The word dysesthesias is derived from the Greek "dys," which means "bad," and "aesthesis," which means "sensation." Thus, dysesthesias are "bad sensations" and the word refers to pain or uncomfortable sensations, often described as burning, tingling, or numbness.
Dysesthesias is a symptom of pain or abnormal sensation(s) that typically cause hyperesthesia, paresthesiae, or peripheral sensory neuropathy. Dysesthesias can be due to lesions (an abnormal change) in sensory nerves and sensory pathways in the central nervous system (CNS, consisting of the brain and the spinal cord). The pain or abnormal sensations in dysesthesias is often described as painful feelings of tingling, burning, or numbness. Dysesthesias can simply be described as a burning pain that is worse where touch sensation is poorest.
Dysesthesias can also be caused by lesions in peripheral nerves (the peripheral nervous system , or PNS, which consists of nerves that are outside the brain or spinal cord). Peripheral nerves travel to muscles and organs providing a nerve supply. Dysesthesias due to a lesion in the PNS usually occurs below the level of the lesion. There is a broad spectrum of diseases, disorders, and medications that cause dysesthesias. There are two broad categories of dysesthesias called paresthesiae and peripheral sensory neuropathy. Some of the common causes of dysesthesias within these categories will be considered.
Paresthesias (abnormal neurological sensations that include numbness, tingling, burning, prickling, and increased sensitivity, or hyperesthesia) can include several conditions such as carpal tunnel syndrome , thoracic outlet syndrome , multiple sclerosis , strokes (cerebrovascular accidents), Guillain-Barré syndrome , transverse myelitis , and compartment syndrome/Volkmann's contracture.
Carpal tunnel syndrome
Carpal tunnel syndrome is caused by entrapment of the median nerve at the wrist. There is limited available space for the median nerve. There is a disease process (i.e. osteoarthritis) that entraps the nerve. Symptoms include paresthesiae of the first three fingers usually present overnight and typically relieved by shaking or elevating the hands. Symptoms progress to sensory loss and weakness of muscles. Treatment usually includes overnight splinting, diuretics (to reduce swelling), or surgery.
Thoracic outlet syndrome
Thoracic outlet syndrome is a condition caused by compression of nerves (and blood vessels) located between the armpit and the base of the neck. The neurologic symptoms associated with thoracic outlet syndrome include dysesthesias (numbness and tingling), weakness, and fatigability. The damage occurs in nerves leaving the spinal cord located behind the neck. Symptoms worsen with arm elevation above the level of the shoulder. Approximately 50% of persons affected report a history of a single traumatic event (i.e., motor vehicle accident) that caused a neck injury.
Multiple sclerosis/transverse myelitis
Multiple Sclerosis is an inflammatory process that involves white matter. There is focal neurologic deficit which can progress. The condition can go in remission but other attacks usually occur causing neurologic deficits. Transverse myelitis (usually associated with an inflammatory process) can cause back pain , leg weakness, and sensory disturbance. Transverse myelitis can occur after viral infections or may even occur as a feature of multiple sclerosis.
Stroke (cerebrovascular accident)
There are two major arteries implicated with stroke . These include the carotid arteries (in the neck and travels into the brain) and the basilar artery (an artery located in the base of the skull). The dysesthesias associated with carotid artery stroke consists of tingling and numbness on one side of the body. Stroke associated with the basilar artery can cause dysesthesias (tingling or numbness) in the cheeks, mouth, or gums.
Guillain-Barré syndrome (also called acute inflammatory demyelinating polyneuropathy) is an immune mediated disorder that follows some infectious process (such as infectious mononucleosis, herpes viruses, cytomegalo-virus, and mycoplasma), and is the most frequent caused of acute flaccid paralysis throughout the world. Initial symptoms consist of "pins-and-needles sensations" in the feet, lower back pain, and weakness (which develop within hours or days). Weakness is prominent in the legs. Progression of symptoms can occur abruptly and patients may have serious involvement of nerves responsible for respiration and swallowing, which may be life-threatening. The condition is serious and could cause rapid deterioration. Patients usually require hospitalization and treatment with high doses of human immunoglobulin and plasmapheresis (exchange of patient's plasma for the protein called albumin).
Compartment syndrome/Volkmann contracture
Compartment syndrome refers to any condition that causes a decrease in compartment size or increased compartment pressure. Compartment syndromes can be caused by crush injuries, internal bleeding, fractures, snake bites, burns, and excessive exercise . Ifa compartment (or area) is injured (i.e., a crushing injury to hand), the trauma will decrease the normal area of the hand (due to bleeding). This results in an increase in compartmental pressure which could impair blood flow to the area, causing irreversible tissue ischemia (tissue death). Compartment syndrome can occur from injuries to the upper extremity which can affect the forearm and hand since these areas have naturally occurring compartments made by anatomical structures such as muscle. Excessive swelling due to traumatic injury can cause nerves and blood vessels to be compartmentalized (in a sense, crushed against) muscle from abnormal swelling or internal bleeding. If left untreated the dead muscle and nerve tissue is replaced with fibrous tissue causing a Volk-mann ischemic contracture (contractures of fingers or in severe cases the forearm). In severe cases there is a loss of nerve tissue. Damage shows signs in 30 minutes and measurable functional loss after 12 to 24 hours.
Peripheral neuropathies are conditions that cause injury to nerves that supply sensation to the legs and arms. This category of dysesthesias can include conditions such as amyloidosis, Charcot-Marie-Tooth syndrome, diabetes, leprosy, syphilis, and Lyme disease .
Amyloid neuropathies/hereditary neuropathies
There are several types of amyloid neuropathies, and they are all associated with diseases that deposit a protein (amyloid) in nerves and even other tissues (like blood vessels). Sensory nerves are damaged causing dysesthesias. These disorders are inherited, occur in midlife, and represent the most relevant inherited neurologic diseases. These include Charcot-Marie-Tooth disease and amyloid neuropathies. Charcot-Marie-Tooth disease refers to inherited disease that causes nerve degeneration usually in the second to fourth decades of life. Patients exhibit impairment of sensory function, and the nerves of the toes and feet are affected (can lead to foot drop.)
Diabetes (metabolic neuropathy)
The most frequent neuropathy world wide is diabetes. Peripheral neuropathy can be detected in approximately 70% of long-term diabetics. The cause of nerve involvement is unclear, but it is thought that a faulty mechanism (deleterious to nerve cells) is related to high blood glucose levels. The symptoms are insidious and typically include dysesthesias evoked by regular activity (i.e., bothersome tingling of toes under bed sheets). The pain can be throbbing or it may be a continuous burning type of dysesthesias. Additionally, person may describe abrupt, quick "lightning" pains which may affect the feet and legs.
Leprosy is an infectious disease transmitted by a bacterium called Mycobacterium leprae. The World Health Organization (WHO) estimates that there are 2.5 million persons affected by leprosy. The organism proliferates in coolest regions of skin (i.e., ears, face, fingers), causing a selective loss of pain sensation (dysesthesias) in cold areas of skin.
Neurosyphilis refers to a disease caused by untreated syphilis infection that invades the central nervous system years after initial infection. In the United States the number of cases of neurosyphilis has risen from 10,000 in 1956 to over 50,000 in 1990. Approximately 28% of patients have ataxia , 23% have stroke, and 10% of affected persons describe "lightning" pains. Additionally 10% have headaches and 36% have cranial neuropathy. Treatment attempts include antimicrobial therapy.
Lyme disease (Boreliosis)
Lyme disease is an infection transmitted by an arthropod (a tick which harbors the infectious bacterium called Borrelia burdorferi ). The bacteria can be transmitted to a human by the bite of infected deer ticks, and in 2002 caused 23,000 infections in the United States. After the initial symptoms ("bulls-eye" rash, fever, fatigue , muscle aches, and joint aches), early disease can cause neurologic symptoms such as lymphocytic meningitis, cranial neuropathy (especially facial nerve palsy), and radiculoneuritis. Patients may also have musculoskeletal pain that includes muscle pain (myalgia) and joint aches (arthralgia). Late symptoms include encephalopathy , sleep disturbances, fatigue, and personality changes.
Other causes of dysesthesias
Toxic neuropathies can occur due to medications (used to treat illnesses), metal exposures, substance abuse, and exposure to industrial poisons/chemicals. For drug (medications) or chemical exposure induced neuropathies the cause (mechanism of damage) is usually obscure. Medications that can cause neuropathies include (but are not limited to) antivirals, chloramphenicol (antibiotic), cisplatin (anticancer), ethambutol (antitubercolosis), hydralazine (antihypertensive), isoniazid (antitubercolosis), metronidazole (antifungal), phenytoin (antiepileptic), pyridoxine (vitamin B-6), gold therapy, and vincristine/vinblastin (anticancer) therapy. Metals that can cause neuropathies include arsenic, lead, mercury, and thallium (a metal in rodenticides such as Gizmo mouse killer). Heavy metals such as lead found in lead-based paint in the automobile industry and manufacture of storage batteries and printing can cause neuropathies. Lead neuropathy can occur due to drinking bootleg whiskey distilled in lead pipes, or hand mixing of lead-based paints by artists. Occupational exposure in farming to arsenic-containing sprays, pesticides, and weed killers can cause arsenic neuropathy. Accidental ingestion of arsenic-containing rodenticides can cause arsenic neuropathy.
Chemical abuse with alcohol or by glue or nitrous oxide inhalation can cause neuropathies. Severe peripheral neuropathies can result from exposure to household and industrial chemicals.
Thallium neuropathy can occur in manufacturers of optic glass, industrial diamonds, and prisms. Thallium is also used as an additive in internal combustion engines. Accidental ingestion of thallium and subsequent neuropathy also occurs with rodent killer substances (rodenticides).
Before development of AIDS , persons with HIV infection can develop chronic inflammatory peripheral neuropathy. However, the most prevalent neuropathy associated with HIV infection is sensory neuropathy of AIDS, which causes pain on the soles of the feet and discomfort when walking. The pain is intense and affected persons may have motor impairment. The condition is caused by degeneration of sensory nerve fibers.
Another condition called herpes zoster or shingles (caused by the varicella zoster virus which causes chicken pox) can cause a latent nerve neuropathy with localized cutaneous eruptions during periods of reactivation. There are over 500,000 cases of shingles estimated to occur annually in the United States. The abnormal skin sensations are localized and range from itching to tingling to severe pain. Treatment typically includes antiviral medications. Pain can persist for months or even years.
The cause of Bell's palsy is unclear. It is thought to be due to an infectious process, possibly viral, that involves a nerve in the face called the facial nerve. Pain is often sudden and patients often describe a "numbing of the face" sensation.
The ingestion of a certain fish (ciguatera) and some shellfish can be the cause of acute peripheral neuropathy (paresthesia). The typical causes among ciguatera include red snapper and barracuda from waters in the West Indies, Florida and Hawaii. Shellfish, clams scallops and mussels from the waters of Alaska, New England and the west coast are also causative biologic toxins. The neuropathy is followed after a few hours from the initial symptoms of nausea and vomiting. Paresthesiae occurs around the face and spreads to limbs. The problem can quickly progress to respiratory paralysis (paralysis of the muscles responsible for respiration) which could be a life-threatening condition.
Neuropathy can result due to vitamin deficiencies such as vitamin B-12, vitamin B-1 and vitamin E. Vitamin B-12 deficiency can cause dysesthesias (sensation of "pins-and-needles" and numbness) in the feet and hands. Usually patients are diagnosed since they have a blood disorder called macrocytic megaloblastic anemia. Patients who have a bowel problem called malabsorption may loose ingested fat substances in the feces undigested, causing a loss of essential vitamins and nutrients. Fat containing molecules like vitamin E may be lost causing a neuropathy with symptoms similar to vitamin B-12 deficiency. Vitamin B-1 deficiency can likely occur due to alcoholism. The neuropathy is mostly sensory and patients describe a painful hypersensitivity of the feet. In advanced cases there may be weakness in the limbs or even paralysis leading to wrist drop or foot drop .
Nerve root compression
Radiculopathy , commonly caused by disk herniation (nerve root compression) is generally accompanied by muscle weakness, sensory loss and absent tendon reflexes. Herpes zoster radiculopathy is a lesion in the nerve root characterized by a burning pain and skin eruptions in dermatomal distribution. The inflammatory reaction precipitates stimulation of nerves producing a burning pain that precedes and often accompanies the skin eruptions.
General Concepts of pain management: Acute vs. chronic pain
There are several key concepts for pain management. Pain is best treated early and a vigilant search for the cause is imperative. Pain scales should be utilized in order to gauge progression of pain (i.e. getting worse or better). Unrelieved pain is implicated with negative physiological and psychological conditions. For acute pain an opioid (morphine) is a suitable agent to control moderate to severe pain. Acute pain is usually a symptom of injury or illness and serves a biological purpose (i.e. to provoke treatment of the injury). Additionally, acute pain causes anxiety, has identifiable pathology (disease) and is present less than six months. In cases of chronic pain, the dysesthesias is the problem itself and serves no biological function. Chronic pain syndromes with dysesthesias are often implicated with depression due to chronicity (long-term illness). Chronic pain may or may not have identifiable pathology and is present for more than six months.
Management of Pain
The first step to management of patients with neuropathic pain is to gain a good explanation of the cause and origin of the pain. Tricyclic antidepressants have an important role for the treatment of neuropathic pain (especially the "burning pain" associated with diabetes). These medications seem to be effective in several "pain" syndromes. Tricyclics tend to help with "burning" type pains, lacinating pains and cutaneous hyperalgesia. Tricyclics have an analgesic effect, thought to be mediated by alterations in brain chemistry (two specific neurotransmitters called serotonin and norepinephrine). Anticonvulsants (antiepileptic medications) can help reduce lacinating pain. Topical local aesthetic preparations (i.e. EMLA cream, eutectic mixture of local anesthetics) can penetrate skin and temporarily relieve neuropathic pain. The use of long term opioid treatment is unclear and should be reserved to selective cases. The use of capsaicin (the active substance extracted from hot pepper, can relieve pain (if placed on skin) in approximately 33% of patients with painful post-herpetic neuralgia and diabetic neuropathy.
Canale, S. Terry. Campbell's Operative Orthopedics, 10th ed. St. Louis: Mosby, Inc., 2003.
DeLee, Jesse, G., and David Drez. Delee and Drez's Orthopedic Sports Medicine, 2nd ed. Philadelphia: Saunders, 2003.
Goetz, Christopher G., et al., eds. Textbook of Clinical Neurology, 1st ed. Philadelphia: W. B. Saunders Company, 1999.
Goldman, Lee, et al. Cecil's Textbook of Medicine, 21st ed. Philadelphia: W. B. Saunders Company, 2000.
Marx, John A., et al., eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis: Mosby, Inc., 2002.
Noble, John, et al., eds. Textbook of Primary Care Medicine. 3rd ed. St. Louis: Mosby, Inc., 2001.
Pascuzzi, Robert, M. "Peripheral neuropathies in clinical practice." Medical Clinics of North America 87, no. 3 (May 2003).
National Institute of Neurological Disorders. <http://www.ninds.nih.gov>.
NIH Neurological Institute. PO Box 5801, Bethesda, MD 20824. 301-496-5751 or 1-800-352-9424. <http://www.ninds.nih.gov>.
Laith Farid Gulli, M.D.
Nicole Mallory, M.S., PA-C
Alfredo Mori, M.B., B.S.
Gulli, Laith; Mallory, Nicole; Mori, Alfredo. "Dysesthesias." Gale Encyclopedia of Neurological Disorders. 2005. Encyclopedia.com. (June 26, 2016). http://www.encyclopedia.com/doc/1G2-3435200126.html
Gulli, Laith; Mallory, Nicole; Mori, Alfredo. "Dysesthesias." Gale Encyclopedia of Neurological Disorders. 2005. Retrieved June 26, 2016 from Encyclopedia.com: http://www.encyclopedia.com/doc/1G2-3435200126.html