Traumatic brain injury week 7 Flashcards

1
Q

How many people sustain a TBI in the US annually?

A

btwn 1.5 and 1.7 million people sustain a TBI in the US annually

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2
Q

What is the incidence of deaths due to TBI in the US annually?

Hospitalizations due to TBI?

A

52,000 deaths

275,000 hospitalizations

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3
Q

What is the leading cause of TBI? Particularly in what age group?

What cause of TBI results in the largest percentage of TBI related deaths? Particularly in what age group?

People aged ___ and older have the highest rates of TBI-related hospitalizations and death.

What is one of the leading causes of child maltreatment deaths in the US?

What is the leading cause of TBI for active duty military personnel in war zones?

A
  • Falls are the leading cause (esp. in those > 60 years old)
  • Motor vehicle crashes and traffic-related incidents result in the largest percentage of TBI-related deaths (31.8%) among all age groups
  • People aged 75 and older have the highest rates of TBI-related hospitalizations and death.
  • Shaken Baby Syndrome, a form of abusive head trauma and inflicted TBI, is a leading cause of child maltreatment deaths in the U.S.
  • Blasts are a leading cause of TBI for active duty military personnel in war zones.
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4
Q

Which of the two is worse: decorticate or decerebrate rigidity?

What may transition from decorticate to decerebrate rigidity signify?

A

Decerebrate rigidity is a worse clinical sign and transition from decorticate to decerebrate could signify brain herniation.

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5
Q

What is the Glascow Coma Scale (GCS)?

What is it out of?

What are the score ranges of GCS for severe, moderate, and mild TBI? How may duration of post-traumatic amensia affect the classification of severity of a TBI?

A

The Glascow Coma Scale (GCS) clinical tool designed to assess coma and impaired consciousness (15-point test)

  • Severe TBI (GCS scores of 3 to 8)
  • Moderate TBI (scores 9-12)
  • Mild TBI ( scores 13-15)

Duration of post-amnesia may indicate a worst TBI than is told by the GCS score (go with the more severe category).

Duration of post amnesia: Mild < 24 hours, Moderate 1-6 days, severe 7 days or more.

Amnesia tells us there is cortical damage.

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6
Q

What are the 8 types of TBI?

A

Types of TBI (not mutually exclusive categories)

  1. Concussion
  2. Contusion/ Intracerebral hemorrhage
  3. Coup-Contrecoup Injury
  4. Subdural hematoma
  5. Epidural hematoma
  6. Subarchnoid hemorrage
  7. Diffuse Axonal Injury
  8. Second Impact Syndrome: “Recurrent TBI”
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7
Q

What is a concussion caused by?

What are the danger signs of a concussion?

How do the danger signs of a concussion differ in children?

A
  • type of TBI, caused by a bump, blow, or jolt to the head
  • can also occur from a fall or a blow to the body that causes the head and brain to move quickly back and forth.
  • Health care professionals may describe a concussion as a “mild” TBI because concussions are usually not life-threatening. However, long term effects can be serious.

Danger signs of a Concussion

  • Headache that gets worse and does not go away
  • Weakness, numbness or decreased coordination
  • Repeated vomiting or nausea
  • Slurred speech
  • Drowsiness
  • Dilated pupil (s)
  • Convulsions or seizures
  • Cannot recognize people or places
  • Confusion, restlessness, or agitation
  • Unusual behavior
  • Loss of consciousness (even a brief loss of consciousness should be taken seriously and the person should be carefully monitored). LOC IS THE WORST SIGN OF CONCUSSION.

Danger Signs in Children Same as for adult but also include:

  • constant crying and inability to be consoled
  • Refusal or unwilling to nurse or eat
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8
Q

What is a cerebral contusion?

Where in the brain do they typically occur?

What symptoms/problems are often present in individuals who have suffered a contusion?

What clinical parameter must be assessed in contusion and why? At what time after the contusion is this parameter at its worst?

How is contusion treated?

In what type of injury does contusion commonly occur in?

A

Cerebral Contusion

  • Occurs in 20-30% of severe TBIs
  • can be associated with multiple microhemorrhages; numerous small contusions from broken capillaries that occur in grey matter under the cortex: (multiple petechial hemorrhages or multifocal hemorrhagic contusion)
  • occur under the site of impact especially in brain regions near sharp ridges on the inside of the skull (under frontal and temporal lobes and on roof of the orbit). (frontal lobes may hit crista galli, temporal lobes on sphenoid bone, for example)
  • Attention, emotional and memory problems (associated with damage to frontal and temporal lobes) are common in head trauma survivors.
  • Frequently associated with edema and are especially likely to cause increases in intracranial pressure (ICP) and crushing of delicate brain tissue and vasculature.
  • Swelling is worst at around four to six days after the injury.
  • Cerebral swelling very dangerous; therefore treatment includes medications to prevent swelling and/or surgery to reduce it (craniotomy).
  • Contusions commonly occur in coup-contrecoup injuries
  • Clinical Signs and symptoms depend on the contusion’s location in the brain.
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9
Q

What is mass effect? Why does it occur? Why is it dangerous?

A

mass effect: brain tissue and structures must shift to accommodate swelling and/or blood.

  • Hemorrhage or edema can cause this
  • Physical mass can:

– directly compress vascular structures, resulting in ischemia and infarct

– directly impinge upon other vital structures

– herniate different parts of the brain

– Stretch or compress cranial nerves

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10
Q

What is a coup-contrecoup injury?

What type of TBI is it associated with?

What lobes of the brain are most commonly affected in a coup-contrecoup injury?

A
  • a coup injury occurs under the site of impact with an object
  • a contrecoup injury occurs on the side opposite the area that was impacted
  • Both associated with cerebral contusion
  • Inertia is involved in the injuries (e.g. when the brain keeps moving after the skull is stopped by a fixed object or when the brain remains still after the skull is accelerated by an impact with a moving object).
  • Frontal, occipital and temporal poles most common sites of injury
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11
Q

What is the most common type of intracranial traumatic lesion?

A

subdural hemorrhage

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12
Q

What type of brain injury is present in the attached pic? How can you tell?

A

A 26 year-old man was brought to the hospital agitated and confused following a motor vehicle accident. Frontal Pole Contusion. Axial CT scans without contrast. Note the areas of traumatic contusion, which consist of hemorrhage (stars) and surrounding edema (White circle), in both frontal lobes. There is also a “mass effect” on the anterior horns of the lateral ventricles (decreased ventricular volume) (arrows)

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13
Q

What characteristic shape does a subdural hemorrhage have on imaging?

In what age group are subdural hemorrhages most common and why?

What may occur to the brain as a result of an expanding subdural hematoma?

What is the mortality rated of acute subdural hematomas?

A
  • Acute subdural hematomas are the most common type of intracranial traumatic lesion (see characteristic crescent shape structure representing blood below the dura compressing brain tissue).
  • They are especially common in the elderly, in whom they may occur following insignificant and often forgotten head trauma.
  • This is one the most common etiologies because as the brain atrophies during aging, the “bridging veins” that connect the cortex to the draining venous sinuses stretch, and are more easily torn from minor trauma, resulting in a subdural hematoma.
  • Slow venous bleeding (under low pressure) such that the hematoma may develop over time.
  • Clinically, subdural hematomas may present in a variety of ways. If the patient develops an expanding subdural hematoma, brain tissue must shift to accommodate the mass. Since the cranial volume is a constant, part of the cranial contents may herniate through the tentorial incisura (uncal herniation) or under the Falx cerebri (cingulated herniation) to make room for the mass.
  • The mortality rates of an acute subdural hematoma are as high as 90%.
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14
Q

Name the types of herniation and classify them as supratentorial or infratentorial.

A

Supratentorial herniation

  1. Uncal (transtentorial) : common
  2. Central: diencephalon and more of temporal lobes herniate through tentorial notch
  3. Cingulate: gyrus pushed under falx cerebri
  4. Transcalvarial (brain herniates out through skull fracture or surgical site)

Infratentorial herniation

  1. Upward (upward cerebellar)
  2. Tonsillar (downward cerebellar)
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15
Q

What signs/symptoms does herniation frequently present with?

A

Brain herniation frequently presents with:

  • abnormal posturing (decerebrate or decorticate)
  • Low Glascow Coma Scales (three to five)
  • One or both pupils may be dilated and fail to constrict in response to light (midbrain compression &/or stetching CN III).
  • Compression of cardiovascular/respiratory control centers in medulla can cause cardio/respiratory arrest
  • Vomiting may occur: compression of vomiting center in medulla (area postrema)
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16
Q

What artery is commonly affected in epidural hemorrhages? Where does bleeding occur?

What happens to the underlying brain tissue as a result?What is the treatment?

A

Epidural Hematoma

During a traumatic skull injury a meningeal vessel (commonly middle menigeal artery) running in the periosteal layer of the dura can tear causing bleeding into epidural space, compressing underlying brain. Is fatal unless treated surgically.

17
Q

What type of hemorrhage is present in the attached pic? How do you know?

A

Subdural. Note the crescent shape. More importantly, note the lining of dura mater on the perimeter and the bleed underneath it.

18
Q

What kind of hemorrhage is present? How do you know?

A

CT scan demonstrating lens shaped epidural hematoma/. Note there is not a lining of dura with bleeding underneath as is seen in subdural hemorrhages. The opposite is seen (blood on the outside of dura-hence epidural). Note the mass effect.

19
Q

Where is blood visualized on imaging in a subarachnoid hemorrhage?

A

Subarachnoid hemorrhage: Blood spreads throughout the cisterns and fissures surrounding the brain in the subarachnoid space.

20
Q

Identify the injuries on the attached CT image.

A

intraparenchymal hematoma (contusion)

subdural

subarachnoid

21
Q

What is diffuse axonal injury (DAI) caused by?

Where does it most often occur (white matter, gray matter)?

What happens to the axons in DAI and why?

What part of the axon does damage occur?

A
  • result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated (as may occur in auto accidents, falls, assaults, and Shaken baby syndrome.
  • Occurs especially in white matter tracts such as corpus callusom, subcortical white matter, brainstem tracts, etc
  • major cause of damage is disruption of axons
  • caused by shearing injury: brain regions of differing densities and distances from the axis of rotation slide over one another, stretching axons that traverse these junctions between areas of different density. Occurs especially at junctions between white and gray matter.
  • is related to excitotoxic mechanisms, particularly glutamate and NMDA receptors.
  • Axonal damage often occur at the node of Ranvier, resulting in a traumatic defect in the axonal membrane
  • Causes a biochemical cascade with leakage of glutamate in the extracellular space leading to glial cell and axonal swelling, and finally necrosis or axonal degeneration.
22
Q

How is DAI detected on imaging? Explain the reasons for the difficulties with imaging of DAI.

What finding on imaging can allow one to infer DAI has occured?

Why may someone with DAI appear fine and deteriorate later?

A
  • difficult to detect because it does not show up well on CT scans or MRI. MRI more sensitive but may miss DAI, because it identifies the injury using signs of edema, which may not be present initially.
  • Its presence can be inferred when small bleeds are visible in the corpus callosum or cerebral cortex. MRI is more useful than CT for detecting characteristics of DAI in the subacute and chronic stages.
  • Newer studies such as Diffusion tensor Imaging (DTI) and Diffusion weighted imaging (DWI) are able to demonstrate the degree of white matter fiber tract injury even when the standard MRI is negative.
  • Because axonal damage is largely a result of secondary biochemical cascades, it has a delayed onset, so a person with DAI who initially appears well may deteriorate later.
  • Thus , injury is frequently more severe than is realized and DAI should be suspected in any patients whose CT scans appear normal but who have severe symptoms such as unconsciousness
23
Q

What are the potential complications of TBI?

A
  1. altered conciousness
  2. abnormal posturing such as decerebrate (extensor) or decorticate (flexor) rigidity
  3. seizures
  4. infections
  5. cranial nerve damage
  6. recurrent TBI (aka second impact syndrome)
24
Q

Altered consciousness: Moderate to severe TBI can result in prolonged or permanent changes in a person’s state of consciousness, awareness or responsiveness. Define the following altered states of conciousness:

coma (what GCS scale defines it?)

vegetative state

minimally concious state

locked-in syndrome

A

Coma (CGS of 8 or less): person unconscious, unaware of anything and unable to respond to any stimulus. This results from widespread damage to all parts of the cortex. After a few days to a few weeks, a person may emerge from a coma or progress to a vegetative state.

Vegetative state: caused by widespread damage to the brain. The person is unaware of his or her surroundings, but may groan or have open eyes or reflex responses. A vegetative state can be permanent, but individuals may progress to a minimally conscious state.

Minimally conscious state: condition of severely altered consciousness but with some evidence of self-awareness or awareness of one’s environment. Often a transitional state from a coma or vegetative condition to greater recovery.

Locked-in- syndrome: person is fully conscious/aware of surroundings and awake, but can’t move or speak. May be able to communicate with vertical eye movement. This state results from damage limited to the lower brainstem. (Note: more commonly due to a basilar artery infarct)

25
Q

How may derebrate and decorticate rigidity be treated?

Some people with TBI will have seizures within what time period? This results in administering what type of medication post TBI?

A
  1. Abnormal posturing such as decerebrate (extensor) or decorticate (flexor) rigidity

• May be treated with spasticity medications

  1. Some people with TBI will have seizures within the first week due to anoxia, bleeds, brain damage, etc. Therefore, antiseizure meds given as a preventative measure. More-serious injuries may result in recurring seizures, called post-traumatic epilepsy
26
Q

Why can TBI lead to infection? What type of infection may result?

Injuries to the base of the skull can damage cranial nerves resulting in what consequences?

A
  1. Skull fractures or penetrating wounds can tear the meninges, thereby enabling bacteria to enter the brain causing meningitis.
  2. Injuries to the base of the skull can damage cranial nerves resulting in:
  • Damage to the olfactory nerves (I)
  • Loss of vision (II)
  • Damage to the nerves controlling eye movements (III, IV, VI), which can cause double vision
  • Loss of facial sensation (V)
  • Paralysis of facial muscles (VII)
27
Q

TBI may increase risk of what neurodegenerative diseases?

A

A TBI may increase the risk of neurodegenerative diseases including:

  • Alzheimer’s disease: progressive loss of memory and other cognitive skills (i.e. dementia)
  • Parkinson’s disease
  • Dementia pugilistica — most often associated with repetitive blows to the head in career boxing — which causes dementia and Parkinson’s symptoms (Pugilistica parkinsonism) ; Example: Muhammed Ali
28
Q

What is chronic traumatic encephalopathy?

Who is at risk for it?

What are the potential symptoms?

A

RECURRENT TBI (OR SECOND IMPACT SYNDROME) AKA CHRONIC TRAUMATIC ENCEPHALOPATHY (CTE)

can occur in football, hockey players, etc and can cause Chronic Traumatic Encephalopathy (CTE): this is neuronal degeneration after mild but repetitive brain injury. Many neurological symptoms can occur ranging from emotional changes (aggression, depression, suicide and suicidal thoughts, apathy), sleep disturbance, balance problems, etc.

29
Q

Presence of the _____ allele increases tendency for development of dementia/Alzheimer’s Disease and associated neuropathology

A

Presence of the Apo E allele (epsilon 4) increases tendency for development of dementia/Alzheimer’s Disease and associated neuropathology

30
Q

How is TBI treated initially? What is the most important aspect of treatment?

A

Initial Treatment of TBI

Most Important Aspect of treatment is to manage increased ICP. A device may be placed surgically in the cranial cavity to monitor ICP.

  1. Intubation and mechanical ventilation to support breathing and help keep ICP down.
  2. If signs of brain herniation exist, mannitol or other hyperosmolar diuretic given to draw fluid out of brain.
  3. If bleeding present in cranial cavity (lesion with mass effect on CT scan), surgical decompression (Decompressive craniectomy where a portion of the skull is removed), removal or drainage.
  4. In severe cases (extensive swelling and damaged brain tissue), portion of brain may be surgically removed making room for viable tissue.
  5. Hypothermia: reduce O2 demands of brain
  6. Sedatives and Paralytics to place patient in a drug-induced coma: used to minimize agitation/secondary injury and reduce O2 demand of brain.
  7. Ventriculostomy (aka external ventricular drain): catheter placed into the ventricles to drain (CSF) externally.
  8. In an open head injury skull fractures may need to be repaired and damaged tissue removed.
  9. Head up position at all times
31
Q

What is the overall goal of surgical treatment?

Ventriculostomy or external ventricular drain (EVD) may be placed to alleviate what kind of hydrocephalus? (in the context of TBIs)

A
  1. The overall goal of all surgical treatment is to prevent secondary injury by helping to maintain blood flow and oxygen to the brain and minimize swelling and increased ICP.
  2. A ventriculostomy or external ventricular drain (EVD) or ventricular catheter, is placed into the ventricles, to drain (CSF) externally. This would relieve the external (communicating) hydrocepahlus: CSF cannot flow out through arachnoid granulations due to increased ICP
32
Q

Potential Effects of Severe TBI

  • extended period of unconsciousness (coma)
  • amnesia after the injury.
  • almost half (43%) have a related disability one year after the injury.

Wide range of short- or long-term issues affecting:

  • Cognitive Function (e.g., attention and memory)
  • Motor function (e.g., extremity weakness, spasticity, impaired coordination and balance)
  • Sensation (e.g., hearing, vision, impaired perception and touch)
  • Emotion (e.g., depression, anxiety, aggression, impulse control, personality changes)

Approximately 5.3 million Americans are living with a TBI-related disability; consequences of severe TBI can affect all aspects of an individual’s life (relationships with family and friends, ability to work, do household tasks, drive, and/or participate in other ADLs).

A
33
Q

What does treatment of medically stable patients post TBI consist of?

A

Inpatient/Outpatient Rehabilitation (Physical Medicine and Rehab, OT, PT, Speech and Language therapies, Cognitive therapies, etc)