Notalgia paresthetica

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Notalgia paresthetica is a chronic sensory neuropathy. Notalgia paresthetica is a common localized itch, affecting mainly the interscapular area especially the T2-T6 dermatomes, but occasionally with a more widespread distribtuion, involving the shoulders, back, and upper chest.[1]:402 The characteristic symptom is pruritus (itch or sensation that makes a person want to scratch) on the back, usually on the left hand side below the shoulder blade (mid to upper back). It is occasionally accompanied by pain, paresthesia (pins and needles), and/or hyperesthesia (unusual or pathologically increased sensitivity of the skin to sensory stimuli, such as pain, heat, cold, or touch), which results in a well circumscribed hyperpigmentation of a skin patch in the affected area.

The causes or origin of this condition (etiology) have not yet been completely defined. [2] Patients are usually older persons, and commonly find themselves scratching their back on doorposts etc, as the location can be hard to reach.

The correlation of notalgia paresthetica localization with corresponding degenerative changes in the spine suggest that spinal nerve impingement may be a contributing cause.

Many treatments have been tried, including local anesthetics, topical corticosteroids, and topical capsaicin. [3] Some patients treated with capsaicin reported pain, burning, or tingling sensations with treatment, and symptoms returned within a month of ceasing treatment.[4] Oxcarbazepine was reported to have reduced severity of symptoms in a few cases, but this was a reduction of symptoms rather than a cure. [5] One patient has been treated with “paravertebral nerve blocks, with bupivacaine and methylprednisolone acetate injected into the T3-T4 and T5-T6 intervertebral spaces” [6] Most recently intradermal injections of botulinum toxin type A (Botox) have been tried with some success. Even though botulinum normally wears off in three to six months, the treatment appears to be long term, and it has been theorised that botulinum type A effects lasting change in pain signaling.[7]

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