Causes and mechanisms of development
The development of herniation syndrome is most often associated with severe traumatic brain injury (TBI). As a result of trauma, mass lesions creating a pronounced mass effect can form. One of the most frequent triggers is acute subdural hematoma located along the convexity of the hemisphere.
In the early postoperative period following surgical removal of the hematoma, displacement may persist due to residual blood accumulation and concomitant pneumocephalus. The pressure from these structures leads to a severe shift of hemispheric tissue in the opposite direction. Additionally, displacement can occur against the background of severe polytrauma accompanied by intrathoracic or intra-abdominal hemorrhage.
Types of herniation according to neuroimaging
According to computed tomography (CT) and magnetic resonance imaging (MRI), several key patterns of brain structure displacement are distinguished:
- Subfalcine herniation (under the falx cerebri). Manifests as unilateral displacement of the cingulate gyrus (gyrus cinguli) and parts of the superior frontal gyrus under the lower edge of the falx cerebri.
- Transtentorial herniation (uncal/tentorial). Characterized by the displacement of the medial temporal lobe, specifically the uncus (uncus), into the tentorial notch (incisura tentorii). This leads to deformation of the midbrain and effacement of the suprasellar cistern.
- Cerebellar tonsillar herniation. Descent of the cerebellar tonsils into the foramen magnum occurs, which causes direct compression of the medulla oblongata.
Diffuse cerebral edema
A special condition in severe polytrauma and shock is diffuse brain swelling (diffuse brain swelling). Its most important feature is that the displacement of midline structures may be completely absent.
On native CT scans, edema manifests with the following signs:
- Total loss of visualization and effacement of the cortical sulci.
- Compression (disproportionate narrowing) of the ventricular system.
- Diffuse decrease in X-ray density (attenuation) of the cortex, basal ganglia, and thalami. The structures remain distinguishable, but their reduced density indicates hypoxic-ischemic injury resulting from systemic hypotension.
Complications and secondary injuries
Tissue displacement inevitably entails compression of the major arteries supplying the brain. As a consequence, acute cerebral infarctions develop. Most frequently, follow-up CT scans (usually after 48 hours) reveal ischemic zones in:
- The anterior cerebral artery (ACA) territory;
- The posterior cerebral artery (PCA) territory.
In addition, transtentorial herniation directly deforms the brainstem, disrupting the body's vital functions.
Prognostic assessment based on MRI
MRI is used for precise assessment of injury severity and prognosis. In an unfavorable course of trauma, the following patterns are revealed:
- On T2-weighted images (T2 WI), a diffusely altered MR signal from the cortex throughout the edematous tissue is visible.
- On diffusion-weighted images (DWI) and ADC maps (ADC map), total restriction of diffusion is registered throughout the cerebrum. Notably, the cerebellar tissue may remain intact.
- MR angiography (MR angiography) shows an almost complete absence of intracranial arterial blood flow.
A combination of such neuroimaging findings indicates an extremely unfavorable prognosis, which typically ends in death within the next 24 hours.
Briefly: answers to topical questions
What types of brain herniation are distinguished based on neuroimaging?
Based on neuroimaging, the following types of brain herniations are distinguished:
- Subfalcine herniation — displacement of the cingulate gyrus (gyrus cinguli) and part of the superior frontal gyrus under the falx cerebri.
- Transtentorial herniation (superior, tentorial) — displacement of the mediiobasal part of the temporal lobe and dislocation of the uncus (uncus) relative to the tentorial notch (incisura tentorii).
- Tonsillar herniation (inferior, cerebellar tonsillar herniation) — downward displacement of the cerebellar tonsils through the foramen magnum into the spinal canal.
Which parts of the brainstem undergo compression in various types of herniation?
In various types of herniation, different parts of the brainstem undergo compression.
- In transtentorial herniation (superior), deformation and compression of the upper parts of the brainstem, specifically the midbrain, occur.
- In tonsillar herniation (inferior), direct compression of the caudal part of the brainstem occurs, which is accompanied by severe impairment of its functions.
Specifically, which cranial nerves and vessels are compressed in the tentorial notch during transtentorial herniation?
In transtentorial herniation, sources directly indicate compression of the oculomotor nerve, which can lead to pupil dilation and paresis of extraocular muscles. Vessel compression during herniation can lead to infarctions in the posterior and anterior cerebral artery territories; the development of infarctions in the left PCA and left ACA territories is indicated on dynamic CT scans.
Which basal cisterns are deformed or effaced during transtentorial herniation?
In transtentorial herniation, according to neuroimaging data, deformation and effacement of the suprasellar cistern occur. In general, with an increase in intracranial volume and the development of herniation syndrome at the compensation stage, radiological observation shows narrowing of the basal cisterns, as well as compression of the ventricles and effacement of cortical sulci.
What pathological processes and mass lesions can act as causes of herniation syndrome?
The causes of herniation syndrome are various pathological processes and mass lesions:
- Hematomas — acute subdural, subcortical, putaminal, and cerebellar hematomas.
- Tumors — mass lesions in the cerebral hemisphere or in the posterior cranial fossa.
- Cerebral edema (including swelling-edema) — develops in traumatic brain injury, meningitis, meningoencephalitis, cerebral ischemia, hypoxia, as well as in hepatic coma and sunstroke.
- Hemorrhages — for example, hemorrhage into the cerebellum.
To memorize the sequence of assessing herniations on CT, move from top to bottom: first, look for the displacement of gyri under the falx cerebri (subfalcine), then evaluate the tentorial notch and uncus (transtentorial), and finally check the cerebellar tonsils.
Class and exam questions
Is midline shift always present in severe cerebral edema?
No. In diffuse brain edema (e.g., against the background of hypotension and shock), the ventricles and sulci are compressed from both sides, so midline shift may be absent.
Why do cerebral infarctions occur in transtentorial herniation?
The displacing structures of the temporal lobe compress the major vessels, leading to secondary ischemia and the formation of acute infarctions, most commonly in the anterior and posterior cerebral artery territories.
Which MRI findings indicate critical impairment of cerebral blood supply?
A critical condition is indicated by total diffusion restriction on DWI/ADC maps in the cerebral tissue and the absence of intracranial arterial blood flow visualization on MR angiography.
What else to study on this topic
- Anatomical grading of diffuse axonal injury (DAI) and lesions in the substantia nigra.
- Differences between spiral CT angiography and traditional angiography in penetrating injuries.
- Mechanisms of brain edema development in blunt cerebrovascular injury.
- Radiological classification of temporal bone fractures.
- Clinical significance and prognosis in mild traumatic brain injury.
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