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Cutaneous dysaesthesia

Author: Dr Eileen J McManus, Advanced Neurology Trainee, Waikato Hospital, Hamilton, New Zealand. Technical Editor: Elaine Mary Luther, Medical Student, Ross University School of Medicine, Barbados. DermNet NZ Editor in Chief: Adjunct A/Prof. Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy edited by Gus Mitchell. February 2020.


What is cutaneous dysaesthesia?

Cutaneous dysaesthesia is a condition defined as an unpleasant and abnormal sensation in the skin. In the mouth, a similar sensation is called oral dysaesthesia

It can be classified as generalised or localised. There are multiple variants of localised cutaneous dysaesthesia, which differ in location, duration, and symptom severity.

Who gets cutaneous dysaesthesia?

Anyone can get cutaneous dysaesthesia. There is a possible female predominance in some variants, such as scalp dysaesthesia and notalgia paraesthetica [1].

What causes cutaneous dysaesthesia?

Generalised cutaneous dysaesthesia is associated with neurological diseases, including:

  • Autoimmune disorders, such as acute inflammatory demyelinating polyneuropathy and multiple sclerosis
  • Peripheral neuropathies, which may be hereditary or metabolic or induced by infection or toxin
  • Thalamic infarcts
  • Alcohol or drug withdrawal
  • Endocrine diseases, most commonly diabetes.

Localised dysaesthesia often follows nerve trauma, impingement, or irritation. This can be intracranial (in trigeminal trophic syndrome), spinal, or peripheral.

  • Trauma might be iatrogenic (including surgery) or spontaneous (due osteoarthritis, hyperostosis, a fracture, tumour, arterial ischaemia, or tight clothing) [2].
  • Infections can also cause nerve injury including herpes zoster, herpes simplex, and leprosy [1].
  • Dysaesthesia associated with syringomyelia may be due to impairment of supra-spinal pathways, disinhibition of sympathetic neurons, and aberrant spreading of nociceptive afferent nerves (the fibres that send information to the brain) [3].

Other reported causative associations with cutaneous dysaesthesia are described below.

  • Notalgia paraesthetica has been linked with multiple endocrine neoplasia type 2A (MEN2A) caused by RET gene mutations [4].
  • Brachioradial pruritus is often exacerbated by sun exposure [5].
  • Meralgia paraesthetica has been associated with type 2 diabetes and obesity [6].
  • Substance P, a neuropeptide, is postulated to play a key role in trichodynia by promoting mast cell degranulation and neurogenic inflammation in the hair follicle [7].
  • Psychological stress and generalised anxiety disorder can aggravate symptoms or result in somatisation [8]. See Psychosocial factors in dermatology.

What are the clinical features of cutaneous dysaesthesia?

Dysaesthesia or paraesthesia describes positive cutaneous symptoms such as pruritus, burning, crawling, stinging, hyperaesthesia, allodynia, and pain; and negative symptoms such as anaesthesia or cold sensation. One or all of these symptoms may be present.

The examination of the affected area may be normal or there may be signs of the underlying disease if any, or secondary to rubbing and scratching (if itchy).

Generalised cutaneous dysaesthesia

Generalised cutaneous dysaesthesia presents with dysaesthesia affecting most or all of the skin surface. Symptoms can be exacerbated by temperature change, heat, or the touch of clothing. Dysaesthesia often leads to anxiety and depression [9].

Localised cutaneous dysaesthesia

Localised cutaneous dysaesthesia presents with symptoms confined to one area.

  • Symptoms can be unilateral or bilateral.
  • The skin may appear normal.
  • Secondary dermatological changes associated with pruritus may include excoriations, bruising, hyperpigmentation, and lichenification.
  • If nerve impingement involves sympathetic pathways as well as sensory nerves, localised dysaesthesia may be accompanied by hyperhidrosis.

Signs of cutaneous dysaesthesia

How is localised cutaneous dysaesthesia classified?

Localised cutaneous dysaesthesia has been classified in the following conditions.

  • Brachioradial pruritus affects the skin overlying the brachioradialis muscle of the forearm, that is, on the dorsolateral aspect of the arm around the elbow [10].
  • Glossodynia or burning mouth syndrome is confined to the oral mucocutaneous membrane and is a form of oral dysaesthesia [8].
  • Genital dysaesthesia may affect the vulva (dysaesthetic vulvodynia) or scrotum (male genital dysaesthesia and scrotodynia) [8]. Perineal dysaesthesia may be accompanied by erythema. See also Pudendal nerve entrapment syndrome.
  • Meralgia paraesthetica affects the anterolateral thigh, the distribution of the lateral femoral cutaneous nerve.
  • Notalgia paraesthetica affects the skin between the scapula and vertebrae (T2–T6). Forward flexion or extension of the arms may worsen symptoms [11].
  • Scalp dysaesthesia affects the skin overlying the occipitofrontalis muscle and scalp aponeurosis (C5–C6) [1]. This is sometimes referred to as trichodynia (literally, painful hair) when associated with hair loss or an inflammatory condition of the scalp.
  • Hand-foot syndrome is a form of cutaneous dysaesthesia affecting hands and feet during chemotherapy
  • The trigeminal trophic syndrome usually affects the ala of the nose (V2 branch of the trigeminal nerve) with subsequent rubbing and picking causing ulceration. The trigeminal trophic syndrome can also involve the buccal mucosa, the tongue, or eye. The tip of the nose (innervated by a branch of V1) is often spared [1].

What are the complications of cutaneous dysaesthesia?

The main complication of cutaneous dysaesthesia is decreased quality of life and impact on mood and mental health.

How is cutaneous dysaesthesia diagnosed?

Generalised cutaneous dysaesthesia

Generalised cutaneous dysaesthesia is a clinical diagnosis after a detailed history and examination have excluded a primary dermatological disease. If there is evidence of an underlying neurological, metabolic, or endocrine disease, further investigations may be undertaken [9].

Serological tests may include testing for the following:

  • Glycosylated haemoglobin (HBA1c)
  • Complement (C3, C4)
  • Antinuclear antibody (ANA)
  • Antineutrophil cytoplasmic antibodies (ANCA)
  • Antibodies to Borrelia burgdorferi (found in Lyme disease)
  • Human immunodeficiency virus (HIV) and viral hepatitis
  • C-reactive protein (CRP)
  • Iron studies
  • Folate
  • Vitamin B12
  • Vitamin E
  • Heavy metal levels
  • Angiotensin-converting enzyme (ACE).

Other tests may include:

  • Nerve conduction studies to look for demyelinating or axonal neuropathy
  • Cerebrospinal fluid (CSF) analysis for oligoclonal bands if demyelination is suspected
  • Magnetic resonance imaging (MRI) of the brain and cervical spine if demyelination or ischaemia is suspected.

Localised cutaneous dysaesthesia

The diagnosis of localised cutaneous dysaesthesia is based on clinical suspicion. A comprehensive history and examination are needed to identify any underlying cause. For instance, hyperreflexia, weakness, or autonomic dysfunction can indicate a spinal cord pathology.

When meralgia paraesthetica is suspected, the following manoeuvres are useful [9].

  • The pelvic compression test is performed with the patient lying on their side with their symptomatic side facing up. The examiner applies a downward, compression force to the pelvis and maintains pressure for 45 seconds. If the patient reports an alleviation of symptoms, the test is considered positive for meralgia paresthetica.
  • The Tinel sign is elicited by lightly tapping over the lateral cutaneous nerve of the thigh as it exits the inguinal ligament region. It is positive if the symptoms are reproduced.

Other diagnostic tests may include:

  • Serology: antinuclear antibody (ANA), antineutrophil cytoplasmic antibodies (ANCA), C-reactive protein (CRP)
  • Skin biopsy
  • Imaging: plain X-rays, or MRI of the cervical/thoracic spine to eliminate disc herniation, spinal lesions, or fractures.

What is the differential diagnosis for cutaneous dysaesthesia?

The differential diagnosis of cutaneous dysaesthesia should be broadened if the skin is normal or abnormal (eg, lichenification might be due to eczema, nasal ulceration might be due to skin cancer).

Somatisation is sometimes implicated with cutaneous sensory disorders such as compulsive skin picking.

What is the treatment for cutaneous dysaesthesia?

Cutaneous dysaesthesia is difficult to treat effectively. Management depends on the cause, body site, and severity of symptoms.

Symptomatic therapy may include:

  • Capsaicin cream
  • Local anaesthetic patches
  • Topical amitriptyline 1% with ketamine 0.5% [12]
  • Low-dose tricyclic [1] or another antidepressant [7]
  • Antiepileptics including gabapentin, pregabalin, and carbamazepine
  • Antipsychotic medications such as venlafaxine and pimozide
  • Physiotherapy.

Additional treatments may include:

What is the outcome for cutaneous dysaesthesia?

Prognosis depends on aetiology, symptom severity, and treatment response. There is no effect on life expectancy.

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Related information

 

References

  1. Shumway NK, Cole E, Fernandez KH. Neurocutaneous disease: Neurocutaneous dysesthesias. J Am Acad Dermatol 2016; 74: 215–28. PubMed
  2. Savk E, Savk O, Bolukbasi O, Culhaci N, Dikicioğlu E, Karaman G, Sendur N. Notalgia paresthetica: a study on pathogenesis. Int J Dermatol 2000; 39: 754–60. PubMed
  3. Saito H. Segmental dysesthesia with segmental hyperhidrosis. Japanese J Auton Nerv Syst 2019; 56: 33–6. Journal (Japanese language). doi.org/10.32272/ans.56.1_033.
  4. Verga U, Fugazzola L, Cambiaghi S, Pritelli C, Alessi E, Cortelazzi D, Gangi E, Beck‐Peccoz P. Frequent association between MEN 2A and cutaneous lichen amyloidosis. Clin Endocrinol (Oxf) 2003; 59: 156–61. PubMed
  5. Waisman M. Solar pruritus of the elbows (brachioradial summer pruritus). Arch Dermatol 1968; 98: 481–5. PubMed
  6. Parisi TJ, Mandrekar J, Dyck PJ, Klein CJ. Meralgia paresthetica: relation to obesity, advanced age, and diabetes mellitus. Neurology 2011; 77: 1538–42. PubMed
  7. Rebora A. Trichodynia: a review of the literature. Int J Dermat 2016; 55: 382–4. PubMed
  8. Gupta MA, Vujcic B, Gupta AK. Dissociation and conversion symptoms in dermatology. Clin Dermatol 2017; 35: 267–72. PubMed
  9. Landerholml ÅH, Hansson PT. Mechanisms of dynamic mechanical allodynia and dysesthesia in patients with peripheral and central neuropathic pain. Eur J Pain 2011; 15: 498–503. PubMed
  10. Fisher M. Brachioradial pruritus: a case report and review of the literature. Cutis 2008; 81: 37–40. PubMed
  11. Pérez-Pérez LC. General features and treatment of notalgia paresthetica. Skinmed 2011; 9: 353–8. PubMed
  12. Winhoven SM, Coulson IH, Bottomley WW. Brachioradial pruritus: response to treatment with gabapentin. Br J Dermatol 2004; 150: 786–7. PubMed
  13. Brzezinski P, Zawar V, Chiriac A. Trichodynia silenced effectively with propranolol. Int J Trichology 2019; 11: 41–2. PubMed
  14. Savk E, Savk O, Sendur F. Transcutaneous electrical nerve stimulation offers partial relief in notalgia paresthetica patients with a relevant spinal pathology. J Dermatol 2007; 34: 315–9. PubMed

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