Brain edema, swelling, and liquefaction
These conditions represent three stages of a single pathological process driven by water retention. Macroscopically, the brain increases in volume, its cut surface appears moist and shiny, the gyri flatten, and the ventricles are compressed.
Two key types of edema are distinguished by their development mechanism:
- Vasogenic: occurs due to pathological hyperpermeability of the microvasculature.
- Cytotoxic: caused by intracellular metabolic disorders.
At the microscopic level, white matter suffers more severely than gray matter. Upon transitioning to the liquefaction stage, the neural tissue acquires a porous structure, myelin fibers disintegrate, and serous fluid accumulates in perivascular spaces.
Hydrocephalus
Excessive accumulation of CSF in the cranial cavity can be congenital (e.g., in Chiari malformation) or acquired.
According to its distribution, the process is divided into:
- Generalized hydrocephalus: CSF accumulates everywhere.
- Obstructive: a physical barrier to outflow exists. If the blockage is at the level of the interventricular foramen (foramen of Monro), one lateral ventricle enlarges; at the cerebral aqueduct level, both lateral ventricles and the third ventricle; at the level of the foramina of Luschka and Magendie, the entire system is affected.
- Communicating (non-obstructive): there are no obstacles between the ventricles and the subarachnoid space.
Pathomorphology: ependymal epithelium flattens and desquamates, the white matter turns into a narrow band, and the cortex of the frontal, parietal, and temporal lobes may be destroyed down to a thin film.
Traumatic brain injury (TBI)
Brain injuries resulting from mechanical impact are divided into primary (at the moment of impact) and secondary (hematomas, edema). A massive release of excitotoxic amino acids (glutamate) plays a crucial role in the pathogenesis of cellular dysfunction, causing a decrease in ATP and organelle destruction.
Main forms of closed TBI:
- Concussion: functional brainstem disorder without permanent structural defects, accompanied by amnesia.
- Contusion (Contusio cerebri): local hemorrhagic softening on prominent cortical areas. A contrecoup lesion often forms on the side opposite to the zone of physical contact. Ends with the formation of cysts or glial scars.
- Diffuse axonal injury: fiber tearing due to rotational and acceleration forces. Specific axonal retraction balls form, triggering retrograde neuronal degeneration.
Intracranial hematomas
Hemorrhages are the most frequent complication of head injuries. They are classified by location:
- Epidural hematoma: blood accumulates between the skull and the dura mater (most commonly in the temporal region). Develops upon impact with a small-surface-area object on a stationary head. Source: rupture of meningeal arteries.
- Subdural hematoma: located beneath the dura mater. Associated with the rupture of pial veins. Upon impact of a moving head against an obstacle, it frequently occurs on the contralateral (opposite) side. In its chronic form, it becomes surrounded by a fibrous capsule.
- Intracerebral hematoma: forms in the parenchyma of the frontal or temporal lobes. The mechanism of blood extravasation may be rhexis (direct vessel rupture), diapedesis (oozing through the wall), or arrosion (necrotic melting of the vessel wall).
Complications of brain injuries
In addition to compression by tissues and hematomas, injuries are fraught with concomitant pathologies. Extracranial mechanisms of secondary injury include systemic hypoxia, arterial hypotension, and anemia.
About 10% of survivors of severe TBI (especially with depressed skull fractures) suffer from post-traumatic epilepsy. Open skull base fractures carry a high risk of direct infection from the paranasal sinuses or middle ear cavity, leading to purulent meningitis and intracranial abscesses.
Briefly: answers to topical questions
What types of cerebral edema are distinguished by their pathogenetic mechanism?
Based on the pathogenetic mechanism, two main types of cerebral edema are distinguished, driven by water-electrolyte metabolism disorders, increased osmotic pressure, and slowed blood flow:
- Vasogenic edema — develops with increased permeability of the microvascular wall and/or elevated filtration pressure.
- Cytotoxic edema — observed in metabolic disorders.
What types of intracranial hemorrhages are classified by anatomical location?
By the anatomical location of blood spread, intracranial hemorrhages are classified into the following types:
- Intracerebral hemorrhage — parenchymal hemorrhage (intracerebral hematoma).
- Intraventricular hemorrhage — accumulation of blood in the ventricular system.
- Subarachnoid hemorrhage — accumulation of blood beneath the arachnoid mater.
- Subdural hemorrhage — formation of a subdural hematoma.
- Epidural hemorrhage — formation of an epidural hematoma.
- Mixed forms — subarachnoid-parenchymal, parenchymal-ventricular, and others.
They are also divided into three broader groups: meningeal, intracerebral, and subarachnoid-parenchymal hemorrhages.
What types of brain herniation syndromes exist?
The following main types of brain herniation syndromes exist:
- Uncal herniation (transtentorial herniation) — displacement of the mediobasal part of the temporal lobe medially and downward beneath the tentorium cerebelli.
- Tonsillar herniation (tonsillar herniation) — downward displacement of the cerebellar tonsils through the foramen magnum into the spinal canal.
- Subfalcine herniation (Subfalcine herniation) — displacement of the cingulate gyrus beneath the lower edge of the falx cerebri to the contralateral side.
Which clinico-morphological stroke forms belong to cerebrovascular diseases?
The main clinico-morphological stroke forms include hemorrhagic and ischemic strokes.
- Hemorrhagic stroke — a polyetiological disease characterized by non-traumatic intracranial hemorrhage. Accounts for 15–20% of all cases.
- Ischemic stroke (cerebral infarction) — detected 4 times more frequently than hemorrhagic stroke and accounts for 80–85% of all disease cases.
It is impossible to reliably differentiate these forms based solely on clinical presentation; neuroimaging is required.
Which vessels form the cerebral arterial circle (Circle of Willis)?
The cerebral arterial circle (circulus arteriosus cerebri Willisii) is formed by the following vessels:
- Anterior communicating artery (a. communicans anterior);
- Anterior cerebral artery (a. cerebri anterior) — proximal (A1) segment;
- Internal carotid artery (a. carotis interna) — distal segment;
- Posterior communicating artery (a. communicans posterior);
- Posterior cerebral artery (a. cerebri posterior) — proximal (P1) segment;
- Basilar artery (a. basilaris) — bifurcation region.
This vascular ring provides a closed collateral blood supply to the brain.
To remember the connection between subdural hematoma and movement: «Epidural — Epicenter» (blow to a stationary head, blood is localized locally above the meninges), «Subdural — Shifting» (head in motion stops abruptly, the brain shifts, tearing veins beneath the meninges).
Class and exam questions
What is the microscopic difference between brain swelling and brain edema?
Macroscopically they are indistinguishable. However, microscopically during liquefaction (pronounced edema) the nervous tissue becomes porous, myelin fibers are completely destroyed, and serous fluid accumulates abundantly around cells and vessels.
What are Duret hemorrhages?
These are multiple secondary hemorrhages in the brainstem. They are localized perivascularly around the cerebral aqueduct and along the median raphe, arising as a consequence of severe compression and displacement of brain structures.
How do axonal spheroids form?
They occur in diffuse axonal injury when, due to sudden acceleration or head rotation, nerve fibers rupture. Axoplasm protrudes at the site of such a rupture, forming characteristic spheroids.
What else to study on this topic
- Pathogenesis of excitotoxicity and ultrastructural neuronal changes (chromatolisis)
- Morphological evolution and organization of chronic subdural hematoma
- Specifics of open and scalp traumatic brain injuries
- Formation of a vicious circle in elevated intracranial pressure
- Differences in congenital hydrocephalus in Chiari and Dandy–Walker syndromes
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