Neurobehavioral Assessments of Cerebral Vasospasm - Animal Models of Acute Neurological Injuries: Injury and Mechanistic Assessments - page 543

rupture and subarachnoid clot formation on short- and long-term
behavioral outcome remains unanswered. Also, it is still unclear
how behavioral outcome is affected by surgery or endovascular
treatment, whether there is a difference in the outcome between
the patients who do or do not suffer SAH with or without
vasospasm, as well as how the behavioral outcome is affected
by development of postoperative delayed ischemic neurological
defi cits (DINDs) with or without coexisting vasospasm.
There are many mechanisms of brain injury that are unleashed
by rupture of an intracranial aneurysm with violent high-pressure
fl ow of highly oxygenated blood and formation of a blood clot in
the subarachnoid space. Acutely, it is a dramatic increase of intrac-
ranial pressure (ICP) with a decrease of cerebral perfusion pressure
(CPP) ( 19 ), with the possibility of developing acute hydrocephalus,
intracerebral and intraventricular bleeding, “no-fl ow phenome-
non,” as well as just recently confi rmed development of early
vasospasm ( 20 ). Subacutely, other insults to the brain occur as the
result of different factors released locally from the blood, plasma,
and clot, as well as the early infl ammatory reaction, “no-refl ow
phenomenon,” electrolyte, and/or hormonal imbalance (e.g., the
salt waste syndrome) ( 6, 21 ). The next aSAH-associated events
occur in a delayed fashion (days 3-14) and these include delayed
cerebral vasospasm ( 14, 22 ) and, for a long time considered being
closely linked to it, clinical vasospasm (also referred to as DIND)
( 14 ). But, the fi ndings of several recent studies revitalized interest
in events other than vasospasm aSAH-related mechanisms ( 17, 18,
23 ) that can result in DINDs. Recently, this concept gained con-
siderable interest after Dreier et al. ( 24, 25 ) proposed a new path-
omechanism leading to DIND that does not require the presence
of delayed cerebral vasospasm. These so-called spreading cortical
ischemias (CSIs) that develop in the presence of blood in the suba-
rachnoid space and decreased local availability of nitric oxide (NO)
have recently been confi rmed to exist in a patient after aSAH
and are associated with clinical deterioration and the presence
of CT-confi rmed cortical infarctions ( 24-26 ). The chronic (occur-
ring after more than 2 weeks after aSAH) reasons for clinical
deterioration are hydrocephalus and emotional distress and/or
depression. Of course, surgical trauma and blood fl ow changes
evoked by the endovascular intervention add yet another insult
due to decreased cerebral blood fl ow during cerebral arteriography
( 27 ) as well as an aneurysm repair both surgically or endovascularly
( 6, 13 ). However, the list of events that can affect the neurobehav-
ioral outcome of aSAH and its treatments does not end here.
The adjunct treatments of aSAH, such as CSF diversion via ven-
triculostomy, lumbar drainage or ventriculo-peritoneal shunt place-
ment, administration of nimodipine, or triple H-therapy ( 28-31 ),
may also impact neurobehavioral outcome.