Clinical Approach to Neuropathy and GBS

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Eugene Blake
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1 Clinical Approach to Neuropathy and GBS Definitions Polyneuropathy Pathological process affecting peripheral nerves. Mononeuropathy A single nerve affected. Mononeuritis multiplex Multiple mononeuropathy or Multifocal neuropathy. Plexopathy Disease involving the plexus Radiculopathy Disease of nerve roots Peripheral Nerve Disorders Mononeuropathies (entrapment, trauma, etc) Mononeuritis multiplex (DM, vasculitis) Plexopathies (immune, neoplastic) Radiculopathies (discs, immune) Peripheral Neuropathies Mechanisms of damage Demyelination Myelin sheath disrupted o GBS Post Diphtheric HSMN Axonal degeneration Axon damage o DM, Alcohol, Toxic neuropathies Wallerian degeneration Nerve section Compression Focal demyelination o Entrapment-Carpel tunnel syndrome Infarction Arteritis o Polyarteritis nodosa Churg-Strauss synd. DM Infiltration Infiltration Leprosy Sarcoidosis

Diabetes Mellitus Metabolic disorders Infectious agents Vasculitis Toxins Drugs Autoimmunity Inherited Causes Workup of a patient with suspected Peripheral Neuropathy History Time course (acute,

2 Diabetes Mellitus Metabolic disorders Infectious agents Vasculitis Toxins Drugs Autoimmunity Inherited Causes Workup of a patient with suspected Peripheral Neuropathy History Time course (acute, subacute,chronic, episodic) Negative numbness Postive tingling, pain Weakness and loss of function Balance Postural dizziness PMH?DM Medication Social, toxins, diet Family history Workup of a patient with suspected Peripheral Neuropathy Examination Gait (foot drop, high step, unsteady Romberg positive) Cranial Nerves ( facial, bulbar, or neck weakness, tonic pupils) Limbs Pes cavus, Clawing, Wasting, fasiculation Flaccidity, palpable nerves Distal weakness (radiculopathy) Reduced or absent DTRs

Glove and stocking sensory loss Systemic rash, BP Workup of a patient with suspected Peripheral Neuropathy Neurophysiology Demyelination (low velocities, latencies) Axonal change (low amp SNAPs and

3 Glove and stocking sensory loss Systemic rash, BP Workup of a patient with suspected Peripheral Neuropathy Neurophysiology Demyelination (low velocities, latencies) Axonal change (low amp SNAPs and CMAPs) Neuronopathy (very low or absent NAP) CSF (raised protein) NERVE BIOPSY (Aetiology not existence of neuropathy) General Subtype specific 1. Diabetes mellitus 2. Renal insufficiency 3. Hypothyroidism 4. Vitamin B12 deficiency 5. Systemic vasculitis Treatment General Pain Antiepileptic drugs Antidepressants Tramadol Preventative and palliative Weight reduction foot care Good shoes Ankle-foot orthoses as needed

4 Mononeuropathy Focal lesion involving a single nerve CAUSES OF MONONEUROPATHY: Trauma: wrong injection into a nerve,. Infective: leprosy, herpes zoster. Vascular: polyarteritis nodosa. Metabolic: diabetes mellitus. Electro diagnostic studies Localize site of injury Determine severity of lesion Mononeuropathy Multiplex Separate/noncontiguous involvement Pattern Frequently evolves quickly Mononeuropathy Multiplex Urgent assessment for vasculitis Polyarteritis nodosa Churg-Strauss disease Connective tissue diseases Rheumatoid arthritis Sjogren s syndrome Guillan barre syndrome Guillain-Barré syndrome (GBS) is an acute, frequently severe, and fulminant polyradiculoneuropathy that is autoimmune in nature. Males are at slightly higher risk for GBS than females. Guillain-Barré syndrome has been reported to follow vaccinations epidural anesthesia thrombolytic agents It has been associated with some systemic processes, such as Hodgkin's disease SLE Sarcoidosis, and infection with Campylobacter, Lyme disease, EBV, CMV, HSV, mycoplasma, and recently acquired HIV infection

5 Clinical symptoms The initial symptoms are SENSORY CHANGES: paresthesia,numbness, burning,tingling,shocklike, WEAKNESSascending and symmetrical, lower limbs involved first, proximal muscles involved earlier; develops acutely and progresses, varying severity deficits peak by 4 weeks after initial symptoms; recovery begins 2-4 weeks after progression stops The lower cranial nerves frequently involved, causing bulbar weakness. Bilteral facial nerve involvement in more than 50% of cases. Bladder dysfunction rarely occur in severe cases. Hypotonia and areflexia Autonomic involvement is common Loss of vasomotor control with wide fluctuation in blood pressure, postural hypotension, and cardiac dysrhythmias. DIFFERENTIAL DIAGNOSIS porphyria Critical illness polyneuropathy Diptheria Vasculitis Toxins arsenic,thallium,organophosphorus,lead. DISORDER OF NEUROMUSCULAR JUNCTION Botulism Myaesthenia gravis Tick paralysis

6 DIAGNOSTIC STUDIES Electrophysiologic studies are the most specific and sensitive tests for diagnosis of the disease,shows demylinating or axonal pattern. cerebrospinal fluid (CSF): an elevated protein TREATMENT The main modalities of therapy for Guillain-Barré syndrome include Plasmapheresis or Administration of intravenous immune globulin Ventilatory support. Treatment Pain relieve Monitor for hemodynamic instability and arrhythmias proper positioning, increasing upright tolerance and endurance, active muscle strengthening, mobility skills ##############################################################################

Aetna Nerve Conduction Study Policy

Aetna Nerve Conduction Study Policy Policy Aetna considers nerve conduction velocity (NCV) studies medically necessary when both of the following criteria are met: 1. Member has any of the following indications: