 Headache accompanied by fever or signs of
meningeal irritation, such as stiff neck and
sensitivity to light, should be evaluated and
treated immediately for possible infectious
meningitis, since patients with this condition can
deteriorate rapidly if untreated.
Idiopathic intracranial hypertension or pseudotumor
cerebri
 a condition of unknown cause characterized by
headache and elevated intracranial pressure with
no mass lesion
 most common in adolescent females
 treated with acetazolamide or, when severe, with
shunting procedures.
Temporal arteritis
 Also called giant cell arteritis
 Treatable cause of headache
 Seen most commonly in elderly individuals
 Vasculitis affects the temporal arteries and other
vessels, including those supplying the eye. The
temporal artery is characteristically enlarged and
firm.
 Diagnosis is made by measurement of the blood
erythrocyte sedimentation rate (ESR) and by
temporal artery biopsy.
 Prompt diagnosis and treatment with steroids is
essential to prevent possible vision loss.
INTRACRANIAL MASS LESIONS
 Anything abnormal that occupies volume within
the cranial vault functions as a mass.
 Examples include tumor, hemorrhage, abscess,
edema, hydrocephalus, and other disorders.
 Intracranial mass lesions can cause neurologic
symptoms and signs by the following
mechanisms:
1. Compression and destruction of adjacent
regions of the brain can cause
neurologic abnormalities.
2. A mass located within the cranial vault
can raise the intracranial pressure,
which causes certain characteristic
symptoms and signs.
3. Mass lesions can displace nervous
system structures so severely that they
are shifted from one compartment into
another—a situation called herniation.
Mass lesions can cause both local tissue damage and
remote effects through mechanical distortion of adjacent
structures. Mass effect
 any distortion of normal brain geometry due to a
mass lesion
 can be as subtle as a mild flattening, or
effacement, of sulci next to a lesion, seen on
MRI scan but producing no symptoms
 Depending on location and size, a mass can
produce neurologic abnormalities due to local
damage
 For example, a lesion located in the primary
motor cortex will cause contralateral weakness.
If the mass distorts or irritates blood vessels or
meninges, it may cause headache. Compression
of blood vessels can also cause ischemic
infarction, and erosion through blood vessel
walls can cause hemorrhage.
 Disruption of the blood–brain barrier results in
extravasation of fluid into the extracellular
space, producing vasogenic edema
 Compression of the ventricular system can
obstruct CSF flow, producing hydrocephalus
 Lesions can provoke abnormal electrical
discharges in the cerebral cortex, resulting in
seizures
 Remote effects may result from functional
changes in regions receiving important synaptic
connections from the damaged areas.
 Large masses can produce dramatic midline
shift of brain structures away from the side of
the lesion.
 Displacement and stretching of the upper
brainstem impairs function of the reticular
activating systems, causing impaired
consciousness and, ultimately, coma.
 The pineal calcification is a useful landmark for
measuring extent of midline shift at the level of
the upper brainstem. The amount of pineal shift
has been shown to correlate with impairment of
consciousness.
 In the extreme, mass effect causes brain
structures to shift from one compartment into
another, leading to herniation.
ELEVATED INTRACRANIAL PRESSURE
 The contents of the intracranial space are
confined by the hard walls of the bony skull.
 Of the three residents of this cavity—
cerebrospinal fluid, blood, and brain tissue—not
one is compressible (although they can be
deformed).
 Therefore, whenever there is a space-occupying
or mass lesion within the skull, something must
leave the skull to accommodate the extra
volume.
 Smaller lesions can be accommodated by a
decrease in intracranial CSF and blood without
causing much rise in intracranial pressure (flat
part of the curve in Figure 5.16)
 Larger lesions overcome this compensatory
mechanism, and the intracranial pressure
eventually begins to rise steeply. This can
ultimately lead to herniation and death (the
rightmost part of the curve in Figure 5.16).
rise to nausea and vomiting in elevated
intracranial pressure are not known.
 Vomiting occasionally occurs suddenly and
without much nausea. This is called projectile
vomiting.
 Elevated intracranial pressure is transmitted
through the subarachnoid space to the optic
nerve sheath, obstructing axonal transport
and venous return in the optic nerve.
 Ophthalmoscopic exam may reveal
papilledema, in which there is engorgement
and elevation of the optic disc, sometimes
accompanied by retinal hemorrhages

 Severely elevated intracranial pressure can cause

decreased cerebral blood flow and brain
ischemia.
 Cerebral blood flow depends on cerebral
perfusion pressure
 Cerebral perfusion pressure = mean arterial
pressure minus the intracranial pressure
(A) Funduscopic view of retina from a normal subject (left eye). Note
o (CPP = MAP – ICP) sharp margins of the optic disc.
o as the intracranial pressure increases,
cerebral perfusion pressure decreases.
 Autoregulation of cerebral vessel caliber can
compensate for modest reductions in cerebral
perfusion pressure, leading to relatively stable
cerebral blood flow. However, large increases in
intracranial pressure can exceed the capacity of
autoregulation, leading to reduced cerebral blood
flow and brain ischemia.
 Depending on the type of lesion, intracranial
pressure can change suddenly or more slowly,
over a period of days to weeks. If left untreated,
severely elevated intracranial pressure causes (B) Papilledema in a patient with elevated intracranial pressure (left
irreversible brain damage and death, sometimes eye).
within a few hours.
 It is essential for clinicians to recognize the This was a 43-year-old man who developed headaches, visual
blurring, and horizontal diplopia. Lumbar puncture revealed an
symptoms and signs of elevated intracranial opening pressure of 40 cm H2O. Magnetic resonance venogram
pressure so that appropriate treatment can be revealed a bilateral sigmoid sinus venous thrombosis. Blood studies
instituted without delay. showed an elevated anticardiolipin antibody. The patient was treated
 Headache associated with intracranial mass successfully with chronic oral anticoagulation.
lesions is often worse in the morning, since brain
edema increases overnight from the effects of
gravity on a patient in the reclining position.
 Altered mental status, especially irritability This classic sign of elevated intracranial pressure takes
and depressed level of alertness and attention, is several hours to days to develop and is often not present
in the acute setting.
often the most important indicator of elevated
intracranial pressure. The mechanisms giving  Transient or permanent optic nerve injury can
occur in association with papilledema, leading to
visual blurring or visual loss.
  Areas of decreased vision most commonly then 0.25 g/kg every 6 hours, edema and other fluids
(or, alternatively, hypertonic from CNS while
include an increased blind spot or a concentric saline) aiming for serum Na+ maintaining cerebral
visual field deficit affecting mainly the >138 mEq/L and osmolarity perfusion
300–310 mOsm/L
peripheral margins of the visual field whilemaintaining normal
 Diplopia (double vision) can occur as a result of volume status and normal
downward traction on CN VI, causing unilateral bloodpressure. Furosemide
may also be added
or bilateral abducens nerve palsies. Ventricular drainage Minutes Removal of CSF
 Cushing’s triad—hypertension, bradycardia, decreases intracranial
pressure
and irregular respirations—is another classic If other measures fail, try 1 hour Causes cerebral
sign of elevated intracranial pressure. barbiturate-induced coma. vasoconstriction and
 Hypertension may be a reflex mechanism to reduced metabolic
demands
maintain cerebral perfusion pressure, Hemicraniectomy (removal Immediate Decompresses intracranial
bradycardia may be a reflex response to the of skull overlying mass cavity
hypertension, and irregular respirations are lesion) Experimental
Steroids Hours Reduces cerebral edema,
caused by impaired brainstem function. possibly by strengthening
 a variety of changes in vital signs other than blood–brain barrier
May also work by other
Cushing’s triad can be seen as a result of mechanisms
brainstem dysfunction, including hypotension Often used with brain
and tachycardia. tumors
Not shown to improve
outcome in acute head
Goals of treating elevated intracranial pressure trauma, stroke, or
hemorrhage
 To reduce intracranial pressure to safe levels,
providing time to treat the underlying disorder
o Normal intracranial pressure in adults BRAIN HERNIATION SYNDROMES
 less than 20 cm H2O, or  Intracranial tumors, hemorrhage, edema, and
less than 15 mm Hg (torr) other masses cause a displacement of
 1 cm H2O = 0.735 mm Hg; 1 intracranial structures called mass effect.
mm Hg = 1.36 cm H2O  Herniation occurs when mass effect is severe
 To keep cerebral perfusion pressure above 50 enough to push intracranial structures from one
mm Hg so that cerebral blood flow is maintained compartment into another.
 The three most clinically important herniation
Measurement of Intracranial Pressure syndromes are caused by
 Intracranial pressure can be measured in o herniation through the tentorial notch –
clinically stable patients during lumbar transtentorial herniation
puncture); however, lumbar puncture should not o herniation centrally and downward –
be performed in patients suspected of having
central herniation
severely elevated intracranial pressure, since this
o herniation under the falx cerebri –
carries a risk of precipitating herniation.
subfalcine herniation
 In critically ill patients, intracranial pressure can
be monitored continuously with a ventricular
drain, intraparenchymal monitor, subarachnoid
bolt, or a variety of other devices placed
neurosurgically within the cranium and
connected to a pressure transducer.

Treatment Measures for Elevated Intracranial

Pressure
TIME TO
PROPOSED
ONSET
INTERVENTION MECHANISM/
OF
COMMENTS
EFFECT
Elevate head of bed 30°, and Immediate Promotes venous drainage
maintain head straight
Immediate Promotes venous
drainage to avoid obstructing
jugular venous return.
Intubate and hyperventilate 30 seconds Causes cerebral
to pCO2 of 25–30 mm Hg vasoconstriction Transtentorial Herniation
IV mannitol 1 g/kg bolus, 5 minutes Promotes removal of
  herniation of the medial temporal lobe,
especially the uncus (uncal herniation),
inferiorly through the tentorial notch).

Uncal herniation
 heralded by the clinical triad of a “blown”
pupil, hemiplegia, and coma.

Blown pupil
 Compression of the oculomotor nerve (CN III),
usually ipsilateral to the lesion, produces first a
dilated, unresponsive pupil (a blown pupil),
and, later, impairment of eye movements.
 dilated pupil is ipsilateral to the lesion in 85%
of cases.
Hemiplegia
 Compression of the cerebral peduncles can
cause hemiplegia (paralysis of half of the
body).
 Corticospinal tract crosses to the opposite side
as it descends through the medulla into the
spinal cord at the pyramidal decussation. Thus,
often the hemiplegia is contralateral to the
lesion either because of uncal herniation
compressing the ipsilateral corticospinal tract in
the mid-brain, or because of a direct effect of
the lesion on the ipsilateral motor cortex, or
because of both.
 Sometimes in uncal herniation, the midbrain is
pushed all the way over until it is compressed
by the opposite side of the tentorial notch. In
these cases the contralateral corticospinal tract
is compressed, producing hemiplegia that is
ipsilateral to the lesion. This is called
Kernohan’s phenomenon.
Coma
 Distortion of the midbrain reticular formation
leads to decreased level of consciousness and,
ultimately, to coma.
 The posterior cerebral arteries may be
compressed as they pass upward through the
tentorial notch. The result can be infarction in
the posterior cerebral artery territory.
 Uncal transtentorial herniation can be unilateral
or bilateral and is caused by supratentorial mass
lesions. Occasionally, large mass lesions in the
posterior fossa can cause upward transtentorial
herniation.