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Neuropsychiatric Aspects of Traumatic Brain Injury

Neuropsychiatric Aspects of Traumatic Brain Injury

Special Report: Neuropsychiatry

Each year, more than 2 million
individuals in the United States
sustain a traumatic brain injury
(TBI), leading to more than 500,000
hospital admissions and 80,000 survivors
with persistent neurologic disabilities.
The population at highest risk for
TBI is in the 15- to 24-year age range,
with a male-to-female ratio of approximately
3:2. The most common causes
of TBI include motor vehicle accidents,
falls, assaults, and sporting accidents.
In patients older than 65, the most
common cause is a fall.1

Risk factors for TBI include substance
abuse and psychiatric conditions
associated with impulsive behaviors,
such as bipolar disorder, cluster B personality
disorders, and attention-deficit/
hyperactivity disorder (ADHD). These
pre-injury psychiatric conditions are
associated with high-risk behaviors that
can lead to TBI. More than 50% of TBIs
involve alcohol intoxication, and 30%
to 60% of patients are intoxicated at
the time of injury.2

TBI involves the application of force
to the brain that results in structural or
metabolic alterations manifested by
altered consciousness or focal neurologic
deficits of varying severity and duration.
An initial score on the Glasgow Coma
Scale of 13 to 15 constitutes a mild TBI,
while a score of 9 to 12 represents moderate
TBI, and a score below 9 is severe
TBI. Mild TBI accounts for about 80%
of all cases, with moderate and severe
cases each being responsible for 10%.

The American Congress of Rehabilitation
Medicine has further refined the
definition of mild TBI, stating that it is
any traumatically induced disruption of
brain function with limited loss of
consciousness (30 minutes or less) or
post-traumatic amnesia for less than 24
hours (Table).3 Given the fact that most
TBIs are mild, clinicians may encounter orbitofrontal and anterior temporal
cortex tend to be selectively damaged.4 Additional diffuse axonal injury (DAI)
occurs at the white-gray matter junction
and in connecting pathways
throughout the brain.5 Often undetectable
through structural neuroimaging
methods such as CT and MRI, DAI
results from shearing forces applied to
the brain during rapid acceleration and
deceleration of the head.

These acceleration-deceleration
mechanics do not require the blunt
force impact that occurs when a moving
head strikes a stationary object or vice
versa. They can also occur through
rotational mechanics, such as whiplash
injuries. Thus, the absence of external
stigmata of injury or structural neuroimaging
abnormalities does not rule out
the presence of a TBI. It is these mild
TBIs that while leaving few, if any, lasting
neurologic or cognitive sequelae,
may lead to disruptive psychiatric
syndromes that are far from mild.

Secondary injuries from edema or
hemorrhage result from increased
intracranial pressure in severe trauma.
However, TBI may also activate intracellular
processes involving excitatory
amino acids that lead to cell death.6 This
process is initiated within hours of
injury, although the cascade of events
that ultimately cause cell death may take
days or weeks. The precise mechanism
that mediates excitotoxic cell death is
not understood, but it is possible that prolonged excitation of neurons may
secondarily cause intracellular metabolic
disruption. While clinical trials of
excitatory amino acid antagonists have
been disappointing,7 these studies have
targeted a more severely injured population.
The clinical manifestation of
this process in mild TBI may be the
progressive emergence of neuropsychiatric
symptoms over several days or
weeks following injury.8

Cognitive deficits

Given the reliance of higher cognitive
functions on distributed rather than
focal processing, DAI tends to
profoundly affect the executive cognitive
functions even in the absence of
neurologic or focal cortical deficits.
Acquired deficits in attention, concentration,
and vigilance may resemble
those of ADHD, although the postinjury
onset or worsening of these
deficits helps clarify the cause. Deficits
in executive cognitive functioning may
particularly affect persons in occupations
that are highly dependent on rapid
decision making and the complex use
of information.


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