These include increased temperature and tenderness of the mucosa in the affected area, which is otherwise normal in every regard.Patient often reports symptoms of paresthesia, pain, and throbbing. Physical examination may be normal, but hypoesthesia, hyperesthesia, and allodynia may be found. The features of atypical facial pain can be considered according to the Socrates pain assessment method (see table). Causes
Health care associated
Sometimes dental treatment or surgical procedures in the mouth appear to precede the onset of AFP, or sometimes persons with AFP will blame clinicians for their pain. Organic disease
Many persons with AFP blame organic disease for their pain.Research in individuals with AFP showed that there is increased cerebral activity (demonstrated during positron emission tomography), possibly suggesting that there is an overactive alerting mechanism to peripheral stimuli. It has been theorized that this can trigger neuropeptides to be released, and the formation of free radicals (capable of damaging cells), the release of eicosanoids (e.g. prostaglandins). There is some suggestion that AFP is an early form of trigeminal neuralgia.Pain may be referred from other parts of the head or other parts of the body to cause facial pain. Nowhere in the body is referred pain more well illustrated than in the face, and this is due to the richly and complexly innervated nature of the head and neck. "Neuralgia-inducing cavitational osteonecrosis"
Neuralgia-inducing cavitational osteonecrosis (NICO) is a controversial term, and it is questioned to exist by many.
There is also an increased risk of skin infection and mechanical compression, leading to problems like limb ischemia. There is also a risk of intoxication by cutaneous absorption of topical products, for example salicylate intoxication (similar to aspirin overdose) due to keratolytics.The condition is not thought to be painful or in itself distressing to the child. Nursing usually takes place in a neonatal intensive care unit, and good intensive care seems to have improved the prognosis markedly. The collodion membrane should peel off or "shed" 2 to 4 weeks after birth, revealing the underlying skin disorder. The condition can resemble but is different from harlequin type ichthyosis. Long term course
The appearance can be caused by several skin diseases, and it is most often not associated with other birth defects. In most cases, the baby develops an ichthyosis or ichthyosis-like condition or other rare skin disorder. Most cases (approximately 75%) of collodion baby will go on to develop a type of autosomal recessive congenital ichthyosis (either lamellar ichthyosis or congenital ichthyosiform erythrodema).In around 10% of cases the baby sheds this layer of skin and has normal skin for the rest of its life. This is known as self-healing collodion baby. The remaining 15% of cases are caused by a variety of diseases involving keratinization disorders. Known causes of collodion baby include ichthyosis vulgaris and trichothiodystrophy. Less well documented causes include Sjögren-Larsson syndrome, Netherton syndrome, Gaucher disease type 2, congenital hypothyroidism, Conradi syndrome, Dorfman-Chanarin syndrome, ketoadipiaciduria, koraxitrachitic syndrome, ichthyosis variegata and palmoplantar keratoderma with anogenital leukokeratosis.