Troubled Mind: The Lowdown on Increased ICP

Other reliable early indicators of increasing ICP include severe headache and persistent vomiting. A severe headache will commonly occur in the setting of a subarachnoid hemorrhage, typically following the rupture of an aneurysm. Free blood will irritate the meninges, causing the classic “thunderclap” or “worst headache of my life.” Vomiting, which can be projectile, occurs as the area of the brain that controls emesis is compressed and irritated.

When patients decline to verbal or pain or are unresponsive on the AVPU scale, they are typically in the later stages of increasing ICP. Besides a declining level of consciousness, other late signs include seizures, a blown pupil, posturing and Cushing reflex. Seizures can occur for a variety of reasons, including metabolic abnormalities or toxic injections; however, in these cases it is typically the result of either direct cortex compression by an expanding hematoma or mass, or irritation of brain tissue by free blood increasing edema. The “blown” pupil, or mydriasis, is the result of compression of the third cranial nerve that controls papillary constriction, eyelid elevation and most of the extraocular muscles. The parasympathetic fibers that control constriction run along the outside of the nerve and so are the first to be compressed with increasing ICP. Interruption of the parasympathetic flow allows for unopposed sympathetic stimulation to the pupil and resulting dilation. Posturing occurs as the corticospinal tracts of the spinal cord, within which motor fibers lie, are compressed during herniation, along with the pontine and midbrain structures that influence them.

A particularly late finding is the Cushing reflex, which indicates a significantly increased ICP. It is characterized by increased systolic blood pressure, bradycardia and inadequate respirations. Hypertension develops as autoregulatory mechanisms attempt to generate an adequate MAP to maintain CPP and perfuse the brain. Specifically, sympathetic nervous system stimulation results in alpha-1 adrenergic receptor stimulation and subsequent arterial vasoconstriction, increased systemic vascular resistance, and increased blood pressure. This resultant increase in blood pressure is detected by baroreceptors in the aortic and carotid sinuses, which in turn activate a parasympathetic response via the vagus nerve. Increased vagal tone results in bradycardia, an attempt to correct the developing hypertension. Inadequate respirations occur as a result of herniation of the brain stem causing compression of the respiratory control centers in the medulla oblongata.⁷

Cerebral herniation occurs when increased ICP displaces the brain within the cranial vault, pressing it up against structures such as the tentorium cerebelli or through the cranial foramen. There are numerous specific mechanisms by which cerebral herniation can occur (Figure 2).^8,9 Cingulate herniation, the most common type, occurs when the middle lobe of the brain herniates under the falx cerebelli. Uncal (transtentorial) herniation occurs when the uncus of the brain is pressed up against the tentorium cerebelli as the brain is forced through the tentorial hiatus. Central transtentorial herniation occurs when pressure is exerted on the brain from above, herniating the brain across the tentorium cerebelli. Cerebellotonsillar herniation occurs when the cerebellum herniates through the foramen magnum, resulting in compression of the brain stem. Upward transtentorial herniation occurs when the cerebellum herniates upward through the tentorial opening. Transcalvarial herniation occurs when increased ICP forces brain tissue out through a fracture or surgical site in the cranium.

Signs and Symptoms of Increased ICP

Early in the development of increased ICP, the associated signs and symptoms are related to the effects on the cerebral cortex and upper brain stem. Systolic blood pressure and pulse pressure will increase as the brain attempts to maintain a MAP sufficient to produce an adequate CPP. The heart rate will decrease, and bradycardia may develop. Alteration in the respiratory pattern, such as Cheyne-Stokes respirations, may occur. An altered mental status and decreased level of consciousness will develop. The patient may exhibit decorticate, or flexor, posturing.

As ICP continues to increase and the middle brain stem is generally affected, central neurogenic hypoventilation can develop, along with a wide pulse pressure and bradycardia. The pupils may be sluggish to light or nonreactive, and the patient may exhibit decerebrate, or extensor, posturing.