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Dysesthesia
From Wikipedia, the free encyclopedia
Dysesthesia (dysaesthesia) comes from the Greek word "dys", meaning "not-normal" and "aesthesis", which
means "sensation" (abnormal sensation). It is defined as an unpleasant, abnormal sense of touch. It often
presents as pain[1] but may also present as an inappropriate, but not discomforting, sensation. It is caused by
lesions of the nervous system, peripheral or central, and it involves sensations, whether spontaneous or evoked,
such as burning, wetness, itching, electric shock, and pins and needles.[1] Dysesthesia can include sensations in
any bodily tissue, including most often the mouth, scalp, skin, or legs.[1]
It is sometimes described as feeling like acid under the skin. Burning dysesthesia might accurately reflect an
acidotic state in the synapses and perineural space. Some ion channels will open to a low pH, and the acid
sensing ion channel has been shown to open at body temperature, in a model of nerve injury pain. Inappropriate,
spontaneous firing in pain receptors has also been implicated as a cause of dysesthesia.
Patients suffering from dysesthesia can become incapacitated with pain, despite no apparent damage to the skin
or other tissue. Patients suffering from dysesthesia also often suffer from psychological disorders.
Contents
1 Types of dysesthesia
2 Causes
3 Comparison to phantom limb and other disorders
4 Recent research
4.1 Studies
5 Living with dysesthesia
6 Treatment
7 See also
8 References
9 Further reading
10 External links
Types of dysesthesia
Dysesthesia can generally be described as a class of neurological disorders. It can be further classified
depending on where it manifests in the body, and by the type of sensation that it provokes.
Cutaneous dysesthesia is characterized by discomfort or pain from touch to the skin by normal stimuli,
including clothing. The unpleasantness can range from a mild tingling to blunt, incapacitating pain.
Scalp dysesthesia is characterized by pain or burning sensations on or under the surface of the cranial skin.
Scalp dysesthesia may also present as excessive itching of the scalp.
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Occlusal dysesthesia, or "phantom bite," is characterized by the feeling that the bite is "out of place" (occlusal
dystopia) despite any apparent damage or instability to dental or oromaxillofacial structures or tissue. Phantom
bite often presents in patients that have undergone otherwise routine dental procedures. Short of compassionate
counseling, evidence for effective treatment regimes is lacking.
Causes
Dysesthesia is commonly seen in diabetic patients, and can be relieved by using creams containing
capsaicin.
Dysesthesia may be seen in patients suffering from GuillainBarr syndrome.
Dysesthesia is among symptoms of neuropathy (along with paresthesias, gait disturbance, weakness, and
absent DTRs).
Dysesthesia, along with polyneuropathy can be a symptom of nerve damage caused by Lyme Disease.[2]
The dysesthetic sensations continue after the successful antibiotic treatment of Lyme disease.
Dysesthesia is a common symptom of a withdrawal from alcohol or other drugs.
Dysesthesia is also a common symptom of Multiple Sclerosis, or MS. It is an effect of spinal cord
injury.[3]
Many patients suffering from occlusal dysesthesia have reported recent oral surgery before the onset of
dysesthetic pain.[4]
Late-onset GM2 gangliosidosis may also present as burning dysesthesia.[5]
Chemotherapy-induced peripheral neuropathy is a progressive, enduring and often irreversible tingling
numbness, intense pain, and hypersensitivity to cold, beginning in the hands and feet and sometimes
involving the arms and legs caused by some chemotherapy agents.[6]
Dysesthesia may be caused by a thalamic stroke involving the ventral postero-lateral (VPL) nucleus. It's
typically seen in Dejerine-Roussy syndrome with hemi-sensory loss and severe dysesthesia of the affected
area.
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Recent research
There are a number of hypotheses regarding the basis of occlusal dysesthesia. Some researchers believe the
disorder is a psychological one, while others believe it to be a psychosomatic disorder.[4] Joseph Marbach
hypothesized that the symptoms were rooted in psychiatric disorders. Marbach suggested that occlusal
dysesthesia would occur in patients with underlying psychological problems (such as schizophrenia) after
having undergone dental treatment. More recently, two studies have found that occlusal dysesthesia is
associated with somatoform disorders in which the patients obsess over the oral sensations.
Similarly, Marbach later proposed that occlusal dysesthesia may be caused by the brain talking to itself,
causing abnormal oral sensations in the absence of external stimuli. According to this model, the symptoms of
dysesthesia are catalyzed by dental amputation, for example the extraction of a tooth, whereby the brain loses
the ability to distinguish between its memory of the bite and the actual, new bite. The patient, unable to
recognize his or her own bite, becomes especially attentive to these perceived oral discrepancies. Finally and
most recently, Greene and Gelb suggested that instead of having a psychological root, dysesthesia may be
caused by a false signal being sent from the peripheral nervous system to the central nervous system. However,
the reviewers note that no method exists for determining sensor nerve thresholds, and so sensory perception in
the mouth is often measured by interdental thickness discrimination (ITD), or the ability to differentiate
between the sizes of objects (thin blocks) placed between teeth. In one study, occlusal dysesthesia patients
showed greater ability to differentiate these thicknesses than control, healthy individuals, but these differences
were not statistically significant.
Studies
Bennett et al. produced an artificial peripheral mononeuropathy in rats by surgically constricting the
sciatic nerve.[7] These rats showed an increased response to noxious radiant heat, were nocifensive when
placed on a cold metal floor, protected their hind paws, and had suppressed appetite. Additionally, the
paws of many of these rats were inappropriately warm or cool to the touch, and many of the rats overgrew
claws on the affected paws as well. These results indicate that the rats exhibited hyperalgesia, allodynia,
and dysesthesia.
In a study in which researchers cut spinal nerves in rats, researchers found these rats exhibited a longer
duration in spontaneous foot lifting, hypersensitivity to mechanical stimuli, allodynia, and
hyperalgesia.[8] Additionally, the receptive field neurons in this nerve pathway showed spontaneous firing
in low-threshold nociceptors, suggesting that nerve damage can cause dysesthesia.
In women suffering from chronic pain or itchy scalps without any apparent physical cause, about half
were suffering from psychiatric disorders. For the majority of these women, their symptoms of scalp
dysesthesia were alleviated or removed by treatment with low doses of antidepressants.[9]
Landerholm et al. hypothesized that dynamic mechanical allodynia (DMA) might be the hyperbole of
dynamic mechanical dysesthesia (DMD), mediated by peripheral nerves. When the researchers artificially
blocked nerves in patients suffering from peripheral neuropthic pain or central post-stroke pain, DMA
symptoms in many of the patients transitioned into DMD symptoms. Additionally, the researchers
determined that the number of mechanocreceptive fibers associated with the nociceptive system was
responsible for the differentiation of DMA to DMD.[10]
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Ochoa et al. recorded intraneural signals in subjects with post-ischaemic paraesthesiae. The researchers
found the signals to be spontaneous. The frequency of the signals paralleled the intensity and timing of
the paresthetic sensations reported by the patients. These results suggest that paresthetic sensations are the
result of inappropriate firing frequency and timing by impulses from sensory cells.[11]
Tuskiyama et al. assessed occlusal dysesthesia patients using an interdental thickness discrimination test
and a psychological examination. The researchers found that occlusal dysesthesia patients could not
discriminate the thickness of material in their bite any better than normal dental patients, but that the
occlusal dysesthesia patients were significantly more likely to exhibit psychological disorders.[12]
Treatment
Daily oral muscle physical therapy, or the administration of antidepressants have been reported as effective
therapy for occlusal dysesthesia patients.[4] Tooth grinding, and the replacement or removal of all dental work
should be avoided in patients with occlusal dysesthesia,[4] despite the frequent requests for further surgery often
requested by these patients.
Antidepressants are also often prescribed for scalp dysesthesia.
Prakash et al. found that many patients suffering from burning mouth syndrome (BMS), one variant of occlusal
dysesthesia, also report painful sensations in other parts of the body. Many of the patients suffering from BMS
met the cclassification of restless leg syndrome (RLS). About half of these patients also had a family history of
RLS. These results suggest that some BMS symptoms may be caused by the same pathway as RLS in some
patients, indicating that dopaminergic drugs regularly used to treat RLS may be effective in treating BMS as
well.
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See also
Paresthesia
Scalp dysesthesia
References
1. IASP Pain Terminology (http://www.iasp-pain.org/AM/Template.cfm?
Section=General_Resource_Links&Template=/CM/HTMLDisplay.cfm&ContentID=3058).
2. Klempner, M. S., Hu, L. T., Evans, J., Schmid, C. H., Johnson, G. M., Trevino, R. P., . . . Weinstein, A. (2001). Two
controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. New England
Journal of Medicine, 345(2), 85-92.
3. [1] (http://ms.about.com/od/signssymptoms/g/dysesthesia.htm).
4. Hara, E. S., Matsuka, Y., Minakuchi, H., Clark, G. T., & Kuboki, T. (2012). Occlusal dysesthesia: a qualitative
systematic review of the epidemiology, aetiology and management. Journal of Oral Rehabilitation, 39(8): 630-638. [2]
(http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2842.2012.02300.x/pdf)
5. Chow, G. C. S., Clarke, J. T. R., & Banwell, B. L. (2001). Late-onset GM2 gangliosidosis presenting as burning
dysesthesias. Pediatric Neurology, 25(1).
6. del Pino BM. Chemotherapy-induced Peripheral Neuropathy
(http://www.cancer.gov/aboutnci/ncicancerbulletin/archive/2010/022310/page6). NCI Cancer Bulletin. Feb 23,
2010;7(4):6.
7. Bennett, G. J., & Xie, Y. K. (1988). A PERIPHERAL MONONEUROPATHY IN RAT THAT PRODUCES
DISORDERS OF PAIN SENSATION LIKE THOSE SEEN IN MAN. Pain, 33(1).
8. Djouhri, L., Fang, X., Koutsikou, S., & Lawson, S. N. (2012). Partial nerve injury induces electrophysiological changes
in conducting (uninjured) nociceptive and nonnociceptive DRG neurons: Possible relationships to aspects of peripheral
neuropathic pain and paresthesias. Pain, 153(9).
9. Hoss, D., & Segal, S. (1998). Scalp dysesthesia. Archives of Dermatology, 134(3). doi: 10.1001/archderm.134.3.327
10. Landerholm, A. H., & Hansson, P. T. (2011). Mechanisms of dynamic mechanical allodynia and dysesthesia in patients
with peripheral and central neuropathic pain. European Journal of Pain, 15(5).
11. Ochoa, J. L., & Torebjork, H. E. (1980). PARAESTHESIAE FROM ECTOPIC IMPULSE GENERATION IN HUMAN
SENSORY NERVES. Brain, 103(DEC).
12. Tsukiyama, Y., Yamada, A., Kuwatsuru, R., & Koyano, K. (2012). Bio-psycho-social assessment of occlusal
dysaesthesia patients. Journal of Oral Rehabilitation, 39(8).
13. [Copyright 2001 by David Berg http://www.painonline.org/dyses.htm].
14. [3] (http://www.calmclinic.com/anxiety/types/dysesthesia).
Further reading
External links
Chiari & Syringomyelia Foundation (http://www.CSFinfo.org)
.By Dhiraj kumar
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Categories: Symptoms and signs: Cognition, perception, emotional state and behaviour
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