Spinal Cord Injury (SCI) Study
Guide: Pathophysiology &
Assessment
Section 1: Pathophysiology of Spinal Cord
Injury
Q1: What is the primary difference between the primary
injury mechanism and the secondary injury mechanism in
spinal cord trauma?
Answer: * Primary Injury: The immediate physical damage to the
spinal cord tissue caused by the mechanical forces of the initial trauma
(e.g., transection, contusion, compression, or shear forces from fracture-
dislocations). It is irreversible and occurs at the moment of impact.
Secondary Injury: A progressive cascade of destructive cellular,
chemical, and vascular events that begins minutes after the
primary trauma and can last for weeks. This cascade expands the
initial lesion area and worsens neurological outcomes.
Q2: Which cellular and biochemical events characterize the
phase of secondary injury following an acute SCI?
Answer: The secondary injury cascade includes:
Vascular disruptions: Local hemorrhage, vasospasm, thrombosis,
and loss of autoregulation leading to profound ischemia.
Electrolyte imbalances: Mass influx of intracellular calcium
($Ca^{2+}$) and extracellular efflux of potassium ($K^+$),
disrupting cellular homeostasis.
Excitotoxicity: Excessive release of glutamate into the
extracellular space, overactivating NMDA and AMPA receptors.
Oxidative stress: Generation of free radicals and reactive oxygen
species (ROS) that cause lipid peroxidation of cellular membranes.
Inflammation: Infiltration of microglia, macrophages, and
neutrophils that release pro-inflammatory cytokines, causing
further apoptosis of neurons and oligodendrocytes.
Q3: Define spinal shock, including its typical clinical
presentation and duration.
Answer: Spinal shock is a temporary physiological state that occurs
immediately following acute spinal cord injury. It is characterized by the
, temporary loss of all reflex activity, motor function, and sensation below
the level of the injury. Clinically, patients present with flaccid paralysis
and absent deep tendon reflexes (areflexia), including the loss of the
bulbo cavernosus reflex. It typically lasts from several days to several
weeks and resolves when reflex arcs below the injury level begin to
recover (often signaled by the return of the bulbocavernosus reflex).
Q4: How does neurogenic shock differ pathophysiologically
and clinically from spinal shock?
Answer: * Spinal shock is a neurological and electrical phenomenon
involving the loss of spinal reflexes and motor/sensory function below a
lesion. It can occur with any spinal injury level.
Neurogenic shock is a hemodynamic condition caused by the loss
of autonomic nervous system signals (sympathetic tone) due to a
cervical or high thoracic ($T6$ or above) SCI. Clinically, it results in
a distributive shock state marked by the classic triad of
hypotension, bradycardia, and peripheral vasodilation (warm, dry
extremities).
Q5: What causes the classic triad of symptoms seen in
neurogenic shock?
Answer: The disruption of the descending sympathetic pathways in the
spinal cord ($T1–L2$) leaves the parasympathetic nervous system (via
the vagus nerve) unopposed.
Hypotension: Caused by massive systemic vasodilation and loss
of vascular tone due to decreased sympathetic input to the
peripheral blood vessels.
Bradycardia: Resulting from the loss of cardiac accelerator nerve
input ($T1–T4$), allowing the vagus nerve to slow down the heart
rate unchecked.
Poikilothermia/Warm extremities: Due to the loss of vasomotor
control, the body cannot constrict peripheral blood vessels to
conserve heat, leading to peripheral warmth initially but core
hypothermia as heat dissipates.
Q6: Explain the mechanism of autonomic dysreflexia (AD),
including the level of injury at which it typically occurs.
Answer: Autonomic dysreflexia is a life-threatening syndrome that
occurs in individuals with spinal cord injuries at or above the $T6$ level.
It is triggered by a noxious stimulus below the level of injury (most
commonly a distended bladder, impacted bowel, or skin irritation).
The stimulus sends afferent pain signals up the spinal cord, triggering a
massive, unmodulated sympathetic reflex response below the lesion level. This
, causes severe, widespread vasoconstriction. The brain detects the resulting
dangerous rise in blood pressure via baroreceptors and attempts to
compensate by sending descending inhibitory signals; however, these signals
are blocked by the spinal cord lesion. The brain can only use the vagus nerve to
slow the heart rate, resulting in bradycardia and vasodilation above the level of
injury, while severe vasoconstriction and hypertension persist below the level
of injury.
Q7: Why is autonomic dysreflexia considered a medical
emergency, and what is the immediate first-line
management sequence?
Answer: AD is an emergency because the uncontrolled paroxysmal
hypertension can lead to hemorrhagic stroke, retinal detachment,
myocardial infarction, or seizures. The immediate clinical sequence is:
1. Sit the patient fully upright (90 degrees) to induce orthostatic
pooling of blood and lower blood pressure.
2. Loosen any tight clothing, binders, or orthoses.
3. Identify and remove the triggering stimulus: Check the
urinary drainage system for kinks or irrigate the catheter; if not
catheterized, perform a bladder scan/catheterization. If the bladder
is empty, check for bowel impaction (using lidocaine jelly) or skin
lesions/pressure ulcers.
4. Administer rapid-acting antihypertensives (e.g., nitropaste or
sublingual nifedipine) if the systolic blood pressure remains
elevated above 150 mmHg after addressing the primary triggers.
Q8: Describe the role of glutamate excitotoxicity in
secondary spinal cord damage.
Answer: Following mechanical trauma, dying cells burst and dump large
quantities of the excitatory neurotransmitter glutamate into the
extracellular fluid. Astrocytes also lose their ability to reabsorb glutamate
due to energy depletion. This excess glutamate continuously stimulates
post-synaptic NMDA and AMPA receptors on neighboring intact neurons
and oligodendrocytes. This overactivation triggers a massive,
pathological influx of extracellular calcium ($Ca^{2+}$), activating
intracellular proteases, lipases, and nucleases that systematically
degrade cellular structures, leading to widespread apoptotic and necrotic
cell death.
Q9: How does ischemia contribute to the expansion of the
spinal cord lesion during the acute post-injury phase?
Answer: Mechanical trauma disrupts microscopic capillaries within the
spinal cord gray matter, causing focal hemorrhage and thrombosis.
Guide: Pathophysiology &
Assessment
Section 1: Pathophysiology of Spinal Cord
Injury
Q1: What is the primary difference between the primary
injury mechanism and the secondary injury mechanism in
spinal cord trauma?
Answer: * Primary Injury: The immediate physical damage to the
spinal cord tissue caused by the mechanical forces of the initial trauma
(e.g., transection, contusion, compression, or shear forces from fracture-
dislocations). It is irreversible and occurs at the moment of impact.
Secondary Injury: A progressive cascade of destructive cellular,
chemical, and vascular events that begins minutes after the
primary trauma and can last for weeks. This cascade expands the
initial lesion area and worsens neurological outcomes.
Q2: Which cellular and biochemical events characterize the
phase of secondary injury following an acute SCI?
Answer: The secondary injury cascade includes:
Vascular disruptions: Local hemorrhage, vasospasm, thrombosis,
and loss of autoregulation leading to profound ischemia.
Electrolyte imbalances: Mass influx of intracellular calcium
($Ca^{2+}$) and extracellular efflux of potassium ($K^+$),
disrupting cellular homeostasis.
Excitotoxicity: Excessive release of glutamate into the
extracellular space, overactivating NMDA and AMPA receptors.
Oxidative stress: Generation of free radicals and reactive oxygen
species (ROS) that cause lipid peroxidation of cellular membranes.
Inflammation: Infiltration of microglia, macrophages, and
neutrophils that release pro-inflammatory cytokines, causing
further apoptosis of neurons and oligodendrocytes.
Q3: Define spinal shock, including its typical clinical
presentation and duration.
Answer: Spinal shock is a temporary physiological state that occurs
immediately following acute spinal cord injury. It is characterized by the
, temporary loss of all reflex activity, motor function, and sensation below
the level of the injury. Clinically, patients present with flaccid paralysis
and absent deep tendon reflexes (areflexia), including the loss of the
bulbo cavernosus reflex. It typically lasts from several days to several
weeks and resolves when reflex arcs below the injury level begin to
recover (often signaled by the return of the bulbocavernosus reflex).
Q4: How does neurogenic shock differ pathophysiologically
and clinically from spinal shock?
Answer: * Spinal shock is a neurological and electrical phenomenon
involving the loss of spinal reflexes and motor/sensory function below a
lesion. It can occur with any spinal injury level.
Neurogenic shock is a hemodynamic condition caused by the loss
of autonomic nervous system signals (sympathetic tone) due to a
cervical or high thoracic ($T6$ or above) SCI. Clinically, it results in
a distributive shock state marked by the classic triad of
hypotension, bradycardia, and peripheral vasodilation (warm, dry
extremities).
Q5: What causes the classic triad of symptoms seen in
neurogenic shock?
Answer: The disruption of the descending sympathetic pathways in the
spinal cord ($T1–L2$) leaves the parasympathetic nervous system (via
the vagus nerve) unopposed.
Hypotension: Caused by massive systemic vasodilation and loss
of vascular tone due to decreased sympathetic input to the
peripheral blood vessels.
Bradycardia: Resulting from the loss of cardiac accelerator nerve
input ($T1–T4$), allowing the vagus nerve to slow down the heart
rate unchecked.
Poikilothermia/Warm extremities: Due to the loss of vasomotor
control, the body cannot constrict peripheral blood vessels to
conserve heat, leading to peripheral warmth initially but core
hypothermia as heat dissipates.
Q6: Explain the mechanism of autonomic dysreflexia (AD),
including the level of injury at which it typically occurs.
Answer: Autonomic dysreflexia is a life-threatening syndrome that
occurs in individuals with spinal cord injuries at or above the $T6$ level.
It is triggered by a noxious stimulus below the level of injury (most
commonly a distended bladder, impacted bowel, or skin irritation).
The stimulus sends afferent pain signals up the spinal cord, triggering a
massive, unmodulated sympathetic reflex response below the lesion level. This
, causes severe, widespread vasoconstriction. The brain detects the resulting
dangerous rise in blood pressure via baroreceptors and attempts to
compensate by sending descending inhibitory signals; however, these signals
are blocked by the spinal cord lesion. The brain can only use the vagus nerve to
slow the heart rate, resulting in bradycardia and vasodilation above the level of
injury, while severe vasoconstriction and hypertension persist below the level
of injury.
Q7: Why is autonomic dysreflexia considered a medical
emergency, and what is the immediate first-line
management sequence?
Answer: AD is an emergency because the uncontrolled paroxysmal
hypertension can lead to hemorrhagic stroke, retinal detachment,
myocardial infarction, or seizures. The immediate clinical sequence is:
1. Sit the patient fully upright (90 degrees) to induce orthostatic
pooling of blood and lower blood pressure.
2. Loosen any tight clothing, binders, or orthoses.
3. Identify and remove the triggering stimulus: Check the
urinary drainage system for kinks or irrigate the catheter; if not
catheterized, perform a bladder scan/catheterization. If the bladder
is empty, check for bowel impaction (using lidocaine jelly) or skin
lesions/pressure ulcers.
4. Administer rapid-acting antihypertensives (e.g., nitropaste or
sublingual nifedipine) if the systolic blood pressure remains
elevated above 150 mmHg after addressing the primary triggers.
Q8: Describe the role of glutamate excitotoxicity in
secondary spinal cord damage.
Answer: Following mechanical trauma, dying cells burst and dump large
quantities of the excitatory neurotransmitter glutamate into the
extracellular fluid. Astrocytes also lose their ability to reabsorb glutamate
due to energy depletion. This excess glutamate continuously stimulates
post-synaptic NMDA and AMPA receptors on neighboring intact neurons
and oligodendrocytes. This overactivation triggers a massive,
pathological influx of extracellular calcium ($Ca^{2+}$), activating
intracellular proteases, lipases, and nucleases that systematically
degrade cellular structures, leading to widespread apoptotic and necrotic
cell death.
Q9: How does ischemia contribute to the expansion of the
spinal cord lesion during the acute post-injury phase?
Answer: Mechanical trauma disrupts microscopic capillaries within the
spinal cord gray matter, causing focal hemorrhage and thrombosis.
