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Bedside tests that establish loss of all brainstem reflexes can show
that the destructive storm has indeed run its course, because the
brainstem is often the last structure to be compromised in this
process. Confirmatory tests and, in particular, various sorts of an-
giography (measurements of cranial blood flow) can be very useful
in confirming that the gross infarction that is required for a diagno-
sis of total brain failure has actually occurred.11
When the preserved areas of the brain do not support any recogniz-
able function, this lack of total anatomical annihilation is less
troubling. As the President’s Commission noted in its report, the
neurological standard for death requires an irreversible loss of all
brain functions, not complete anatomical destruction of the tissue.13
Isolated metabolic or electrical activity in dispersed cells cannot be a
sign that a patient is still alive; after all, such activity, supporting no
function of the whole organism, can continue even in some cells of
a corpse after the heart has stopped beating.
As critics have pointed out, however, the physiological facts are not
so simple.14 In some cases, the preserved tissue in a body with total
brain failure actually does support certain isolated functions of the
brain. Most notably, some patients with total brain failure do not
exhibit the condition known as “diabetes insipidus.” This condition
develops when a hormone known as AD H (anti-diuretic hormone)
is not released by a part of the brain known as “the posterior pitui-
38 | CO NTRO VERSIES IN THE D ETERMINATIO N O F D EATH
because its (extradural) arterial source is distinct from that which feeds other tis-
sue of the brain. The damage that is due to the rise in intracranial pressure, which
leads to total brain failure, can spare these extradural arteries so that a portion of
pituitary is preserved. For discussion of this point, see E. F. Wijdicks and J. L.
Atkinson, “Pathophysiologic Responses to Brain D eath,” in Brain D eath, ed. E. F.
Wijdicks (Philadelphia: Lippincott Williams & Wilkins, 2001).