Mr.C’s numbness of his feet is most likely due to symmetric polyneuropathy affecting the distal axons. Although diabetic neuropathy is most frequently symmetric, it may also be focal (more common in Type II older diabetics) and often involves the autonomic nervous system (Inzucchi & Sherwin, 2008). Our initial introduction to Mr. C indicated he had numbness to both feet for an unspecified period of time. Mr. C’s symptoms of numbness to both feet is not unusual for diabetics as peripheral neuropathies are present in approximately 50% of all diabetics (Inzuccchi & Sherwin, 2008). What types of neuropathy are there and how do they differ? The simplest definition of neuropathy as defined by Stedman’s Medical Dictionary (2005) includes, “any disorder that affects the nervous system, specifically diseases involving the cranial nerves, peripheral or autonomic nervous systems” (p.999). The peripheral nervous system (PNS) is a large communication network which relays information from the brain and spinal cord (CNS) to every other part of the body and sends sensory information back the CNS. “Damage to the peripheral nervous system interferes with vital connections [similar to] static on a telephone line” (http://www.ninds.nih.gov/), causing a distortion and sometimes interruption in the messages between the brain and the rest of the body. Individuals who present with peripheral neuropathies have decreased nerve growth factor that impacts the degree of possible nerve regeneration. Acute neuropathy has a better prognosis towards resolution than chronic neuropathy. “Chronic, more insidious neuropathies may be mediated by metabolic factors, whereas the more acute, self-limiting neuropathies most likely have a vascular component” (Inzuccchi & Sherwin, 2008, p. 1745). Autonomic neuropathies are complex and carry a poor prognosis. They accompany other pathologic complications in the various organs impacted. For example, the parasympathetic nervous system is responsible for cardiovascular complications such as diminished heart rate and myocardial ischemia, whereas altered gastrointestinal function such as diarrhea is impacted by an impaired sympathetic inhibition (Inzuccchi & Sherwin, 2008). Other autonomic presentations may be include the loss of sweating, postural hypotension, sexual dysfunction, bowel and bladder dysfunction, and impaired gastric emptying (NINDS, 2008). There are more than 100 different types of peripheral neuropathies. Identifying these neuropathies is simplified by placing the various pathologies into a classification system that identifies the different nerve fibers that are affected. According to Boss (2006) neuropathies may be classified into three broad categories; 1. Generalized symmetric polyneuropathies; 2. Generalized neuropathies; 3. focal or multiple neuropathies. (p. 594) Generalized symmetric polyneuropathies (GSPN) include symmetrical sides of the body (e.g. numbness to both feet) and may include the sensory, motor, or autonomic fibers. Polyneuropathies refer to diffuse disorders of many peripheral nerves. Further, GSPN may be furthered divided into distal axonal polyneuropathy or demyelinating polyneuropathy. Distal axonal (sensori-motor) neuropathy is the most common neuropathy in diabetics (Boss, 2006). All somatic nerves are impacted as well as the distal sensori-motor nerves in the feet and hands (Inzuccchi & Sherwin, 2008). Both the small unmyelinated C fibers that transmit pain and temperature, as well as the larger myelinated fibers (touch, vibration, and proprioception) are affected (Inzuccchi & Sherwin, 2008). A more complex range of symptoms occur as a result of sensory nerve damage (NINDS, 2008). Initially, people are asymptomatic as changes are very subtle but with progression of nerve degeneration people complain of burning pain, tingling, and numbness of the feet. In addition to the general symptoms, damage to the small nerve fibers cause decreased somatic pain and temperature sensation. Over time, damage to large sensory nerve fibers will result in a continuous decline in individuals ability to discriminate light touch, vibration, and sense of position (Inzuccchi & Sherwin, 2008; NINDS, 2008). The two primary causes are diabetes mellitus and alcoholism. Diabetic polyneuropathy is often related tot the degree and duration of uncontrolled diabetes. Diabetic neuropathy is usually chronic and is often as a result of metabolic factors. General symptoms include weakness or sensory loss in the sensory nerves first. Often diabetics will experience neuropathies in both their hands and feet referred to as “stocking and glove sensory loss ” (NINDS, 2008). Axonal polyneuropathies related to alcoholism usually involves a nutritional deficiency with the most significant impact on thiamine loss. With the correction of this deficiency and abstinence from alcohol an improvement in symptoms occur (Shy, 2008). Individuals with axonal polyneuropathies recover over a prolonged period of time depending on the axonal regrowth. Axons grow approximately 1-3 mm/day therefore regrowth is over an extended period of time and is dependent upon the length of the nerve fiber damaged (Zochodone, personal communication, date unknown). As well, those with axonal neuropathy often experience muscle wasting further complicating recovery. Demyelinating polyneuropathy occurs less often and includes the myelin and Schwann cells. The axon is preserved, however there is loss of the myelin sheath. Demyelination can be internodal or paranodal (Shy, 2008). In general, the predominant symptom is weakness with more motor than sensory involvement. For example, Guillain-Barre syndrome is an acquired inflammatory disease resulting in demyelinating neuropathy of the peripheral nerves (Boss, 2008). Guillain- Barre is often preceded by an illness or vaccination and is “characterized by acute onset of a motor paralysis, usually of an ascending nature” (Boss, 2006). It is thought that the neuropathic nature of this illness is “both a humoral and cell-mediated immunologic reaction directed by the peripheral nerve myelin” (Boss, 2006). Gillian-Barre has an acute onset of ascending weakness, flaccidity, and areflexia involving both spinal and cranial nerves, as well as sudden autonomic alterations including pain and numbness (Shy, 2008). People who have demyelinating polyneuropathies generally will experience recovery however, 20% will have persistent disabilities (Shy, 2008). Inherited polyneuropathies affect both the sensory and motor neurons. Charcot Marie Tooth Disease, leukodystrophy, Freidrich’s ataxia are example of inherited polyneuropathies (Shy, 2008). “Generalized neuropathies affect the cell body of only one type of peripheral neuron” (Boss, 2006, p. 594). Focal, asymmetric or distal symmetric distributions are considered generalized neuropathies. Sensory neuropathies affect the dorsal root ganglion causing numbness. This numbness may result in a focal or multifocal neuropathy affecting both the sensory and motor fibers. Generally these neuropathies present with pain, have a sudden onset, and commonly occur in nerves of the oculomotor, median, radial, and lateral popliteal (Inzuccchi & Sherwin, 2008). Focal neuropathy may also be referred to as mononeuropathy and is a disorder of one peripheral nerve, root or plexus territory (Zochodne, personal communication, date unknown). Focal neuropathies may present with motor or sensory symptoms. Mononeuropathies may be a result of trauma, compression or entrapment, root disorders, plexus disorders, or cranial neuropathies. For example Bell’s Palsy is a result of cranial nerve involvement whereas foot drop involves the peroneal nerve causing the inability to dorsiflex foot. Carpel tunnel syndrome, ulnar nerve compression, and sciatic nerve compression are examples of focal neuropathies as well. Nerve compression may lead to either demyelination or injury to the axon. Injury may be caused from repetitive use syndrome or trauma to the nerve (http://www.medicinenet.com). The primary signs and symptoms of focal neuropathies are dermatomal numbness, pain, and possible muscle atrophy in Wallerian degeneration caused by a lack of nerve input to the muscle (Zochodne, personal communication, date unknown). Sensory neuropathies include leprosy, industrial solvent poisoning that effect the sensory neurons, hereditary disorders, and toxicity to chemicals such as chloramphenicol. Motor neuropathy affects the anterior horn of the spinal tract causing muscle weakness that can affect one or both sides of the body. Examples of motor neuropathies include amyotrophic lateral sclerosis (ALS) or poliomyelitis (Boss, 2006, p. 594). References Boss, B.J. (2006). Alterations of neurologic function. In McCance & Huether, Pathophysiology: The biologic basis for disease in adults and children (5th ed.). Philadelphia: Elsevier Mosby. National Institute of Neurological Disorders and Stroke (2008). Peripheral neuropathy fact sheet. Retrieved on May 25, 2008 form http://www.ninds.nih.gov/ Shy, M.E. (2008). Peripheral neuropathies. In Goldman & Ausiello, Cecil Medicine (23rd ed.). Philadelphia: Saunders Elsevier.