Intracranial Hemorrhage

Intracranial Hemorrhage: Types, Imaging Features, and Clinical Pearls

Intracranial hemorrhage is a life-threatening neurologic emergency commonly encountered in trauma, neurosurgery, emergency medicine, and perioperative care. Rapid recognition of the type of hemorrhage, its mechanism, and its clinical presentation is essential for diagnosis, management, and exam performance. The four major categories include epidural hematoma, subdural hematoma, subarachnoid hemorrhage, and intraparenchymal hemorrhage.

Summary Table: Key Differences

Epidural Hematoma (EDH)

An epidural hematoma results from arterial bleeding between the dura mater and the inner table of the skull, most commonly due to rupture of the middle meningeal artery, often secondary to a temporal bone fracture.

Clinically, epidural hematomas are classically associated with a lucid interval, in which the patient briefly regains consciousness before rapid neurologic deterioration. As bleeding progresses, increased intracranial pressure may lead to transtentorial (uncal) herniation, producing ipsilateral cranial nerve III palsy with a fixed and dilated pupil.

On imaging, epidural hematomas appear as a lentiform (biconvex) hyperdensity on CT and do not cross suture lines, as the dura is tightly adherent at sutures.

Subdural Hematoma (SDH)

Subdural hematomas are caused by rupture of bridging veins, leading to venous bleeding between the dura and arachnoid mater. This mechanism iscommon in elderly patients, chronic alcohol users, and cases of shaken baby syndrome.

Because venous bleeding is slower, symptoms may evolve over hours to days. Subdural hematomas cross suture lines and appear as a crescent-shaped collection on CT imaging. Significant hemorrhage can result in midline shift and secondary brain injury.

Subarachnoid Hemorrhage (SAH)

Subarachnoid hemorrhage most commonly results from rupture of a saccular (berry) aneurysm or, less commonly, an arteriovenous

 malformation (AVM). The most frequent aneurysm location is the anterior communicating artery (AComm), followed by the anterior cerebral artery (ACA).

Patients classically describe a “worst headache of my life”, often with sudden onset. Lumbar puncture reveals bloody or xanthochromic cerebrospinal fluid if CT imaging is nondiagnostic.

A critical delayed complication of SAH is cerebral vasospasm, which typically occurs 4–10 days after hemorrhage and can lead to ischemic infarction. Nimodipine is used prophylactically to reduce the risk of vasospasm-related neurologic decline.

Sentinel Headache in Subarachnoid Hemorrhage

Retrospective studies show that up to 40% of patients experience a sentinel headache days to weeks before a

neurysmal rupture. This headacherepresents a minor leak from an aneurysm and serves as a warning sign. Risk factors for SAH include smoking, hypertension, alcohol use, and estrogen depletion.

Intraparenchymal (Intracerebral) Hemorrhage

Intraparenchymal hemorrhage occurs within the brain tissue itself and is most commonly caused by chronic systemic hypertension. Anotherimportant etiology is cerebral amyloid angiopathy, particularly in elderly patients.

Hypertensive hemorrhages are classically associated with Charcot-Bouchard microaneurysms of the lenticulostriate vessels and most frequently involve the basal ganglia and internal capsule.

Posturing and Herniation Syndromes

Increased intracranial pressure and herniation syndromes may produce characteristic posturing patterns:

• Decerebrate posturing (arm extension, internal rotation) indicates damage at or below the midbrain

• Decorticate posturing (arm flexion, clenched fists) reflects severe injury above the midbrain, within the cerebral hemispheres

The classic triad of transtentorial herniation includes:

1. Ipsilateral fixed and dilated pupil

2. Decerebrate posturing

3. Coma