Central Nervous System Trauma Flashcards

1
Q

Define concussion, or mild traumatic brain injury

A

A concussion, or mild traumatic brain injury, is an alteration in mental status caused by biomechanical forces that may or may not cause loss of consciousness. One need not be rendered unconscious to have sustained a concussion.

The pathophysiology and mechanism of concussion differ from that of severe TBI only in degree, and the regions of the brain affected tend to be confined to the junction of the grey and white matter immediately beneath the cortex where gradient echo MRI often detects shearing lesions of DAI

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2
Q

What are the peak age groups in which head injuries occur and what are the mechanisms whereby these injuries are received?

A

Peak age group: 24-35 years

Causes (most common listed first):
MVA, Recreation, Violence, Falls, Bicycles, SBS

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3
Q

What is the goal of treatment in head injuries?

A
The goal of treatment is to reduce secondary injury to the brain by minimizing ICP and maximizing oxygen/metabolite delivery
•	intubation
•	controlled ventilation
•	osmotic diuretics (mannitol)
•	ventricular catheters
•	drug-induced coma
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4
Q

What is the reason for the control of intracranial pressure in the treatment of head injury?

A
  • Once the volume of the brain rises past the point at which all the compressible compartments of the brain have been maximally compressed (i.e. venous system and CSF compartments), a small change in volume will lead to substantial increases in ICP
  • Once ICP increases to a pressure that is equal or greater to the mean arterial pressure, blood vessels will be compressed and blood supply compromised
  • High ICP can lead to herniation syndromes that result in abrupt neurological condition changes
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5
Q

What are the signs and symptoms of increased intracranial pressure?

A

“lucid interval” with headache, n/v, vomiting, progressive lethary, loss of consciousness.

Subfalcine herniation
Uncal herniation
Tonsilar herniation

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6
Q

What is the Glasgow Coma Scale, and how is it used in predicting injury severity and outcome, and the elements of the clinical evaluation of concussion?

A

Used to determine the likelihood that a patient has an intracranial mass lesion and the likelihood of a good outcome, moderate disability, severe disability or death. The patient is assigned a score for eye opening, motor response and verbal response. The score is added up and the two tables are used to assess risk of a lesion and to predict prognosis. Other components of the evaluation include: 24 hour monitoring after incident, CT scan for intracranial bleed if LOC observed, Careful neuro exam, Mental status exam

Mild score = 15-13
Moderate = 12-9
Severe = 8-3

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7
Q

What are the five of the most common symptoms of concussion?

A
  1. Headache
  2. Dizziness
  3. Poor attention
  4. Inability to concentrate
  5. Memory problems
  6. Fatigue
  7. Irritability
  8. Depressed mood
  9. Intolerance of bright light or loud noise
  10. Sleep disturbance
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8
Q

Linear skull fracture

A

High impact injury. Outcome is good if there is no underlying impact injury

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9
Q

Depressed skull fracture

A

High impact injury resulting in comminuted bone fragments. May require surgery for debris or for cosmetic reasons

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10
Q

Basilar skull fracture

A

High velocity blunt injury. Fracture may extend through cribiform plate or petrous bone causing CSF leak.

Signs/Symptoms: Meningitis, CSF leak from ears and nose, Orbital (raccoon eyes) or mastoid bruising (battle sign), Subconjuctival hemorrhage, Facial nerve palsy

Outcome is good if meningitis is treated and if there are no underlying injuries

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11
Q

Diastatic skull fracture

A

High impact injury separates skull at suture lines. Outcome is good if there are no underlying injuries

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12
Q

Growing fractures of injury

A

Skull fracture and dural tears in infants allow the arachnoid to herniate into the fracture. The herniation moves with CSF pulsations and causes further bone loss over months. Outcome is good after surgical correction

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13
Q

Epidural hematoma

A

Intracranial, extradural bleeding most often from the middle meningeal artery following an impact injury. There is a “lucid interval” followed by progressive obtundation and coma. Imaging shows a lentinular shape lesion. Mortality is

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14
Q

Subdural hematoma

A

Translation acceleration resulting in a rupture of bridging veins. There is a gradual onset of symptoms associated with increased cranial pressure. Generally slow bleeds. Imaging shows a crescent-shaped lesion. Mortality is 40-60%. Subdural hematomas are often associated with cerebral contusions and increase intracranial pressure, causing a mass effect

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15
Q

Cerebral contusion

A

High velocity translational and/or impact injury causes superficial hemorrhagic contusions commonly at the rough surfaces of the skull (anterior cranial fossa and wing of the sphenoid). Imaging shows a wedge-shaped lesion. Mortality is

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16
Q

Diffuse axonal injury

A

High velocity rotational injury stretches/tears axons. Once enough axons tear, you get DAI. Pts are rendered unconscious following injury. Invisible on the CT/MRI. Mortality as high as 80%

“Retraction balls of Cajal”

17
Q

Secondary head trauma

A

Primary trauma→ massive depolarization of neurons → excitotoxicity and glutamate transporter reversal → vasogenic and cytotoxic edema → increased ICP → reduced blood supply → no oxygen leading to further excitotoxicity and glutamate transporter reversal → ischemia and damage

18
Q

Subfalcine herniation

A
  • cingulate gyrus moves under falx cerebri, kinking anterior cerebral artery
  • stroke in anterior cerebral a. distribution
19
Q

Uncal herniation

A
  • medial temporal lobe moves across tentorial edge and down into posterior fossa compressing midbrain and ipsilateral cerebral peduncle
  • ipsilateral third nerve palsy and contralateral hemiparesis = blown pupil
  • may be associated with Duret hemorrhages in brainstem that lead to neurologic consequences
20
Q

Tonsilar herniation

A
  • cerebellar tonsils herniate downward into foramen magnum and compress medulla
  • abnormal cardiac and respiratory responses
  • Cushing’s reflex (bradycardia, HTN and high ICP)
21
Q

Biomechanics of a concussion

A
  • Regardless of the direction of the force, frontal & temporal lobes are most affected
  • Rotational (angular) forces are more damaging than Translational (linear)
  • Linear (translational) forces also cause skull fractures and contrecoup contusions
22
Q

Pathophysiology of a concussion

A

Biomechanical forces cause tissue deformation, shearing and fluid wave propagation through the hemisphere. Irritation leads to rapid, chaotic electrical depolarization across the cortex

Neurotransmitters / neurochemicals are released in excessive (excitotoxic) amounts, driving up cellular metabolism (hyperglycolysis) and lactic acid levels

Na – K pump failure and axonal stretch injury lead to Calcium influx and axonal swelling or disintegration

Rotational injuries lead to diffuse shearing of small vessels
Diffuse axonal injury is underlying lesion

23
Q

What is Second Impact Syndrome?

A

Catastrophic brain swelling occurring if concussions happen near each other in time.
Intracranial vasodilation and cerebrovascular congestion – vascular autoregulation dysfunction