Secondary Effects and Sequelae of CNS Trauma

Main Text

Preamble

Traumatic brain injury is not a single “one and done” event. A veritable “cascade” of adverse pathophysiologic events continues to develop after the initial injury. Some—such as progressive hemorrhagic injury—occur within the first 24 hours after trauma. Others (e.g., brain swelling and herniation syndromes) may take a day or two to develop.

Secondary effects of CNS trauma are defined as those that occur after the initial injury. These secondary effects are often more devastating than the initial injury itself and can become life threatening. Whereas many of the primary effects of CNS trauma (e.g., cortical contusions and axonal injuries) are permanent injuries, some secondary effects are either preventable or treatable.

Many potentially serious secondary effects are at least partially reversible if recognized early and treated promptly. Emergent imaging assessment, together with aggressive management of elevated intracranial pressure (ICP), perfusion alterations, and oxygenation deficits, may help mitigate both the immediate and long-term effects of brain trauma.

Chapter 2 focused on the primary effects of traumatic brain injury (TBI). In this chapter, we consider a broad spectrum of secondary effects that follow brain trauma, beginning with herniation syndromes.

Herniation Syndromes

Preamble

Brain herniations occur when one or more structures is displaced from its normal or “native” compartment into an adjacent space. They are the most common secondary manifestation of any expanding intracranial mass, regardless of etiology.

Relevant Anatomy

Bony ridges and dural folds divide the intracranial cavity into three compartments: Two supratentorial hemicrania (the right and left halves) and the posterior fossa (3-1).

The falx cerebri is a broad, sickle-shaped dural fold that attaches superiorly to the inside of the skull on either side of the midline, where it contains the superior sagittal sinus (SSS).

The concave inferior “free” margin of the falx contains the inferior sagittal sinus. As it courses posteriorly, the inferior margin of the falx forms a large open space above the corpus callosum and cingulate gyrus. This open space allows potential displacement of brain and blood vessels from one side toward the other [subfalcine herniation (SFH)].

The tentorium cerebelli extends inferolaterally from its confluence with the falx, where their two merging dural folds contain the straight sinus. The straight sinus courses posteroinferiorly toward the sinus confluence with the SSS and transverse sinuses (3-2).

The tentorium has two concave medial edges that contain a large U-shaped opening called the tentorial incisura. “Transtentorial” displacement of brain structures and accompanying blood vessels from the supratentorial compartment or posterior fossa can occur in either direction—up or down—through the tentorial incisura.

Relevant Physiology

Once the sutures fuse and the fontanelles close, brain, CSF, and blood all coexist in a rigid, unyielding “bone box.” The cerebral blood volume (CBV), perfusion, and CSF volume exist in a delicate balance within this closed box. Under normal conditions, pressures within the brain parenchyma and intracranial CSF spaces are equal.

When extra volume (blood, edema, tumor, etc.) is added to a cranial compartment, CSF in the sulci and subarachnoid cisterns is initially squeezed out. The ipsilateral ventricle becomes compressed and decreases in size. As intracranial volume continues to increase, the mass effect eventually exceeds the brain’s compensatory capacity, and ICP begins to rise.

If a mass becomes sufficiently large, brain, CSF spaces, and blood vessels are displaced from one intracranial compartment into an adjacent one, resulting in one or more cerebral herniations.

In turn, cerebral herniations may cause their own cascade of secondary effects. Parenchyma, cranial nerves, &/or blood vessels can become compressed against the adjacent unyielding bone and dura. Secondary ischemic changes, frank brain infarcts, cranial neuropathies, and focal neurologic deficits may develop.

Subfalcine Herniation

Terminology and Etiology

SFH is the most common brain herniation and the easiest to understand. Here, an enlarging supratentorial mass in one hemicranium causes the brain to begin shifting toward the opposite side. Herniation occurs as the affected hemisphere pushes across the midline under the inferior “free” margin of the falx, extending into the contralateral hemicranium (3-3). The cingulate gyrus and accompanying anterior cerebral artery (ACA) herniate under the falx anteriorly, but posterosuperiorly, the falx is wider and more rigid, anatomically limiting their displacement (3-5).

Imaging

Mass effect displaces the brain from one side toward the other (“midline shift”). The ipsilateral ventricle appears compressed and displaced across the midline, while the contralateral ventricle enlarges (3-4). The cingulate gyrus and accompanying ACAs also herniate under the falx (3-6).

Complications

Early complications of SFH include unilateral hydrocephalus, seen on axial NECT as enlargement of the contralateral ventricle. As the mass effect increases, the lateral ventricles become progressively more displaced across the midline. This displacement initially just deforms, then kinks, and eventually occludes the foramen of Monro.

As herniation progresses, the choroid plexus in the contralateral ventricle continues to secrete CSF. Because the foramen of Monro is obstructed, CSF has no egress, and the contralateral ventricle enlarges while the ipsilateral ventricle is compressed by the mass effect.

If SFH becomes severe, the herniating ACA can become pinned against the inferior “free” margin of the falx cerebri and then occluded, causing secondary infarction of the cingulate gyrus.

Descending Transtentorial Herniation

Transtentorial herniations are brain displacements that occur through the tentorial incisura. Although these displacements can occur in both directions (from top down or bottom up), descending herniations from supratentorial masses are far more common than ascending herniations.

Terminology and Etiology

Descending transtentorial herniation (DTH) is the second most common type of intracranial herniation syndrome. DTH is caused by a hemispheric mass that initially produces side-to-side brain displacement (i.e., SFH). As the mass effect increases, the uncus of the temporal lobe is pushed medially and begins to encroach on the suprasellar cistern. With progressively increasing mass effect, both the uncus and hippocampus herniate inferiorly through the tentorial incisura.

DTH can be unilateral or bilateral. Unilateral DTH occurs when a hemispheric mass effect pushes the uncus and hippocampus of the ipsilateral temporal lobe over the edge of the tentorial incisura (3-7). In bilateral DTH, both temporal lobes are displaced medially (3-9).

“Complete” or “central” descending herniation occurs when the supratentorial mass effect becomes so severe that the hypothalamus and optic chiasm are flattened against the skull base, both temporal lobes are herniated, and the whole tentorial incisura is completely plugged with displaced tissue (3-11) (3-12).

Imaging

Axial CT scans in early unilateral DTH show that the uncus is displaced medially and the ipsilateral aspect of the suprasellar cistern is effaced (3-8). As DTH increases, the hippocampus also herniates medially over the edge of the tentorium, compressing the quadrigeminal cistern and pushing the midbrain toward the opposite side of the incisura. In severe cases, the temporal horn can even be displaced almost into the midline.

With bilateral DTH, both temporal lobes herniate medially into the tentorial hiatus (3-10). With central descending herniation, both hemispheres are so swollen that the whole central brain is flattened against the skull base (3-13). All the basal cisterns are obliterated as the hypothalamus and optic chiasm are crushed against the sella turcica, and the suprasellar and quadrigeminal cisterns are completely effaced (3-14).

In complete (central) bilateral DTH, the midbrain is compressed and squeezed medially from both sides. Sagittal images show that the midbrain is also pushed inferiorly through the tentorial incisura, displacing the pons downward. The angle between the midbrain and pons is progressively reduced from nearly 90° to almost 0°(3-14). In terminal central herniation, the pons eventually pushes the cerebellar tonsils inferiorly through the foramen magnum (3-15).

Complications

Even mild DTH can compress the third cranial (oculomotor) nerve as it exits from the interpeduncular fossa and courses anterolaterally toward the cavernous sinus. This may produce a pupil-involving third nerve palsy.

Other, more severe complications may occur with DTH. As the temporal lobe is displaced inferomedially, it pushes the posterior cerebral artery (PCA) below the tentorial incisura. The PCA can become kinked and eventually even occluded as it passes back up over the medial edge of the tentorium, causing a secondary PCA (occipital) infarct (3-28) (3-29).

Severe bilateral DTH may cause pressure necrosis of the uncus and hippocampus (3-11), causing a secondary hemorrhagic infarct in the midbrain or pons (Duret hemorrhage) (3-7).

With complete central DTH, perforating arteries that arise from the circle of Willis are compressed against the central skull base and also occlude, causing multiple hypothalamic and basal ganglia infarcts.

In a vicious cycle, the hemispheres become more edematous, and ICP soars. If the rising pressure exceeds intraarterial pressure, perfusion is drastically reduced and eventually ceases, causing brain death (BD).

Ascending Transtentorial Herniation

Two types of herniations occur with posterior fossa masses: Ascending transtentorial herniation (ATH) and tonsillar herniation.

Terminology and Etiology

In ATH, the cerebellar vermis and hemispheres are pushed upward (“ascend”) through the tentorial incisura into the supratentorial compartment. The superiorly herniating cerebellum first flattens and displaces, then effaces the quadrigeminal cistern and compresses the midbrain (3-16).

Imaging

Axial NECT scans show that CSF in the superior vermian cistern and cerebellar sulci is effaced. The quadrigeminal cistern is first compressed and then obliterated by the upwardly herniating cerebellum. As the herniation progresses, the tectal plate becomes compressed and flattened (3-17). In severe cases, the dorsal midbrain may actually appear concave instead of convex. The most common complication of ATH is acute intraventricular obstructive hydrocephalus caused by compression of the cerebral aqueduct (3-17).

Tonsillar Herniation

Terminology and Etiology

In tonsillar herniation, the cerebellar tonsils are displaced inferiorly and become impacted into the foramen magnum (3-18). Tonsillar herniation can be congenital (e.g., Chiari 1 malformation) or acquired.

Acquired tonsillar herniation occurs in two different circumstances. The most common cause is an expanding posterior fossa mass pushing the tonsils downward into the foramen magnum.

Inferior tonsillar displacement also occurs with intracranial hypotension. Here, the tonsils are pulled downward by abnormally low intraspinal CSF pressure (see Chapter 38).

Imaging

Diagnosing tonsillar herniation on NECT scans may be problematic. The foramen magnum usually contains CSF that surrounds the medulla and cerebellar tonsils. Herniation of one or both tonsils into the foramen magnum obliterates most or all of the CSF in the cisterna magna (3-19).

Tonsillar herniation is much more easily diagnosed on MR. In the sagittal plane, the normally horizontal tonsillar folia become vertically oriented, and the inferior aspect of the tonsils becomes pointed. Tonsils > 5 mm below the foramen magnum are generally abnormal, especially if they are peg-like or pointed (rather than rounded) (3-15).

In the axial plane, T2 scans show that the tonsils are impacted into the foramen magnum, obliterating CSF in the cisterna magna and displacing the medulla anteriorly (3-19).

Complications

Complications of tonsillar herniation include obstructive hydrocephalus and tonsillar necrosis.

Other Herniations

The vast majority of cerebral herniations are subfalcine, descending/ascending transtentorial, and tonsillar herniations. Other, less common herniation syndromes are transalar and transdural/transcranial herniations.

Transalar Herniation

Transalar herniation occurs when the brain herniates across the greater sphenoid wing (GSW) or “ala” and can be either ascending (the most common) or descending.

Ascending transalar herniation is caused by a large middle cranial fossa mass(3-20). The middle cerebral artery (MCA) branches and sylvian fissure are elevated, and the superior temporal gyrus is pushed above the GSW (3-21).

Descending transalar herniation is caused by a large anterior cranial fossa mass. Here, the gyrus rectus is forced posteroinferiorly over the GSW, displacing the sylvian fissure and shifting the MCA backward.

Transdural/Transcranial Herniation

This rare type of cerebral herniation, sometimes called a “brain fungus” by neurosurgeons, can be life threatening. For transdural/transcranial herniation to occur, the dura must be lacerated, a skull defect (fracture or craniotomy) must be present (3-22), and ICP must be elevated (3-23).

Traumatic transdural/transcranial herniations typically occur in infants or young children with a comminuted skull fracture that deforms inward with impact, lacerating the dura-arachnoid. When ICP increases, the brain can herniate through the torn dura and across the skull fracture into the subgaleal space (3-24).

Edema, Ischemia, and Vascular Injury

Preamble

TBI can unleash a cascade of physiologic responses that may adversely affect the brain more than the initial trauma. These responses include diffuse brain swelling, excitotoxic responses elicited by glutamatergic pathway activation, perfusion alterations, and a variety of ischemic events, including territorial infarcts.

Posttraumatic Brain Swelling

Cerebral edema is a major contributor to TBI morbidity. Massive brain swelling with severe intracranial hypertension is among the most serious of all secondary traumatic lesions. Mortality approaches 50%, so early recognition and aggressive treatment of this complication are imperative.

Etiology and Epidemiology

Focal, regional, or diffuse brain swelling develops in 10-20% of patients with TBI. Whether this is caused by increased tissue fluid (cerebral edema) or elevated blood volume (cerebral hyperemia) secondary to vascular dysautoregulation is unclear. In some cases, the trigeminal system may mediate brain swelling associated with subdural bleeding, providing the link between small-volume, thin subdural bleeds and swelling of the underlying brain.

Clinical Issues

Children, young adults, and individuals with repetitive concussive or subconcussive injuries are especially prone to developing posttraumatic brain swelling and are almost twice as likely as older adults to develop this complication. Although gross enlargement of one or both hemispheres occasionally develops rapidly after the initial event, delayed onset is more typical. Severe cerebral edema generally takes between 24-48 hours to develop.

In some cases, aggressive measures for control of ICP fail to restore cerebral metabolism and improve neurologic outcome. Decompressive craniectomy as a last resort is often performed, but evidence for reduced risk of death or dependence in severe TBI is lacking.

Imaging

The appearance of posttraumatic brain swelling evolves over time. Initially, mild hemispheric mass effect with sulcal/cisternal compression is seen on NECT scans (3-25).

During the early stages of brain swelling, gray matter-white matter differentiation is relatively preserved. Although the ipsilateral ventricle may be slightly compressed, subfalcine displacement is generally minimal. However, if the mass effect is disproportionately greater than the maximum width of an extraaxial collection, such as a subdural hematoma (SDH), early and potentially catastrophic swelling of the underlying brain parenchyma should be suspected and treated emergently (3-26).

MR shows swollen gyri that are hypointense on T1WI and hyperintense on T2WI. Diffusion-weighted scans show restricted diffusion with low apparent diffusion coefficient (ADC) values.

As brain swelling progresses, the demarcation between the cortex and underlying white matter becomes indistinct and eventually disappears (3-31). The lateral ventricles appear smaller than normal, and the superficial sulci are no longer visible (3-32).

POSTTRAUMATIC BRAIN SWELLING

Epidemiology

• 10-20% of TBI

• Can be focal, regional, or diffuse

• Most common in children, young adults

• Potentially catastrophic

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