The most recent revision of the UKs Department of Health Code of Practice governing use of that procedure for the diagnosis of death reaffirms the preconditions for its consideration. These are:

There should be no doubt that the patients condition – deeply comatose, unresponsive and requiring artificial ventilation – is due to irreversible brain damage of known cause. There should be no evidence that this state is due to depressant drugs. Primary hypothermia as the cause of unconsciousness must have been excluded, and
Potentially reversible circulatory, metabolic and endocrine disturbances likewise. Potentially reversible causes of apnoea (dependence on the ventilator), such as muscle relaxants and cervical cord injury, must be excluded.With these pre-conditions satisfied, the definitive criteria are:

Fixed pupils which do not respond to sharp changes in the intensity of incident light. No corneal reflex. Absent oculovestibular reflexes – no eye movements following the slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric reflex test). No response to supraorbital pressure. No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation. No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5 minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and diffusion oxygenation during the disconnection (so the brainstem respiratory centre is not challenged by the ultimate, anoxic, drive stimulus).
Tay syndrome should not be confused with the Tay–Sachs disease. : 485   It is an autosomal recessive congenital disease. : 501  In some cases, it can be diagnosed prenatally. IBIDS syndrome is nonphotosensitive. Cause
The photosensitive form is referred to as PIBIDS, and is associated with ERCC2 and ERCC3. Photosensitive forms
All photosensitive TTD syndromes have defects in the nucleotide excision repair (NER) pathway, which is a vital DNA repair system that removes many kinds of DNA lesions. This defect is not present in the nonphotosensitive TTDs. These type of defects can result in other rare autosomal recessive diseases like xeroderma pigmentosum and Cockayne syndrome. DNA repair
Currently, mutations in four genes are recognized as causing the TTD phenotype, namely TTDN1, XPB, XPD and TTDA. Individuals with defects in XPB, XPD and TTDA are photosensitive, whereas those with a defect in TTDN1 are not. The three genes, XPB, XPD and TTDA, encode protein components of the multi-subunit transcription/repair factor IIH (TFIIH). This complex factor is an important decision maker in NER that opens the DNA double helix after damage is initially recognized. NER is a multi-step pathway that removes a variety of different DNA damages that alter normal base pairing, including both UV-induced damages and bulky chemical adducts. Features of premature aging often occur in individuals with mutational defects in genes specifying protein components of the NER pathway, including those with TTD (see DNA damage theory of aging). Diagnosis
Treatment
See also
Skin lesion
List of cutaneous conditions

References
External links
NIH document on Tay syndrome