Edema, Swelling, and Liquefaction of Brain Tissue
These conditions represent three stages of a single pathological process rooted in water retention. Macroscopically, the brain increases in volume, its cross-section appears moist and shiny, gyri are flattened, and ventricles are compressed.
There are two key types of edema based on their developmental mechanism:
- Vasogenic: arises from pathological increases in microvascular permeability.
- Cytotoxic: caused by intracellular metabolic disturbances.
Microscopically, white matter suffers more severely than gray matter. As it progresses to the liquefactive stage, neural tissue acquires a porous structure, myelin fibers disintegrate, and serous fluid accumulates in perivascular spaces.
Hydrocephalus
Excessive accumulation of cerebrospinal fluid (CSF) within the cranial cavity can be congenital (e.g., associated with Chiari malformation) or acquired.
Depending on distribution, the process is classified into:
- Generalized hydrocephalus: CSF accumulates throughout the entire ventricular system.
- Obstructive (non-communicating): a physical barrier blocks CSF outflow. If the block is at the interventricular foramen (foramen of Monro), one lateral ventricle dilates; at the cerebral aqueduct (aqueduct of Sylvius), both lateral and third ventricles dilate; at the foramina of Luschka and Magendie, the entire ventricular system is affected.
- Communicating (non-obstructive): no obstruction exists between the ventricular system and the subarachnoid space.
Pathomorphology: ependymal lining flattens and desquamates, white matter is reduced to a narrow band, and the cortex of the frontal, parietal, and temporal lobes may be destroyed down to a thin membrane.
Traumatic Brain Injury (TBI)
Brain injuries from mechanical force are divided into primary (occurring at impact) and secondary (hematomas, edema). A massive release of excitotoxic amino acids (glutamate) plays a crucial role in cellular dysfunction, causing ATP depletion and organelle destruction.
Main forms of closed TBI:
- Concussion: functional brainstem disorder without permanent structural defects, accompanied by amnesia.
- Contusion (Contusio cerebri): localized hemorrhagic softening on protruding areas of the cortex. A contrecoup lesion often forms on the side opposite the site of physical impact. Resolves with the formation of cysts or glial scars.
- Diffuse axonal injury (DAI): tearing of nerve fibers due to rotational and acceleration forces. Characteristic retraction balls (axonal spheroids) form, triggering retrograde neuronal degeneration.
Intracranial Hematomas
Hemorrhages are the most frequent complication of head trauma and are classified by anatomical location:
- Epidural hematoma: blood accumulates between the skull and the dura mater (most frequently in the temporal region). Develops upon impact by a small-surface object against a stationary head. Source: rupture of meningeal arteries.
- Subdural hematoma: located beneath the dura mater. Associated with bridging vein tears. Frequently occurs on the contralateral side when a moving head strikes an object. In chronic cases, it becomes surrounded by a fibrous capsule.
- Intracerebral hematoma: forms within the parenchyma of the frontal or temporal lobes. Mechanisms of bleeding include rhexis (direct vascular rupture), diapedesis (oozing through the vessel wall), or arrosion (necrotic dissolution of the vessel wall).
Complications of Brain Injuries
In addition to tissue compression and hematomas, trauma carries a high risk of secondary systemic and local pathologies. Extracranial mechanisms of secondary injury include systemic hypoxia, arterial hypotension, and anemia.
- Post-traumatic epilepsy: develops in about 10% of survivors of severe TBI (especially with depressed skull fractures).
- Infections: open skull base fractures carry a high risk of direct contamination from paranasal sinuses or the middle ear cavity, leading to purulent meningitis and intracranial abscesses.