Study
NR 325 Exam1 STUDY GUIDE (1)Guide_
GlendaNR325_
Portionn.Exam 1
Topics
5
Acute Intracranial Problems 3
Head Injury
Spinal Cord Injury
Seizures
Brain Tumors
Bacterial Meningitis
Stroke
Migraine Headache
Multiple Sclerosis
Parkinson’s Disease
Myasthenia Gravis
Amyotrophic Lateral Sclerosis
Huntington’s Disease
Alzheimer’s disease
Trigeminal Neuralgia
Guillain-Barré
Glaucoma
Cataract
Otitis Media
Meniere disease
Increased Intracranial Pressure
Highlight: Any patient, who becomes unconscious acutely, regardless of the cause, should be suspected of
having increased ICP.
• Mechanisms of increased ICP
Highlight: Mechanisms of Increased Intracranial Pressure
Increased ICP is a potentially life-threatening situation that results from an increase in any or all of the three
components (brain tissue, blood, CSF) within the skull. Elevated ICP is clinically significant because it
diminishes CPP, increases risks of brain ischemia and infarction, and is associated with a poor prognosis.5
Common causes of increased ICP include a mass (e.g., hematoma, contusion, abscess, tumor) and cerebral
edema (associated with brain tumors, hydrocephalus, head injury, or brain inflammation).
These cerebral insults, which may result in hypercapnia, cerebral acidosis, impaired autoregulation, and
systemic hypertension, increase the formation and spread of cerebral edema. This edema distorts brain tissue,
further increasing the ICP, and leads to even more tissue hypoxia and acidosis. Fig. 57-3 illustrates the
progression of increased ICP.
It is critical to maintain CBF to preserve tissue and thus minimize secondary injury. Sustained increases in
ICP result in brainstem compression and herniation of the brain from one compartment to another.
1
, Study
NR 325 Exam1 STUDY GUIDE (1)Guide_
GlendaNR325_
Portionn.Exam 1
Displacement and herniation of brain tissue can cause a potentially reversible process to become irreversible.
35
Ischemia and edema are further increased, compounding the preexisting problem. Compression of the
brainstem and cranial nerves may be fatal. (Fig. 57-4 illustrates types of herniation.) Herniation forces the
cerebellum and the brainstem downward through the foramen magnum. If compression of the brainstem is
unrelieved, respiratory arrest will occur due to compression of the respiratory control center in the medulla.
FIG. 57-3 Progression of increased intracranial pressure (ICP).
Cerebral Edema
As shown in Table 57-2, there are a variety of causes of cerebral edema (increased accumulation of fluid in
the extravascular spaces of brain tissue). Regardless of the cause, cerebral edema results in an increase in
2
, Study
NR 325 Exam1 STUDY GUIDE (1)Guide_
GlendaNR325_
Portionn.Exam 1
tissue volume that can increase ICP. The extent and severity of the original insult are factors that determine
35
the degree of cerebral edema. There are three types of cerebral edema: vasogenic, cytotoxic, and interstitial.
The same patient may have more than one type.
FIG. 57-4 Herniation. A, Normal relationship of intracranial structures. B, Shift of intracranial
structures.
• Clinical Manifestations
Glenda: The clinical manifestations of increased ICP can take many forms, depending
on the cause, location, and rate of increases in ICP.
Highlight: The level of consciousness (LOC) is the most sensitive and reliable
indicator of the patient's neurologic status.
Note: The change in level of consciousness (LOC) is an indicator of increased intracranial pressure (ICP) and suggests
that immediate action by the nurse is needed to prevent complications.
Highlight: Ocular Signs.
Compression of cranial nerve (CN) III, the oculomotor nerve, results in dilation of the pupil on the same side
(ipsilateral) as the mass lesion, sluggish or no response to light, inability to move the eye upward, and ptosis of the
eyelid. These signs can be the result of the brain shifting from midline, compressing the trunk of CN III, and paralyzing
the muscles controlling pupillary size and shape. In this situation, a fixed, unilateral, dilated pupil is considered a
neurologic emergency that indicates herniation of the brain.
3
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NR 325 Exam1 STUDY GUIDE (1)Guide_
GlendaNR325_
Portionn.Exam 1
35
Decrease in Motor Function.
As the ICP continues to rise, the patient manifests changes in motor ability. A
contralateral (opposite side of the mass lesion) hemiparesis or hemiplegia may
develop, depending on the location of the source of the increased ICP. If painful
stimuli are used to elicit a motor response, the patient may localize to the stimuli or
withdraw from it.
Noxious stimuli may also elicit decorticate (flexor) or decerebrate (extensor)
posturing (Fig. 57-5). Decorticate posture consists of internal rotation and adduction
of the arms with flexion of the elbows, wrists, and fingers as a result of interruption of
voluntary motor tracts in the cerebral cortex. Extension of the legs may also be seen.
A decerebrate posture may indicate more serious damage and results from disruption
of motor fibers in the midbrain and brainstem. In this position, the arms are stiffly
extended, adducted, and hyperpronated. There is also hyperextension of the legs with
plantar flexion of the feet.
Headache.
Although the brain itself is insensitive to pain, compression of other intracranial
structures, such as the walls of arteries and veins and the cranial nerves, can produce
headache. The headache is often continuous but worse in the morning. Straining,
agitation, or movement may accentuate the pain.
Vomiting.
Vomiting, usually not preceded by nausea, is often a nonspecific sign of increased ICP.
This is called unexpected vomiting and is related to pressure changes in the cranium.
Projectile vomiting may also occur and is related to increased ICP.
FIG. 57-5 Decorticate and decerebrate posturing. A, Decorticate response.
Flexion of arms, wrists, and fingers with adduction in upper extremities.
Extension, internal rotation, and plantar flexion in lower extremities. B,
Decerebrate response. All four extremities in rigid extension, with
hyperpronation of forearms and plantar flexion of feet. C, Decorticate
response on right side of body and decerebrate response on left side of body.
D, Opisthotonic posturing.
4
NR 325 Exam1 STUDY GUIDE (1)Guide_
GlendaNR325_
Portionn.Exam 1
Topics
5
Acute Intracranial Problems 3
Head Injury
Spinal Cord Injury
Seizures
Brain Tumors
Bacterial Meningitis
Stroke
Migraine Headache
Multiple Sclerosis
Parkinson’s Disease
Myasthenia Gravis
Amyotrophic Lateral Sclerosis
Huntington’s Disease
Alzheimer’s disease
Trigeminal Neuralgia
Guillain-Barré
Glaucoma
Cataract
Otitis Media
Meniere disease
Increased Intracranial Pressure
Highlight: Any patient, who becomes unconscious acutely, regardless of the cause, should be suspected of
having increased ICP.
• Mechanisms of increased ICP
Highlight: Mechanisms of Increased Intracranial Pressure
Increased ICP is a potentially life-threatening situation that results from an increase in any or all of the three
components (brain tissue, blood, CSF) within the skull. Elevated ICP is clinically significant because it
diminishes CPP, increases risks of brain ischemia and infarction, and is associated with a poor prognosis.5
Common causes of increased ICP include a mass (e.g., hematoma, contusion, abscess, tumor) and cerebral
edema (associated with brain tumors, hydrocephalus, head injury, or brain inflammation).
These cerebral insults, which may result in hypercapnia, cerebral acidosis, impaired autoregulation, and
systemic hypertension, increase the formation and spread of cerebral edema. This edema distorts brain tissue,
further increasing the ICP, and leads to even more tissue hypoxia and acidosis. Fig. 57-3 illustrates the
progression of increased ICP.
It is critical to maintain CBF to preserve tissue and thus minimize secondary injury. Sustained increases in
ICP result in brainstem compression and herniation of the brain from one compartment to another.
1
, Study
NR 325 Exam1 STUDY GUIDE (1)Guide_
GlendaNR325_
Portionn.Exam 1
Displacement and herniation of brain tissue can cause a potentially reversible process to become irreversible.
35
Ischemia and edema are further increased, compounding the preexisting problem. Compression of the
brainstem and cranial nerves may be fatal. (Fig. 57-4 illustrates types of herniation.) Herniation forces the
cerebellum and the brainstem downward through the foramen magnum. If compression of the brainstem is
unrelieved, respiratory arrest will occur due to compression of the respiratory control center in the medulla.
FIG. 57-3 Progression of increased intracranial pressure (ICP).
Cerebral Edema
As shown in Table 57-2, there are a variety of causes of cerebral edema (increased accumulation of fluid in
the extravascular spaces of brain tissue). Regardless of the cause, cerebral edema results in an increase in
2
, Study
NR 325 Exam1 STUDY GUIDE (1)Guide_
GlendaNR325_
Portionn.Exam 1
tissue volume that can increase ICP. The extent and severity of the original insult are factors that determine
35
the degree of cerebral edema. There are three types of cerebral edema: vasogenic, cytotoxic, and interstitial.
The same patient may have more than one type.
FIG. 57-4 Herniation. A, Normal relationship of intracranial structures. B, Shift of intracranial
structures.
• Clinical Manifestations
Glenda: The clinical manifestations of increased ICP can take many forms, depending
on the cause, location, and rate of increases in ICP.
Highlight: The level of consciousness (LOC) is the most sensitive and reliable
indicator of the patient's neurologic status.
Note: The change in level of consciousness (LOC) is an indicator of increased intracranial pressure (ICP) and suggests
that immediate action by the nurse is needed to prevent complications.
Highlight: Ocular Signs.
Compression of cranial nerve (CN) III, the oculomotor nerve, results in dilation of the pupil on the same side
(ipsilateral) as the mass lesion, sluggish or no response to light, inability to move the eye upward, and ptosis of the
eyelid. These signs can be the result of the brain shifting from midline, compressing the trunk of CN III, and paralyzing
the muscles controlling pupillary size and shape. In this situation, a fixed, unilateral, dilated pupil is considered a
neurologic emergency that indicates herniation of the brain.
3
, Study
NR 325 Exam1 STUDY GUIDE (1)Guide_
GlendaNR325_
Portionn.Exam 1
35
Decrease in Motor Function.
As the ICP continues to rise, the patient manifests changes in motor ability. A
contralateral (opposite side of the mass lesion) hemiparesis or hemiplegia may
develop, depending on the location of the source of the increased ICP. If painful
stimuli are used to elicit a motor response, the patient may localize to the stimuli or
withdraw from it.
Noxious stimuli may also elicit decorticate (flexor) or decerebrate (extensor)
posturing (Fig. 57-5). Decorticate posture consists of internal rotation and adduction
of the arms with flexion of the elbows, wrists, and fingers as a result of interruption of
voluntary motor tracts in the cerebral cortex. Extension of the legs may also be seen.
A decerebrate posture may indicate more serious damage and results from disruption
of motor fibers in the midbrain and brainstem. In this position, the arms are stiffly
extended, adducted, and hyperpronated. There is also hyperextension of the legs with
plantar flexion of the feet.
Headache.
Although the brain itself is insensitive to pain, compression of other intracranial
structures, such as the walls of arteries and veins and the cranial nerves, can produce
headache. The headache is often continuous but worse in the morning. Straining,
agitation, or movement may accentuate the pain.
Vomiting.
Vomiting, usually not preceded by nausea, is often a nonspecific sign of increased ICP.
This is called unexpected vomiting and is related to pressure changes in the cranium.
Projectile vomiting may also occur and is related to increased ICP.
FIG. 57-5 Decorticate and decerebrate posturing. A, Decorticate response.
Flexion of arms, wrists, and fingers with adduction in upper extremities.
Extension, internal rotation, and plantar flexion in lower extremities. B,
Decerebrate response. All four extremities in rigid extension, with
hyperpronation of forearms and plantar flexion of feet. C, Decorticate
response on right side of body and decerebrate response on left side of body.
D, Opisthotonic posturing.
4
