Neuro Module 2 Flashcards
(89 cards)
1
Q
Define stroke
A
-Interruption in blood flow to CNS
“Brain attack”
2
Q
Hemorrhagic vs. ischemic stroke
A
- Less common than ischemic
- Some debate over how many cases of stroke are hemorrhagic
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
4
Q
Pathology of hemorrhagic stroke
A
- Primary destruction of neurons from hemorrhage
- Secondary destruction from potential rise in ICP
- Hematoma expands creating pressure
5
Q
Causes of hemorrhagic stroke
A
- HTN (small vessel bleeding)
- Anticoag or bleeding disorders
- Cocaine use
6
Q
How does cocaine cause hemorrhagic stroke?
A
- Causes vasoconstriction and elevates BP
- Constriction alone may occlude BV
7
Q
Common locations of hemorrhagic stroke:
A
Smaller blood vessels of:
- Thalamus
- Putamen (basal ganglia)
- Cerebellum
- Brainstem
8
Q
Which type of stroke is MC?
A
Ischemic
9
Q
What causes an ischemic stroke?
A
- Extracranial embolism
- Intracranial thrombus
10
Q
Where do most extracranial emboli of ischemic stroke arise?
A
Heart
11
Q
Where do most intracranial thrombus of ischemic stroke arise?
A
- Cerebral branches of Circle of Willis
- ICA
- Small vessels of posterior circulation
12
Q
What is the goal of ischemic stroke treatment?
A
Get blood flowing ASAP via thrombolytic treatment
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
14
Q
What is the primary site of irreversible necrosis in ischemic stroke?
A
Neuron
15
Q
In ischemic stroke, how does ischemia trigger cascade of events to cell death?
A
Ischemia causes failure of Na/K pump
16
Q
How long does it take for cell necrosis to begin in ischemic stroke?
A
20 minutes
17
Q
Steps of irreversible necrosis in ischemic stroke
A
- Neuron depolarized causing influx of Ca/ion channel dysfunction
- Ca influx leads to release of degradative enzymes
- Neuron cell membrane destroyed, releasing more substances to perpetuate inflammation/cell necrosis
18
Q
What is the secondary site of reversible damage in ischemic stroke?
A
Penumbra (shadow surrounding primary site of necrosis)
19
Q
Within what time period can the ischemic penumbra be attacked by cascade of necrosis?
A
Within hours
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
21
Q
How long do neuro symptoms last in TIAs?
A
Less than 1 hour (minutes)
22
Q
Where does the Circle of Willis receive blood from?
A
ICA and vertebral/basilar arteries
23
Q
Functions of Circle of Willis
A
- Origin of major brain BVs
- Anastomosis pathways
- Small perforating arteries
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
25
What does the anterior cerebral artery supply?
Medial (sagittal) regions of each hemisphere
26
Motor and sensory of ACA?
- Medial motor and sensory strips
| - Lower body
27
Motor effects of ACA infarction
- Lower extremity contralateral hemiparesis
- Urinary incontinence
- Possible motor disorders a/w basal ganglia
28
Sensory effects of ACA infarction
Lower extremity contralateral hemiparesthesia (abnormal sensation) OR hemianesthesia (loss of sensation)
29
Define akinetic mutism and how it occurs
- 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
30
What does the middle cerebral artery supply?
Lateral aspect of each hemisphere
31
Motor and sensory areas of MCA
- Lateral motor and sensory strips
- Trunk and upper extremities
- Portion of optic tract (potential visual changes possible!)
32
Possible effects of MCA infarction
Depends on location
- Major trunk occlusion = everything involved w/MCA
- Superior branches = global/Broca's aphasia
- Inferior branches = Wernicke's and visual hemianopsia
33
What are the classic MCA infarct signs/symptoms and where does this infarct occur?
- Global/Broca's aphasia
| - Occurs w/infarct in the MCA's superior branches
34
Describe hemisphere loss with MCA infarction
Dominant and non-dominant loss
35
Motor changes a/w MCA infarct
- Contralateral hemiparesis or hemiplegia (lower extremity is spared!)
- Conjugate gaze (horizontal, eyes deviate toward side of lesion)
- Apraxia (MC w/dominant infarct)
36
What parts of the body are spared by an MCA infarct?
Lower extremity
37
When is apraxia MC seen in MCA infarct?
Dominant hemisphere loss
38
What is the MC form of apraxia?
Ideomotor (inability to perform steps in voluntary movement)
39
Sensory changes with MCA infarct
- Contralateral hemiparesthesia or hemianesthesia
- Contralateral astereoagnosis
- Hemianopsia
40
What is astereoagnosis?
Inability to interpret object by touch
41
Dominant hemisphere loss with MCA infarct consists of:
- 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
Non-dominant hemisphere loss with MCA infarct consists of:
- 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
What does the posterior cerebral artery supply?
- Occipital lobe
| - Inferior regions of temporal lobe
44
What changes occur with PCA infarct?
- 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
What is the internal capsule?
- Subcortical region
| - Pathway of myelinated axons leaving and entering cerebral cortex
46
Define acute concussion
Transient impairment of neurologic function that resolves spontaneously
47
Difference between acute concussion and mild TBI?
- Acute concussion: functional disturbance
| - Mild TBI: structural injury
48
Clinical symptoms of acute concussion
- May or may NOT involve loss of consciousness
| - Symptoms resolve in predictable sequential pattern
49
What does imaging of acute concussion show?
NO structural abnormalities
50
Grading of concussions
- Many systems out there
| - Current guidelines do not support universal grading scales
51
Current theories regarding pathophys of acute concussion:
1. Metabolic changes
2. Cerebral BF decrease
3. Transient microscopic damage to individual neurons (from mechanical forces on the cells)
52
Current guidelines on return to play after acute concussion:
NO same day return to play
53
Describe the risk of post-concussion syndrome
Severity of immediate acute symptoms is NOT correlated with risk of post-concussion syndrome
54
What are the risk factors for post-concussion syndrome?
- Female
| - Older age
55
Describe second impact syndrome
- 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
Describe chronic traumatic encephalopathy
- Complication of concussion
- Progressive neurodegenerative a/w repeated brain trauma
- Often not found until after death
57
Complications of concussion
- Second impact syndrome
- Chronic traumatic encephalopathy
- Depression
- Mild cognitive impairments
58
Describe traumatic brain injury
- 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
Who is affected by TBI?
Young males
60
What defines the severity of a TBI?
Glasgow coma scale
61
What is the Glasgow Coma scale?
- 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
What is the Rancho Los Amigos scale?
- Levels of cognitive functioning
- Measures awareness, cognition, behavior and interaction with the environment
- Level 1 is unresponsive
- Level 10 appropriate responses
63
What is the leading cause of TBI?
MVA
64
What are the types of "tissue strain" in the brain?
- Compressive
- Tensile
- Shearing
65
Mechanisms of injury for TBI
1. Impact loading
2. Impulsive loading
3. Static or quasistatic loading
66
Describe impact loading of TBI
- A mechanism of injury
- Head collides with object
- Speed is contributing factor
- e.g. MVA hitting windshield
67
Describe impulsive loading of TBI
- A mechanism of injury
- Sudden acceleration/deceleration WITHOUT significant physical contact
- e.g. MVA but head doesn't hit anything
68
Describe static or quasistatic loading of TBI
- A mechanism of injury
- Mechanical loading on brain but speed isn't a factor
- Squeezing or slow crush injury
69
Primary injury vs secondary injury TBI
- Primary: direct gross tissue damage
| - Secondary: cellular damage that occurs from immune/inflammation response to initial injury
70
Define intracranial hemorrhage
- Vascular rupture
| - Different potential regions of vascular disruption
71
Types of intracranial hemorrhage
- Epidural
- Subdural (MC)
- Subarachnoid (release of blood into CSF)
- Intracerebral
72
What is the MC type of intracranial hemorrhage?
Subdural (60-80% of TBIs)
73
Describe coup and contrecoup contusions
- 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
What can be a/w shaken baby syndrome?
Coup and contrecoup contusions (combo of vascular and tissue damage)
75
Describe diffuse axonal injury
- Extensive tensile damage to white matter of brain
- Axons are stretched and damaged
- Grades 1-3
76
What is the onset of secondary injury of TBI?
Acute or gradual (hours to days) after initial injury
77
Physiology of secondary TBI injury
- Excitatory NT (amino acids) released from damaged neurons
| - Resulting in inflammation, swelling, altered neuronal cell membrane function, cell death
78
Effects of sympathetic, parasympathetic, cytokines in secondary TBI injury
- Sympathetic: excessive activity leading to further cell death
- Parasympathetic: behavior suppression/LOC
- Cytokines: lead to cell death
79
Elevated ICP in secondary TBI injury can lead to:
- Cerebral hypoxia, ischemia, edema
- Hydrocephalus
- Brain herniation
80
Describe Alzheimer's disease
- Severe cerebral cortex atrophy (widened sulci and shrinkage of gyri)
- Occiptal pole often spared
- MC form of dementia
81
What parts of the cerebral cortex are involved in Alzheimer's?
Mostly every part, but occipital pole is often spared
82
Primary functional CNS loss of Alzheimer's
Loss of dendrite size and synapses
83
Describe neuritic plaques and neurofibrillary tangles
- Classic pathological findings in Alzheimer's
| - Found in other diseases as well as normally
84
What are neuritic plaques?
- Spherical accumulation of amyloid surrounded by degenerating or dystrophic nerve endings (neurites)
- Found in Alzheimer's
85
What are neurofibrillary tangles?
- Intracellular protein tangles that disrupt normal cytoskeletal architecture (causing neuronal cell death)
- Found in Alzheimer's and CTE
86
What is amyloid?
Fibrous protein deposits
87
What is amyloid angiopathy?
- Amyloid deposition in walls of small to medium cortical and leptomeningeal arteries
- A/w Alzheimer's and can be cause of lacunar stroke
88
Where is the internal capsule located?
Located between thalamus and basal ganglia
89
What is the internal capsule supplied by?
Small perforating arteries
