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cytokines and a disruption of the blood-brain barrier, which causes

the development of vasogenic (extracellular) brain edema; impaired

cerebral autoregulation and ischemia in the setting of hypoxia and

hypotension; tissue acidosis and an influx of electrolytes, which

causes cytotoxic (intracellular) brain edema; and the loss of neurons,

glial cells, and presynaptic terminals from neurochemical and oxygen

free radical reactions.17.18

Table 4- 1 8 defines the most common types of TBI and describes

the clinical findings. The management of these conditions is discussed

later in General Management and in Table 4-2 1 .

Spil/al Cord II/jury

Spinal cord injury (SCI) and the resultant para- or quadriplegia are

typically due to trauma or, less frequently, impingement of the spinal

cord from abscess, ankylosing spondylitis, or tumor. Primary SCI, the

direct trauma at the time of injury, can be described according to

location or mechanism of injury29:

1 .

Location. SCI may involve the cervical, thoracic, or lum-

bar spines.

2.

Mechanism of injury. SCI may result from blunt or penetrat-

ing injuries. Blunt forces include ( I ) forward hyperOexion, causing the

discontinuity of the posterior spinal ligamenrs. disc herniation, and

NERVOUS SYSTEM

307

Table 4-18. Clinical Findings and General Management of Traumatic

Brain Injuries

Injury

Definition

Clinical Findings

Cerebral

Shaking of the brain sec-

Brief loss of consciousness or

concussion

ondary (Q acceleration

"dazed" presentation,

deceleration forces, usuheadache, dizziness, irritaally as a result of a fall or

bility, inappropriate laughduring sports activity.

ter, decreased concentration

Can be classified as mild or

and memory, rerro- or anreclassic.

grade amnesia, altered gait

Signs and symptoms of

cerebral concussion are

reversible.

Cerebral

Bruise (small hemorrhage)

See Cerebral concussion,

contusion

secondary to accelerationabove

deceleration forces or

beneath a depressed skull

fracture. most commonly

in the frontal or temporal

areas.

Cerebral

Tear of the cortical surface

SIS dependent on area

laceration

secondary to accelerationinvolved, JCr, and degree

deceleration forces, comof mass effect

monly in occurrence with

cerebral contusion over

the anterior and middle

fossa where [here are

sharp bony surfaces.

Diffuse

Occurs with widespread

Coma, abnormal posturing

axonal

white matter shearing

(if severe), other SIS depeninjury

secondary to high-speed

dent on area involved, ICP,

IDAI)

accelerarion-decelera -

and degree or mass effect

tion forces, usually as a

result of a motor vehicle

accident.

Can be classified as mild

16-24 hrs of coma),

moderare (greater than

24 hrs coma), or severe

(days ro weeks of coma).

308

AClITE CARE HANDBOOK I:OR PHYSICAL THERAPISTS

Table 4-18. Continued

Injury

Definition

Clinical Findings

Epidural

Blood accumulation in the

Headache, altered COIlhematoma

epidural space secondsciousness, abnormal

(EDH)

ary ro tearing of

posture, contralateral

meningeal arteries that

hemiparesis, and other

compresses deep brain

SIS dependent on specific

structures.

location of rhe lesion,

Associated with cranial

ICP, and degree of mass

fractures, particularly

effect

the thin temporal bone

and frontal and middle

meningeal tears.

Subdural

Blood accumulation in the

See Epidural hemaroma,

hematoma

subdural space that comabove

(SDH)

presses brain structures

as a result of traumatic

rupture or tear of cerebral veins, increased

intracranial hemorrhage, or cominued

bleeding of a cerebral

contusion.

The onset of symptoms

Can present with a "lucid"

may be acute (up to 24

interval before loss of conhrs), subacme (2 days to

sciousness for a second time

3 wks), or chronic (3

wks to 3-4 mas).

Intracere

Blood accumulation in the

See Epidural hematoma,

bral

brain parenchyma secabove

hematoma

ondary to acceleration

(ICH)

deceleration forces, the

shearing of cortical

blood vessels, or beneath

a fracmre.

NERVOUS SYSTEM

309

Injury

Definirion

Clinical Findings

May also arise as a complicarion of hypertension or

delayed bleeding with

progression of blood into

the dural, arachnoid, or

ventricular spaces.

ICP = intracranial pressure, SIS = signs and symploms.

Sources: Data from JV Hickey (ed). The Clinical Practice of Neurological and Neurosurgical Nursing (4th ed). Philadelphia: Lippincon, 1997; and SA Mayer, LP Rowland.

Head Injury. In LJ> Rowland (ed). Merrirr's Neurology ( I Orh cd). Philadelphia: Lippincan, Williams & Wilkins, 2000.

vertebral dislocation or fracture; (2) hyperextension, causing discontinuity of the anrerior spinal ligaments, disc herniation, and vertebral dislocation or fracture; and (3) axial compression, rotation, contusion, laceration, or transection. Penetrating forces, such as gunshot or stab wounds, may be ( 1 ) low velocity, in which the spinal cord and

protective structures are injured directly, or (2) high velocity, in which

a concussive force injures the spinal cord, and the protective structures remain intact.

Seco/ldary SCI is a complex series of pathologic vascular and

innammatory responses to primary SCI, which further compound

the original injury over the course of several days. A summary of

secondary SCI includes ( 1 ) vasospasm of superficial spinal vessels,

intra parenchymal hemmorhage and disruption of the blood-brain

and spinal cord barrier, complicated by neurogenic shock and loss

of autoregulation, and (2) increased calcium levels, which stimulate frce radical production to cause further ischemia, the release of catecholamines and opioids, and the accumulation of activated

microglia and macrophages.29,3o

The severity of SCI is most commonly classified by the American