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Pathophys II MHM - Exam 3 > Neuro Module 2 > Flashcards

Neuro Module 2 Flashcards

1
Q

Define stroke

A

-Interruption in blood flow to CNS

“Brain attack”

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2
Q

Hemorrhagic vs. ischemic stroke

A
  • Less common than ischemic

- Some debate over how many cases of stroke are hemorrhagic

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3
Q

Why is there a debate over how many cases of stroke are hemorrhagic?

A

Unsure whether we’re seeing increases because of improved CT imaging or increased anticoagulant

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4
Q

Pathology of hemorrhagic stroke

A
  • Primary destruction of neurons from hemorrhage
  • Secondary destruction from potential rise in ICP
  • Hematoma expands creating pressure
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5
Q

Causes of hemorrhagic stroke

A
  • HTN (small vessel bleeding)
  • Anticoag or bleeding disorders
  • Cocaine use
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6
Q

How does cocaine cause hemorrhagic stroke?

A
  • Causes vasoconstriction and elevates BP

- Constriction alone may occlude BV

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7
Q

Common locations of hemorrhagic stroke:

A

Smaller blood vessels of:

  • Thalamus
  • Putamen (basal ganglia)
  • Cerebellum
  • Brainstem
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8
Q

Which type of stroke is MC?

A

Ischemic

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9
Q

What causes an ischemic stroke?

A
  • Extracranial embolism

- Intracranial thrombus

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10
Q

Where do most extracranial emboli of ischemic stroke arise?

A

Heart

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11
Q

Where do most intracranial thrombus of ischemic stroke arise?

A
  • Cerebral branches of Circle of Willis
  • ICA
  • Small vessels of posterior circulation
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12
Q

What is the goal of ischemic stroke treatment?

A

Get blood flowing ASAP via thrombolytic treatment

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13
Q

What is the window of time for treating ischemic stroke?

A
  • Initial research says less than 3 hrs

- Recent research says 4.5 hrs

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14
Q

What is the primary site of irreversible necrosis in ischemic stroke?

A

Neuron

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15
Q

In ischemic stroke, how does ischemia trigger cascade of events to cell death?

A

Ischemia causes failure of Na/K pump

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16
Q

How long does it take for cell necrosis to begin in ischemic stroke?

A

20 minutes

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17
Q

Steps of irreversible necrosis in ischemic stroke

A
  1. Neuron depolarized causing influx of Ca/ion channel dysfunction
  2. Ca influx leads to release of degradative enzymes
  3. Neuron cell membrane destroyed, releasing more substances to perpetuate inflammation/cell necrosis
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18
Q

What is the secondary site of reversible damage in ischemic stroke?

A

Penumbra (shadow surrounding primary site of necrosis)

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19
Q

Within what time period can the ischemic penumbra be attacked by cascade of necrosis?

A

Within hours

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20
Q

Define TIA and what causes it

A
  • Transient ischemic attack
  • Temporary loss of blood flow
  • Neuro deficits resolve within 24 hours
  • Caused by athero, emboli, arterial dissection, cocaine, etc.
  • Increases risk of stroke
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21
Q

How long do neuro symptoms last in TIAs?

A

Less than 1 hour (minutes)

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22
Q

Where does the Circle of Willis receive blood from?

A

ICA and vertebral/basilar arteries

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23
Q

Functions of Circle of Willis

A
  • Origin of major brain BVs
  • Anastomosis pathways
  • Small perforating arteries
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24
Q

What are the small perforating arteries?

A
  • Group of BVs that contribute to subcortical regions of brain
  • Regions are: diencephalon, internal capsule, pons, cerebellum
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25
Q

What does the anterior cerebral artery supply?

A

Medial (sagittal) regions of each hemisphere

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26
Q

Motor and sensory of ACA?

A
  • Medial motor and sensory strips

- Lower body

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27
Q

Motor effects of ACA infarction

A
  • Lower extremity contralateral hemiparesis
  • Urinary incontinence
  • Possible motor disorders a/w basal ganglia
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28
Q

Sensory effects of ACA infarction

A

Lower extremity contralateral hemiparesthesia (abnormal sensation) OR hemianesthesia (loss of sensation)

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29
Q

Define akinetic mutism and how it occurs

A
  • Damage to frontal lobe
  • Conscious alert pt who retains ability to move/speak but fails to do so
  • Damaged pathways inhibit motivation/increase apathy causing passiveness to interact or respond
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30
Q

What does the middle cerebral artery supply?

A

Lateral aspect of each hemisphere

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31
Q

Motor and sensory areas of MCA

A
  • Lateral motor and sensory strips
  • Trunk and upper extremities
  • Portion of optic tract (potential visual changes possible!)
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32
Q

Possible effects of MCA infarction

A

Depends on location

  • Major trunk occlusion = everything involved w/MCA
  • Superior branches = global/Broca’s aphasia
  • Inferior branches = Wernicke’s and visual hemianopsia
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33
Q

What are the classic MCA infarct signs/symptoms and where does this infarct occur?

A
  • Global/Broca’s aphasia

- Occurs w/infarct in the MCA’s superior branches

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34
Q

Describe hemisphere loss with MCA infarction

A

Dominant and non-dominant loss

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35
Q

Motor changes a/w MCA infarct

A
  • Contralateral hemiparesis or hemiplegia (lower extremity is spared!)
  • Conjugate gaze (horizontal, eyes deviate toward side of lesion)
  • Apraxia (MC w/dominant infarct)
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36
Q

What parts of the body are spared by an MCA infarct?

A

Lower extremity

37
Q

When is apraxia MC seen in MCA infarct?

A

Dominant hemisphere loss

38
Q

What is the MC form of apraxia?

A

Ideomotor (inability to perform steps in voluntary movement)

39
Q

Sensory changes with MCA infarct

A
  • Contralateral hemiparesthesia or hemianesthesia
  • Contralateral astereoagnosis
  • Hemianopsia
40
Q

What is astereoagnosis?

A

Inability to interpret object by touch

41
Q

Dominant hemisphere loss with MCA infarct consists of:

A
  • Apraxia
  • Broca’s aphasia (comprehends but can’t speak - area 44, 45)
  • Wernicke’s aphasia (speaks but can’t comprehend - area 22)
  • Global aphasia (involves both parietal/temporal and frontal lobes)
42
Q

Non-dominant hemisphere loss with MCA infarct consists of:

A
  • Anosognosia (neglect)
  • Construct apraxia
  • Dressing apraxia
  • Motor/sensory dysprosodia (“musical” aspects of speech)
  • Confusion
  • Extinction (inability to focus on 2 stimuli)
  • Unintentional fabrication of info
43
Q

What does the posterior cerebral artery supply?

A
  • Occipital lobe

- Inferior regions of temporal lobe

44
Q

What changes occur with PCA infarct?

A
  • Hemianopsia (visual field contralateral to lesion)
  • Visual agnosia (inability to recognize an object)
  • Prosopagnosia (difficulty recognizing familiar faces)
  • Alexia (can’t read)
  • Possible memory impairments
45
Q

What is the internal capsule?

A
  • Subcortical region

- Pathway of myelinated axons leaving and entering cerebral cortex

46
Q

Define acute concussion

A

Transient impairment of neurologic function that resolves spontaneously

47
Q

Difference between acute concussion and mild TBI?

A
  • Acute concussion: functional disturbance

- Mild TBI: structural injury

48
Q

Clinical symptoms of acute concussion

A
  • May or may NOT involve loss of consciousness

- Symptoms resolve in predictable sequential pattern

49
Q

What does imaging of acute concussion show?

A

NO structural abnormalities

50
Q

Grading of concussions

A
  • Many systems out there

- Current guidelines do not support universal grading scales

51
Q

Current theories regarding pathophys of acute concussion:

A
  1. Metabolic changes
  2. Cerebral BF decrease
  3. Transient microscopic damage to individual neurons (from mechanical forces on the cells)
52
Q

Current guidelines on return to play after acute concussion:

A

NO same day return to play

53
Q

Describe the risk of post-concussion syndrome

A

Severity of immediate acute symptoms is NOT correlated with risk of post-concussion syndrome

54
Q

What are the risk factors for post-concussion syndrome?

A
  • Female

- Older age

55
Q

Describe second impact syndrome

A
  • Complication of concussion
  • If still symptomatic and allowed to play, increased risk of 2nd impact
  • Bleeding risk and increased ICP due to hematoma
  • Immediate medical emergency
  • Doesn’t matter if 2nd impact is minor
56
Q

Describe chronic traumatic encephalopathy

A
  • Complication of concussion
  • Progressive neurodegenerative a/w repeated brain trauma
  • Often not found until after death
57
Q

Complications of concussion

A
  • Second impact syndrome
  • Chronic traumatic encephalopathy
  • Depression
  • Mild cognitive impairments
58
Q

Describe traumatic brain injury

A
  • Acute trauma induced damage to the brain
  • Complex range of symptoms and management
  • Head injury does NOT mean TBI but is often used interchangeably
59
Q

Who is affected by TBI?

A

Young males

60
Q

What defines the severity of a TBI?

A

Glasgow coma scale

61
Q

What is the Glasgow Coma scale?

A
  • 15 point scale based on overall social capability or dependence on others
  • Describes level of consciousness in a person with TBI
  • Mild is 13-15
  • Severe is 3-8
62
Q

What is the Rancho Los Amigos scale?

A
  • Levels of cognitive functioning
  • Measures awareness, cognition, behavior and interaction with the environment
  • Level 1 is unresponsive
  • Level 10 appropriate responses
63
Q

What is the leading cause of TBI?

A

MVA

64
Q

What are the types of “tissue strain” in the brain?

A
  • Compressive
  • Tensile
  • Shearing
65
Q

Mechanisms of injury for TBI

A
  1. Impact loading
  2. Impulsive loading
  3. Static or quasistatic loading
66
Q

Describe impact loading of TBI

A
  • A mechanism of injury
  • Head collides with object
  • Speed is contributing factor
  • e.g. MVA hitting windshield
67
Q

Describe impulsive loading of TBI

A
  • A mechanism of injury
  • Sudden acceleration/deceleration WITHOUT significant physical contact
  • e.g. MVA but head doesn’t hit anything
68
Q

Describe static or quasistatic loading of TBI

A
  • A mechanism of injury
  • Mechanical loading on brain but speed isn’t a factor
  • Squeezing or slow crush injury
69
Q

Primary injury vs secondary injury TBI

A
  • Primary: direct gross tissue damage

- Secondary: cellular damage that occurs from immune/inflammation response to initial injury

70
Q

Define intracranial hemorrhage

A
  • Vascular rupture

- Different potential regions of vascular disruption

71
Q

Types of intracranial hemorrhage

A
  • Epidural
  • Subdural (MC)
  • Subarachnoid (release of blood into CSF)
  • Intracerebral
72
Q

What is the MC type of intracranial hemorrhage?

A

Subdural (60-80% of TBIs)

73
Q

Describe coup and contrecoup contusions

A
  • Primary injury TBI
  • Combo of vascular and tissue damage
  • Coup: injury at site of direct impact
  • Contrecoup: injury at site opposite of direct impact
  • Can be a/w shaken baby syndrome
74
Q

What can be a/w shaken baby syndrome?

A

Coup and contrecoup contusions (combo of vascular and tissue damage)

75
Q

Describe diffuse axonal injury

A
  • Extensive tensile damage to white matter of brain
  • Axons are stretched and damaged
  • Grades 1-3
76
Q

What is the onset of secondary injury of TBI?

A

Acute or gradual (hours to days) after initial injury

77
Q

Physiology of secondary TBI injury

A
  • Excitatory NT (amino acids) released from damaged neurons

- Resulting in inflammation, swelling, altered neuronal cell membrane function, cell death

78
Q

Effects of sympathetic, parasympathetic, cytokines in secondary TBI injury

A
  • Sympathetic: excessive activity leading to further cell death
  • Parasympathetic: behavior suppression/LOC
  • Cytokines: lead to cell death
79
Q

Elevated ICP in secondary TBI injury can lead to:

A
  • Cerebral hypoxia, ischemia, edema
  • Hydrocephalus
  • Brain herniation
80
Q

Describe Alzheimer’s disease

A
  • Severe cerebral cortex atrophy (widened sulci and shrinkage of gyri)
  • Occiptal pole often spared
  • MC form of dementia
81
Q

What parts of the cerebral cortex are involved in Alzheimer’s?

A

Mostly every part, but occipital pole is often spared

82
Q

Primary functional CNS loss of Alzheimer’s

A

Loss of dendrite size and synapses

83
Q

Describe neuritic plaques and neurofibrillary tangles

A
  • Classic pathological findings in Alzheimer’s

- Found in other diseases as well as normally

84
Q

What are neuritic plaques?

A
  • Spherical accumulation of amyloid surrounded by degenerating or dystrophic nerve endings (neurites)
  • Found in Alzheimer’s
85
Q

What are neurofibrillary tangles?

A
  • Intracellular protein tangles that disrupt normal cytoskeletal architecture (causing neuronal cell death)
  • Found in Alzheimer’s and CTE
86
Q

What is amyloid?

A

Fibrous protein deposits

87
Q

What is amyloid angiopathy?

A
  • Amyloid deposition in walls of small to medium cortical and leptomeningeal arteries
  • A/w Alzheimer’s and can be cause of lacunar stroke
88
Q

Where is the internal capsule located?

A

Located between thalamus and basal ganglia

89
Q

What is the internal capsule supplied by?

A

Small perforating arteries

Pathophys II MHM - Exam 3 (5 decks)

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