Other Types of TBI


A cerebral or intracranial (inside the skull) hemorrhage occurs when blood leaks from a damaged vessel into brain tissue. The size of a hemorrhage can range from tiny to large and symptoms depend on the size and location of the damage. Bleeding usually develops within minutes of a TBI but it can develop hours to days after the initial injury.


Infarction is the medical term for stroke. Infarctions associated with TBI occur when an artery to the brain is compressed by the swelling of surrounding tissues, preventing the flow of blood-borne oxygen and nutrients to brain cells. Most TBI-induced strokes involve the posterior cerebral artery and affect the occipital and temporal lobes causing loss of peripheral vision and speech or language problems.


A subdural hematoma (SDH) is slow bleeding outside the brain, usually over the surface of the frontal or parietal lobe. Typically, it is caused by damage to a vessel carrying venous blood (i.e., blood that has passed through capillaries and distributed oxygen to the tissues). An acute hematoma may develop slowly, taking minutes to days to manifest. If large enough, it can exert a dangerous amount of pressure on the brain, necessitating surgery to drain the accumulated blood and relieve pressure.

An epidural hematoma (EDH) occurs outside the brain and is usually caused by a damaged artery. Arteries carry blood under high pressure; therefore, a large EDH can cause pressure to build up within minutes, even seconds. This condition requires immediate surgery to relieve pressure and prevent severe permanent damage or death.

Subarachnoid hemorrhage (SAH) refers to a small amount of bleeding that spreads thinly over the surface of the brain. This usually is an incidental finding detected on a CT scan and has little significance. SAH is more significant when caused by the bursting of an aneurysm (weakened blood vessel) in the brain, such as during a stroke.

Late Secondary Complications of TBI

Complications can develop in the brain weeks or even months after the initial injury. The most common late secondary complications are hydrocephalus and chronic subdural hematoma.

There are several pockets in the brain called ventricles. Cerebrospinal fluid (CSF) produced in these ventricles surrounds and coats the surface of the brain and spinal cord. CSF is constantly produced and reabsorbed into the bloodstream. TBI can disrupt this process. If too much fluid builds up in the ventricles and enlarges them, a condition called hydrocephalus results, creating pressure on brain tissues and preventing nerve cells from functioning properly.

A chronic subdural hematoma (SDH), or hygroma, is a focal brain injury characterized by an accumulation of blood or spinal fluid on the surface of the brain that exerts pressure on brain tissues. Increased pressure inside the skull (intracranial pressure or ICP) can produce several complications, including weakness on the opposite side of the body, speech difficulties, and confusion. Although chronic SDH often resolves on its own, persistent symptoms may require surgery to relieve pressure.

Intracranial Pressure (ICP)

In the days and weeks after a traumatic brain injury, patients are monitored closely for any sign of increased intracranial pressure (ICP), a dangerous complication in which the brain's soft tissues become squeezed against the skull. This occurs when trauma to the head causes damaged blood vessels to leak or form clots (hematomas) or produces an imbalance in the amount of cerebrospinal fluid (CSF) in the ventricles.

Because the skull is rigid and the space between it and the brain is small, there is no room for expansion. Extra fluid or clots in the brain (intercerebral clots) or the space between it and the skull (subdural or extradural clots) produce increased pressure, which can damage the brain in two ways: (1) by squeezing it against the skull or (2) by compressing its blood vessels to the point where circulation is impeded. Either complication can be fatal.

Publication Review By: Stanley J. Swierzewski, III, M.D.

Published: 01 Sep 2001

Last Modified: 18 Nov 2011