Hyperpathia

Hyperpathia: Description, Causes and Risk Factors: Hyperpathia is a clinical symptom of certain neurological disorders wherein nociceptive stimuli evoke exaggerated levels of pain. This should not be confused with allodynia, where normally nonpainful stimuli evoke pain. HyperpathiaHyperpathia is quite different from dysesthetic pain. It follows a gradient which is the opposite of dysesthesia, a gradient which increases proximally on the body. This gradient which increases where touch sensation is most retained and where dysesthesia is least, and the fact that the pain is not bizarre but rather retains the ordinary character, seems to suggest hyperpathia might merely be a failure of inhibition. This is in contrast to dysesthesia, which is of wildly different character from nociceptive pain, so different as to defy explanation. Causalgia and hyperpathia both involve cutaneous sensory loss, raised pain threshold, and the hyperpathic burning pain. Psychogenic tenderness of surface is not associated with cutaneous sensory loss, patients feels the stimulus normally but more intensely since their pain threshold is lowered by suggestion, attention, emotion, attitudes or past experience. Risk Factors: The mechanisms of hyperpathia are substantially different to those of nociceptive pain.
  • Novel impulse generators develop at various sites, and these are not stimulus-dependent.
  • In peripheral nerve, it has been shown that ectopic impulse generation (EIG) develops as a result of the expression of abnormal sodium channels. This can be modified by neurotrophic growth factors (a potential target for new treatments).
  • Abnormal chemical sensitivities develop in damaged primary sensory neurons, notably to catecholamines. Whilst this can be readily demonstrated in experimental preparations, the clinical relevance remains uncertain.
  • Degenerative and then regenerative changes in the spinal cord may lead to aberrant connectivity, and possibly a permanently reorganised, irreversible state.
  • Damage at one level in the nervous system may lead to secondary pathophysiological changes at more rostral levels. This has important implications when targeting treatments for hyperpathia.
When taking a history, the examiner should always determine by examination or ask the Central Pain patient whether the pain under discussion is dysesthetic or not. If the pain is not dysesthetic, hyperpathia will apply to it. Symptoms: Patients often find it difficult to describe the quality ofhyperpathia; it is outside their previous experience of pain.Sensory loss may be mild and overshadowed by allodynia(all stimuli producing pain), hyperalgesia and hyperpathia (delayed perception, summation and painful aftersensation).Rarely, (eg trigeminal neuralgia) there is nodemonstrable sensory loss.There may be signs of sympathetic dysfunction, andoccasionally dystrophic changes. The onset of pain maybe delayed, the commonest example being central poststrokepain (thalamic), which may start months or yearsafter the initiating stroke.Pain is often of mixed nociceptive and neuropathictypes, for example, mechanical spinal pain with radiculopathyor myelopathy. It is not generally recognized thatnociceptive spinal pain can radiate widely, mimicking aroot distribution. It can be difficult to identify the dominantpain type and treat appropriately. Such patientsrequire careful examination, imaging and neurophysiologicalinvestigation. Diagnosis: A thorough diagnostic laboratory work up includes complete blood cell count, sedimentation rate, general chemistry profile, thyroid function tests, vitamin B12 and folate serum level, fasting blood sugar, glycosylated hemoglobin, seroprotein electrophoresis with immunofixation. Lyme disease antibody titers, hepatitis virus B and C screening titers, antinuclear antibodies, rheumatoid factor, Sj

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