Peripheral neuropathy
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types of neuropathy classification and management
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Peripheral neuropathy
- 1. Dr. Anoop.K.R Dept of General Medicine
- 2. Generalized term including disorders of any cause affecting PNS May involve sensory nerves, motor nerves, or both May affect one nerve (mononeuropathy), several nerves together (polyneuropathy) or several nerves not contiguous (Mononeuropathy multiplex)
- 3. Further classified into those that primarily affect the cell body (e.g., neuronopathy or ganglionopathy), myelin (myelinopathy), and the axon (axonopathy)
- 4. Disease Diabetes1 2 Paraproteinaemia2 3 Alcohol misuse1 Renal failure1 Vitamin B-12 deficiency1 HIV infection1 Chronic idiopathic axonal neuropathy4 Prevalence 11-41% (depending on duration, type,and control) 9-10% 7% 4% 3.6% 16% (depending on the population studied, usually much lower) 10-40% of different hospital series BMJ 2010:341:c6100
- 5. Loss of function “- symptoms” Disordered function “+ symptoms” Sensory “Large Fiber” ↓ Vibration ↓ Proprioception Hyporeflexia Sensory ataxia Paresthesias Sensory “Small Fiber” ↓ Pain ↓ Temperature Dysesthesias Allodynia The clinical response to sensory nerve injury
- 6. Loss of function “- symptoms” Disturbed function “+ symptoms” Motor nerves Large fibre Wasting Hypotonia Weakness Hyporeflexia Orthopedic deformity Fasciculation Cramps The clinical response to motor nerve injury
- 7. Loss of function “- symptoms” Disturbed function “+ symptoms” Autonomic nerves ↓ Sweating Hypotension Urinary retention Impotence Vascular color changes ↑ Sweating Hypertension The clinical response to autonomic nerve injury
- 9. By far the majority of the toxic, metabolic and endocrine causes NCVs: CMAPs ↓ 80% lower limit of normal w/o or min velocity or distal motor latency change. Legs>> arms. EMG: Signs of denervation (acute, chronic) and reinnervation
- 10. Unusual by comparison with axonopathies Clues: hypertrophic nerves on exam global arreflexia weakness without wasting motor >> sensory deficits NCS can discriminate inherited from acquired NCS: Distal motor latency prolonged (>125% ULN) Conduction velocities slowed (<80% LLN) May have conduction block EMG: Reduced recruitment w/o much denervation
- 11. SJOGREN’S SYNDROME VIT B12 NEUROPATHY CISPLATIN PYRIDOXINE NEUROTOXICITY FRIEDEREICH’S ATAXIA
- 12. PAIN- burning,shock like,stabbing,pric kling,shooting,la ncinating Allodynia Decreased pinprick sensation Tight band like pressure Insensitive to heat and cold Diminished temperature sensation
- 13. Heriditary sensory neuropathy Lepromatous leprosy Diabetes mellitus Amyloidosis(early familial&primary) Tangier disease Fabry’s disease-pain predomonates Dysautonomia-riley-day syndrome HIV & antiretroviral therapy neuropathy
- 14. Global sensory loss Carcinomatous sensory neuropathy Hereditary sensory neuropathy Diabetic sensory neuropathy Vacor intoxication Xanthomatous neuropathy of primary biliary cirrhosis
- 15. Immune neuropathies Heriditary motor sensory neuropathies Acute intermittent porphyria Diphtheritic neuropathy Lead neuropathy Brachial neuritis Diabetic lumbosacralplexus neuropathy
- 16. Acute-pandysautonomia -botulism -porphyria -GBS -Amiodarone -vincristine Chronic-amyloid,diabetes,sjogren’s,HSN 1&3,chagas,paraneoplastic
- 17. ?MONONEUROPATH Y Focal involvement of a single nerve Weakness & sensory loss in the territory of a single peripheral nerve Pain along the pathway of the nerve Direct trauma compressio n entrapment Vascular lesions neoplasms
- 18. Random pattern of nerve involvement In distribution of separate nerves,asymmetric May/may not be painful Not length dependent Isolated reflex loss CAUSES—inflammatory-leprosy,sarcoid Vascular-Diabetes Pressure,Trauma,Infiltration Vasculitis- PAN,SLE,RA,scleroderma Immune-vaccination
- 19. MC type –Distal symmetric polyneurpathy Burning sensation,tingling,numbness Length dependent pattern Starts in feet,distal stocking glove pattern Fairly symmetric Symmetrically decreased reflexes Sensory>motor
- 20. Diabetes mellitus Alcohol Vit B12 deficiency HIV Although more than one nerve involved one will be prominant
- 21. Lumbosacral polyradiculopathy/stenosis Myelopathy-structural -nonstructural Vascular insufficiency-exercise related cramps,aching pain>numbness Orthopedics –stress #,plantar fascitis
- 22. ?POLYRADICULOPATHY Disease of multiple peripheral nerve roots Asymmetric with erratic distribution-proximal in one,distal in another Pain is a common feature ?MONORADICULOPATHY Root disease by disease of spinal column Changes in distribution of spinal nerve root
- 23. ?SENSORY NEURONOPATHY Ganglion cells predominantly affected Both proximal & distal involvement Sensory ataxia is common No weakness But awkward movement d/t sensory disturbances ?MOTOR NEURONOPATHY Disorder of ant horn cells Weakness,fasciculation,atrophy Not properly a process of peripheral NP
- 24. ?PLEXOPATHY Asymmetric Painful onset Multiple nerves in a single limb Rapid onset of weakness,atrophy Isolated reflex loss
- 25. a/c idiopathic polyneuritis Peripheral nerve+cranial nerve involvement Self limiting painful ophthalmoplegia CAUSES-TB meningitis osteomyelitis skull otitis media syphilitic meningitis sarcoidosis carcinomatous meningitis
- 26. 1.syndrome of a/c ascending motor paralysis a.acute idiopathic polyneuritis b.IMN with polyneuritis c.diphtheria d.hepatitis with polyneuritis e.porphyria f.TOCP poisoning g.paraneoplastic h.post vaccinial
- 27. 2.syndome of subacute sensorymotor NP A.Deficiency=alcoholic beriberi pellagra vit B12 B.Toxins=arsenic,lead,Hg,Pb C.Drugs=nitrofurantoin,INH dapsone,disulfiram clioquinol D.Uremic E.DM,PAN,sarcoidosis A,B,C,D====SYMMETRIC
- 28. 3.C/C sensorimotor polyneuropathy syndrome GENETIC ACQUIRED Peronealmuscle atrophy/CMT leprosy Dejerine sottas disease Diabetes mellitus Hereditary sensory NP uremia Portugeseamyloidosis/ andrade’s disease carcinoma Refsum’s disease myeloma A beta lipoproteinemia paraproteinemia Tangier’s disease amyloidosis Metachromaticleucodystrophy
- 29. RECURRENT POLYNEUROPATHY Relapsing CIDP Porphyria Refsum’s disease HNPP GBS Beriberi Toxic neuropathy
- 30. SENSORY ATAXIC NEUROPATHY Sensory NP(polyganglionopathy) Paraneoplastic sensory NP=sjogren’s =idiopathic Toxic=cisplatin =vit B6 excess Demyelinating polyradiculopathy=MGUS =Millerfisher
- 32. DM hypothyroidism chronic renal failure liver disease intestinal malabsorption malignancy connective tissue diseases [HIV] drug use Vitamin B6 toxicity alcohol and dietary habits •Weight loss, malaise, and anorexia.
- 33. Diabetes and Pre-Diabetes Alcohol neuropathy Chemotherapy ◦ Platinum-based Paraproteinemia Vasculitis and Connective Tissue Diseases Heavy metals and other toxins HIV Amyloidosis Porphyria
- 34. Axonal Vincristine Paclitaxel Nitrous oxide Colchicine Probenecid Isoniazid Hydralazine Metronidazole Pyridoxine Didanosine Lithium Alfa interferon Dapsone Axonal - continued.. Phenytoin Cimetidine Disulfiram Chloroquine Ethambutol Amitriptyline Demyelinating Amiodarone Chloroquine Suramin Gold Neuronopathy Thalidomide Cisplatin Pyridoxine
- 35. ETIOLOGICAL CLASSIFICATION 1.metabolic-DM,amyloidosis,porphyria 2.infections-leprosy,HIV,CMV,syphilis, diphtheria,lymedisease 3.immune- GBS,CIDN,MMN 4.hereditary-CMT 5.Toxic-drugs,alcohol,heavymetals 6.vasculitis-PAN,CSS,cryoglobulinemia 7.paraneoplastic-lung 8.nutritional- B1,B6,B12
- 36. ◦ Guillain-Barré syndrome ◦ Chronic inflammatory demyelinating polyradiculoneuropathy ◦ Diabetes mellitus ◦ Porphyria ◦ Osteosclerotic myeloma ◦ Waldenstrom's macroglobulinemia ◦ Monoclonal gammopathy of undetermined significance ◦ Acute arsenic polyneuropathy ◦ Lymphoma ◦ Diphtheria ◦ HIV/AIDS ◦ Lyme disease ◦ Hypothyroidism ◦ Vincristine (Oncovin, Vincosar PFS) toxicity
- 37. The temporal course of a neuropathy varies, based on the etiology. ◦ With trauma or ischemic infarction, the onset will be acute, with the most severe symptoms at onset. ◦ Inflammatory and some metabolic neuropathies have a subacute course extending over days to weeks. ◦ A chronic course over weeks to months is the hallmark of most toxic and metabolic neuropathies.
- 38. A chronic, slowly progressive neuropathy over many years occurs with most hereditary neuropathies or with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Neuropathies with a relapsing and remitting course include CIDP, acute porphyria, Refsum's disease, hereditary neuropathy with liability to pressure palsies (HNPP), familial brachial plexus neuropathy, and repeated episodes of toxin exposure.
- 39. Ischemic neuropathies often have pain as a prominent feature. Small-fiber neuropathies often present with burning pain, lightning-like or lancinating pain, aching, or uncomfortable paresthesias (dysesthesias).
- 40. Dying-back (distal symmetric axonal) neuropathies initially involve the tips of the toes and progress proximally in a stocking- glove distribution.
- 41. Peripheral neuropathy can present as restless leg syndrome. Proximal involvement may result in difficulty climbing stairs, getting out of a chair, lifting and bulbar involvement can also be seen
- 42. The clinical assessment should include: ◦ careful past medical history, looking for systemic diseases that can be associated with neuropathy, such as diabetes or hypothyroidism.
- 43. All patients should be questioned regarding ◦ HIV risk factors ◦ diet (nutrition) ◦ vitamin use (especially B6) ◦ possibility of a tick bite (Lyme disease) ◦ Constitutional symtoms (malignancy)
- 44. Acute onset (within days) Subacute onset (weeks to months) Chronic course/ insidious onset Relapsing/ remitting course Guillain-Barré syndrome Maintained exposure to toxic agents/medications Hereditary motor sensory neuropathies Guillain-Barré syndrome Acute intermittent porphyria Persisting nutritional deficiency Dominantly inherited sensory neuropathy CIDP Critical illness polyneuropathy Abnormal metabolic state CIDP HIV/AIDS Diphtheric neuropathy Paraneoplastic syndrome Toxic Thallium toxicity CIDP Porphyria
- 45. A cranial nerve examination can provide evidence of mononeuropathies. Funduscopic examination may show abnormalities such as optic pallor, which can be present in leukodystrophies and vitamin B12 deficiency.
- 47. Cardiovagal ◦ Heart rate variability Adrenergic ◦ Valsalva maneuver Induces BP changes and monitors pulse reaction Postganglionic sudomotor function ◦ QSART
- 48. Screening laboratory tests may be considered for all patients with DSP (Level C). Tests with the highest yield of abnormality: 1. blood glucose (fasting) 2. serum B12 with metabolites (methylmalonic acid, homocysteine) 3. SPEP(serum protein electrophoresis) (Level C).
- 49. ANA, RF, Anti-dsDNA, Anti-Ro, Anti-La, ANCA screen, cryoglobulins Urine for heavy metals, porphyrins IFE/urine IFE/ plasma light chain analysis
- 50. BLOOD TC,DC,ESR Urea,electrolytes,LFT RBS,HbA1C Serum protein electrophoresis Auto Ab=ANA,Antiganglioside,Antineuronal Vit B 12 level DNA analysis=chr 17 duplication-HMSN1&1A =chr 17 deletion -HLPP
- 51. URINE BJ protein Porphyria Heavy metals CSF ANALYSIS NERVE CONDUCTION STUDY Variation in axonal,demyelinating neuropathy Conduction block-CIDP,GBS,MMN EMG-muscle denervation changes Sensory threshold Thermal & vibration threshold
- 52. Antibodies against Gangliosides GM1 : Multifocal motor neuropathy GM1, GD1a : Guillain-Barré syndrome GQ1b : Miller Fisher variant Antibodies against Glycoproteins Myelin-associated glycoprotein : MGUS Antibodies against RNA-binding proteins Anti-Hu, antineuronal nuclear antibody 1: Malignant inflammatory polyganglionopathy
- 53. (1) Confirming the presence of neuropathy, (2) Locating focal nerve lesions, (3) Nature of the underlying nerve pathology
- 55. Distal motor latency prolonged Nerve conduction velocity slow Reduced action potential
- 56. The limitations of EMG/NCS should be taken into account when interpreting the findings. ◦ There is no reliable means of studying proximal sensory nerves. ◦ NCS results can be normal in patients with small- fiber neuropathies ◦ Lower extremity sensory responses can be absent in normal elderly patients. EMG/NCS are not substitutes for a good clinical examination.
- 57. IMAGES CXR-sarcoidosis,malignancy Skeletal survey-multiple myeloma Screening for malignancy AUTONOMIC FUNCTION TESTS Diagnostic tests imp in Asymmetric,motor predominant,rapid onset,demyelinating neuropathy
- 58. VASCULITIS GIANT AXONAL NPthy AMYLOIDOSIS Infantile neuroaxonal dystrophy SARCOIDOSIS CMT 1&3 LEPROSY CIDPolyradiculoneuropathy KRABBE’S Paraprotein neuropathy METACHROMATIC LEUKODYSTROPY
- 59. In vasculitis, amyloid neuropathy, leprosy, CIDP, Inherited disorders of myelin, and rare axonopathies The Sural nerve is selected most commonly The superficial peroneal nerve – alternative; :advantage of allowing simultaneous biopsy of the peroneus brevis muscle through the same incision. This combined nerve and muscle biopsy procedure increases the yield of identifying suspected vasculitis
- 60. “For symptomatic patients with suspected polyneuropathy, skin biopsy may be considered to diagnose the presence of a polyneuropathy, particularly SFSN.”
- 61. Slow progression ◦ Treat causative factors if possible ◦ If rapidly progressing IVIG Immunomodulating agents Symptom Management
- 62. Tricyclic antidepressants ◦ Amitryptilin, nortryptilin Calcium channel alpha-2-delta ligands ◦ Gabapentin, pregabalin SNRI’s ◦ Duloxetine, venlafaxine Topical Agents ◦ Lidocaine, Capsaicin
- 63. Antiepileptic Drugs ◦ Carbamazepine, phenytoin, lacosamide SSRI’s Opioid analgesics Tramadol Miscellaneous ◦ Botulinum toxin ◦ Mexiletine ◦ Alpha lipoic acid
- 64. Physical Therapy ◦ Gait and balance training Assistive devices Safe environment Footwear at all times Foot hygiene
- 66. Thanks