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![ DM
•Weight loss, malaise, and anorexia.
hypothyroidism
chronic renal failure
liver disease
intestinal
malabsorption
malignancy
connective tissue
diseases
[HIV]
drug use
Vitamin B6 toxicity
alcohol and dietary
habits](https://image.slidesharecdn.com/approachtoperipheralneuropathy-140921053534-phpapp02/75/Approach-to-peripheral-neuropathy-18-2048.jpg)
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Approach to peripheral neuropathy
- 1. Dr. Parag Moon Senior resident Dept of neurology GMC Kota
- 2. Generalized termincluding 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 classifiedinto 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. The clinical responseto sensory nerve injury Loss of function “- symptoms” Disordered function “+ symptoms” Sensory “Large Fiber” ↓ Vibration ↓ Proprioception Hyporeflexia Sensory ataxia Paresthesias Sensory “Small Fiber” ↓ Pain ↓ Temperature Dysesthesias Allodynia
- 6. The clinical responseto motor nerve injury Loss of function “- symptoms” Disturbed function “+ symptoms” Motor nerves Large fibre Wasting Hypotonia Weakness Hyporeflexia Orthopedic deformity Fasciculation Cramps
- 7. The clinical responseto autonomic nerve injury Loss of function “- symptoms” Disturbed function “+ symptoms” Autonomic nerves ↓ Sweating Hypotension Urinary retention Impotence Vascular color changes ↑ Sweating Hypertension
- 8. Focal involvementof a single nerve and implies a local process: Direct trauma compression or entrapment vascular lesions neoplastic compression or infiltration
- 9. simultaneous /sequentialdamage to multiple noncontiguous nerves. Ischemia caused by vasculitis Microangiopathy in diabetes mellitus Less common causes : Granulomatous, leukemic, or neoplastic infiltration, Hansen's disease (leprosy) and sarcoidosis.
- 10. Characterized bysymmetrical, distal motor and sensory deficits that have a graded increase in severity distally and by distal attenuation of reflexes, Rarely predominantly proximal:(E.g: acute intermittent porphyria). The sensory deficits generally follow a length-dependent stocking-glove pattern
- 12. By farthe 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
- 13. Unusual bycomparison 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
- 18. DM •Weightloss, malaise, and anorexia. hypothyroidism chronic renal failure liver disease intestinal malabsorption malignancy connective tissue diseases [HIV] drug use Vitamin B6 toxicity alcohol and dietary habits
- 19. Diabetes andPre-Diabetes Alcohol neuropathy Chemotherapy ◦ Platinum-based Paraproteinemia Vasculitis and Connective Tissue Diseases Heavy metals and other toxins HIV Amyloidosis Porphyria
- 20. 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
- 21. ◦ 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
- 22. The temporalcourse 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.
- 23. 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.
- 24. Ischemic neuropathiesoften have pain as a prominent feature. Small-fiber neuropathies often present with burning pain, lightning-like or lancinating pain, aching, or uncomfortable paresthesias (dysesthesias).
- 25. Dying-back (distalsymmetric axonal) neuropathies initially involve the tips of the toes and progress proximally in a stocking-glove distribution.
- 26. Peripheral neuropathycan 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
- 27. The clinicalassessment should include: ◦ careful past medical history, looking for systemic diseases that can be associated with neuropathy, such as diabetes or hypothyroidism.
- 28. All patientsshould be questioned regarding ◦ HIV risk factors ◦ diet (nutrition) ◦ vitamin use (especially B6) ◦ possibility of a tick bite (Lyme disease) ◦ Constitutional symtoms (malignancy)
- 29. Acute onset (withindays) 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
- 30. A cranialnerve 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.
- 31.
- 32. Cardiovagal ◦Heart rate variability Adrenergic ◦ Valsalva maneuver Induces BP changes and monitors pulse reaction Postganglionic sudomotor function ◦ QSART
- 33. Screening laboratorytests 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).
- 34. ANA, RF,Anti-dsDNA, Anti-Ro, Anti-La, ANCA screen, cryoglobulins Urine for heavy metals, porphyrins IFE/urine IFE/ plasma light chain analysis
- 35. 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
- 36. (1) Confirmingthe presence of neuropathy, (2) Locating focal nerve lesions, (3) Nature of the underlying nerve pathology
- 38. Distal motor latencyprolonged Nerve conduction velocity slow Reduced action potential
- 39. The limitationsof 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.
- 40. 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
- 41. “For symptomatic patientswith suspected polyneuropathy, skin biopsy may be considered to diagnose the presence of a polyneuropathy, particularly SFSN.”
- 42. Slow progression ◦ Treat causative factors if possible ◦ If rapidly progressing IVIG Immunomodulating agents Symptom Management
- 43. Tricyclic antidepressants ◦ Amitryptilin, nortryptilin Calcium channel alpha-2-delta ligands ◦ Gabapentin, pregabalin Calcium channel blocker • Prialt SNRI’s ◦ Duloxetine, venlafaxine Topical Agents ◦ Lidocaine, Capsaicin
- 44. Antiepileptic Drugs ◦ Carbamazepine, phenytoin, lacosamide SSRI’s Opioid analgesics Tramadol Miscellaneous ◦ Botulinum toxin ◦ Mexiletine ◦ Alpha lipoic acid NMDA receptors unsuccessful ◦ Namenda, Dextromethorphan
- 45. First linedrugs • Lidoderm 5% patch • Tricyclic antidepressants • Gabapentin • Pregabalin p.o. • Duloxetine Second line • Carbamazepine • Phenytoin • Venlafaxine • Tramadol
- 46. Physical Therapy ◦ Gait and balance training Assistive devices Safe environment Footwear at all times Foot hygiene
- 48.
- 49. Clinical Approachto Peripheral Neuropathy: Anatomic Localization and Diagnostic Testing Adina R. Alport et al : Continuum Lifelong Learning Neurol 2012;18(1):13–38. An Approach to the Evaluation of Peripheral Neuropathies;Mark B. Bromberg; SEMINARS IN NEUROLOGY/VOLUME 30, NUMBER 4 2010