Neuro Mod 8 Flashcards
Primary injury to the spinal cord?
Direct physical impact immediately damages spinal cord cells (neurons/glial cells) and causes necrosis
Secondary injury to the spinal cord occurs within ______
hours
Secondary injury to the spinal cord?
Cellular necrosis from primary injury causes immune/inflammatory cascade, neuro excitatory responses to ischemia (further damage area adjacent to primary injury)
Medical strategies for primary spinal cord injury?
Stabilize injury, address emergency life threatening concerns
Medical strategies for secondary spinal cord injury?
Neuroprotective therapy to minimize: acute-phase procedural/surg intervention, systemic pharm agents, cell-based therapies
-high dose IV steroids used in past (unclear evidence, guidelines do not support)
What is spinal shock?
Acute loss of motor, sensory, reflex functions below level of injury:
-areflexia (including bulbocavernosus reflex)
-flaccid paralysis (all muscles below injury, bowel/bladder dysfunction, resp. dysfunction if high cervical injury)
-Complete anesthesia
When does spinal shock occur?
Immediately after acute spinal cord injury
*not usual w gradual injury (tumors, etc.)
Phase 1 of spinal shock?
Areflexia/hyporeflexia: immediate
Phase 2 of spinal shock?
Initial reflex return: first one to return is bulbocarvernosus (w/in 24-48 hr), usually a marker for end of spinal shock
*deep tendon reflexes remain absent
How to check for bulbocarvernosus reflex?
compress glans penis or clitoris and observe for anal sphincter contraction
*another method: tug on foley catheter
Phase 3 of spinal shock?
Early hyperreflexia: some DTRs return gradually (1-4wks) after injury and are hyper reflexic (transition phase from hyporeflexia to hyperreflexia)
Phase 4 of spinal shock?
Final hyperreflexia/spasticity: all DTR below level of injury return/are hyperreflexic
*flaccid paralysis is replaced by hypertonicity/spasticity 1-12 months post injury
What is neurogenic shock a result of?
acute spinal cord injury or sometimes non-traumatic causes of SCI (anesthesia, infection, toxins, etc)
How does neurogenic shock manifest?
Hypotension, bradyarrhythmia, temp dysregulation
Neurogenic shock occurs in what % of SCI?
</=10%
Neurogenic shock is associated w/ what kind of SCI?
cervical high thoracic (SCI above T6)
Neurogenic shock is ____ ____ if not managed immediately?
Potentially fatal
Pathophys of neurogenic shock?
Disrupts sympathetic pathways in upper SC, leads to severe loss of sympathetic function while parasympathetic is intact
Loss of sympathetic tone allows for ______ parasympathetic activity
Unopposed
What does unopposed parasympathetic activity lead to?
Hypotension (systolic <100), Bradycardia, Hypothermia
Management goal of neurogenic shock?
Restore hemodynamics
How to manage hypotension w/ neurogenic shock?
(MAP 85-94), IV fluids, vasopressors, inotropes (inc strength of cardio contraction)
*too much fluid can cause overload/pulm edema
How to manage bradycardia w/ neurogenic shock?
Anticholinergics (atropine, glycolpyrolate)
What is autonomic dysreflexia?
Extreme HTN w/ bradycardia
*potentially life threatening
Autonomic dysreflexia is a complication of SCI above the T6 level and rare if it occurs below _____
T10
What % of SCI will develop autonomic dysreflexia?
20-70%
A hx of autonomic dysreflexia is a potential complication for what?
Med procedures, surgeries, labor
Pathophys of autonomic dysreflexia?
Cutaneous or visceral stimulation below level of injury –> stimulates sympathetic reflex activity
Cutaneous/visceral stimulation of autonomic dysreflexia pathophys?
Bladder/rectum: distend, foley catheter, impaction
Cutaneous: pain, cold, pressure ulcers, etc.
Injuries: fx, etc.
UTIs
Sympathetic reflex activity of autonomic dysreflexia pathophys?
Massive vasoconstriction in lower 2/3 of body and extreme HTN –> stimulates parasympathetics to inhibit sympathetics in brainstem via barorecptors to compensate
Parasympathetic signals in autonomic dysreflexia pathophys cannot descend past _______
level of injury (allows sympathetic reflexes to remain active below this point, massive vasoconstriction and HTN persist here)
Treatment for autonomic dysreflexia?
Immediately sit patient up to decrease BP, Do not lay pt down, remove irritating stimuli asap
*bladder distention is mc cause: evaluate catheter
*bowel: constipation/impaction
*skin: clothes, pressure sores
If unable to resolve irritating stimuli causing autonomic dysreflexia, what should be done?
Transfer to emergency medical system ASAP
If not treated promptly, autonomic dysreflexia can lead to what?
Seizures, cerebral hemorrhage/stroke, potential death
What two areas do descending motor tracts originate in the CNS?
Motor cortex (primary motor area) or Brainstem (red nucleus, tectum, vestibular nuclei, reticular nuclei)
What are the two major descending motor tract pathways?
Lateral and medial (anterior) motor tracts
Lateral motor tracts & their control?
Lateral corticospinal tract & rubrospinal tract
Control fine motor movements of distal extremities
Anterior/medial motor tracts & their control?
Tectospinal, anteriomedial corticospinal, reticulospinal, vestibulospional tracts
Control axial/trunk and reflexes
Lateral corticospinal and rubrospinal tracts travel ________ in the _______ of the spinal cord
Next to each other in the lateral column
Lateral corticospinal tract pathway?
Motor cortex output –> internal capsule –> ipsilateral anterior brainstem –> cross midline in lower medulla –> descend in lateral spinal column –> terminate in anterior horn motor neurons to supply UE/LE muscles
*controls fine motor movement
What is a result of a lesion in the lateral corticospinal tract above the medulla (stroke, tumor of motor cortex, internal capsule, anterior brain stem)?
Contralateral hemiparesis
What is a result of a lesion in the lateral corticospinal tract below the medulla (SCI or MS/ALS in lateral spinal cord)?
Ipsilateral hemiparesis below lesion
Function of rubrospinal tract?
Supports fine motor movement, promotes UE flexors/inhibits US extensors
*more involved in UE than LE
Pathway of rubrospinal tract?
Originates in red nucleus of midbrain –> descends lateral column of spinal tract just anterior to lateral corticospinal tract –> terminates at anterior horn motor neurons that supply UE/LE
An isolated rubrospinal tract lesion is rare and would not cause ________
hemiparesis
A lesion in the lateral column (that affects both rubrospinal and lateral corticospinal tracts would result in what?
Hemiparesis
What is decerebrate posturing?
UE and LE extended
What is decorticate posturing?
UE flexed, LE extended
Decorticate and decerebrate posturing are associated with ____ outcomes
poor
Brainstem damage involving the red nucleus and below would result in what?
Decerebrate posturing
*red nucleus decreases UE flexor tone/allows UE extensor tone to dominate at elbow
Which is more severe/has a worse outcome: decerebrate or decorticate posturing?
Decerebrate
Brainstem damage above the red nucleus would result in what?
Decorticate posturing
*loss of normal cortex inhibition to red nucleus, excessive flexor tone of UE to dominate