Decreased perfusion pressure can also
occur when systemic blood pressure drops, such
as when assuming a standing position. Some
patients with increased ICP develop brief bi-
lateral visual loss when they stand, called vi-
sual obscurations, presumably due to failure
to autoregulate the posterior cerebral blood
flow. Failure of perfusion pressure can also
occur focally (i.e., in a patient with an otherwise
asymptomatic carotid occlusion who develops
symptoms in the ipsilateral carotid distribu-
tion on standing because of the resulting small
drop in blood pressure). If the patient has bi-
lateral chronic carotid occlusions, transient loss
of consciousness may result.
16
Patients with elevated ICP from mass lesions
often suffer sudden rises in ICP precipitated
by changes in posture, coughing, sneezing, or
straining, or even during tracheal suctioning
(plateau waves).
17
The sudden rises in ICP can
reduce cerebral perfusion and produce a variety
of neurologic symptoms including confusion,
stupor, and coma
18
(Table 3–2). In general, the
symptoms last only a few minutes and then re-
solve, leading some observers to confuse these
with seizures.
Finally, the loss of compliance of the intra-
cranial system to further increases in volume
and the rate of change in ICP plays an important
role in the response of the brain to increased
ICP. Compliance is the change in pressure
caused by an increase in volume. In a normal
brain, increases in brain volume (e.g., due to a
small intracerebral hemorrhage) can be com-
pensated by displacement of an equal volume of
CSF from the compartment. However, when a
mass has increased in size to the point where
there is little remaining CSF in the compart-
ment, even a small further increase in volume
can produce a large increase in compartmental
pressure. This loss of compliance in cases where
diffuse brain edema has caused a critical in-
crease in ICP can lead to the development of
plateau waves. These are large, sustained in-
creases in ICP, which may approach the mean
arterial blood pressure, and which occur at in-
tervals as often as every 15 to 30 minutes.
19,20
They are thought to be due to episodic arterial
vasodilation, which is due to systemic vasomo-
tor rhythms, but a sudden increase in vascular
volume in a compartment with no compliance,
even if very small, can dramatically increase
ICP.
21
These sudden increases in ICP can
thus cause a wide range of neurologic parox-
ysmal symptoms (see Table 3–2). When pres-
sure in neighboring compartments is lower,
this imbalance can cause herniation (see be-
low).
22
Table 3–2 Paroxysmal Symptoms That May Result From a Sudden
Increase in Intracranial Pressure
Impairment of consciousness
Opisthotonus, trismus
Trancelike state
Rigidity and tonic extension/flexion
Unreality/warmth
of the arms and legs
Confusion, disorientation
Bilateral extensor plantar responses
Restlessness, agitation
Sluggish/absent deep tendon reflexes
Disorganized motor activity, carphologia
Generalized muscular weakness
Sense of suffocation, air hunger
Facial twitching
Cardiovascular/respiratory disturbances
Clonic movements of the arms and legs
Headache
Facial/limb paresthesias
Pain in the neck and shoulders
Rise in temperature
Nasal itch
Nausea, vomiting
Blurring of vision, amaurosis
Facial flushing
Mydriasis, pupillary areflexia
Pallor, cyanosis
Nystagmus
Sweating
Oculomotor/abducens paresis
Shivering and ‘‘goose flesh’’
Conjugate deviation of the eyes
Thirst
External ophthalmoplegia
Salivation
Dysphagia, dysarthria
Yawning, hiccoughing
Nuchal rigidity
Urinary and fecal urgency/incontinence
Retroflexion of the neck
Adapted from Ingvar.
18
Structural Causes of Stupor and Coma
93
Conversely, when a patient shows early signs
of herniation, it is often possible to reverse the
situation by restoring a small margin of com-
pliance to the compartment containing the mass
lesion. Hyperventilation causes a fall in arterial
pCO
2
, resulting in arterial and venous vaso-
constriction. The small reduction in intracranial
blood volume may reverse the herniation syn-
drome dramatically in just a few minutes.
The Role of Vascular Factors and
Cerebral Edema in Mass Lesions
As indicated above, an important mechanism
by which compressive lesions may cause symp-
toms is by inducing local tissue ischemia. Even
in the absence of a diffuse impairment of ce-
rebral blood flow, local increases in pressure
and tissue distortion in the vicinity of a mass le-
sion may stretch small arteries and reduce their
caliber to the point where they are no longer
able to supply sufficient blood to their targets.
Many mass lesions, including tumors, inflam-
matory lesions, and the capsules of subdural
hematomas, are able to induce the growth of new
blood vessels (angiogenesis).
23
These blood ves-
sels do not have the features that characterize
normal cerebral capillaries (i.e., lack of fenes-
trations and tight junctions between endothelial
cells) that are the basis for the blood-brain bar-
rier. Thus, the vessels leak; the leakage of
Tight junction
Astrocyte foot
Vesicular transport
across endothelial cells
Capillary endothelial cells
A
C
B
Astrocyte foot
Edematous astrocyte
Edematous
neuron
Edematous
capillary
endothelial
cells
Opened tight
junctions and
escaping plasma
Figure 3–1. A schematic drawing illustrating cytotoxic versus vasogenic edema. (A) Under normal circumstances, the brain
is protected from the circulation by a blood-brain barrier, consisting of tight junctions between cerebral capillary endo-
thelial cells that do not permit small molecules to penetrate the brain, as well as a basal lamina surrounded by astrocytic
end-feet. (B) When the blood-brain barrier is breached (e.g., by neovascularization in a tumor or the membranes of sub-
dural hematoma), fluid transudates from fenestrated blood vessels into the brain. This results in an increase in fluid in the
extracellular compartment, vasogenic edema. Vasogenic edema can usually be reduced by corticosteroids, which decrease
capillary permeability. (C) When neurons are injured, they can no longer maintain ion gradients. The increased intracel-
lular sodium causes a shift of fluid from the extracellular to the intracellular compartment, resulting in cytotoxic edema.
Cytotoxic edema is not affected by corticosteroids. (From Fishman, RA. Brain edema. N Engl J Med 293 (14):706–11,
1975. By permission of Massachusetts Medical Society.)
94
Plum and Posner’s Diagnosis of Stupor and Coma