CHAPTER FOUR
TRAUMATIC BRAIN INJURY AND INCREASED INTRACRANIAL PRESSURE

CEREBRAL CONTUSIONS, DIFFUSE AXONAL INJURY, AND THE SHAKEN BABY SYNDROME

CEREBRAL CONTUSIONS

Contre coup contusions

A contusion is hemorrhagic necrosis of brain tissue. When the head is abruptly brought to a stop against a solid object, such as the dashboard or the ground, the brain continues to move for an instant, hitting the inside the now stationary skull. The soft brain is easily contused and lacerated by the hard bony ridges at the base of the skull or by the tentorium cerebelli and falx cerebri. Contusions usually involve the surface of the brain, especially the crowns of gyri, and are more frequent in the orbital surfaces of the frontal lobes and the tips of the temporal lobes. Acute contusions show hemorrhagic necrosis and brain swelling. Gradually, macrophages remove necrotic brain tissue and blood. Eventually, the contusion evolves into a yellowish plaque characterized by loss and atrophy of brain tissue, glial scarring, hemosiderin deposition, and loss of axons in the underlying white matter. A cerebral contusion can be distinguished from a cerebral infarct because, in the infarct, the superficial cortex is usually preserved, whereas in the contusion, it is the first to be destroyed. Contusions may correspond to the site of impact ("coup" contusions) -from the French word "blow"- or develop opposite the impact ("contre coup" contusions). In falls, contre coup are more frequent than coup contusions. A fall to the back with the occiput hitting the ground causes contusions in the inferior frontal and temporal lobes.

DIFFUSE AXONAL INJURY

Diffuse axonal injury (DAI) is a special traumatic lesion, which occurs most frequently in motor vehicle accidents and following blows to the unsupported head. In the course of such injuries, the cerebrum goes into a back and forth gliding motion, pivoting around the upper brainstem. The brainstem, together with the cerebellum, is held firmly fixed by the tentorium, and the falx prevents side-to-side motion. Axons are stretched but do not snap from this injury; their sudden deformation causes changes in the axonal cytoskeleton (compaction of neurofilaments, loss of microtubules) that lead to an arrest of the fast axoplasmic flow. Components of this flow, including mitochondria and other organelles, accumulate proximal to the lesion and cause axonal swellings. Some axons with mild lesions probably recover but many eventually rupture. It takes several hours from trauma to axonal rupture. The cascade of reactions that lead to the formation of axonal swellings is probably initiated by influx of calcium through the stretched axolemma. The swellings are located at nodes of Ranvier where the axolemma is more liable to deform because there is no myelin. Brain damage is most severe along midline structures (corpus callosum, brainstem) where the shear forces are greatest, and at the cortex-white matter junction because of the change in the consistency of brain tissue.

Clinically, patients with severe DAI become unconscious immediately after the injury and either remain comatose or go into a persistent vegetative state. Cerebral concussion is thought to be a mild form of DAI without permanent pathology. The loss of consciousness in concussion is probably due to a functional disturbance of the reticular activating substance of the upper brainstem. This is the part of the CNS that is subjected to the highest twisting force during sagittal rotation of the hemispheres. In severe TBI, DAI is compounded by widespread vascular injury and other traumatic lesions which cause cerebral edema and HIE.

DAI-corpus callosum hemorrhages	DAI-brainstem hemorrhages

DAI is rarely a pure lesion, and, clinically, its effects are difficult to separate from other concurrent  TBI pathology. When severe, it can depress consciousness in the acute phase and can cause lasting impairment of memory and cognition. The MRI shows small hypointense lesions corresponding to traumatic microbleeds. While being the only marker of DAI, the microbleeds may not correlate with the degree of axonal damage. In acute DAI, the brain is either normal or shows petechial hemorrhages in the corpus callosum, centrum semiovale, dorsolateral brainstem, and other areas, due to tearing of blood vessels. These vascular lesions should be distinguished from secondary brainstem hemorrhages that occur with herniations (see further on).

DAI-axonal swellings. BAPP immunostain.	DAI. Severe white matter degeneration.

Microscopically, the damaged white matter shows axonal swellings. These can occur anywhere but are particularly common in the parasagittal parts of the brain, the corpus callosum, fornix, internal capsule, and the brain stem. Axonal swellings can be detected with H&E and silver stains 15 hours after the injury. Immunostains with antibodies to Beta Amyloid Precursor Protein (BAPP) can detect the axonal lesions in 2-3 hours after the injury. BAPP is produced by neurons as a reaction to injury. It flows down the axon and accumulates at points of axonal constriction or transection. Axonal swellings may persist for years. Distal to the swellings, axons and myelin degenerate and gliosis develops over time. Severe DAI may cause decrease of white matter volume, atrophy of the corpus callosum, and dilatation of the lateral ventricles.

THE SHAKEN BABY SYNDROME

Shaken baby syndrome. Retinal and optic nerve hemorrhages.	Shaken baby syndrome. Retinal and optic nerve hemorrhages.

The shaken baby syndrome describes a pattern of child abuse which is the second most common cause of death in children under one year of age, after the sudden infant death syndrome. It often causes a combination of subdural hematoma, subarachnoid hemorrhage, contusions, DAI, and retinal hemorrhage. Infants with these injuries are usually brought to the Emergency Department with a nonspecific clinical picture of hypotonia, listlesness, vomiting, irritability, and lethargy. The diagnosis may be missed unless a skeletal survey and fundoscopic examination are done. In the past, these lesions were attributed to shaking. Shaking sets the head into a dangling motion and can cause whiplash spinal cord injury. Movement of the brain inside the skull causes subdural and subarachnoid hemorrhage, contusions, white matter hemorrhages (gliding hemorrhages) , tears of the corpus callosum, and DAI. In actuality, many child abuse injuries are a combination of shaking and blunt impact, and the latter is also important in their pathogenesis. Thus, the term "shaking-impact syndrome" is closer to reality. Retinal hemorrhages and hemorrhages within the optic nerve sheathes are an important component of the shaken baby syndrome and correlate with the severity of brain damage.They are probably caused by shaking of the globe and tearing of delicate retinal vessels. Retinal hemorrhages are extremely uncommon in accidental brain injury. Documentation of retinal hemorrhage by fundoscopic examination is important in the clinical evaluation of such cases.

INTRACEREBRAL HEMATOMA

Severe head trauma can also cause deep intracerebral hematomas and brain necrosis. Traumatic intracerebral hematomas are often multiple. They are found more commonly in the frontal and temporal white matter. They are probably due to rupture of intrinsic vessels as result of angular rotation of the brain.

POSTTRAUMATIC CEREBRAL ISCHEMIA

A large proportion of patients with severe or fatal TBI also have cerebral infarcts. Most of these infarcts are in vascular territories and a few affect watershed zones. The underlying causes are intracranial hypertension, vascular compression from herniations, vasospasm, traumatic vascular tears, dissecting hematomas and other vascular lesions. Global HIE is also a frequent finding in severe TBI. It is caused by a combination of systemic hypotension and intracranial hypertension, leading to cerebral hypoperfusion. Cardiovascular collapse and other systemic changes may result from the effects of DAI on the medulla. Infarcts and HIE greatly increase morbidity and mortality in TBI.

Further reading

Marino R,Gasparotti R, Manzoni D, et al. Posttraumatic cerebral infarction in patients with moderate or severe head trauma. Neurology 2006;67:1165-71. PubMed

Updated: November, 2006.