Neurotrauma & Increased Intracranial Pressure

Vocabulary practice flashcards covering key definitions, classification, pathophysiology, signs, and syndromes associated with neurotrauma, traumatic brain injuries, intracranial hemorrhage, and spinal cord injuries.

Linear Skull Fracture

A non-displaced fracture of the skull that is generally not problematic unless it occurs in an area such as the temporal bone, where underlying vessels can be lacerated.

Depressed Skull Fracture

A skull fracture involving downward depression of bone into brain tissue, often resulting from a severe blow to the head with a blunt object.

Comminuted Skull Fracture

A type of skull fracture that causes fragmentation and downward displacement of bone into brain tissue.

Basilar Skull Fracture

Fractures occurring at the base of the skull (usually in the temporal or frontal areas), often presenting as an open head injury with symptoms such as Battle's sign, Raccoon's eyes, and CSF drainage.

Battle's Sign

Unilateral ecchymosis or bruising over the mastoid area behind the auricle of the ear, which can appear immediately or days after a basilar skull fracture.

Raccoon (Eyes) Sign

Bilateral periorbital ecchymosis or bruising, especially indicative of a basilar skull fracture in the absence of direct orbital trauma.

Traumatic Brain Injury (TBI)

An injury to the brain caused by sudden trauma, such as direct violent head impact or an object penetrating the scalp, skull, or brain tissue.

Primary Brain Injury

Direct damage to brain tissues and blood vessels occurring at the moment of injury, including skull fractures, contusions, hematomas, lacerations, and nerve damage.

Secondary Brain Injury

Damage to neurons not initially injured in the traumatic event, caused by a cascade of physiologic and biochemical events from intracranial conditions (e.g., cerebral edema, vasospasm) or extracranial conditions (e.g., hypoxia, hypotension).

Cerebral Concussion

A head injury characterized by temporary loss of neurological function and disruption of synaptic activity with no structural damage, often caused by acceleration-deceleration forces.

Diffuse Axonal Injury (DAI)

Widespread brain injury caused by direct damage to axons or disruption of axonal processes, leading to microscopic hemorrhages throughout brain tissue that are not usually visible on diagnostic testing.

Moderate Diffuse Axonal Injury

A form of DAI involving minute brain bruising and shearing of brain fibers, accounting for 20% of severe head injuries, presenting with transient loss of consciousness, persistent confusion, headache, and potential coma lasting >24 hours without brainstem injury signs.

Severe Diffuse Axonal Injury

Severe DAI involving disruption of multiple axons in both cerebral hemispheres extending into the brainstem, characterized by GCS < 8 for more than 6 hours, increased ICP from edema, and rare full recovery.

Subdural Hematoma

The most common traumatic mass-effect lesion (accounting for 20-40% of severe head injuries), resulting from venous bleeding (rupture of bridging veins) into the potential space between the dura mater and arachnoid mater.

Acute Subdural Hematoma

A subdural hematoma that manifests within 48 hours after injury, characterized by altered consciousness, ipsilateral pupillary changes, contralateral focal motor symptoms, and signs of increased ICP.

Chronic Subdural Hematoma

A subdural hematoma occurring over 2 weeks after injury, common in alcoholics and the elderly due to brain atrophy, presenting with progressive headache, personality changes, ataxia, incontinence, and seizures.

Epidural Hematoma

A neurosurgical emergency caused by rapid arterial bleeding between the skull and dura mater (70%-80% due to meningeal artery injury from temporal or parietal skull fractures), classically presenting with brief LOC followed by a lucid interval and rapid neurological deterioration.

Subarachnoid Hemorrhage

Bleeding into the subarachnoid space that mixes with cerebrospinal fluid, most commonly presenting with the textbook complaint of 'the worst headache of my life'.

Kernig Sign

A clinical sign of meningeal irritation where passive extension of the knee elicits pain or limited extension when both the hip and knee are flexed to 90 degrees.

Brudzinski Sign

A clinical sign of meningeal irritation where passive forward flexion of the neck causes involuntary flexion of the hips and knees.

Cerebral Contusion

Bruising or bleeding on the surface of the brain (most common in frontal, temporal, and occipital lobes) caused by deformation, rotation, or acceleration-deceleration forces.

Coup and Contrecoup Injury

A dual-focal brain contusion pattern where 'coup' is the primary impact site ('blow') and 'contrecoup' is the secondary injury site on the opposite side of the brain ('counter-blow').

Central Cord Syndrome

A spinal cord syndrome usually caused by hyperextension of the cervical spine, resulting in upper extremity motor weakness and incontinence, with lower extremities relatively spared.

Anterior Cord Syndrome

A spinal cord injury caused by lack of perfusion to the anterior cord (often from flexion forces), resulting in loss of motor function, pain, light touch, and temperature sensation below the lesion, while proprioception and vibration sensation remain preserved.

Brown-Séquard Syndrome

A spinal cord syndrome caused by hemitransection of the cord (typically from penetrating trauma), producing ipsilateral loss of motor function and sensation, and contralateral loss of pain and temperature sensation.

Cauda Equina Syndrome

Compression of nerve roots at the lower end of the spinal cord (below L2), presenting with incontinence, lower extremity weakness, and saddle anesthesia.

Spinal Shock

A temporary loss of reflex, motor, sensory, and autonomic function below the level of a spinal cord lesion, manifesting as flaccidity, anesthesia, priapism, loss of bowel/bladder control, and hypotension with hypothermia.

Autonomic Dysreflexia

An exaggerated, uninhibited sympathetic response occurring in patients with spinal cord injuries at T6 or higher after spinal shock resolves, triggered by stimuli such as a full bladder and producing severe hypertension, bradycardia, and sweating above the lesion.