Week 5 - Concussion and SCI Flashcards

1
Q

what are the 2 main types of concussion injuries?

A
  1. Coup-contrecoup injury
  2. torque (rotational) injury
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2
Q

Coup-contrecoup injury

A

contusion from impact (coup) causes a movement of the brain to impact the opposite side of the skull (contrecoup)

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3
Q

Torque (rotational) injury

A
  • head and neck twists, causing shear stress on neurons
  • neurons of the reticular formation most often affected
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4
Q

Concussion pathophysiology

A
  • many neurons injured due to blow and/or shearing
  • spontaneous AP firing (axons begin to leak ions)
  • excess excitatory NT release (glutamate)
  • many neurons stimulated (EPSP)
  • massive increase in metabolic activity
  • increased demand for blood (glucose) but also a transient decrease in blood to the brain after a concussion
  • imbalance of nutrient supply and demand (hours-days)
  • neurons are damaged; remain in a low metabolic state for a period of time
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5
Q

Acute concussion symptoms

A
  • confusion
  • memory loss
  • loss of consciousness
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6
Q

Chronic concussion symptoms

A
  • headache
  • dizziness
  • nausea
  • sensitivity to noise or light
  • fatigue
  • vision disturbances
  • emotional disturbances
  • sleep disturbances
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7
Q

Concussion treatment

A
  • rest completely
  • avoid activity that could cause excess brain movement
  • rehab with support
  • avoid repeated concussion
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8
Q

Chronic Traumatic Encephalopathy

A
  • from repeated concussion
  • damage build up
  • neuronal death
  • brain atrophy
  • dementia
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9
Q

Spinal Cord Injury (SCI)

A
  • obstructs the transmission of neural messages through the spinal cord; loss of somatic and autonomic control of the trunk, limbs, and viscera below the site of the injury
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10
Q

Phases of SCI: primary injury

A
  • sudden trauma to the spine
  • acute spinal cord compression, shear stress, severing (partial vs complete)
  • acute impact to neurons, glial cells, and neural parenchyma
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11
Q

Phases of SCI: secondary injury

A

Primary injury triggers secondary
- involves cascade of biochemical/metabolic and mechanical changes within the neural tissues
- secondary injury is a consequence of these downstream effects (hemorrhage and inflammation)

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12
Q

SCI secondary injury sub-classifications

A
  1. acute phase
  2. sub-acute phase
  3. chronic phase
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13
Q

SCI secondary injury: acute phase

A

(0-48hrs)
- hemorrhage, inflammation and edema result in local ischemia
- neural toxicity induces cellular damage
- demyelination and cell death begins

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14
Q

SCI secondary injury: sub-acute phase

A

(first two-weeks)
- further neurotoxicity, inflammation, cell death, scar tissue formation
- any undamaged tracts begin to resume function (incomplete injury)
- axonal regrowth and sprouting begins if possible

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15
Q

SCI secondary injury: chronic phase

A

( days to years)
- continued cell death and scar tissue formation
- cyst development
- axonal degeneration and demyelination
- continued regrowth and sprouting if possible

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16
Q

Systemic effects of SCI

A
  • bradycardia in response to acute cervical and upper thoracic SCI
  • hypotension
  • pulmonary: ventilation severely impaired in injuries above C5
  • bowel and bladder function
  • Hyperreflexia (spasticity): disinhibition of spinal reflex arcs
  • thermoregulation
  • autonomic dysreflexia
17
Q

Autonomic dysreflexia

A

uncontrolled SNS response to an afferent stimulus below the level of the SCI

18
Q

Autonomic dysreflexia result

A

widespread vasoconstriction BELOW the level of the injury;
- increased BP
- baroreceptors sense and send signal to medulla
- parasympathetic response ABOVE level of injury; decreased HR and vasodilation