Polyneuropathy

Polyneuropathies may be classified in different ways, such as by cause,[1] by presentation,[3] or by classes of polyneuropathy, in terms of which part of the nerve cell is affected mainly: the axon, the myelin sheath, or the cell body.[7][8]

Action potential propagation in myelinated neurons is faster than in unmyelinated neurons(left)

• Distal axonopathy, is the result of interrupted function of the peripheral nerves.[9] It is the most common response of neurons to metabolic or toxic disturbances, and may be caused by metabolic diseases such as diabetes, kidney failure, connective tissue disease, deficiency syndromes such as malnutrition and alcoholism, or the effects of toxins or drugs such as chemotherapy. They may be divided according to the type of axon affected (large-fiber, small-fiber, or both), the most distal portions of axons are usually the first to degenerate, and axonal atrophy advances slowly toward the nerve's cell body, however if the cause is removed, regeneration is possible, although the prognosis depends on the duration and severity of the stimulus. People with distal axonopathies usually present with sensorimotor disturbances such as amyotrophic lateral sclerosis[10]
• Myelinopathy, is due to a loss of myelin or of the Schwann cells.[11] This demyelination slows down or completely blocks the conduction of action potentials through the axon of the nerve cell(neurapraxia).[12] The most common cause is acute inflammatory demyelinating polyneuropathy AIDP, the most common form of Guillain–Barré syndrome[13](although other causes include chronic inflammatory demyelinating polyneuropathy )[14]
• Neuronopathy is the result of issues in the peripheral nervous system (PNS) neurons. They may be caused by motor neurone diseases, sensory neuronopathies, toxins, or autonomic dysfunction. Neurotoxins such as chemotherapy agents may cause neuronopathies.[15]

Among the signs/symptoms of polyneuropathy, which can be divided (into sensory and hereditary) and are consistent with the following:[3]

• Sensory polyneuropathy – ataxia, numbness, muscle wasting and paraesthesiae.
• Hereditary polyneuropathy – scoliosis and hammer toes

The causes of polyneuropathy can be divided into hereditary and acquired and are therefore as follows:[1]

• Inherited -are hereditary motor neuropathies, Charcot–Marie–Tooth disease, and hereditary neuropathy with liability to pressure palsy
• Acquired -are diabetes mellitus, vascular neuropathy, alcohol abuse, and vitamin B12 deficiency

Human T Cell

In regards to the pathophysiology of polyneuropathy, of course, the former depends on which polyneuropathy. For instance in the case of chronic inflammatory demyelinating polyneuropathy, one finds that it is a autoimmune disease. Here, T cells involvement has been demonstrated, while in terms of demyelination, antibodies alone are not capable.[16]

Micrograph of a muscle biopsy

The diagnosis of polyneuropathies begins with a history and physical examination to ascertain the pattern of the disease process (such as-arms, legs, distal, proximal) if they fluctuate, and what deficits and pain are involved. If pain is a factor, determining where and how long the pain has been present is important, one also needs to know what disorders are present within the family and what diseases the person may have. Although diseases often are suggested by the physical examination and history alone, tests that may be employed include: electrodiagnostic testing, serum protein electrophoresis, nerve conduction studies, urinalysis, serum creatine kinase (CK) and antibody testing (nerve biopsy is sometimes done).[3][2]

Other tests may be used, especially tests for specific disorders associated with polyneuropathies, quality measures have been developed to diagnose patients with distal symmetrical polyneuropathy (DSP).[17]

Methylprednisolone

In the treatment of polyneuropathies one must ascertain and manage the cause, among management activities are: weight decrease, use of a walking aid, and occupational therapist assistance. Additionally BP control in those with diabetes is helpful, while intravenous immunoglobulin is used for multifocal motor neuropathy.[3]

According to Lopate, et al., methylprednisolone is a viable treatment for chronic inflammatory demyelinative polyneuropathy (which can also be treated with intravenous immunoglobulin). The authors also indicate that prednisone has greater adverse effects in such treatment, as opposed to intermittent (high-doses) of the aforementioned medication.[3][21]

According to Wu, et al., in critical illness polyneuropathy supportive and preventive therapy are important for the affected individual, as well as, avoiding (or limiting) corticosteroids.[22]

• Dimachkie, Mazen M.; Barohn, Richard J. (7 April 2013). "Chronic Inflammatory Demyelinating Polyneuropathy". Current Treatment Options in Neurology. 15 (3): 350–366. doi:10.1007/s11940-013-0229-6. ISSN 1092-8480. PMC 3987657. PMID 23564314.
• Katirji, Bashar; Kaminski, Henry J.; Ruff, Robert L. (2013-10-11). Neuromuscular Disorders in Clinical Practice. Springer Science & Business Media. ISBN 9781461465676. Retrieved 26 August 2016.
• Said, Professor Gérard (2014). Peripheral Neuropathy & Neuropathic Pain: Into The Light. tfm Publishing Limited. p. 17. ISBN 9781910079027. Retrieved 3 August 2016.