Porth's Essentials of Pathophysiology, 4e - page 944

926
U N I T 1 0
Nervous System
The signs and symptoms produced by an intracere-
bral hematoma depend on its size and location in the
brain. Signs of increased ICP can be manifested if the
hematoma is large and encroaching on vital structures.
A hematoma in the temporal lobe can be dangerous
because of the potential for lateral herniation.
Concussions
A cerebral concussion can be defined as a transient neu-
rogenic dysfunction caused by mechanical force to the
brain.
7,10–12
Acceleration–deceleration is the mechanism
of injury, usually due to a nonpenetrating force such as
a sudden blow to the head. There may be a momen-
tary loss of consciousness without demonstrable symp-
toms, except for residual amnesia. Microscopic changes
can often be detected in neurons and neuroglia within
hours of injury, but brain imaging is usually negative.
Although recovery usually takes place within 24 hours,
mild symptoms, such as headache, irritability, insomnia,
and poor concentration and memory, may persist for
months. This is known as the
postconcussion syndrome.
The amnesia or memory loss usually includes an interval
of time preceding the injury (retrograde amnesia) and
following the injury (anterograde amnesia). The dura-
tion of retrograde amnesia correlates with the severity
of the brain injury.
Traditionally, the diagnosis and management of con-
cussion has relied heavily on the person’s self-reporting
of symptoms. Because symptom resolution often pre-
cedes cognitive recovery and because many persons don’t
report symptoms in an effort to return to their normal
activities, additional neurophysiologic testing and moni-
toring can be useful. Neurophysiologic tests commonly
evaluate decision-making ability, reaction time, attention,
memory, and cognitive processing speed in an objective
fashion. CT or MRI imaging is usually reserved for cases
in which intracranial bleeding is suspected. Treatment,
which is largely supportive, includes both physical and
mental rest. Once symptoms have resolved, the person
may begin shortened work days with decreased work
demands. Students may benefit from short periods of
reading and studying with frequent breaks. Athletes are
advised to follow a slow stepwise return to play.
The complications of concussion, although rare, are
potentially serious. Currently, the clinical and neuro-
pathic consequences of repeated mild head injury are
known as
chronic traumatic encephalopathy
. The dis-
orders often manifests years or decades after the incit-
ing head injuries with effects on behavior, cognition,
and movement. Cognitive changes may occur early in
the disease course and include loss of executive func-
tion and poor memory. A widely feared complication
of concussion is the
second-impact syndrome
. It is
thought to occur when someone who is still recovering
from a recent concussion suffers a second head trauma.
Significant morbidity and even death can result from
edema caused by cerebral congestion that occurs.
Diffuse Axonal Injury
Diffuse axonal injury is caused by shearing of fragile
axons by acceleration-deceleration forces at the time of
trauma.
1,4,7
The difference in acceleration–deceleration
gradient on certain areas of the brain, permits generation
of rotational forces that cause axonal shearing injury.
It is characterized by distinct and microscopic findings,
including axonal swelling, that are widely distributed in
the cerebral hemispheric white matter, corpus callosum,
and upper brain stem.
Diffuse axonal injury is characterized clinically by
functional cerebral impairment, which may range from
confusion to coma and death. The clinical diagnosis of
diffuse axonal injury is based on immediate onset of
unconsciousness in a person with significant cerebral
trauma and no intracranial lesion noted on CT scan.
Current treatment modalities focus on supportive care,
especially for the unconscious person. Studies indicate
that axonal injury evolves over a period of hours or
days, suggesting that there may be an opportunity to
arrest its progression and preserve axonal integrity.
Manifestations of Diffuse
Brain Injury
Diffuse (global) brain injury, whether due to head
trauma or other pathologic processes, is manifested by
alterations in sensory, motor, and cognitive function and
by changes in the level of consciousness. In contrast to
a localized injury, which causes focal neurologic defi-
cits without altered consciousness, global injury nearly
always results in altered levels of consciousness, rang-
ing from inattention to stupor or coma. Severe injury
that seriously compromises brain function may result in
brain death.
Epidural
hematoma
Cerebral contusions
Subarachnoid
hemorrhages
FIGURE 37-9.
Computed tomography scan of brain in traumatic
brain injury, showing hemorrhagic cerebral contusions in right
temporal and bifrontal lobes, subarachnoid hemorrhages, and
epidural hematoma.
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