alcoholism are the most common causes of peripheral neuropathy in the United States </li></ul><ul><li>The most common presentation of peripheral neuropathy is distal symmetric sensorimotor dysfunction </li></ul>
  24. 24. Hereditary <ul><li>Charcot-Marie-Tooth Disease and Related Neuropathies </li></ul><ul><li>Type I – most common (~1:400) ~ 50% of hereditary neuropathy, autosomal dominant, demyelination and onion bulb </li></ul><ul><li>Type 2 – axonal atrophy and degeneration </li></ul><ul><li>Type 3 – Dejerine-Sottas disease, congenital hypomyelination, classic onion bulbs, severe form relatively rare, autosomal dominant sporadic or </li></ul><ul><li>recessive </li></ul><ul><li>Type 4 – all forms have hypomyelination </li></ul>
  25. 25. Hereditary <ul><li>X-Linked Charcot-Marie-Tooth Disease </li></ul><ul><li>Hereditary Neuropathy with Liability to Pressure Palsies: HNPP = tomaculous neuropathy </li></ul><ul><li>Hereditary Sensory and Autonomic Neuropathies (types 1, 2, 3, 4, 5) </li></ul><ul><li>Familial Amyloid Polyneuropathies (types I, II, III, IV) </li></ul>
  26. 26. Hereditary Disorders of Lipid Metabolism <ul><li>Metachromatic Leukodystrophy - widespread myelin degeneration of central & peripheral nervous systems and abdominal organ dysfunction, deficiency of arylsulfatase A results in the accumulation of sulfatides in various tissues </li></ul><ul><li>Krabbe’s Disease (Globoid Cell Leukodystrophy) widespread degeneration of the CNS white matter with collection of globoid cells = macrophages </li></ul>
  27. 27. Hereditary Disorders of Lipid Metabolism <ul><li>Adrenoleukodystrophy - progressive dementia, optic atrophy, cortical blindness, seizures and spasticity </li></ul><ul><li>Refsum’s Disease - increased phytanic acid, retinitis pigmentosa, cerebellar dysfunction, increased protein in CSF </li></ul><ul><li>Tangier Disease - rare autosomal recessive disorder, deficiency of HDL </li></ul>
  28. 28. Hereditary Disorders of Lipid Metabolism <ul><li>Cerebrotendinous Xanthomatosis (Cholestanolosis) - progressive dementia, spasticity, ataxia, cataracts, deposition of xanthomas on tendons, increased cholestanol -derivative from cholesterol </li></ul>
  29. 29. Hereditary Ataxia <ul><li>Friedreich’s Ataxia </li></ul><ul><li>Vitamin E deficiency </li></ul><ul><li>Abetalipoproteinemia </li></ul><ul><li>(Bassen-Kornzweig Disease) </li></ul><ul><li>Ataxia-Telangiectasia </li></ul><ul><li>Spinocerebellar Ataxias </li></ul><ul><li>Marinesco-Sjögren-Garland Syndrome </li></ul>
  30. 30. Hereditary Neuropathies <ul><li>Cockayne’s Syndrome </li></ul><ul><li>Giant Axonal Neuropathy </li></ul><ul><li>Infantile Neuroaxonal Dystrophy </li></ul><ul><li>Porphyria : inherited disorders caused by defects in heme biosynthesis, acute abdominal pain, agitation, hallucinations, seizures; later manifestation of motor weakness in the upper or lower limbs, may be asymmetric, cranial nerves and autonomic system can be involved </li></ul>
  31. 31. Acquired Neuropathies <ul><li>Immune-Mediated Polyneuropathies </li></ul><ul><li>Neuropathies Associated with Infections </li></ul><ul><li>Neuropathies Associated with Endocrinopathies </li></ul><ul><li>Neuropathies Associated with Systemic Diseases </li></ul><ul><li>Neuropathies Associated with Malignancies </li></ul><ul><li>Toxic Neuropathies </li></ul><ul><li>Neuropathies Related to Nutritional Deficiencies </li></ul><ul><li>Chronic Idiopathic Sensory or Sensorimotor Polyneuropathy </li></ul>
  32. 32. Immune-Mediated <ul><li>Acute Inflammatory Demyelinating Polyradiculo-neuropathy (AIDP) – Guillain Barre Syndrome </li></ul><ul><ul><li>The most common cause of acute generalized weakness </li></ul></ul><ul><ul><li>Usually a preceding infectious process: viral, bacterial </li></ul></ul><ul><ul><li>Ascending paralysis </li></ul></ul><ul><ul><li>CSF: elevated protein in 80% of patient </li></ul></ul><ul><ul><li>(+) anti-GM1 antibodies </li></ul></ul><ul><ul><li>EMG & NCS: conduction block, prolongation or absence of F-waves, reduced conduction velocity, prolonged motor latencies </li></ul></ul><ul><li>Treatment </li></ul><ul><ul><li>IVIg </li></ul></ul><ul><ul><li>Plasmapheresis </li></ul></ul><ul><ul><li>Rehabilitation </li></ul></ul>
  33. 33. CIDP <ul><li>Chronic Acquired Demyelinating Polyneuropathies </li></ul><ul><ul><li>Chronic Inflammatory Demyelinating Polyneuropathies </li></ul></ul><ul><ul><li>(CIDP) </li></ul></ul><ul><ul><li>Distal Acquired Demyelinating Symmetric (DADS) </li></ul></ul><ul><ul><li>Multifocal Acquired Demyelination Sensory and Motor Neuropathy (MADSAM) </li></ul></ul><ul><ul><li>Multifocal Motor Neuropathy (MMN) </li></ul></ul>
  34. 34. CIDP <ul><li>May be associated with preceding drug use, vaccination, infections, other autoimmune or collagen vascular disease or monoclonal gammopathies </li></ul><ul><li>Peak incidence: 40-60 years </li></ul><ul><li>Progressive weakness, usually symmetric, relapsing with sensory changes, absent reflexes </li></ul><ul><li>Variants: 80% - both motor and sensory involvement, 10% - pure motor, 5-10% - pure sensory </li></ul>
  35. 35. CIDP <ul><li>Laboratory Features: </li></ul><ul><ul><li>Electrodiagnostic (EMG & NCS) abnormality similar to GBS </li></ul></ul><ul><ul><li>Increased CSF protein concentration is the most frequently abnormal finding (>45mg/dl) </li></ul></ul><ul><ul><li>Nerve biopsy exhibits demyelination </li></ul></ul><ul><li>Rx: </li></ul><ul><ul><li>Prednisone </li></ul></ul><ul><ul><li>IVIg: 66% - 95% of patients respond to initial IVIg </li></ul></ul><ul><ul><li>Plasmapheresis </li></ul></ul><ul><ul><li>Cytotoxic agents - Cyclophosphamide or Cyclosporin </li></ul></ul><ul><ul><li>Rehabilitation </li></ul></ul><ul><li>Only 1/3 of the patients achieve complete remission off medications </li></ul>
  36. 36. Immune-Mediated: Vasculitis <ul><li>Primary Vasculitis </li></ul><ul><ul><li>Large Vessel: Giant cell (temporal) </li></ul></ul><ul><ul><li>arteritis </li></ul></ul><ul><ul><li>Medium and small vessel vasculitis (Polyarteritis nodosa, Churg-Strauss syndrome, Wegener’s granulomatosis, Microscopic polyangiitis, Isolated angiitis of the nervous system) </li></ul></ul><ul><li>Secondary Vasculitis associated with </li></ul><ul><ul><li>Connective tissue disorders: RA, SLE </li></ul></ul><ul><ul><li>Malignancies: small cell CA lung, lymphoma </li></ul></ul><ul><ul><li>Infections: herpes varicella zoster, CMV, HIV, hepatitis </li></ul></ul><ul><ul><li>Cryoglobulinemia </li></ul></ul>
  37. 37. Autoimmune Connective Tissue Diseases <ul><li>Sjögren’s Syndrome </li></ul><ul><li>Rheumatoid Arthritis </li></ul><ul><li>Systemic Lupus Erythematosus </li></ul><ul><li>Polyarteritis Nodosa </li></ul><ul><li>Scleroderma </li></ul><ul><li>Mixed Connective Tissue Disease </li></ul>
  38. 38. Immune-Mediated <ul><li>Sarcoidosis : multisystem granulomatous disorder affecting several organs, central & peripheral nervous system - involved in ±5% of patients </li></ul><ul><li>Idiopathic Perineuritis </li></ul><ul><li>Hypereosinophilia Syndrome </li></ul><ul><li>Isaac’s Syndrome - neuromyotonia, continuous muscle fiber activity syndrome </li></ul>
  39. 39. Infectious <ul><li>Leprosy (Hansen’s Disease) : 10 10 million cases, mycobacterium leprae </li></ul><ul><li>Lyme’s Disease : spirochete transmitted by ticks, Borrelia burgdorferi, erythema migrans </li></ul><ul><li>Diptheria : neuropathy occurs in ±20% of </li></ul><ul><li>cases associated with circulatory and </li></ul><ul><li>myocardial failure; bacterial toxin causes </li></ul><ul><li>demyelination may cause cranial neuropathies </li></ul><ul><li>HIV: can be associated to the viral infection, nutritional deficiencies and medications – </li></ul><ul><li>Nucleoside reverse transcriptase inhibitors (NRTIs), or &quot;d-drugs&quot;, are most frequently associated with peripheral neuropathy </li></ul>
  40. 40. Infectious <ul><li>Human T-Lymphotropic Virus-I (HTLV-I) </li></ul><ul><li>CMV </li></ul><ul><li>Epstein-Barr virus </li></ul><ul><li>Herpes Varicella Zoster virus </li></ul><ul><li>Hepatitis B and C </li></ul>
  41. 41. Endocrinopathies <ul><li>Diabetes Mellitus: 70% of the patients demonstrate the distal symmetric form, sensory or mixed </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Acromegaly </li></ul><ul><li>Hypothyroidism – myxedema deposition </li></ul>
  42. 42. Systemic Diseases <ul><li>Uremic Neuropathy </li></ul><ul><li>Gastrointestinal Diseases: Crohn’s disease, gluten-induced enteropathy </li></ul><ul><li>Liver Diseases: primary biliary cirrhosis </li></ul><ul><li>COPD </li></ul><ul><li>Gout </li></ul><ul><li>Critical Illness Polyneuropathy </li></ul>
  43. 43. Malignancies <ul><li>Paraneoplastic Neuropathies : anti-Hu syndrome </li></ul><ul><li>Cryptogenic Sensory or Sensorimotor Polyneuropathy : 29% related to Gastric malignancy </li></ul><ul><li>Neuropathies Related to Tumor Infiltration : neurofibromatosis, local infiltration by tumor tissue </li></ul><ul><li>Noninfiltrative Neuropathies Associated with Lymphoproliferative Disorders and Monoclonal Gammopathies </li></ul>
  44. 44. Malignancies <ul><li>Acquired Amyloidosis </li></ul><ul><li>Monoclonal Gammopathy of Uncertain Significance : IgM is the most common in patients with neuropathy, accounts for >90% </li></ul><ul><li>Neuropathies Associated with Bone Marrow Transplantation and Graft-vs-Host Disease </li></ul>
  45. 45. Toxic Neuropathies <ul><li>Chemotherapy : anti-nucleosides, vincristine, cisplatin, paclitaxel and the podophyllotoxins </li></ul><ul><li>Other medications : amiodarone, chloroquine, sulfa medications, vitamin B6 intoxication </li></ul><ul><li>Industrial and Environmental Agents : hexacarbon inhalation </li></ul><ul><li>Heavy Metal Intoxication : arsenic, lead, mercury </li></ul><ul><li>Ethanol : alcoholism - 30% of all cases of generalized polyneuropathy </li></ul>
  46. 46. Nutritional Deficiencies <ul><li>Thiamine (Vitamin B1) </li></ul><ul><li>Pyridoxine (Vitamin B6) </li></ul><ul><li>Cobalamin (Vitamin B12) </li></ul><ul><li>Folic Acid </li></ul><ul><li>Vitamin E </li></ul><ul><li>Postgastrectomy Syndromes </li></ul><ul><li>Hypophosphatemia </li></ul><ul><li>Jamaican Neuropathy </li></ul><ul><li>Alcoholic Neuropathy </li></ul>
  47. 47. Focal Peripheral Neuropathies <ul><li>Median Nerve – carpal tunnel syndrome, AIN </li></ul><ul><li>Ulnar nerve – cubital tunnel syndrome </li></ul><ul><li>Radial Nerve – radial tunnel syndrome, PIN </li></ul><ul><li>Peroneal Nerve – fibular head, drop foot </li></ul><ul><li>Tibial Nerve – tarsal tunnel syndrome </li></ul><ul><li>Cranial neuropathies: trigeminal, facial, recurrent and superior laryngeal – vagus, phrenic, spinal accessory, hypoglossal </li></ul>
  48. 48. Treatment <ul><li>Acquired : treat the cause </li></ul><ul><li>Medications : </li></ul><ul><ul><li>Anti-seizures medications: Lyrica, Neurontin </li></ul></ul><ul><ul><li>Anti-depressant medications: Cymbalta (SNRI) </li></ul></ul><ul><ul><li>TCA’s: Amitriptyline, Nortriptyline </li></ul></ul><ul><ul><li>Lidoderm Patch 5%: post-herpetic neuralgia </li></ul></ul><ul><ul><li>Topical: Capsaicin </li></ul></ul>
  49. 49. Treatment <ul><li>Rehabilitation </li></ul><ul><ul><li>physical therapy </li></ul></ul><ul><ul><li>occupational therapy </li></ul></ul><ul><ul><li>therapeutic exercises to strengthen muscles, improve balance, coordination and propioception, desensitization techniques </li></ul></ul><ul><ul><li>TENS - pain control </li></ul></ul>
  50. 50. References <ul><li>Asbury AK, Thomas PK. Peripheral nerve disorders 2. Oxford: Butterworth Heinemann Ltd; 1995. </li></ul><ul><li>Bollensen E, Schipper HI, Steck AJ. Motor neuropathy with activity of monoclonal IgM antibody to GD1a ganglioside. J Neurol . 1989;236:353-355. </li></ul><ul><li>Chiba A, Kusunoki S, Obata H, et al. Serum anti-GQ1b antibodies are associated with ophthalmoplegia in Miller-Fisher syndrome and Guillaine-Barre syndrome. Neurology . 1993;43:1911-1917. </li></ul><ul><li>Duane GC, Farrer RG, Dalakas MC, et al. Sensory neuropathy associated with immunoglobulin M to GD1b ganglioside. Ann Neurol. 1992;31:683-685. </li></ul><ul><li>Dyck PJ, Thomas PK, Griffin JW, et al. Peripheral Neuropathy , 3rd Ed. Philadelphia: WB Saunders; 1993. </li></ul><ul><li>Kelly JJ Jr, Kyle RA, Miles JM, et al. The spectrum of peripheral neuropathy in myeloma. Neurology . 1981;31:24-31. </li></ul><ul><li>Kelly JJ Jr, Kyle RA, Obrien PC, et al. The prevalence of monoclonal gammopathy in peripheral neuropathy. Neurology . 1981;31:1480-1483. </li></ul><ul><li>Kinsella LJ, Lange DJ, Trojaborg W, et al. The clinical and electrophysiological correlates of elevated anti-GM1 antibody titers. Neurology . 1994;44:1278-1282. </li></ul><ul><li>Kyle RA, Greip PR. Amyoloidosis (AL): clinical and laboratory features of 229 cases. Mayo Clin Proc . 1983;58:665-683. </li></ul><ul><li>Latov N. Pathogenesis and therapy of neuropathies associated with monoclonal gammopathies. Ann Neurol. 1995;37(S1):S32-42. </li></ul><ul><li>Latov N, Steck AJ. Neuropathies associated with glycoconjugate antibodies and IgM monoclonal gammopathies. In: Asbury A, Thomas PK (eds). Peripheral Nerve Disorders II . Boston: Butterworth-Heinemann;1995:153-173. </li></ul><ul><li>Ogino M, Orazio N, Latov N. IgG anti-GM1 antibodies from patients with acute motor neuropathy are predominantly of the IgG1 and IgG3 subclasses. J Neuroimmunol . 1995; 58:77-80. </li></ul><ul><li>Pestronk A, Li F, Griffin J, et al. Polyneuropathy syndromes associated with serum antibodies to sulfatide and myelin associated glycoprotein. Neurology . 1991; 41:357-362. </li></ul><ul><li>van den Berg LH, Hays AP, Nobile-Orazio E, et al. Anti-MAG and anti-SGPG antibodies in neuropathy. Muscle Nerve . 1996;19:637-643. </li></ul>
  51. 51. Thanks !