Pathophysiology of Nervous System Trauma Flashcards

1
Q

What is the definition of traumatic brain injury?

A

Any form of external injury that affects the normal function of the brain, either transiently or permanently

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2
Q

Who are the most vulnerable populations for TBI and what is the most common cause of non-fatal TBI?

A

Children and adolescents whose cranial cavities are not fully formed, also adults >75

Leading cause of TBIs is falls

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3
Q

What is the most important outcome of TBI and what patient factors influence recovery?

A

Disability

Patient pre-injury functioning, socioeconomic status, and access to rehabilitation services have a large effect on recovery

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4
Q

What are the two classifications of TBI related to timing of trauma?

A

Primary injury - damage caused by mechanical force, occurring at the moment of injury

Secondary injury - damage not caused directly by primary event, but superimposed on brain already affected by primary injury (i.e. bruising, swelling, herniation, all sequellae)

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5
Q

What are some examples of focal vs diffuse injury in TBI?

A

Focal - scalp injury, skull fracture, or surface contusions

Diffuse injury - diffuse axonal injury, hypoxic-ischemic injury, meningitis, or vascular injury

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6
Q

What is the rating scale of the Glasgow Coma Scale (GCS) and what corresponds to mild, moderate, and severe TBI?

A

3-15

Mild: 13-15
Moderate: 9-12
Severe: 3-8 (<=8 is comatose)

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7
Q

What are the three categories of evaluation for GCS?

A
  1. Eye opening
  2. Verbal response
  3. Motor response
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8
Q

What is the scoring scheme for eye opening on GCS?

A

1 - no opening
2 - opens to pain only (i.e. on forehead)
3 - opens to verbal request
4 - Spontaneously open

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9
Q

What is the scoring scheme for verbal response in GCS?

A
1 - no response
2 - random sounds
3 - random nonsensical word strings
4 - confused response (not oriented)
5 - oriented to time, place, and person
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10
Q

What is the scoring scheme for motor response in the GCS?

A

1 - no response
2 - decerebrate - abnormal extension in response to pain
3 - decorticate - abnormal flexion in response to pain
4 - flexion withdrawal of limb from painful stimulus
5 - touch area of painful stimulus (localizes)
6 - obeys commands

-> most objective scale

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11
Q

What is a closed / blunt head injury? What typically causes them?

A

TBI where skull remains intact. Commonly accidents, falls, acts of violence, sports injuries.

Also, blast-related closed head injuries -> changes in atmospheric pressure, objects dislodged from blasts, or people being thrown into motion by blast

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12
Q

What is a concussion? What are the possible sequellae?

A

A type of closed head injury where there is instant onset transient neurological dysfunction, with or without loss of consciousness

Possible sequellae include post-concussive syndrome. Repetitive concussions may cause chronic traumatic encephalopathy

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13
Q

What is post-concussive syndrome?

A

Prolonged symptoms of concussion lasting longer than usual 7-10 days.

Clinical features: headache, dizziness, nausea, memory disturbance, depression, sleep problems, difficulty concentration, mental fog

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14
Q

What is chronic traumatic encephalopathy (CTE)?

A

Progressive degenerative disease of the brain found in people with severe or repeated blows to the head. Commonly occurs in boxers and football players.

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15
Q

What are common pathological findings of CTE?

A

Neurofibrillary tangles of tau, and amyloid plaques, accompanied by cerebral atrophy, enlarged ventricles (ex vacuo hydrocephalus), and reduced pigmentation of substantia nigra + locus coeruleus.

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16
Q

Where do contusions occur in terms of dural space and which areas of the brain are most susceptible?

A

These are bruises / bleeds in the brain parenchyma, caused by rapid brain displacement and disruption of vascular channels -> hemorrhage. Hemorrhage can extend into subarachnoid space as well.

Crests of gyri are most susceptible, where direct force is the greatest. These are most commonly damaged over rough surfaces (i.e. frontal lobes over orbital ridges)

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17
Q

What are blossoming contusions?

A

Hemorrhagic progression of a contusion ->

Contusions with hemorrhage which expand overtime

or

NEW, non-contiguous contusions

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18
Q

What is diffusion axonal injury (DAI) caused by and what will happen to axons?

A

Rotational / acceleration injuries with whiplash - axons get torn at nodes of Ranvier due to shearing forces.

There will be perivascular microhemorrhages and formation of swollen axons which accumulate beta-amyloid.

19
Q

What will happen to patients in severe DAI, and what areas of the brain are most susceptible?

A

There are unconscious from the moment of injury
-> may remain comatose, vegetative, or severely disabled for life

Areas most susceptible are areas of white matter with long tracts: corpus callosum, midbrain, and deep cerebral white matter

20
Q

What is the definition of an open / penetrating head injury?

A

A head injury in which the dura mater is breached -> usually due to high velocity projectiles or bone fragments from a skull fracture.

21
Q

Define the following skull fracture types:

  1. Linear
  2. Basal
  3. Depressed
  4. Diastatic
  5. Comminuted
A
  1. Linear - fracture lines radiate from site of impact
  2. Basal - fracture of basal skull
  3. Depressed - Skull is depressed into cranial cavity, like a pingpong ball (often in children)
  4. Diastatic - Separation along suture lines
  5. Comminuted - fragmented bone into pieces
22
Q

What is the definition of a displaced skull fracture?

A

A fracture in which the bone is displaced into the cranial cavity greater than the thickness of the bone

23
Q

What clinical signs and symptoms are associated with basilar skull fracture?

A

Raccoon eyes - orbital hematomas

Battle’s sign - bruising near mastoid process

Lower cranial nerve involvement

24
Q

What is the definition of a compound skull fracture?

A

Fracture of skull association with laceration of overlying scalp

25
Q

What are the possible complications of open skull fracture?

A
  1. Intracranial hematoma
  2. CSF leak -> through ear or nose
  3. Damage to cranial nerves
  4. Pneumocephalus - ingress of air
  5. Meningitis - easy entry of infectious agents
26
Q

How can you tell a coup vs contrecoup injury apart?

A

At the level of the brain, you can’t. Just know that the coup injury will be where the fracture is because that’s where the skull was actually hit.

27
Q

Does an epidural hematoma always present acutely? What is the characteristic patient symptomatology?

A

Yes -> it is caused by the rupture of an artery so it will present acutely.

Patient may be knocked out by initial injury, but have a “lucid interval” of 6-12 hours before suddenly dying of transtentorial herniation

28
Q

What causes subdural hematoma and does it always present acutely?

A

Rupture of bridging veins, may present acutely or chronically.

Acute - traumatic, high-energy impact

Chronic - associated with mild trauma, cerebral atrophy, alcoholism, elderly patients

29
Q

How can you tell acute vs subacute vs chronic subdural hematoma apart, and what is the end-stage of subdural hematoma?

A

Via density on CT scan

Acute - clotted blood, appears hyperdense on CT

Subacute - blood becoming liquefied and resorbed from the brain

Chronic - Liquid blood entirely, now very hypodense on CT

End-stage: Area of chronic subdural hematoma becomes filled with only CSF
“subdural hygroma”

30
Q

What pathology can be seen on CT secondary to diffuse axonal injury?

A

“Shearing hemorrhages” - small little contusions due to shearing forces on blood vessels
-> remember the perivascular microhemorrhages

31
Q

What are the causes of vertebral and carotid artery dissection?

A

Carotid artery - hyperextension and rotation of neck (i.e. chiropractor) or direct blow to anterolateral aspect of head

Vertebral - cervical spinal cord fracture

Tears vessel intima and leads to bloodflow into vessel wall.

32
Q

What is the feared complication of vertebral or carotid artery dissection?

A

Ischemic stroke -> Superimposed thrombosis and blockage of blood flow from dissecting blood forming clot

33
Q

What are common secondary brain injuries (vs primary which is what instantaneously happens in TBI)?

A
  1. Cerebral ischemia / hypoxia / hypotension
  2. Cerebral edema / elevated ICP -> brain herniation and death
  3. Seizures are very common due to cortical disruption
  4. Excitotoxicity and reperfusion free radicals
34
Q

How does TBI usually cause hydrocephalus if it causes it?

A

Usually occurs in subarachnoid hemorrhage, where products of blood breakdown and debris impair CSF resorption via arachnoid granulations

35
Q

What is complete vs incomplete spinal cord injury?

A

Complete - all functions below the injured area are lost

Incomplete - preservation of motor or sensory function below the level of the injury

36
Q

What commonly causes cervical vs thoracic vs lumbosacral spinal cord injuries?

A

Cervical - hyperextension / hyperflexion injuries

Thoracic - Crushing, or penetrating injuries

Lumbosacral - older age, including falls most commonly

37
Q

What is ASIA-A vs ASIA-B?

A

ASIA - A = complete, no preservation in S4-S5
ASIA - B = sensory incomplete - S4/S5 preserved (LT, PP, or DAP) + no motor function preserved more than 3 levels below the NLI on either side

(deep anal pressure)

38
Q

What is ASIA-C vs ASIA-D? ASIA-E?

A

ASIA-C = motor incomplete, including voluntary anal contraction OR is sensory incomplete but has sparing of motor function more than 3 levels below NLI. Must have less than half of key muscles below NLI > or equal to 3.

ASIA-D: At least half of key muscles are > or equal to 3 below the NLI

ASIA-E: normal but had prior deficits

39
Q

Where does central cord injury occur and what are the symptoms?

A

Almost exclusively in cervical region. Seen in elderly patients and those with cervical stenosis or severe hyperextension or syringomyelia

-> Greater weakness in arms with relative sparing of legs (lateral corticospinal tract has cervical segments oriented medially)

40
Q

What are the features of Brown-Sequard syndrome?

A

Hemisection

  1. Ipsilateral loss of sensation AT level of lesion (first order neurons lost) + LMN signs AT level of lesion
  2. Ipsilateral UMN signs BELOW level of lesion
  3. Ipsilateral loss of DC-ML BELOW level of lesion
  4. CONTRALATERAL loss of pain and temperature below the level of the lesion
41
Q

When will Horner syndrome happen in Brown-Sequard?

A

When the lesion occurs above T1

SANS to the head and neck is derived in the ILC at the level of T1, and travels in sympathetic trunk to synapse in superior cervical ganglion.

42
Q

What is Conus Medullaris syndrome? Where does this structure ends?

A

Injury of the end of the spinal cord which results in areflexic bladder and bowel and loss of sexual function (loss of sacral cord)

-> Ends at level of LV2

43
Q

What is Cauda Equina syndrome?

A

Injury to lumbosacral NERVE ROOTS below L2 -> areflexic bladder, bowel, and lower limbs

-> this is a peripheral root injury, so there will be lower motor neuron loss. Permanent flaccid paralysis and wasting of lower limb musculature.

44
Q

What commonly causes Cauda Equina syndrome and what sensory loss pattern is very characteristic?

A

Commonly caused by disc hernation or tumors which compress the nerve roots

Saddle anesthesia - loss of sensation around buttocks, inner surfaces of thighs, and perineum