Closed Brain Injuries

Classification and mechanisms of injury

In clinical practice, closed brain injuries are generally divided into three main forms: concussion, contusion, and compression. In practice, these types of injuries are rarely seen in isolation and typically combine with one another, forming a complex polysystemic pathology.

Pathological changes in nervous tissue develop under the influence of several biomechanical and physiological mechanisms:

1. Direct impact. Tissues are damaged directly at the site of application of the traumatic mechanical force.
2. Shock wave and deformation. Mechanical energy propagates within the closed cranial cavity. A contrecoup effect occurs: the brain shifts and collides with the internal bony prominences of the skull on the side opposite to the initial point of force application.
3. Vascular and metabolic disorders. A pathological cascade is triggered: the initial vasospasm is replaced by hyperemia, which transitions into venous congestion. This leads to microcirculatory disorders and impaired normal cerebrospinal fluid circulation. Due to the developing tissue hypoxia, progressive cerebral edema forms.

Clinical picture and critical volumes

The symptom complex of a closed injury consists of two major groups of manifestations:

• General cerebral symptoms. These include various disorders of consciousness (ranging from mild depression to deep coma), severe headache, vomiting, and signs of increased intracranial pressure.
• Focal symptoms. Their character strictly depends on the topical localization of the lesion zone.

For a full clinical picture of compression to appear, the formation of a hematoma with a volume of 30–40 ml is sufficient. Intraventricular hematomas pose a particular danger. With this localization, the critical volume of blood is significantly smaller. The patient's condition deteriorates fulminantly: it is characterized by the very rapid development of cerebral coma, the appearance of pronounced meningeal signs, a sharp rise in body temperature (hyperthermia), and severe cardiovascular and respiratory disorders.

The "lucid interval" phenomenon

A classic manifestation of an intracranial hematoma (e.g., epidural) is the so-called lucid interval (lucid interval). This is a condition where the clinical picture of compression does not develop immediately at the moment of trauma, but hours or even days later. The process proceeds in three stages:

1. Primary loss of consciousness. Occurs immediately after sustaining the injury, is short-lived, and is caused by the concomitant concussion.
2. Lucid interval. The patient's consciousness is fully or partially restored. The intensity of the headache noticeably decreases or disappears entirely. The patient appears relatively stable.
3. Secondary deterioration. The period of illusory well-being ends. The headache returns, rapidly intensifies, and becomes unbearable. Nausea, vomiting, and dizziness join the clinical picture. The psychomotor state changes: the patient becomes markedly lethargic. Depression of consciousness progressively deepens, eventually leading to a coma.

During the stage of secondary deterioration, vital functions change: breathing becomes more frequent (tachypnea appears), the pulse becomes slow (bradycardia) but retains good volume, and blood pressure remains within normal limits or rises slightly.

Focal symptomatology and topical diagnosis

The assessment of focal neurological symptoms (lateralization) is of crucial importance for topical diagnosis, as it allows for the precise determination of the side where the intracranial hematoma is located.

• On the side of the lesion (ipsilaterally): Pupil dilation (mydriasis) is observed due to compression of the oculomotor nerve.
• On the opposite side (contralaterally): The disappearance or reduction of motor reflexes is noted, and motor deficit develops in the form of limb paresis or paralysis.

The classical triad of symptoms in epidural hematoma includes: pupillary dilation on the affected side, contralateral hemiparesis, and bradycardia. Without timely surgical intervention, death inevitably occurs. The direct causes of the fatal outcome are massive compression and edema of the brain tissue, leading to irreversible paralysis of vital centers—the respiratory and vasomotor centers.

Class and exam questions

What else to study on this topic

• The contrecoup mechanism: biomechanics of damage to convexital surfaces.
• Differential diagnosis between cerebral concussion and contusion.
• Pathophysiology of meningeal syndrome in intraventricular hemorrhages.
• Surgical tactics for epidural and subdural hematomas.

Other topics in "CHAPTER 10. GENERAL ISSUES IN TRAUMATOLOGY"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.