Intracranial Hypertension (ICH)

Intracranial hypertension (ICH) manifests when pressure inside the skull is > 20 mmHg. ICH is often idiopathic, but can also occur in conditions such as hydrocephalus and cerebral edema. Cerebral edema shows loss of grey-white differentiation on imaging, and can either be intracellular—due to the movement of fluid from the interstitium into the cells—or interstitial—stemming from increased vessel permeability and subsequent fluid buildup outside brain cells. Two triggers for intracellular edema are hyponatremia and hypoxia. Hyponatremia decreases extracellular osmolality, drawing water into brain cells, while hypoxia damages brain cells, thus reducing Na+/K+ ATPase activity and an influx of water due to sodium accumulation. Interstitial edema leads to vasogenic intracranial hypertension, which can arise from factors like brain tumors (due to the formation of new leaky vessels), head trauma, and inflammation from conditions like meningitis or encephalitis.

Clinically, patients with ICH often report headaches, seizures, and vomiting, and may also exhibit altered mental statuses ranging from confusion to coma. Observing papilledema, diplopia (stretching of CN VI), and the Cushing’s reflex (hypertension, bradycardia, irregular respirations) can also serve as diagnostic indicators. Additionally, elevated intracranial pressure can precipitate gastric (Cushing) ulcers due to increased parasympathetic activity

Brain herniation is a severe complication of intracranial hypertension. Subfalcine herniation involves the cingulate gyrus herniating beneath the falx cerebri, which can compress the ACA and cause contralateral lower extremity motor and sensory deficits. Transtentorial hernias involve the herniation of the inferior occipital lobe and brainstem, which may shear branches of the basilar artery, resulting in Duret hemorrhages. Tonsillar hernias occur when the cerebellar tonsils move into the foramen magnum, which can compress the brainstem and is often fatal.

In uncal herniation, the medial temporal lobe segment herniates past the tentorium cerebelli, causing complications like CN III compression, causing mydriasis due to unopposed sympathetic tone, and a ‘down and out’ orientation due to the unopposed action of CN IV & VI. Uncal hernias can also compress the PCA, causing ipsilateral occipital lobe infarction, as well as contralateral homonymous hemianopsia (with macular sparing). Finally, compression of contralateral cerebral peduncle can cause ipsilateral hemiparesis.

Treatment strategies for intracranial hypertension aim to lower the intracranial pressure. Hyperventilation, which decreases PaCO2 and causes cerebral vasoconstriction, mannitol for osmotic diuresis, and ventriculostomy to drain excess CSF, are all employed in the treatment of ICH

Idiopathic intracranial hypertension (IIH) occurs from a mismatch in CSF production and resorption from an unknown origin. IIH most frequently occurs in obese women aged 15-45 and is not associated with ventricular enlargement. Certain drugs like OCPs, all-trans retinoic acid, tetracyclines, and isotretinoin also increase IIH risk. Symptomatology mirrors intracranial hypertension, with the addition of pulsatile tinnitus. Diagnosis involves lumbar puncture, which shows increased opening pressure. Potential sequelae of IIH includes permanent vision loss from untreated papilledema. Treatment involves acetazolamide and optic nerve sheath fenestration.