Brain herniation
From Wikipedia, the free encyclopedia
| ICD-10 | G93.5 |
|---|---|
| ICD-9 | 348.4 |
| MedlinePlus | 001421 |
| eMedicine | radio/98 |
Herniation, a deadly side effect of very high intracranial pressure, occurs when the brain shifts across structures within the skull. The brain can shift by such structures as the falx cerebri, the tentorium cerebelli, and even through the hole called the foramen magnum in the base of the skull (through which the spinal cord connects with the brain). Herniation can be caused by a number of factors that increase intracranial pressure such as traumatic brain injury. Because herniation puts extreme pressure on parts of the brain, it is often fatal. Therefore, extreme measures are taken in hospital settings to prevent the condition by reducing intracranial pressure.
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[edit] Classification
There are a number of different types of herniation, classified by which structures the brain shifts across: transtentorial, upward, tonsilar, central, cingulate, and transcalvarial herniation.[1]
[edit] Central herniation
In central herniation, (also called "transtentorial herniation") the diencephalon and parts of the temporal lobes of both of the cerebral hemispheres are squeezed through a notch in the tentorium.[1][2]
[edit] Uncal herniation
In uncal herniation, a common subtype of transtentorial herniation, the innermost part of the temporal lobe, the uncus, can be squeezed so much that it goes by the tentorium and puts pressure on the brainstem.[1] The tentorium is a structure within the skull formed by the meningeal layer the dura mater. Tissue may be stripped from the cerebral cortex in a process called decortication (McCaffrey, 2001). The uncus can squeeze the third cranial nerve, which controls parasympathetic input to the eye on the side of the affected nerve. This interrupts the parasympathetic neural transmission, causing the pupil of the affected eye to dilate and fail to constrict in response to light as it should, so a dilated unresponsive pupil is an important sign of increased intracranial pressure.[2] Cranial arteries may be compressed during the herniation.[3] This type of herniation can also damage the brain stem, causing lethargy, slow heart rate, respiratory abnormalities, and pupil dilation (McCaffrey, 2001). Uncal herniation may advance to central herniation.
[edit] Cerebellar herniation
Increased pressure in the posterior fossa can cause the cerebellum to move up through the tentorial opening in upward, or cerebellar herniation.[1] The midbrain is pushed through the tentorial notch. This also pushes the midbrain down.[3]
[edit] Tonsillar herniation
In tonsilar herniation the brainstem moves downward through the foramen magnum.[1] The resulting pressure on the brainstem causes respiratory and cardiac arrest.[3] Downward herniation can stretch branches of the basilar artery, causing them to tear and bleed, known as a Duret hemorrhage. The result is usually fatal.[2]
[edit] Cingulate herniation
In cingulate or subfalcine herniation, the most common type, the innermost part of the frontal lobe is scraped under part of the falx cerebri.[4][1] This does not put as much pressure on the brainstem as the other types of herniation, but it may interfere with blood vessels in the frontal lobes that are close to the site of injury, or it may progress to central herniation.[1][3] Usually occurring in addition to uncal herniation, cingulate herniation presents with abnormal posturing and coma.[3]
[edit] Transcalvarial herniation
In transcalvarial herniation, the brain squeezes through a fracture or a surgical site in the skull.[3]
[edit] Results of herniation
The patient may become paralyzed on the same side as the lesion causing the pressure, or damage to parts of the brain caused by herniation may cause paralysis on the side opposite the lesion.[2] Damage to the midbrain, which contains the reticular activating network that regulates consciousness will result in coma.[2] Damage to the cardio-respiratory centers in the medulla will cause respiratory and cardiac arrest.[2]
[edit] References
- ^ a b c d e f g Shepherd S. 2004. "Head trauma." Emedicine.com. Retrieved on January 28, 2007.
- ^ a b c d e f Cornell. 1998. Introduction to neuropathology. Reaction to injury: Brain histology." Cornell University Medical College.
- ^ a b c d e f Orlando Regional Healthcare, Education and Development. 2004. Overview of adult traumatic brain injuries. Retrieved on January 28, 2007.
- ^ Dawodu ST. 2007. Traumatic brain injury: Definition, epidemiology, pathophysiology. Emedicine.com. Retrieved on January 28, 2007.
