The diagnostic criteria for Dorian Gray syndrome are:

- Signs of dysmorphophobia

- Arrested development (inability to mature)

- Using at least two different medical-lifestyle products and services:

- Hair-growth restoration (e.g. finasteride)

- Antiadiposita to lose weight (e.g. orlistat)

- Anti-impotence drugs (e.g. sildenafil)

- Anti-depressant drugs (e.g. fluoxetine)

- Cosmetic dermatology (e.g. laser resurfacing)

- Cosmetic surgery (e.g. a face-lift, liposuction)

The Dorian Gray syndrome arises from the concurring and overlapping clinical concepts of the narcissistic personality, dysmorphophobia, and paraphilia. Psychodynamically, the man afflicted with DGS presents an interplay among his narcissistic tendencies ("timeless beauty"), his arrested development (inability to psychologically mature), and his use of "medical lifestyle" products and services — hair restoration, drugs (for impotence, weight-loss, and mood modification), laser dermatology, and plastic surgery — in order to remain young.

Although the DGS patient displays diagnostic features of said mental disorders, the syndrome describes a common, underlying psychodynamics of mental illness, which is characterized by narcissistic defences against time-dependent maturation, expressed by actively seeking the timeless beauty of youth. The article "Das Dorian Gray syndrom" (2005) reported that approximately 3.0 per cent of the population of Germany present features of the Dorian Gray syndrome.

In terms of treating the mental aspect of paruresis, such treatment can be achieved by graduated exposure therapy and cognitive behavioral therapy. In graduated exposure therapy, the subject has a trusted person stand outside the restroom at first, and once the fear is overcome the observer is brought closer in, until step by step the phobia is vanquished. The International Paruresis Association provides a detailed discussion of this method on its website.

In addition to gradual exposure therapy, cognitive behavioral therapy is used to change a sufferer's mental approach to the condition, from one of a person who cannot urinate, to a person who can urinate or is not overly fearful when they can't publicly urinate.

There can be serious difficulties with workplace drug testing where observed urine samples are insisted upon, if the testing regime does not recognise and cater for the condition. In the UK, employees have a general right not to be unfairly dismissed, and so have an arguable defence if this arises, but this is not the case everywhere.

There is growing evidence to suggest that some drug testing authorities find paruresis a nuisance, and some implement "shy bladder procedures" which pay no more than lip service to the condition, and where there is no evidence that they have conducted any real research into the matter. In the U.S. Bureau of Prisons, the Code of Federal Regulations provides that "An inmate is presumed to be unwilling if the inmate fails to provide a urine sample within the allotted time period. An inmate may rebut this presumption during the disciplinary process." Although U.S. courts have ruled that failure to treat properly diagnosed paruresis might violate prisoner's constitutional rights, the courts have also "routinely rejected suspicious or unsubstantiated attempts to invoke it in defense of failure to complete drug testing," particularly when there were no medical record or physician testimony to back up the claim of paruresis. The International Paruresis Association stresses the importance of medical documentation of one's condition since "[t]he person who is unable to produce a urine sample is presumed guilty in the absence of any evidence." Some prisons have offered the use of a "dry cell"—i.e., a cell with no toilet facilities, but only a container for the prisoner's waste—as an accommodation to inmates who are hindered by paruresis from providing an observed urine sample.

FBOP Program Statement 6060.08 states, "Ordinarily, an inmate is expected to provide a urine sample within two hours of the request, but the Captain (or Lieutenant) may extend the time if warranted by specific situations (for example, the inmate has a documented medical or psychological problem, is dehydrated, etc.). Staff may consider supervising indirectly an inmate who claims to be willing but unable to provide a urine sample under direct visual supervision. For example, this might be accomplished by allowing the inmate to provide the sample in a secure, dry room after a thorough search has been made of both the inmate and the room." At least six state prison systems — Florida, Massachusetts, Maryland, Michigan, New York and Tennessee — have modified their drug testing regulations to provide accommodations for prisoners with paruresis.

Per the "Handbook of Correctional Mental Health", "No definitive or objective test is available to confirm or refute the presence of paruresis. The absence of prior treatment or the ability to void in some social situations but not in others does not rule it out. Although modalities associated with the treatment of social phobias help some individuals, no universally effective medication or other treatment exists. Coercive interventions, such as forcing fluids while observing a person with paruresis, are ineffective and can cause serious medical complications. Alternatives to observed urine specimen collection for individuals who self-report paruresis include unobserved collections in a dry room, testing of hair specimens, sweat testing with a patch, and blood testing ('Test for Drugs of Abuse' 2002). These alternatives preclude the need for futile attempts to differentiate inmates with true paruresis from those who fabricate complaints."

Trichomegaly is a congenital condition in which the eyelashes are abnormally long, greater than 12mm in the central area and 8mm in the peripheral. The term was first used by H. Gray in 1944 in a publication in the Stanford Medical Bulletin, though he was only the third person to characterize the disorder; the first two reports were published in German in 1926 and 1931 by Reiter and Bab, respectively. Gray suggested the use of the term "movie lashes" to describe this condition, for long lashes were at the time being portrayed in film as a desirable characteristic in women.

Once the diagnosis of polymicrogyria has been established in an individual, the following approach can be used for discussion of prognosis:

A pregnancy history should be sought, with particular regard to infections, trauma, multiple gestations, and other documented problems. Screening for the common congenital infections associated with polymicrogyria with standard TORCH testing may be appropriate. Other specific tests targeting individual neurometabolic disorders can be obtained if clinically suggested.

The following may help in determining a genetic etiology:

Family history

It is important to ask for the presence of neurologic problems in family members, including seizures, cognitive delay, motor impairment, pseudobulbar signs, and focal weakness because many affected family members, particularly those who are older, may not have had MRI performed, even if these problems came to medical attention. In addition, although most individuals with polymicrogyria do present with neurologic difficulties in infancy, childhood, or adulthood, those with mild forms may have no obvious deficit or only minor manifestations, such as a simple lisp or isolated learning disability. Therefore, if a familial polymicrogyria syndrome is suspected, it may be reasonable to perform MRI on relatives who are asymptomatic or have what appear to be minor findings. The presence of consanguinity in a child's parents may suggest an autosomal recessive familial polymicrogyria syndrome.

Physical examination

A general physical examination of the proband may identify associated craniofacial, musculoskeletal, or visceral malformations that could indicate a particular syndrome. Neurologic examination should assess cognitive and mental abilities, cranial nerve function, motor function, deep tendon reflexes, sensory function, coordination, and gait (if appropriate).

Genetic testing

Screening generally only takes place among those displaying several of the symptoms of ABCD, but a study on a large group of institutionalized deaf people in Columbia revealed that 5.38% of them were Waardenburg patients. Because of its rarity, none of the patients were diagnosed with ABCD (Waardenburg Type IV). Nothing can be done to prevent the disease.

Diagnosis can be made solely on the basis of history and physical examination in people who present with only facial asymmetry. For those who report neurological symptoms such as migraine or seizures, MRI scan of the brain is the imaging modality of choice. A diagnostic lumbar puncture and serum test for autoantibodies may also be indicated in people who present with a seizure disorder of recent onset.

Once it has been positively identified, pharmacotherapy follows. Antipsychotic drugs are the frontrunners in treatment for Fregoli and other DMSs. In addition to antipsychotics, anticonvulsants and antidepressants are also prescribed in some treatment courses. If a Fregoli patient has other psychological disorders, treatment often results in the use of trifluoperazine.

There are several causal agents for this disorder; these can be divided into three main categories and include the following:

The occurrence of WS has been reported to be one in 45,000 in Europe. The diagnosis can be made prenatally by ultrasound due to the phenotype displaying pigmentary disturbances, facial abnormalities, and other developmental defects. After birth, the diagnosis is initially made symptomatically and can be confirmed through genetic testing. If the diagnosis is not made early enough, complications can arise from

Hirschsprung's disease.

Metabolic studies are useful, but they are not able identify neural activity within a specific region to specific cognitive processes. Functionality can only be identified at the most general level: Metabolism in cortical and subcortical regions that may contribute to cognitive processes.

At present, there is no established relation between cerebral metabolic rates of glucose or oxygen as measured by PET and patient outcome. The decrease of cerebral metabolism occurs also when patients are treated with anesthetics to the point of unresponsiveness. Lowest value (28% of normal range) have been reported during propofol anesthesia. Also deep sleep represents a phase of decreased metabolism (down to 40% of the normal range)

In general, quantitative PET studies and the assessment of cerebral metabolic rates depends on many assumptions.

PET for example requires a correction factor, the lumped constant, which is stable in healthy brains. There are reports, that a global decrease of this constant emerges after a traumatic brain injury.

But not only the correction factors change due to TBI.

Another issue is the possibility of anaerobic glycolysis that could occur after TBI. In such a case the glucose levels measured by the PET are not tightly connected to the oxygen consumption of the patient's brain.

Third point regarding PET scans is the overall measurement per unit volume of brain tissue. The imaging can be affected by the inclusion of metabolically inactive spaces e.g. cerebrospinal fluidin the case of gross hydrocephalus, which artificially lowers the calculated metabolism.

Also the issue of radiation exposure must be considered in patients with already severely damaged brains and preclude longitudinal or follow-up studies.

Traditional diagnosis included radiographs. The vet may ask for a follow up radiograph with a barium marker to collect more data on digestion to aid in confirmation of PDD. A tissue sample is a more reliable method as well but invasive yet the only definitive diagnosis with live parrots.

The presence of avian bornaviruses may be detected in two ways: Testing fecal samples, cloanal swabs and blood for the presence of the virus or examining the bird's blood for ABV-specific antibodies by western blot or ELISA.

All tests give a percentage of false positives and false negatives so detection of ABV or antibody against it does not mean that PDD will follow. The disease does not follow a clear path of development or transmission.

Parents of a proband

- The parents of an affected individual are obligate heterozygotes and therefore carry one mutant allele.

- Heterozygotes (carriers) are asymptomatic.

Sibs of a proband

- At conception, each sibling of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier.

- Once an at-risk sibling is known to be unaffected, the risk of his/her being a carrier is 2/3.

- Heterozygotes (carriers) are asymptomatic.

Offspring of a proband

- Offspring of a proband are obligate heterozygotes and will therefore carry one mutant allele.

- In populations with a high rate of consanguinity, the offspring of a person with GPR56-related BFPP and a reproductive partner who is a carrier of GPR56-related BFPP have a 50% chance of inheriting two GPR56 disease-causing alleles and having BFPP and a 50% chance of being carriers.

Other family members of a proband.

- Each sibling of the proband's parents is at a 50% risk of being a carrier

OI is "notoriously difficult to diagnose." As a result, many patients have gone undiagnosed or misdiagnosed and either untreated or treated for other disorders. Current tests for OI (Tilt table test, autonomic assessment, and vascular integrity) can also specify and simplify treatment. (See Dr. Julian Stewart's article, "Orthostatic Intolerance: An Overview" for a more detailed description of OI tests.)

Tuber cinereum hamartoma may be associated with Pallister-Hall syndrome, a diagnosis characterized by multiple malformations, including polydactyly and imperforate anus. Neurologic symptoms are less severe in Pallister-Hall than in isolated cases of hamartoma.

The Fregoli delusion, or the delusion of doubles, is a rare disorder in which a person holds a delusional belief that different people are in fact a single person who changes appearance or is in disguise. The syndrome may be related to a brain lesion and is often of a paranoid nature, with the delusional person believing themselves persecuted by the person they believe is in disguise.

A person with the Fregoli delusion can also inaccurately recall places, objects, and events. This disorder can be explained by "associative nodes". The associative nodes serve as a biological link of information about other people with a particular familiar face (to the patient). This means that for any face that is similar to a recognizable face to the patient, the patient will recall that face as the person they know.

The Fregoli delusion is classed both as a monothematic delusion, since it only encompasses one delusional topic, and as a delusional misidentification syndrome (DMS), a class of delusional beliefs that involves misidentifying people, places, or objects. Like Capgras delusion, psychiatrists believe it is related to a breakdown in normal face perception.

Menkes syndrome can be diagnosed by blood tests of the copper and ceruloplasmin levels, skin biopsy, and optical microscopic examination of the hair to view characteristic Menkes abnormalities. X-rays of the skull and skeleton are conducted to look for abnormalities in bone formation. Urine homovanillic acid/vanillylmandelic acid ratio has been proposed as a screening tool to support earlier detection. Since 70% of MNK cases are inherited, genetic testing of the mother can be performed to search for a mutation in the ATP7A gene.

Diagnosis involves consideration of physical features and genetic testing. Presence of split uvula is a differentiating characteristic from Marfan Syndrome, as well as the severity of the heart defects. Loeys-Dietz Syndrome patients have more severe heart involvement and it is advised that they be treated for enlarged aorta earlier due to the increased risk of early rupture in Loeys-Dietz patients. Because different people express different combinations of symptoms and the syndrome was identified in 2005, many doctors may not be aware of its existence, although clinical guidelines were released in 2014-2015. Dr. Harold Dietz, Dr. Bart Loeys, and Dr. Kenneth Zahka are considered experts in this condition.

Brain death is the irreversible end of all brain activity, and function (including involuntary activity necessary to sustain life). The main cause is total necrosis of the cerebral neurons following loss of brain oxygenation. After brain death the patient lacks any sense of awareness; sleep-wake cycles or behavior, and typically look as if they are dead or are in a deep sleep-state or coma. Although visually similar to a comatose state such as persistent vegetative state, the two should not be confused. Criteria for brain death differ from country to country. However, the clinical assessments are the same and require the loss of all brainstem reflexes and the demonstration of continuing apnea in a persistently comatose patient (< 4 weeks).

Functional imaging using PET or CT scans, typically show a hollow skull phenomenon. This confirms the absence of neuronal function in the whole brain.

Patients classified as brain dead are legally dead and can qualify as organ donors, in which their organs are surgically removed and prepared for a particular recipient.

Brain death is one of the deciding factors when pronouncing a trauma patient as dead. Determining function and presence of necrosis after trauma to the whole brain or brain-stem may be used to determine brain death, and is used in many states in the US.

The diagnosis of this condition can be done via the following:

- Flow cytometry

- Bleeding time analysis

The tumor is difficult to detect by CT due to decreased sensitivity of the scan at the level of the sella turcica. MRI is the primary imaging modality for detection, with the lesion being of similar signal intensity to gray matter and non-enhancing with contrast. Lack of enhancement is an important imaging characteristic to help distinguish the tumor from similar masses that can occur in this region. These include germ cell tumors, granulomas of Langerhans cell histiocytosis and hypothalamic astrocytomas, as these lesions usually demonstrate at least partial uptake of contrast.

Cross–McKusick–Breen syndrome (also known as "Cross syndrome", "hypopigmentation and microphthalmia", and "oculocerebral-hypopigmentation syndrome") is an extremely rare disorder characterized by white skin, blond hair with yellow-gray metallic sheen, small eyes with cloudy corneas, jerky nystagmus, gingival fibromatosis and severe mental and physical retardation.

It was characterized in 1967.

Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.

The condition can be prevented by using chloramphenicol at the recommended doses and monitoring blood levels, or alternatively, third generation cephalosporins can be effectively substituted for the drug, without the associated toxicity.