General Principles of Intracranial Pressure

Intracranial Contents Contributing to Intracranial Volume and Pressure

The skull contains three components that contribute to intracranial volume: the brain, its blood supply, and the cerebrospinal fluid (CSF). The brain accounts for approximately 80% of the intracranial volume, the arterial and venous blood approximately 10%, and the CSF approximately 10%. The skull is fixed and can only accommodate small changes in intracranial volume before intracranial pressure rises. Increased intracranial pressure can arise due to increased volume of any of the three intracranial contents (brain, blood volume, or CSF).

Increased intracranial pressure due to increased brain volume—Both focal brain lesions and diffuse brain pathology can lead to increased intracranial pressure (ICP). A focal brain lesion (e.g., stroke, tumor, abscess, demyelination) can cause increased ICP either by mass effect or by obstruction of the ventricular system leading to obstruction of CSF flow. Diffuse cerebral edema (e.g., secondary to severe head trauma, hypoxic-ischemic injury, hyponatremia, meningoencephalitis) raises overall brain volume, increasing ICP.

Increased intracranial pressure due to increased blood volume—Increased blood volume can occur either due to decreased venous outflow (e.g., venous sinus thrombosis) or due to increased arterial blood flow (e.g., due to cerebral vasodilation).

Increased intracranial pressure due to increased cerebrospinal fluid volume—Increased CSF volume (hydrocephalus) can occur due to obstruction of CSF circulation or rarely due to increased CSF production (e.g., due to choroid plexus papilloma). Obstruction of CSF circulation can be caused by a blockage anywhere within the ventricular system (e.g., tumor, intraventricular hemorrhage, congenital aqueductal stenosis) or a blockage of the arachnoid granulations where CSF is absorbed into the venous circulation (e.g., due to meningitis, subarachnoid hemorrhage). Ventricular obstruction causes noncommunicating hydrocephalus: The ventricles cannot communicate with one another to allow for CSF to circulate. In noncommunicating hydrocephalus, only the ventricles proximal to the obstruction will dilate (e.g., obstruction of the third ventricle will lead to dilation of the lateral ventricles but not the fourth ventricle). Obstruction of the arachnoid granulations causes communicating hydrocephalus: The ventricles can still communicate with one another, but CSF cannot be reabsorbed. In communicating hydrocephalus, all of the ventricles will dilate.

If brain volume increases, there is the possibility of limited compensation in the other two compartments (CSF and blood) to maintain constant intracranial volume (Monro-Kellie doctrine). The compensatory mechanisms include displacing CSF into the spinal column, constriction of arterioles, and collapse of veins. However, if intracranial volume increases beyond a certain point, compensation is no longer possible, and ICP rises.

There are two main potential consequences of increased ICP: brain herniation and decreased cerebral perfusion.

Brain Herniation

Brain herniation refers to shift of brain tissue beyond its normal location (Fig. 25–1). Types of herniation include subfalcine, uncal, transtentorial (central), upward, and tonsillar.

Subfalcine herniation—In this type of herniation, the cingulate gyrus herniates beneath the falx cerebri (the interhemispheric dura). This can compress the anterior cerebral arteries, leading to stroke.

Uncal herniation—In this type of herniation, the medial temporal lobe compresses the ipsilateral third nerve causing pupillary dilatation. If uncal herniation progresses to the point of compressing the contralateral midbrain against the tentorium, the contralateral cerebral peduncle can be affected, leading to motor deficits and upper motor neuron signs ipsilateral to the side of uncal herniation (Kernohan’s notch phenomenon). For example, uncal herniation on the left generally first causes left pupillary dilatation due to compression of the left cranial nerve 3. If uncal herniation progresses, the right cerebral peduncle can be compressed against the tentorium, causing hemiparesis contralateral to this peduncle (i.e., on the left) since the corticospinal tract has not yet crossed. Therefore, the hemiparesis is ipsilateral to the side of uncal herniation and the dilated pupil (on the left in this example).

Transtentorial (central) herniation—In this type of herniation, the central components of the brain (thalami, midbrain) herniate downward through the tentorium cerebelli, which can lead to bilateral pupillary dilatation, and can ultimately proceed to coma, cardiorespiratory dysfunction, and death.

Upward herniation—With a large cerebellar mass lesion (or diffuse cerebellar pathology), the cerebellum can herniate upward through the tentorium. This causes brainstem compression leading to coma and pupillary abnormalities (the pupils may be small due to pontine distortion or dilated due to midbrain distortion). Upward herniation may be precipitated by CSF drainage via placement of an extraventricular drain in patients with increased cerebellar volume (e.g., cerebellar tumor or hemorrhage): An upward pressure vector from the expanded cerebellum leads to upward displacement when pressure from above is decreased.

Tonsillar herniation—In this type of herniation, the cerebellar tonsils descend below the foramen magnum, compressing the medulla (coning). This can cause coma, cardiorespiratory dysfunction, and death.

Cerebral Perfusion Pressure

Cerebral perfusion pressure (CPP) is determined by the pressure of the blood reaching the brain (mean arterial pressure [MAP]) and the ICP acting against this blood pressure:

Therefore, if ICP rises at a constant MAP, cerebral perfusion pressure will fall, which can lead to decreased cerebral perfusion.

Symptoms and Signs of Increased Intracranial Pressure

The symptoms and signs of intracranial hypertension depend on the degree to which ICP is elevated and the rapidity with which ICP rises. Symptoms may include headache, blurred vision, nausea/vomiting, and alteration in mental status ranging from somnolence to coma. Headache due to elevated ICP is classically worse in the supine position and improves with standing. Signs of intracranial hypertension can include:

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  Papilledema. Papilledema may not be present acutely since it can take hours to days to develop.

  
  
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  Unilateral or bilateral sixth nerve palsy. This is referred to as a “false localizing sign” in this context, since it appears focal but is a sign of a generalized process (elevated ICP) causing pressure on one or both abducens nerves due to the long intracranial course of this cranial nerve (see “Cranial Nerve 6: The Abducens Nerve” in Chapter 11 for discussion of the signs of sixth nerve palsy).

  
  
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  Cushing’s response: hypertension, bradycardia, and irregular respiration can result from compression of the medulla.

  
  
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  Signs of herniation related to compression of particular structures may be present depending on the location and cause of the responsible lesion(s) (see “Brain Herniation” above).

Treatment of Acutely Increased Intracranial Pressure