With their focus on psychological factors, the ICD-10 criteria support the idea that the cause of PCS is functional. Like the ICD-10, the ICD-9-CM defines PCS in terms of subjective symptoms and discusses the greater frequency of PCS in people with histories of mental disorders or a financial incentive for a diagnosis.The DSM-IV lists criteria for diagnosis of PCD in people who have had a head trauma with persistent post-traumatic amnesia, loss of consciousness, or post-traumatic seizures. In addition, for a diagnosis of PCD, patients must have neuropsychological impairment as well as at least three of the symptoms marked with a check mark in the table at right under "DSM-IV". These symptoms must be present for three months after the injury and must have been absent or less severe before the injury. In addition, the patient must experience social problems as a result, and must not meet criteria for another disorder that explains the symptoms better.Neuropsychological tests exist to measure deficits in cognitive functioning that can result from PCS. The Stroop Color Test and the 2&7 Processing Speed Test (which both detect deficits in speed of mental processing) can predict the development of cognitive problems from PCS. A test called the Rivermead Postconcussion Symptoms Questionnaire, a set of questions that measure the severity of 16 different post-concussion symptoms, can be self-administered or administered by an interviewer. Other tests that can predict the development of PCS include the Hopkins Verbal Learning A test (HVLA) and the Digit Span Forward examination.
Diagnosis
When diagnosing Congenital Erythroipoetic Porphyria (Gunther Disease) one must exclude other forms of porphyria. These include Hepatoerythropoietic Porphyria and rare homozygous variants of Variegate Porphyria, Hereditary Coproporphyria, and STING-associated vasculopathy with onset in Infancy (SAVI). Mild variants may be present similarly to Porphyria Cutanea Tarda.There are four steps in establishing the diagnosis of any porphyria. First, a thorough history (particularly family history) and physical exam are performed with special attention paid to sun-exposed skin. Biochemical measurements of porphyrins and precursors in the urine, feces, and blood are necessary. Specialized labs are helpful in measuring activity of specific enzymes of the heme synthesis pathway and/or DNA and mutational analyses. In CEP, activity of uroporphyrinogen III synthase (the fourth enzyme in the heme biosynthetic pathway) will be markedly decreased.In congenital erythropoietic porphyria, urine aminolavulanic acid and porphobilinogen are typically normal. However, uroporphyrin and coproporphyrin tend to be markedly elevated and moderately elevated, respectively, in the urine more than in the feces. Additionally, fecal protoporphyrin is typically mildly elevated.In the red blood cells, uroporphyrin, coproporphyrin and protoporphyrin are all elevated, distinguishing this form of porphyria from the others. Finally, plasma analysis will demonstrate elevated uroporphyrin and coproporphyrin.Other nonspecific but helpful diagnostic clues are history of cutaneous photosensitivity, blistering, erosions, crusts and ulcerations leading to extensive scarring and deformation of the hands, loss of eyebrows, eyelashes with severe mutilation of cartilaginous structures like the nose, erythrodontia, and variable degree of hematologic involvement ranging from mild hemolytic anemia to intrauterine hydrops fetalis.