neurologic disorders
Polyneuropathy
Diagnosis of Polyneuropathy
Electrodiagnostic tests Laboratory tests, determined by suspected type of neuropathy Polyneuropathy is suspected in patients with diffuse or multifocal sensory deficits, weakness without hyperreflexia, or both. However, if findings are relatively diffuse but began asymmetrically, the cause may be multiple mononeuropathy. Clinicians must ask patients for a thorough description of symptom onset to determine whether symptoms began symmetrically or asymmetrically. For example, patients should be asked whether symptoms appeared in both feet at about the same time (symmetrically) or appeared in one foot, then one hand, then the other foot (asymmetrically). If findings are consistent with polyneuropathy, try to determine whether symptoms began asymmetrically (possibly suggesting multiple mononeuropathy). Clinical findings, particularly tempo of onset, help clinicians diagnose and identify the cause of polyneuropathy, as in the following: Asymmetric neuropathies suggest vasculitis. Symmetric, distal neuropathies suggest toxic or metabolic causes. Slowly progressive, chronic neuropathies tend to be inherited or due to long-term toxic exposure or metabolic disorders. Acute neuropathies suggest an autoimmune cause, vasculitis, a toxin, an infection, or a postinfectious cause or possibly a drug or cancer. Rash, skin ulcers, and Raynaud syndrome in patients with an asymmetric axonal neuropathy suggest a hypercoagulable state or parainfectious or autoimmune vasculitis. Weight loss, fever, lymphadenopathy, and mass lesions suggest a tumor or paraneoplastic syndrome. Axonopathies should be considered in all patients with polyneuropathy. Regardless of clinical findings, electromyography (EMG) and nerve conduction studies are necessary to classify the type of neuropathy and help clinicians tailor laboratory tests based on possible causes. At a minimum, EMG of both lower extremities should be done to assess for asymmetry and full extent of axon loss. Because nerve conduction studies assess primarily large myelinated fibers in distal limb segments, they may be normal, except for prolonged F wave responses,in patients with proximal myelin dysfunction (eg, early in Guillain-Barré syndrome) and in patients with primarily small-fiber dysfunction. In such cases, quantitative sensory or autonomic testing, done at specialized testing centers, or skin punch biopsy may be done depending on the presenting symptoms. Baseline laboratory tests for all patients include Complete blood count Electrolytes Renal function tests Rapid plasma reagin test Measurement of fasting plasma glucose, glycosylated hemoglobin (HbA1C), and sometimes a 2-hour glucose tolerance test Vitamin B12 and folate levels Thyroid-stimulating hormone (TSH) level Some clinicians include serum protein electrophoresis, especially if patients have a painful sensory neuropathy not explained by diabetes. The need for other tests is determined by polyneuropathy subtype (large- or small-fiber). When electrodiagnostic tests and clinical differentiation are inconclusive, tests for all subtypes may be necessary. the approach is the same as that for Diagnosis ; forced vital capacity is measured to check for incipient respiratory failure. In acute or chronic myelin dysfunction, tests for infectious disorders and immune dysfunction, including tests for hepatitis and HIV and serum protein electrophoresis, are done. A Forvasa nervorum compromise or asymmetric axonal polyneuropathies,tests for hypercoagulable states and parainfectious or autoimmune vasculitis, particularly if suggested by clinical findings, should be done; the minimum is Erythrocyte sedimentation rate Serum protein electrophoresis Measurement of rheumatoid factor, antinuclear antibodies, and serum creatine kinase (CK) CK may be elevated when rapid onset of disease results in muscle injury. Other tests depend on the suspected cause: Coagulation studies (eg, protein C, protein S,antithrombin III, anticardiolipin antibody, and homocysteine levels) should be done only if personal or family history suggests a hypercoagulable state. Tests for sarcoidosis, hepatitis C, or granulomatosis with polyangiitis (formerly known as Wegener granulomatosis) should be done only if symptoms and signs suggest one of these disorders. If no cause is identified, nerve and muscle biopsy should be done. An affected sural nerve is usually biopsied. A muscle adjacent to the biopsied sural nerve or a quadriceps, biceps brachii, or deltoid muscle may be biopsied. The muscle should be one with moderate weakness that has not been tested by needle EMG (to avoid misinterpretation of needle artifacts). An abnormality is more often detected when the contralateral muscle has EMG abnormalities, particularly when the neuropathy is somewhat symmetric. Nerve biopsies are useful in symmetric and asymmetric polyneuropathies but are particularly useful in asymmetric axonopathies. If initial tests do not identify the cause of distal symmetric axonopathies, blood levels may be measured or a 24-hour urine collection may be done to check for heavy metals. Hairs or nails may be tested and may confirm heavy metals as the cause. Whether tests for other causes are needed depends on history and physical examination findings. 