Pathophysiology of Central and Peripheral Nervous System Injuries

Introduction to Nervous System Injury Responses

  • Scope and Context: This discussion, led by Hoffman, focuses on the alterations that occur following injury to nerve cells (neurons) within the Nervous System. The primary focus is on the Central Nervous System (CNS), specifically the brain and the spinal cord.

  • Foundational Biological Principles: The CNS responds to injury using the same general mechanisms as other tissues in the body, which include the vascular and cellular responses.

    • Vascular Response: This involves vasodilation to increase blood flow and increased capillary permeability. This allow fluid to move into the interstitial area, delivering necessary cells to the injury site for cleanup and repair.

    • Cellular Response:

      • Chemotaxis: A signal is sent throughout the body to mobilize white blood cells and platelets toward the site.

      • Cellular Adherence: Cells normally contained within the bloodstream adhere to the capillary walls near the injury.

      • Cellular Migration: Cells move out into the interstitial tissue to perform phagocytosis, breaking down damaged cells and invaders (like bacteria from infection).

Traumatic Injury Mechanisms

  • Traumatic Brain Injury (TBI): Leading causes of TBI vary significantly across different population demographics:

    • Elderly: Primarily falls. Even a minor trip onto a hard surface (e.g., cement or a parking lot) can cause significant internal injury.

    • Ages 5 to 24: Primarily vehicular accidents involving acceleration and deceleration forces or direct blows.

    • Under Age 5: Primarily assault and abuse, specifically Shaken Baby Syndrome, which causes sudden acceleration/deceleration movement of the brain within the skull.

  • Coup-Contrecoup Phenomenon:

    • The brain is surrounded by a small space filled with Cerebrospinal Fluid (CSF), which acts as a cushion and lubricant.

    • Coup Injury: This is the injury occurring at the initial point of impact. For example, if the head snaps forward in a car accident, the brain impacts the frontal part of the skull.

    • Contrecoup Injury: Because the skull is a closed space, the brain rebounds and impacts the opposite side of the skull. A blow to the right side may result in a contrecoup injury on the left side; a frontal impact (coup) can cause an occipital injury (contrecoup).

  • Traumatic Spinal Cord Injury:

    • Mechanisms: May involve pressure, swelling, or the physical severing of spinal nerves.

    • Scope of Damage: Injury patterns typically manifest at the point of impact and often extend one or two vertical spaces above and below the actual site of injury.

    • Causes:

      • Motor Vehicle Accidents: Rapid acceleration/deceleration causing cervical spine pressure.

      • Falls: Depending on the point of impact (e.g., falling onto a handrail).

      • Violence: Gunshot wounds or bites involving the spine.

      • Recreational Accidents: Diving accidents or heavy contact in sporting events.

Ischemic, Excitation, and Pressure Injuries

  • Ischemic Injury:

    • Cause: Result of inadequate perfusion leading to hypoxia.

    • Outcome: Leads to necrosis (unplanned cell death). Because neurons are permanent cells, they do not regenerate, and function at that site is lost forever.

    • Patterns:

      • Global: Hypoxia affecting a large portion of the brain, leading to widespread sensory or motor deficits.

      • Focal/Localized: Lack of blood flow to a specific area of the brain or spinal cord.

  • Excitation Injury (Hyperexcitability):

    • Mechanism: A hyper-release of or hypersensitivity to neurotransmitters at the synapse.

    • Clinical Presentation: The most common manifestation is seizure activity. It can also cause muscle twitching or vision disturbances.

    • Metabolic Impact: Over-excited cells have an increased demand for oxygen. If the supply cannot keep up, excitation injuries lead to secondary ischemic effects.

    • End-Stage Posturing: Often seen in comatose patients near death:

      • Decerebrate Posturing: Neurons causing muscle extension are excited, leading to the body reaching out/extending.

      • Decorticate Posturing (Flexion): Neurons responsible for drawing limbs inward are excited, leading to hyper-flexion toward the center of the body.

  • Pressure Injury:

    • Cerebrospinal Fluid (CSF) Blockage: If the normal drainage of CSF is blocked, fluid builds up in the ventricles (reservoirs) or the surface of the brain, putting internal or external pressure on neurons.

    • Cerebral Edema: Result of fluid overload or electrolyte imbalances (e.g., hyponatremia). Fluid moves from the vascular system into interstitial spaces, causing swelling.

    • Lesions: Tumors or growths that occupy limited space in the skull or spinal column, compressing and displacing neurons.

CNS Cellular Support and Long-term Effects

  • Supporting Cells in Injury Response:

    • Astrocytes: Involved in $O_2$ and $CO_2$ exchange and metabolic communication. They stimulate phagocytosis. When permanent nerve cells are lost, astrocytes form scar tissue known as a glial scar (astrogliosis), which is nonfunctional.

    • Microglia: Primarily responsible for the phagocytosis process (destruction and elimination of debris).

    • Glial Nodules: Microglia and astrocytes can combine to form nodules, which are space-occupying lesions that replace functional nerve tissue.

  • Neuropathy: A lasting effect of CNS or PNS injury characterized by abnormal responses like phantom pain, "pins and needles" sensations, or hypersensitivity to stimuli.

Peripheral Nervous System (PNS) and Axonal Alterations

  • Axonal Structure: Consists of the axon, Schwann cells (which create the myelin sheath), and Nodes of Ranvier (gaps that facilitate impulse transmission).

  • Demyelination and Degeneration:

    • Distal Breakdown: If an injury occurs at the distal (far) end of the axon, the myelin sheath breaks down.

    • Total Cell Death: If the entire cell body is destroyed, it cannot regenerate.

    • Segmental Demyelination: If only specific Schwann cells are affected, the myelin may try to regenerate (remyelination). However, the new Schwann cells are often smaller, which alters the action potential.

  • Functional Consequences: Alterations in impulse transmission slow down the action potential or put it out of sync.

    • Motor Neurons: Changes in movement, control, and coordination.

    • Sensory Neurons: Deficits or alterations in sensations, hearing, sight, or taste.

Summary of Clinical Manifestations

  • Global Responses: Mental status changes, confusion, memory loss, coma, and potential death.

  • Focal/Somatic Responses:

    • Efferent System (Motor): Loss of control or coordination.

    • Afferent System (Sensory): Specific sensory deficits depending on the localized part of the brain or spinal segment impacted.