Intracranial pressure

What is the Monroe-Kellie doctrine

Any increase in the volume of one of the intracranial components (blood, CSF or brain) must be offset by a decrease in another to prevent elevation of ICP: this interrelationship is known as the Monro-Kellie doctrine.

Overall cerebral blood flow however, depends on cerebral perfusion pressure, which is defined by this equation:

Cerebral perfusion pressure (CPP) = mean arterial perfusion (MAP) - ICP

How do dx and tx ICP?

Dx: CT/MRI- mass effect, measure pressure w transducer Tx

What are the 2 main types of edema that can occur in the brain?

The two main types of edema are: *Vasogenic edema*: extracellular accumulation of fluid usually due to disruption of blood vessels and BBB, leading to the extravasation of fluid out of blood vessels. Factors such as hydrostatic forces, inflammatory mediators, and endothelial permeability cause opening of the endothelial tight junctions, and subsequent formation of edema. Vasogenic edema is often seen around neoplastic lesions. Vasogenic edema may resolve once the blood vessels and BBB are restored. *Cytotoxic edema*: intracellular accumulation of fluid, due to injury to cells, most commonly associated with hypoxic, ischemic or traumatic damage. Often the result of lack of energy to cells, leading to depletion of adenosine triphosphate (ATP) and subsequent failure of the Na-K ATPase pumps, causing an alteration in selective permeability of cell membranes. Rapid ascent to high altitudes, alterations in systemic osmolality, lead intoxication and liver failure are some other conditions associated with cytotoxic edema.

Describe the various physical postures that can indicate brain damage or loss of function

decorticate posturing lesion is higher--->flexed arms point up to cortex; decerebrate posturing lesion is lower -------> extended arms point down. decerebrate sort of sounds like decelerate----therefore it indicates damage BELOW the midbrain

Compensatory mechanisms that decrease intracranial volume include____________(3 total)

• movement of CSF into the spinal (thecal) sac • increased reuptake of CSF at the arachnoid villi • compression of veins and sinuses

What are some causes of Causes of Raised ICP?

1. Blood volume: arterial (e.g., subdural, epidural, intracranial hemorrhage) or venous (e.g., blockage of venous drainage due to venous thrombosis). (More details about blood vessels and hemorrhage later this week). 2. CSF • Increased production: e.g., due to a choroid plexus tumor • Decreased absorption: e.g., due to damage to arachnoid villi after meningitis, or decreased flow through villi due to decreased cerebral venous drainage (increased venous pressure). • Blockage: e.g., due to cysts or tumors at narrow points in the ventricular system. 3. Brain volume • Brain tumor: details at the end of this week • Edema: cerebral edema is the end result of several neurological diseases.

ICP is normally_______________mm Hg. Elevation in ICP is life-threatening, so mechanisms exist to compensate for at least modest increases in intracranial pressure.

5-15mm Hg

Describe a central herniation

Central herniation: The upper brainstem can be forced downward through the tentorial notch. Mild central herniation can stretch the abducens nerve during its long course over the clivus, producing lateral rectus palsy, either unilaterally or bilaterally, causing diplopia. Paramedian basilar artery branches may rupture during central herniation, causing Duret hemorrhages: this is usually fatal. Larger masses or higher intracranial pressures can lead to transtentorial herniation (bilateral uncal herniation), and can cause a progression of herniation through the foramen magnum. Occasionally, central herniation can occur upwards if the volume increase is in the posterior cranial fossa.

Describe what happens in Uncal or transtentorial herniation and explain why the specific sxs occur

Here : the medial temporal lobe lies closest to free edge of the tentorium and with supratentorial masses, the parahippocampal gyrus and/or uncus can herniate through the tentorial notch. Uncal herniation is heralded by the clinical triad of a "blown" pupil, hemiplegia and coma. -Blow pupil due to CN 3 impingement -Hemiplegia due to impingement of motor pathway(corticospinal tract) ---Coma due to distortion of the midbrain reticular formation leading to decreased LOC and eventually coma

Describe Idiopathic intracranial hypertension

Idiopathic intracranial hypertension (IIH, pseudotumor cerebri, benign intracranial hypertension) is a condition associated with high intracranial pressure and papilledema but with no obvious cause for the increase in ICP. It is typically seen in overweight young women. Its cause is unknown.

Describe the triple flexion posture

In contrast to these postures, triple flexion (like deep tendon reflexes) is a purely spinal cord-mediated posture that can be present even with loss of function of the rest of the CNS. The thigh and knee are flexed and the ankle dorsiflexed. The response can occur after stimulation of the foot or can appear spontaneously.

Describe a subfalcine herniation

Sub falcine herniation: The cingulate gyrus on the medial aspect of the cerebral hemisphere can herniate inferior to the falx cerebri, compressing the anterior cerebral arteries, and resulting in lower limb weakness due to impact on the motor cortex for the lower limb. This herniation can also be clinically silent.

Describe a tonsillar herniation

Tonsillar herniation: The cerebellar tonsils, lying on either side of the medulla, herniate through the foramen magnum, compressing the medulla and adjacent vertebral arteries. This condition is associated with respiratory arrest, blood pressure instability, and if untreated, is rapidly fatal. Increasing pressure from any herniation, if unrelieved, will eventually lead to tonsillar herniation and death. (In certain congenital conditions (e.g., Chiari malformation) there is prolonged tonsillar herniation).

To confirm brain death, care must be taken to_______________. These include hypoxia, hypothermia, hypoglycemia, and drug overdose.

rule out reversible causes of loss of brain function The cause of the patient's condition should be determined and must be compatible with irreversible brain damage (e.g., severe head injury, spontaneous intracranial bleed).

What are some sxs of ICP

• Headache; worse in mornings, aggravated by stooping and bending • Altered mental status: confusion, irritability and depressed level of alertness and attention, and eventual coma. • Nausea/vomiting: occurs with acute rise in ICP • Papilledema usually present if the raised ICP is chronic, and can cause vision loss. • Diplopia: due to downward traction on CN VI palsy may occur since the nerve has a long subdural course along the clivus before entering the cavernous sinus.. • Raised ICP before the cranial sutures have closed can result in rapid enlargement of the head, with variable neurological compromise. • Cushing's triad -hypertension, bradycardia and irregular breathing are considered classic late signs of raised ICP and are due to compromised brainstem function.