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physio exam 3 > Brain injury > Flashcards

Brain injury Flashcards

1
Q

What are the two types of injuries that can occur to the head/brain?

A

Primary/direct injuries and secondary (subsequent injuries)

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2
Q

What is a primary injury?

A

also known as direct injury

- damage caused by impact

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3
Q

What is a secondary injury?

A

occurs because of other factors such as edema, infection, ischemia

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4
Q

What is a mild brain injury?

A

a concussion, may or may not lose concsciousness

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5
Q

What is a moderate brain injury?

A

hemorrhages, edema, cognitive/motor dysfunction

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6
Q

What is a severe brain injury?

A

extensive tissue damage, coma, hematomas

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7
Q

What is the worst brain injury?

A

brain death and persistent vegetative state

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8
Q

What is a stroke?

A

syndrome of acute focal neurologic defecit from a vascular disorder that injures brain tissues

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9
Q

What brain injury is the leading cause of mortality and morbidity?

A

strokes

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10
Q

What is also referred to as a brain attack?

A

a stroke
brain attack = heart attack
*** time is of essence

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11
Q

What are the risk factors of a stroke?

A
  • increases with age, greater in men, african americans
  • heart diseases (hypertension, atrial fibrilation, high cholesterol), sickle cell disease, diabetes
  • substance abuse: alcohol, cocaine, smoking
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12
Q

What are the two types of strokes?

A
  • ischemic stroke

- hemorrhagic stroke

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13
Q

What is the prevalence of an ischemic stroke?

A

it is the most common type of stroke (70-80%)

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14
Q

What happens during an ischemic stroke?

A

the heart pumps blood to the tissues, a blood clot stops the blood supply to the brain causing a decreased amount of oxygen getting to the brain, high cholesterol levels deposit in arteries (can block the artery completely) and then blood doesn’t reach the brain (ischemia)

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15
Q

What is hypoxia?

A

deprivation of oxygen with maintained blood flow

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16
Q

What are ways hypoxia can occur?

A

decrease atmospheric pressure
carbon dioxide poisoning
anemia

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17
Q

What happens if the brain isn’t receiving enough oxygen?

A

the brain is only 2% of the body weight but uses 20% of the oxygen and fuel
If lack of oxygen - mild euphoria or drowsiness, and impaired problem solving skills

*May not be lethal

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18
Q

What is ischemia?

A

reduced/interrupted flow, decrease oxygen, decreased glucose, increase wastes (because the blood isn’t taking the waste from the brain, may be focal (stroke) or global (cardiac arrest)

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19
Q

What can happen during ischemia?

A

It often leads to unconsciousness if it lasts 2-4 minutes

50-75% of the energy by the brain is used to maintain ionic gradients

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20
Q

What are the three ionic gradients effected by ischemia?

A
  • potassium out: hyperexcitability (more K+ oustide cell) of the membrane leads to convulsions
  • sodium accumulates inside: neuronal and interstitial edema leads to cell destruction (because osmolarity is increased)
  • calcium in (i.e. more calcium inside cell): releases NT/enzymes which lead to cell destruction
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21
Q

What if the threshold of injury isn’t reached during an ischemic attack?

A

the damage is reversible if you manage to revive the person rapidly

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22
Q

How can you treat a person with an ischemic stroke?

A

provide oxygen so the metabolic demands decrease, maintain glucose

  • if you cool down the body temperature below normal (32-34 degrees celsius) the brain’s glucose (metabolic requirement) goes down so if the patient goes no longer than four minutes they may be able to be revived
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23
Q

During ischemia there can be an overstimulation of receptors of excitatory amino acids, what does this mean?

A

Gultamate (mostly astrocytes and glial cells) inside of the cell (ICF) has 16X more glutamate than outside, ischemia immobilized transport systems (i.e. no 02, no ATP, carrier molecules don’t work) so glutamate starts leaking out of the cell increasing ECF concentration, glutamate binds to NMDA receptors allowing calcium inside the cell causing a whole cascade of events which will destroy the cells

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24
Q

How can you prevent damage due to glutamate during ischemia?

A

Inhibit excitatory amino acids synthesis/release, block NMDA receptors (glutamate receptors), stabilize membrane potential (lidocaine/barbituates), block enzymes causing cell death

  • a positive feed back cycle - if you block NMDA receptors glutamate can’t act on them so calcium won’t come in
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25
Q

IS survival likely during a hemorrhagic stroke?

A

NO

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26
Q

What are the characteristics of a hemorrhagic stroke?

A
  • fatal, spontaneous hemorrhage in brain tissues
  • occurs suddenly, during activity
  • due to rupture of blood vessels (aneurysms), leading to edema, compression of brain tissue and vasospasm
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27
Q

What are some symptoms of hemorrhagic stroke?

A
  • vomiting
  • headache
  • paralysis
  • sensory and mental changes
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28
Q

What is the progression of a hemorrhagic stroke?

A
  • progresses rapidly to coma and death
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29
Q

What are the manifestations of stroke?

A
  • depends on affected cerebral artery, area supplied (smaller region defecits may be minor, larger region may have larger defecits) and adequacy of collateral circulation (if entire brain is supplied by a few arteries, one artery is blocked so one part of the brain may be effected, others not)
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30
Q

What are the causes of hemorrhagic strokes?

A
  • advancing age
  • hypertension leading to higher blood pressure which may cause an aneurysm
  • arteriovenous malformations, coagulation disorders
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31
Q

What are the three types of deficits that can occur from strokes?

A
  • motor defecits
  • language and speech defecits
  • cognitive deficits
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32
Q

What is motor deficit?

A

weakness/ paralysis on contralateral (opposite side because of the split by the corpus callosum) side (hemiparesis), face, arm, leg

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33
Q

What are language and speech deficits? What are the two types?

A

Dysarthria: imperfect articulation, changes in voice quality/ pitch
Aphasia: inability to communicate spontaneously or to translate thoughts/ideas into meaningful speech

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34
Q

What are cognitive deficits? What are the three types?

A

Memory loss
Hemiinattention/hemineglect: inability to attend to and react to stimuli from other side

Apraxia: impaired ability to carry out learned motor activities
Agnosia: impaired recognition

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35
Q

When a patient (men) undergo a stroke and only shave or wash one side of face, what type of cognitive defecit is this?

A

hemiinattention/hemineglect

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36
Q

What type of cognitive deficit is is when a person forget hows to ride a bike?

A

apraxia

37
Q

What type of cognitive deficit occurs when one cannot recognize their family or friends?

A

agnosia

38
Q

How is a stroke diagnosed?

A

Complete history, physical and neurological exam

  • time of onset, pattern and rapidity of progression, focal symptoms, diseases
  • presence of hemorrhage and ischemia, type of stroke, CT, MRI, PET, SPECT
39
Q

How is a stroke treated?

A

Reperfusion: salvaging brain tissue and minimize long term disability (provide oxygen and glucose)

  • neuroprotectors (limit calcium cascade), hypothermia (decrease metabolic demands)
  • thrombolytic drugs (clot busters): not for hemorrhagic stroke (CT scan) : WHY CT SCAN IS A MUST
40
Q

What are hematomas?

A

vascular injury in brain accompanied with bleeding

41
Q

What are the three major types of hematomas?

A
  • epidural hematoma
  • subdural or subarachnoid hematoma
  • intracerebral hematomas
42
Q

What is an epidural hematoma?

A

Develops between the bones of the skull and dura mater (outermost)
- tear in artery associated with skull fracture, leads to rapid compression of the brain tissues

43
Q

Who are epidural hematomas common in?

A

young people because their dura is not firmly attached

44
Q

What is the process of a epidural hematoma?

A

unconsious -> lucidity (wake up seem normal) -> rapid unconsiousness, ipsilateral (same side) pupil dilation

lucidity doesn’t always occur

45
Q

What is the prognosis or epidural hematomas?

A

good if hematoma is removed before second loss of consciousness, if not immediately removed - deadly

46
Q

What is a subdural hematoma, where does it develop?

A
  • develops between dura mater and arachnoid mater or in CSF filled arachnoid space
  • tearing of small bridging veins that connect surface of cortex to dural sinuses, develops slowly
47
Q

How is a subdural hematoma classified?

A

based on the time it takes for symptoms to appear

48
Q

What is an acute subdural hematoma?

A

within 24 hours: progress rapidly, high mortality rate

49
Q

What is a subacute subdural hematoma?

A

within 2-10 days: improtement -> deterioration

50
Q

What is a chronic subdural hematoma?

A

within weeks: more common in older persons (brain atrophy causes shrinkage from dura which stretches bridging veins)

51
Q

What is an intracerebral hematoma?

A

develops in the brain itself: common in frontal/ temporal lobes, latter dangerous due to secondary herniations

  • may be single/multiple, in association with severe motion during head injury or contusions
52
Q

Who are intracerebral hematomas more common in/

A

older people/alcoholics (fragile blood vessels)

53
Q

What are the signs and symptoms of intracerebral hematomas?

A

depends on size and location

54
Q

What type of hematoma occurs from a motor vehicle accident?

A

intracerebral hematoma

55
Q

How are intracerebral hematomas treated?

A

surgical remooval

56
Q

Why do hematomas lead to problems?

A

increase in intracranial volume/pressure

57
Q

What are the three compartments of the brain?

A

Brain tissue (80%) brain volume - neurons and glial cells

Blood - 10%

CSF - 10%

58
Q

What happens if there is an increase in intracranial volume/ pressure?

A

leads to brain herniation which can cause cell destruction and brain death because there is only so much space in the brain since it is enclosed in the cranium

**the brain can accommodate very small changes - very limited (i.e. change occurs when sneezing)

59
Q

What is a hemorrhagic stroke referred to as?

A

A thunderclap headache because it is sudden sever and explosive
- the blood vessels rupture

think of a blown up balloon - if very small stimulus - pop/explode

vasospasm - can’t transport blood

60
Q

What is a seizure disorder?

A

abnormal behavior (sensory, motor, autonomic) due to electrical discharge from cortical neurons

61
Q

are seizure disorders diseases?

A

no, but they are a symptom of CNS dysfunction: infections, tumors, drug abuse, brain injury, etc

62
Q

what is primary etiology of a seizure disorder?

A

primary/idiopathic etiology - cause cannot be determined

manifest themselves before the age of 20

63
Q

What is secondary etiology of a seizure disorder?

A

Secondary/symptomatic
cause is identifiable (usually from an infection, tumor, drug abuse, etc)

Generally arise after age 20

64
Q

Why do excitatory or inhibitory neuronal transmissions increase or decrease during an epileptic seizure? all postulated

A
  • many ligand gated ion channels (glutamate increase - excitatory. GABA decrease - inhibitory)
  • or NTs, receptors, metabolizing enzymes (too little metabolism of glutamate/ too much metabolism of GABA)
  • Increased - VG ion channels
  • decreased - NT transporters
65
Q

Which of the following could be used as an anti seizure med?

a. GABA agonists (mimic GABA)
b. Glutamate agonists (mimic glutamate)
c. Both

A

A, not b because glutamate is excitatory which worsens seizure disorders

66
Q

What does the NT GABA do during an epileptic seizure?

A

GABA is involved with decreased inhibitory neuronal activity so it reduces the function of inhibiting the seizure

67
Q

What do VG ion channels (Na, Ka and Ca) do during an epileptic seizure?

A

they are involved with increased excitatory neuronal activity , when they are mutated the channels are hyperactive which can decrease the excitation

68
Q

There is a delicate balance of what in the brain?

A

excitatory and inhibitory NTs

69
Q

When the balance of excitatory and inhibitory NTs is disturbed what happens?

A

it brings about an epileptic seizure

70
Q

What happens when there is increased exictatory neruonal activity and decreased inhibitory neuronal activity?

A

Think about a see-saw balance: in both cases the balance shifts towards the excitatory neuronal activity which will lead to generation of seizures

71
Q

What are the two types of seizrues?

A

partial (or focal) seizures and generalized seizures

72
Q

Neurotransmitters are transporters (ex GABA) if the NT transporters are very active in reuptaking the neruotransmitter what happens?

A

will reduce conc. of GABA in they synapse bringing about increased excitation - i.e. reduce inhibitory fnx

73
Q

VG ion channel mutations can lead to hyperactivity of the channels resulting in?

A

increased excitation

74
Q

Where do partial seizures begin?

A

in specific/focal area – localized

75
Q

What is a simple partial seizure

A
  • the manifestations differ in which part of the brain is affected
  • consciousness/responsiveness is not impaired
  • occurs in one hemisphere, symptoms depend on the area
    Think michael jackson dancing
76
Q

What is a complex partial seizure?

A
  • consciousness is impaired, temporal lobe involved
  • begins in one area, may spread to both areas
  • automatisms (picking at clothing), confusion, hallucinations, fear - manifestations
  • hear/smell things that aren’t present
  • impairment of consciousness, affective symptoms (dremy state, blank, vacant expression, deja vu; jamais vu
77
Q

What are secondarily generalized partial seizures?

A
  • focal onset becomes generalized involving deeper structures (thalamus, reticular activating system)
78
Q

Who are generalized seizures generally seen in?

A

young children

79
Q

What part of the brain is affected in a generalized seizure?

A
  • both brain hemispheres are involved at the outset
80
Q

What are the four types of generalized seizures?

A
  • absence seizures
  • atonic seizures
  • myoclonic seizures
  • tonic-clonic seiqures
81
Q

What is an absence seizure?

A

Mostly seen in children, as they grow older they evolve to more complex (atonic, myoclonic, tonic-clonic) or resolve spontaneously

  • generalized non-convulsive epileptic events, disturbances in consciousness
  • blank stare, motionlessness and unresponsiveness
  • automatisms, fluttering eyelids, changes in postural and autonomic tone
82
Q

What are atonic seizures?

A

drop attacks

- sudden loss of muscle tone: jaw drop, drooping of limbs, falling to ground

83
Q

What are myoclonic seizures?

A

brief involuntary muscle contractions: bilateral (both sides) jerkin of muscles of face, trunk or extremities

84
Q

What are tonic-clonic seiqures?

A

Tonic phase: sharp tonic contraction, extremities extended, loss of consciousness, incontinence of bowel/bladder, cyanosis (blue in the face- unable to breathe properly)

Clonic phase: rhythmic bilateral contraction and relaxation of extremities (shaking arms, legs)

Post-ictal phase: unconsciousness regained after reticular activating system begins to function (complete silence in EEG, no activity seems to be going on in patient)

85
Q

What were seizures called when they were first studied?

A

petit mal (absent seizures) an grand mal (tonic seizures)

86
Q

How are seizures diagnosed?

A

history, neurologic exam, CT/MRI, EEF

87
Q

How are seizures treated?

A

protect the patient during seizure, abort seizure activity and treat underlying diseases (i.e. treat secondary disorder first and the seizures might go away)

  • anticonvulsant medications
  • surgical intervention if blood clot forms
88
Q

Is treatment by anticonvulsant medications the same for all types of seizures?

A

No, treatment may vary from one type to another

physio exam 3 (6 decks)

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