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Pathophysiology 2 > Exam 3 - Neuro cerebral cortex pathology > Flashcards

Exam 3 - Neuro cerebral cortex pathology Flashcards

1
Q

Where does Intracerebral Hemorrhage occur? Subarachnoid Hemorrhage?

A

IH=Bleeding into brain parenchyma

SH=bleeding into subarachnoid space

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2
Q

What is the primary cause of neuron destruction in Intracerebral Hemorrhage?

A

Hemorrhage directly destroys neurons

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3
Q

What are the secondary causes of neuron destruction in Intracerebral Hemorrhage?

A
  1. Potential rise in intracranial pressure

2. Hematoma expands creating pressure

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4
Q

What 4 areas does an Intracranial Hemmorhage mainly occur?

A
  1. Thalamus
  2. Putamen (part of basal ganglia)
  3. Cerebellum
  4. Brainstem
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5
Q

What are Subarachoid Hemmorhages often related to? What happens to intracranial pressure?

A

Berry Anuerysms. IC pressure rises dangerously.

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6
Q

What does elevated intracranial pressure in a SAH impair?

A

Impairs cerebral autoregulation (vasoconstriction, microvascular constriction, platelet aggregation)

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7
Q

What is the end result of SAH?

A

Loss of blood flow and cerebral ischemia.

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8
Q

What percent of stroke are ischemic?

A

85%

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9
Q

What are the two location locations/types of strokes?

A
  1. Extracranial Embolism

2. Intracranial Thrombus

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10
Q

Extracranial Embolism most often arises from where?

A

Heart (valve, MI, afib, diliated myopathy, CHF, etc)

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11
Q

Intracranial Thrombus mostly arises from what three areas?

A
  1. Circle of Willis cerebral branches
  2. Internal Carotid Artery
  3. Small vessels of posterior circulation
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12
Q

In primary site of ischemic stroke is the damage reversible or irreversible? Secondary site reversible or irreversible?

A

Primary site=irreversible

Secondary site=reversible

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13
Q

What happens to a neuron at the primary site of damage in an Ischemic Stroke?

A

Neuron depolarized causing influx of Ca++ which causes release of degradative enzymes destroying neuron cell membrane and releasing substances to harm neighboring neurons

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14
Q

Secondary site of damage in Ischemic Stroke called what? (Hint: means “shadow”)

A

Penumbra

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15
Q

Two ways to preserve neurons in secondary site of Ischemia Stroke?

A
  1. Restore blood flow ASAP

2. Meds to block inflammation

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16
Q

Time frame which TIA deficits resolve?

A

Neurological deficits resolve within 24h

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17
Q

What percent of TIA patients will experience a future stroke?

A

30%

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18
Q

How percent of TIA patients will experience a stroke within 90 days?

A

10% will have a stroke within 90 days

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19
Q

Which two arteries supply the Circle of Willis?

A

Internal Carotid Artery and Vetebral Artery

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20
Q

The Anterior Cerebral Artery supplies which lobe and areas of brain? Of body? What do the Perforating Arteries supply?

A

Brain=Prefrontal lobe. Motor and sensory areas.
Body=Lower body

Perforating Arteries supply subcortical areas.

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21
Q

What areas make up the Prefrontal Lobe?

A

9-12, 46, 47

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22
Q

Infarction/Occlution of the ACA results on what 3 types of MOTOR deficit and where on the body?

A
  1. Lower extremity contralateral hemiparesis (motor loss)
  2. Urinary incontinence
  3. Parkinson patterns from basal ganglia damage
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23
Q

Infarction/Occlution of the ACA results on what type of sensory deficit and where on the body?

A

Contralateral lower extremity hemiparaesthesia (abnormal feeling) or hemianesthesia (no sensation)

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24
Q

Infarction/Occlution of the ACA causing Prefrontal Lobe damage causes what?

A

Personality changes. Apathy, poor motivation, perseveration, social inappropriateness.

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25
Q

Akinetic Mutism is due to infarction/occlusion of which artery?

A

ACA

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26
Q

Which 3 lobes does the Middle Cerebral Artery supply? Which aspect of each hemisphere? What area, lobe, and tract?

A

Frontal, Parietal, and Temporal lobes.
Lateral aspect of each hemisphere.

Association areas, Prefrontal Lobe, part of optic tract.

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27
Q

Infarct/occlusion of MCA Superior Branch and Inferior Branch will affect what?

A

Sup Branch=Brocha’s Aphasia

Inf Branch=Wernicke’s and visual hemianopsia

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28
Q

What is the most classic sign of an MCA infarct/occlusion?

A

Global/Brocha’s Aphasia

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29
Q

What number area is Brocha and Wernicke? On which lobe?

A

Frontal lobe.
Wernicke=22
Brocha=44,45

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30
Q

Superior branches of MCA supply which two lobe parts of brain?

A

Lateral Frontal lobe

Lateral Parietal lobe

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31
Q

Inferior branches of MCA supply which two lobe parts of brain?

A

Lateral Temporal lobe

Inferior Parietal lobe

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32
Q

Which two areas are affected in an MCA infarct/occlusion? Which part of body affected? Which part spared?

A

Contralateral hemiparesis or hemiplegia. Areas 4 and 6.

Lower face/trunk and UE affected. Lower extremity spared.

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33
Q

Which area provides conjugate gaze toward opposite side? Which two CNs?

A

Area 8.

CNs 3 and 6.

34
Q

MCA occlusion/infarct cause eyes to deviate toward or away from lesion?

A

Toward lesion

35
Q

Define Apraxia? Dominant or non-dominant? Occurs from infarct/occlusion of which artery? Which area on which lobe?

A

Inability to preform purposeful voluntary movements. MCA infarct/occlusion on Dominant Hemisphere.

Area 6, frontal lobe.

36
Q

Define Hemianopia. Happens with infarct/occlusion of which artery?

A

Loss of half of visual field. MCA infarct/occlusion.

37
Q

Brocha’s Aphasia and Wernicke’s Aphasia occurs when the dominant or non-dominant hemisphere is damaged?

38
Q

Brocha’s Aphasia on which areas and which artery?

A

44, 45. MCA.

39
Q

Wernicke’s Aphasia from which area and which artery?

40
Q

These occur from loss of which hemisphere and which artery occlusion/infart? Agnosia, Construct Apraxia, Dressing Apraxia, Dysprosodia (motor and sensory), Confusion, Extinction

A

Nondominant hemisphere, MCA.

41
Q

Define: Agnosia, Construct Apraxia, Dressing Apraxia

A

Anosognosia=neglect, denial of injury, won’t turn head to contralateral side

Construct Apraxia=can’t draw a clock, etc

Dressing Apraxia=Can’t connect motor to purpose/meaning

42
Q

Define: Dysprosodia (motor and sensory), Confusion, Extinction

A

Motor Dysprosodia=can’t produce right pitch to speech
Sensory Dysprosodia=can’t interpret tone/pitch/meaning of speech
Confusion=lack of familiarity, feeling list
Extinction=Can’t focus on 2 stimuli, usually on left

43
Q

The PCA (posterior cerebral artery) supplies which lobes? (Hint: does part of one lobe and another full lobe)

A

Occipital Lobe

Inferior regions of Temporal Lobe

44
Q

Infarct/Occlusion of the PCA leads to damage to which areas?

A

17=primary visual area

18,19=visual association area

45
Q

Infarct of Area 17 Primary Visual Area on the Occipital Lobe results in what special type of blindness? Lateral or contralateral to lesion?

A

Hemianopia=loss of vision on same side of both eyes.

Contralateral to lesion.

46
Q

Infarct to Areas 18,19 Visual Association Area results in what three problems?

A
  1. Visual Agnosia=can’t recognize object by sight
  2. Prosopagnosia=difficulty recognizing familiar faces
  3. Alexia=can’t read
47
Q 
Define
1. Visual Agnosia
2. Prosopagnosia
3. Alexia
Associated with damage where? (Lobe and area)
A
  1. Visual Agnosia=can’t recognize object by sight
  2. Prosopagnosia=difficulty recognizing familiar faces
  3. Alexia=can’t read
    Occipital Lobe; Areas 18,19 Visual Association Areas
48
Q

Define Visual Agnosia. Which lobe and area?

A

Occipital Lobe, Area 17 Primary Visual Area

49
Q

What is blood supply to Subcortical Regions? (Hint:5)

A

Small branches of Circle of Willis, ACA, MCA, PCA, and Basilar Arteries

50
Q

What is the term for infarct/occlusion of Subcortical Regions?

A

Lacunar Stroke/Small Vessel Stroke

51
Q

What are the two types of trauma to the Cerebral Cortex?

A
  1. Concussion

2. TBI

52
Q

Concussion and TBI are the two examples of what?

A

Trauma to the Cerebral Cortex

53
Q

Define concussion

A

Impairment of neurologic function that spontaneous resolves.

54
Q

Describe how concussion symptoms resolve over time.

A

Symptoms resolve in a predictable pattern. 7-10 days in 80-90% of PTs

55
Q

What do concussions show in standard imaging?

A

No abnormalities

56
Q

Physical symptoms of concussion include

A

LOC, HA, blurry vision, dizzy, sensitive to light and sound, balance issues, tired or no energy, convulsions

57
Q

Emotional symptoms of concussion include

A

Irritable, sad, more emotional than normal, nervous, anxious

58
Q

Sleep issues with concussion?

A

Sleep more and trouble falling asleep

59
Q

Can a PT return to play on the same day of concussion?

60
Q

What are the three Post-Same Day Return to Play criteria for someone AT REST?

A
  1. Asymptomatic
  2. Baseline neuro eval
  3. IMPACT score returns to baseline
61
Q

What is the time frame for Post-Concussion Syndrome? What does it mean for severity and risk?

A

If symptoms last more than 3 months. Longer recovery=more severe concussion and increased risk for other concussion complications.

62
Q

Define Traumatic Brain Injury (TBI)

A

“Acute trauma-induced damage to brain.” Actual structural damage to brain tissue. (Unlike concussion.)

63
Q

TBI is major cause of death in what age? Highest mortality in which range? MVA TBI death in what range?

A

Major cause of death less than 45 y/o. Highest mortality in 15-24.

MVA TBI death=20-24 y/o

64
Q

How to classify TBI severity?

A

Use GCS within 48h.
Mild=13-15
Moderate=9-12
Severe=3-8

65
Q

In TBI is mental status change or LOC under 30 min, between 30min-6h, or more than 6h what is severity?

A

Mild=MS change or LOC under 30 min
Moderate=MS change or LOC between 30min-6h
Severe=MS change or LOC over 6h

66
Q

All Primary Injuries of TBI can lead to what and is leading cause of death?

67
Q

Three causes/classes of Primary Injury in TBI

A
  1. Trauma/Penetrating
  2. Acceleration-Deceleration
  3. Coup-Countercoup injury
68
Q

Primary Injury of TBI from Trauma/Penetrating aka? Describe.

A

Focal Injury. Direct damage to CNS.

69
Q

Primary Injury of TBI from Acceleration-Deceleration Injury aka? Describe.

A

AKA “Diffuse Injury”. Shear, tensile, and compression strains on CNS. Causes Diffuse Axonal Injury.

70
Q

Define Diffuse Axonal Injury? In Primary or Secondary Injury of TBI?

A

In Primary Injury of TBI. Extensive tensile/stretch damage to white matter which damages axons so they don’t function.

71
Q

Primary Injury of TBI from Coup/Countercoup aka? Describe and define. Example?

A

Combo vascular and tissue damage.
Coup=Injury at direct site of impact
Countercoup=injury at opposite site of direct impact, from inertia

Ex: Shaken Baby Syndrome

72
Q

Four types of Intracranial Hemotoma?

A
  1. Epidural=damage to meningeal and dural arteries/veins
  2. Subdural=damage to subdural veins, 60-80% mortality
  3. Subarachnoid=damage to posterior fossa, blood into CSF
  4. Intracerebral=vessel damage in CNS tissue
73
Q

4 Intracranial Hematoma locations/types: Where damage? Which has highest mortality?

  1. Epidural
  2. Subdural
  3. Subarachnoid
  4. Intracerebral
A
  1. Epidural=damage to meningeal and dural arteries/veins
  2. Subdural=damage to subdural veins, 60-80% mortality
  3. Subarachnoid=damage to posterior fossa, blood into CSF
  4. Intracerebral=vessel damage in CNS tissue
74
Q

Describe Secondary Injury in TBI. What two things are promoted?

A

Primary damaged cells release excitatory neurotransmitters and promote inflammation cascade and increased ICP

75
Q

Alzheimers disease gross findings?

A

Severe atrophy of the cortex. Widened sulci, shrunk gyri. Occipital pole often spared.

76
Q

Alzheimers disease cellular findings? Three specific findings?

A

Loss and shrunk neurons. Neuritic Plaques, Neurofibrillary Tangles, Amyloid Angiopathy.

77
Q

Define Neurofibrillary Tangles

A

Intracellular protein deposits which disrupt normal cytoskeletal architecture and cause cell death.

78
Q

Define Neuritic Plaques

A

Sepherical accumulations of amyloid protein surrounded by degenerative or dystrophic nerve endings (neurites)

79
Q

Define Amyloid Angiopathy

A

Deposit of Amyloid Fibrous Protein in small to mid cortical and leptomeningeal arteries. Causes ischemia and hemmorhage.

80
Q

What is the main cause of demetia today?

A

Alzheimers disease

Pathophysiology 2 (15 decks)

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