Neurotrauma and Spinal Cord Injury

Classifications and Causes of Traumatic Head Injury

• Neurotrauma encompasses injuries to the brain and spinal cord, frequently resulting from significant physical force.

• Major causes of traumatic head injury account for $48\%$ of all cases.

• Head injuries are categorized into two primary types based on the nature of the trauma:

  • Blunt (closed, non-missile) trauma: The brain is injured within the skull without the dura mater being breached.
  • Penetrating (open, missile) trauma: An object pierces the skull and the dura mater, entering the brain tissue.

• Causes of blunt trauma include:

  • Contact with the ground, such as during a fall.
  • Contact with a car interior, as seen in Motor Vehicle Crashes (MVC).
  • Blows from objects such as a baseball bat, hammer, thrown brick, lamp, or bottle.

Pathophysiology of Brain Injury

• Head injury pathophysiology is divided into three distinct phases: primary, secondary, and tertiary.
• Primary Injury: Results directly from the impact. This involves neural injury, primary glial injury, and a vascular response.
• Secondary Injury: Develops as a consequence of the initial trauma. It includes cerebral edema, brain swelling, hemorrhage, infection, and increased intracranial pressure (ICP).
• Tertiary Injury: Occurs due to systemic complications such as apnea, hypotension, and altered pulmonary resistance.
• These injuries can be further classified as either focal (localized) or diffuse (widespread).

Focal Brain Injury and Cerebral Contusions

• Focal brain injuries involve specific, grossly observable brain lesions. These includes:

  • Epidural hematoma
  • Subdural hematoma
  • Subarachnoid hemorrhage
  • Intracerebral hemorrhage
  • Cortical contusions

• Cerebral contusions represent the "bruising" of the brain, characterized by the rupture of small blood vessels near the brain surface.

• Contusions are classified by the site of impact:

  • Coup: Injury occurs on the side of the brain where the impact occurred.
  • Contrecoup: Injury occurs on the opposite side of the brain to the point of impact.

• Common sites for contusions include the anterior fossa and middle fossa, specifically affecting the frontal and temporal lobes.

• Impacts in these areas often lead to changes in attention, memory, motivation, affect, emotion, and behavior.

• The severity of a contusion is determined by the force of impact; a smaller area of impact results in a greater severity of injury.

Traumatic Intracranial Hemorrhage and Hematomas

• Intracranial hemorrhages occur within the meningeal layers or the brain tissue. The meninges consist of:
  • Dura mater (outermost layer)
  • Arachnoid mater (middle layer)
  • Pia mater (inner layer, adjacent to the brain)
• Meningeal spaces include the epidural space (extradural, between the skull and dura), the subdural space (between the dura and arachnoid), and the subarachnoid space (between the arachnoid and pia).

Epidural Hematoma

• Also known as extradural hematoma or epidural hemorrhage, this is an accumulation of blood between the skull and the dura.
• Characteristics and pathophysiology:
  • Occurs in $1-2\%$ of major head injuries.
  • Most common in individuals aged $20-40$ years.
  • Usually associated with a temporal bone fracture and the shearing of the middle meningeal artery.
  • $85\%$ are arterial bleeds; $15\%$ result from injury to a meningeal vein or dural sinus.
  • Radiographically, they typically present with a lentiform (biconvex) shape.
  • Pathological consequences include edema, subfalcine herniation (displacement under the falx cerebri), and transtentorial uncal herniation, which can lead to midbrain hemorrhages.
• Symptoms:
  • Often misleading initially.
  • Characterized by an initial "lucid interval" followed by a later decrease in Level of Consciousness (LOC) due to increased ICP.
  • Lethal if untreated, with death typically resulting from increased ICP.

Subdural Hematoma

• This involves the accumulation of blood in the subdural space, usually due to the severance of bridging veins or the dural sinus.
• Bleeding is generally slower and more limited in volume compared to epidural hematomas.
• Classification by onset:
  • Acute: Develops rapidly within $48\,hrs$, usually located at the top of the skull. Occurs in $10-20\%$ of persons with traumatic brain injury.
  • Subacute: Develops over a period of $48\,hrs$ to $2\,weeks$.
  • Chronic: Develops over weeks to months. Most common in the elderly and alcohol abusers due to brain atrophy, which expands the subdural space. A vascular membrane typically forms around the hematoma in approximately $2\,weeks$.
• Clinical manifestations:
  • Depends on the speed of onset.
  • Often non-specific, such as a headache.
  • In the elderly, may manifest as dementia, sometimes confused with senility.
  • There may be little to no evidence of external trauma.
• Pathological effects include deviation of the midline and ventricles, and the threat of transtentorial or subfalcine herniation.

Subarachnoid and Intracerebral Hemorrhage

• Subarachnoid Hemorrhage:
  • Bleeding between the arachnoid and the pia.
  • Caused by bleeding from the brain surface or a rupture of the Circle of Willis.
  • Triggers include trauma or aneurysm.
  • Gross pathology may show flattened convolutions of the brain.
• Intracerebral Hemorrhage:
  • Occurs in $2-3\%$ of persons with head injuries.
  • May be single or multiple lesions, often associated with contusions.
  • Most common in frontal and temporal lobes, but can also occur deep in white matter.
  • Acts as an expanding mass, leading to increased ICP and compression of brain tissue.
  • Penetrating trauma (missile injuries or compound fractures) frequently results in these focal injuries.

Diffuse Brain Injury and Concussion

• Concussions are categorized by severity using various diagnostic guidelines:
• Cantu Guidelines ($2001$):
  • Grade 1 (Mild): No loss of consciousness; post-traumatic amnesia lasts less than $30\,min$.
  • Grade 2 (Moderate): Loss of consciousness lasting less than $5\,min$, or amnesia lasting between $30\,min$ and $24\,hrs$.
  • Grade 3 (Severe): Loss of consciousness lasting more than $5\,min$, or amnesia lasting more than $24\,hrs$.
• Colorado Medical Society:
  • Grade 1: Confusion; no loss of consciousness.
  • Grade 2: Confusion; post-traumatic amnesia; no loss of consciousness.
  • Grade 3: Any loss of consciousness.
• American Academy of Neurology:
  • Grade 1: Confusion; symptoms last less than $15\,min$; no loss of consciousness.
  • Grade 2: Confusion; symptoms last more than $15\,min$; no loss of consciousness.
  • Grade 3: Any loss of consciousness.

Diffuse Axonal Injury (DAI)

• DAI results from a shaking effect or rotational acceleration (twisting), which creates shearing stresses that tear or stretch nerve fibers (axons).
• Most severe axonal damage is peripheral to the brainstem.
• At the time of injury, damage is only visible via electron microscopy.
• Within $12\,hrs$ to several days, damaged axons regress into "retraction balls" visible under a microscope. These increase in number for the first $1-2\,weeks$, then decrease.
• Categories of DAI:
  • Mild DAI: Coma lasts $6-24\,hrs$; characterized by good recovery or moderate disability, though residual deficits may persist. Death is uncommon.
  • Moderate DAI: The most common type; present in $20\%$ of severe head injuries. Involves physiological impairment throughout the cerebral cortex and diencephalon. Coma lasts longer than $24\,hrs$, and recovery is often incomplete.
  • Severe DAI: Present in $16\%$ of severe head injuries. Involves severe mechanical disruption of axons in both hemispheres, the diencephalon, and the brainstem. Patients remain deeply unconscious; prognosis is poor, involving severe disability, persistent vegetative state, or death.

Spinal Cord Trauma Statistics and Mechanisms

• Incidence: Approximately $15,000$ to $17,000\,cases/yr$ in the U.S.
• Demographics: Most commonly affects males aged $16-30$ years.
• Primary causes:
  • MVCs: $55\%$
  • Sports: $18\%$
  • Penetrating injuries: $15\%$
• Mechanisms of injury:
  • Acceleration
  • Deceleration
  • Deformation
• Vertebral column injuries often involve bones, ligaments (e.g., ligamentum flavum, interspinous, anterior/posterior longitudinal ligaments), and joints through fractures, compressions, dislocations, and subluxations.
• Specific fracture types include Burst fractures (from axial compression) and Wedge fractures (from hyperflexion).

Sites and Functional Consequences of Spinal Injury

• Common sites of injury include the cervical spine, cervico-dorsal junction, and thoraco-lumbar junction.
• Level-Specific Manifestations:
  • $C1$ to $C4$: Paralysis of respiratory muscles and all arm/leg muscles; usually fatal. Injuries to the dens (odontoid process) or transverse ligament are critical.
  • $C5$ to $C6$: Lower extremities paralyzed; slight ability to flex upper limbs (part of the brachial plexus).
  • $C6$ to $C7$: Lower extremities paralyzed; part of wrists, shoulder movement, and elbow bending are relatively preserved.
  • $C8$ to $T1$: Lower extremities and torso paralyzed; eyelids droop, loss of forehead sweating; arms relatively normal, hands paralyzed.
  • $T2$ to $T4$: Lower limbs and torso paralyzed; loss of sensation below the nipples.
  • $T5$ to $T8$: Lower limbs paralyzed; loss of sensation below the rib cage.
  • $T9$ to $T11$: Lower limbs paralyzed; loss of sensation below the umbilicus.
  • $T12$ to $L1$: Paralysis and loss of sensation below the groin.
  • $L2$ to $L5$ and $S1$ to $S2$: Different patterns of leg weakness and sensory loss.
  • $S3$ to $S5$: Loss of bladder and bowel control; loss of sensation in the perineum.
• Note: Loss of bladder and bowel control can occur with severe injury at any level of the spinal column.
• The Phrenic nerves (critical for diaphragm function) are associated with the $C3-C5$ levels.

Pathophysiology of Spinal Cord Injuries

• Timeline and Progression:
  • Within minutes: Microscopic hemorrhages appear in central gray matter and pia/arachnoid.
  • Within $2\,hrs$: Hemorrhages increase in size; edema in white matter impairs microcirculation.
  • Within $4\,hrs$: Swelling (ischemia) peaks; disruption of myelin; axonal degeneration occurs. Necrosis consumes $40\%$ of the cord's cross-section.
  • Within $24\,hrs$: Necrosis consumes $70\%$ of the cord's cross-section. Circulation in white matter may return to normal, but remains altered in gray matter.
  • First few days: Progressive cavitation and coagulative necrosis (posttraumatic infarction).
  • Within $3-4\,weeks$: Meninges thicken and the traumatized cord is replaced by acellular collagenous tissue.
• Edema increases the degree of dysfunction, often impeding the assessment of permanent loss.

Clinical Manifestations of Spinal Cord Injury

• Spinal Shock:

  • Caused by spinal cord concussion; results in a period of loss of all normal activity below the lesion.
  • Typically lasts $24-72\,hrs$.
  • Characterized by paralysis, hypotonia (loss of muscle tone), areflexia (loss of reflexes), anesthesia, and loss of bowel/bladder control.
  • Systemic effects include transient decreased Blood Pressure ($BP$), poor venous circulation, and disturbed thermoregulation.
  • End of spinal shock is indicated by the return of reflex activity below the injury (e.g., the bulbocavernosus reflex), potentially followed by hyperreflexia, hypertonia, and clonus.

• Autonomic Hyperreflexia (Dysreflexia):

  • Represents a massive, uncompensated cardiovascular response to stimulation of the sympathetic nervous system (SNS).
  • Can occur any time after spinal shock ends and is life-threatening.
  • Symptoms include:
  • Systolic $BP$ up to $300\,mm\,Hg$
  • Pounding headache
  • Blurred vision
  • Sweating and flushing above the level of the lesion
  • Piloerection (goosebumps)