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Peripheral neuropathy
This document discusses peripheral neuropathy, including: 1. It defines peripheral neuropathy and describes the different types that can affect motor, sensory, or autonomic nerves. 2. It outlines various causes of peripheral neuropathies including hereditary, infectious, inflammatory, metabolic, toxic, and more. 3. It describes the clinical presentations of different types of peripheral neuropathies based on the affected nerves and provides examples.
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Peripheral neuropathy
- 1. Dr. Sabir KumarKhadka Dept of Orthopedics PERIPHERAL NEUROPATHY
- 2. Refers to nervesoutside thebrainand spinal cord. Broken downinto Sensory Motor Autonomic ▪ Parasympathetic ▪ Sympathetic
- 3. May affectone nerve (mononeuropathy), Several nerves together (polyneuropathy) Several nerves not contiguous (Mononeuropathy multiplex) Further classified into those that primarily affect the cell body (e.g., neuronopathy or ganglionopathy), myelin (myelinopathy), and the axon (axonopathy)
- 4. Pathology Acute axonal interruption Lossof motor and sensory function is immediate and complete Detectable at early stage by nerve conduction and EMG. Chronic axonal degeneration Symptoms tend to appear in feet and legs before arms and hands(stocking and glove distribution) NCV:reduction in size of CMAP and SNAP responses Demyelinating neuropathies Focal entrapment most common in nerve entrapment syndrome and blunt soft tissue trauma. Slowing of conduction and complete nerve block Eg: GBS and HMSN
- 5. Possible mechanisms ofperipheral nervedegeneration Demyelination –e.g. Guillain-BarreSyndrome Axonal degeneration - e.g. toxic neuropathies Compression –e.g. carpal tunnelsyndrome Infarction –e.g.diabetes Infiltration –e.g. leprosy and granulomas
- 6. Causes of polyneuropathy Hereditary Hereditarymotor and sensory neuropathy Friedreich ataxia Hereditary sensory neuropathy Infections Viral infections Herpes zoster Neuralgic amyotrophy Leprosy
- 7. Inflammatory Acute inflammatory polyneuropathy Guillainbarre syndrome SLE Nutritional and metabolic Vitamin deficiencies Diabetes Myxoedema Amyloidosis Neoplastic Primary carcinoma Myeloma Toxic Alcohol lead
- 8. Disease Diabetes Paraproteinaemia Alcohol misuse Renal failure VitaminB-12 deficiency HIV infection Chronic idiopathic axonal neuropathy 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
- 9. 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
- 10. Loss of function “-symptoms” Disturbed function “+ symptoms” Motor nerves Wasting Fasciculation Large fibre Hypotonia Cramps Weakness Hyporeflexia Orthopedic deformity The clinical response to motor nerve injury
- 11. Loss of function “-symptoms” Disturbed function “+ symptoms” Autonomic nerves ↓ Sweating Hypotension ↑ Sweating Hypertension Urinary retention Impotence Vascular color changes The clinical response to autonomic nerve injury
- 13. Peripheral nerve compressionand entrapment Carpaltunnelsyndromeisacommon mononeuropathy –Median nerve entrapement Clinicalpresentation Pain, tinglingand paraesthesia on palmaraspectof handandfingers Weaknessof thenar muscles and wasting of abductor pollicis brevis Painmay extend to arm andshoulder Tinel’sand Phalen’stests arepositive.
- 14. Paraesthesia Numbness Burning pain Lossof vibrationsenseand positionsense Difficulty usingsmall objects e.g.needles Subacute with ataxiadue to lossof senseof posture Feet are usuallyaffected first –Stock andGlove
- 15. ClinicalPresentation: Postural hypotension Urinary retention Erectiledysfunction Diarrhoea/constipation Diminished sweating Impaired pupillaryresponse Cardiacarrhythmias Might occurin: Diabetes Amyloidosis Guillain-Barre syndrome
- 16. Clinical presentation: Progressive weaknessorclumsiness Difficulty walking (falling or stumbling) Respiratory difficulties (falling vital capacity) Wasting Foot or wrist drop might be seen Reflexes absent orreduced
- 17. MONONEUROPATHY Focal involvement of asingle nerve Weakness & sensory loss in the territory of a single peripheral nerve Pain along the pathway of the nerve Direct trauma compression entrapment Vascular lesions neoplasms
- 18. Random pattern ofnerve involvement In distribution of separate nerves,asymmetric May/may not be painful Not length dependent Isolated reflex loss Mononeuropathy Multiplex
- 19.
- 20. MC type –Distalsymmetric polyneurpathy Burning sensation,tingling,numbness Length dependent pattern Starts in feet,distal stocking glove pattern Fairly symmetric Symmetrically decreased reflexes Sensory>motor Polyneuropathy
- 21. Diabetes mellitus Alcohol Vit B12deficiency HIV Although more than one nerve involved one will be prominant
- 22. POLYRADICULOPATHY Disease of multipleperipheral 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. SENSORYNEURONOPATHY Ganglion cells predominantlyaffected 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
- 24. PLEXOPATHY Asymmetric Painful onset Multiple nervesin a single limb Rapid onset of weakness,atrophy Isolated reflex loss Brachial plexus traction injury Lumbosacral plexopathy in pelvic trauma Compression by local tumor(pancoast’s tumor)
- 25. Directly related tothe duration and degree of abnormal metabolic control –occurring relatively early indisease Due to metabolic disturbance and accumulation of fructose and sorbitol in Scwanncells Types of Diabeticneuropathy Symmetrical mainly sensoryneuropathy Acute painfulneuropathy Mononeuropathy and mononeuritismultiplex Diabetic amyotrophy Autonomic Neuropathy
- 26. Chronic alcohol abuseleads topolyneuropathy Calf pain iscommon Deficiency in thiamine dueto alcoholism also causes neuropathy Canlead to Wernicke-Korsakoff syndrome Commonpresentation ▪ Eyesigns ▪ Ataxia ▪ Cognitive change ▪ Deliriumtremens ▪ Hypothermia andhypotension
- 27. Acute polyneuropathy –acuteinflammatory or postinfective neuropathy Usually demyelinating but canbe axonal Following Campylobacter jejuni and CMV infections Infection inducesantibody responses against peripheral nerves Paralysis 1-3weeks followinginfection Weaknessof distal limb musclesand/or distal numbness Symptoms progressproximally Lossof tendonreflexes Facial muscleweakness Autonomic features -uncommon Might need ventilatorysupport SCheparin is required to reduce risk of thrombosis Spontaneousrecovery beginsafter several weeks
- 29. DM hypothyroidism chronic renal failure liverdisease intestinal malabsorption malignancy connective tissue diseases [HIV] drug use Vitamin B6 toxicity alcohol and dietary habits • Weight loss, malaise, and anorexia.
- 30. Diabetes and Pre-Diabetes Alcoholneuropathy Chemotherapy ◦ Platinum-based Paraproteinemia Vasculitis and Connective Tissue Diseases Heavy metals and other toxins HIV Amyloidosis Porphyria
- 31. Axonal Vincristine Paclitaxel Nitrous oxide Colchicine Probenecid Isoniazid Hydralazine Metronidazole Pyridoxine Didanosine Lithium Alfainterferon Dapsone Axonal - continued.. Phenytoin Cimetidine Disulfiram Chloroquine Ethambutol Demyelinating Amiodarone Chloroquine Suramin Gold Neuronopathy Thalidomide Cisplatin Amitriptyline Pyridoxine
- 32. The temporal courseof 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 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.
- 33. A chronic, slowlyprogressive 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.
- 34. Ischemic neuropathies oftenhave pain as a prominent feature. Small-fiber neuropathies often present with burning pain, lightning-like or lancinating pain, aching, or uncomfortable paresthesias (dysesthesias).
- 35. Peripheral neuropathy canpresent 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
- 36. The clinical assessmentshould include: ◦ careful past medical history, looking for systemic diseases that can be associated with neuropathy, such as diabetes or hypothyroidism.
- 37. All patients shouldbe questioned regarding ◦ HIV risk factors ◦ diet (nutrition) ◦ vitamin use (especially B6) ◦ possibility of a tick bite (Lyme disease) ◦ Constitutional symtoms (malignancy)
- 38. A cranial nerveexamination can provide evidence of mononeuropathies. Funduscopic examination may show abnormalities such as optic pallor, which can be present in leukodystrophies and vitamin B12 deficiency.
- 39. Tests with thehighest yield of abnormality: 1. blood glucose (fasting) 2.serum B12 with metabolites (methylmalonic acid, homocysteine) 3. SPEP(serum protein electrophoresis)
- 40. BLOOD TC,DC,ESR Urea,electrolytes,LFT RBS,HbA1C Serum protein electrophoresis AutoAb=ANA,Antiganglioside,Antineuronal Vit B12 level DNA analysis=chr 17 duplication-HMSN1&1A =chr 17 deletion -HLPP
- 41.
- 42. NERVECONDUCTION STUDY Variation inaxonal,demyelinating neuropathy Conduction block-CIDP,GBS EMG-muscle denervation changes
- 43. Antibodies against Gangliosides GM1: GM1, GD1a : GQ1b : Multifocal motor neuropathy Guillain-Barré syndrome Miller Fisher variant Antibodies against Glycoproteins Myelin- associated glycoprotein Antibodies against RNA-binding proteins Anti-Hu, antineuronal nuclear antibody 1: Malignant inflammatory polyganglionopathy
- 44. (1) Confirming thepresence of neuropathy, (2) Locating focal nerve lesions, (3) Nature of the underlying nerve pathology
- 45. The limitations ofEMG/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.
- 46. IMAGES CXR-sarcoidosis,malignancy Skeletal survey-multiple myeloma Screeningfor malignancy AUTONOMIC FUNCTION TESTS Diagnostic tests imp in Asymmetric,motor predominant,rapid onset,demyelinating neuropathy
- 47. In vasculitis, amyloidneuropathy, 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
- 48. “For symptomatic patientswith suspected polyneuropathy, skin biopsy may be considered to diagnose the presence of a polyneuropathy, particularly SFSN.”
- 49. Slow progression ◦ Treatcausative factors if possible ◦ If rapidly progressing IVIG Immunomodulating agents
- 50. Tricyclic antidepressants ◦ Amitryptilin,nortryptilin Calcium channel alpha-2-delta ligands ◦ Gabapentin, pregabalin SNRI’s ◦ Duloxetine, venlafaxine Topical Agents ◦ Lidocaine, Capsaicin
- 51. Antiepileptic Drugs ◦ Carbamazepine,phenytoin, lacosamide SSRI’s Opioid analgesics Tramadol Miscellaneous ◦ Botulinum toxin ◦ Mexiletine ◦ Alpha lipoic acid
- 52. Physical Therapy ◦ Gaitand balance training Assistive devices Safe environment Footwear at all times Foot hygiene
- 54.
- 55. REFERENCES APLEY & SOLOMON’SSYSTEM OF ORTHOPAEDICS AND TRAUMA, 10TH EDITION HARRISON’S PRINCIPLE OF INTERNAL MEDICINE,20th EDITION