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Patho- Neuro > Neuro Mod 2 > Flashcards

Neuro Mod 2 Flashcards

1
Q

3 Pathologies of cerebral cortex

A

Stroke
trauma- concussion
degenerative- alzheimers

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2
Q

What is a stroke?

A

A. Interruption in blood flow to CNS….”brain attack”

  1. medical emergency
  2. 3rd leading cause of death in US
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3
Q

5 common symptoms of a stroke

A
  1. Sudden numbness or weakness of the face, arm or leg (especially on one side of the body)
  2. Sudden confusion, trouble speaking or understanding speech
  3. Sudden trouble seeing in one or both eyes
  4. Sudden trouble walking, dizziness, loss of balance or coordination
  5. Sudden severe headache with no known cause
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4
Q

What is the pathology of hemorrhagic stroke?

A

• Bleeding into brain parenchyma
• Primary destruction of neurons from hemorrhage
• Secondary destruction from potential rise intracranial pressure
(i) Hematoma expands creating pressure

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5
Q

What are 3 causes of injury with hemorrhagic stroke?

A
  • Small vessel bleeding from HTN
  • Anticoagulation therapy
  • Cocaine use
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6
Q

What are the 2 type of thrombus/emboli occlusion?

A

extracranial embolism

intracranial thrombus

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7
Q

What is an extracranial embolism?

A

most arise from heart (valve, MI, afib, dilated myopathy, CHF)

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8
Q

What is an intracranial thrombus

A

cerebral branches of Circle of Willis, internal carotid artery, small vessels of posterior circulation

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9
Q

What is the medical priority with thrombolytic intervention? (2)

A

(i) Window of time (to significantly improve the chances if positive outcome)
1. Initial research: < 3 hour “window of time” to administer thrombolytic
2. More recent efforts: expand window of time to 4.5 hours
a. Protocols limit time when thrombolytic agent can be given (i.e. none after 3 hrs)

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10
Q

What is the pathology of ischemic stroke?

A

cascade of inflammatory events occurs within seconds to minutes
primary site of irreversible necrosis - cellular level:ischemic damage to neuron
secondary site of reversible damage (penumbra=shadow) - within hrs the secondary site can be attacked by cascade of events in primary site

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11
Q

What is the pathology that occurs at the cellular level of ischemic stroke? (4)

A
  1. neuron becomes 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 in the immediate area
  4. within hrs/days - cytokines and other factors are released which promote additional inflammation/cell destruction
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12
Q

What are the goals of treatment with ischemic stroke?

A

preserve neurons in the secondary site by
restoring blood flow as soon as possible
medication to block cascade of inflammation

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13
Q

What are the RF for Stroke?

A 
FH of stroke, heart attack or TIA
Age>55
HTN>140/90
elevated cholesterol/hyperlipidemia total >200
cigarette smoker
DM
obesity - BMI>30
co-existing cardiovascular disease
previous stroke
high levels of homocysteine
use of birth control pills or other hormone therapy
heavy or binge drinking 
use of illicit drugs such as cocaine
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14
Q

What is a TIA?

A

transient ischemic attack
transient loss of blood flow
neuro symptoms usually last <1hr
TIA definitions neuro deficits resolve within 24 hrs

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15
Q

Causes of TIA?

A 
numerous causes
atherosclerosis
emboli
arterial dissection
arteritis
cocaine
other drugs
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16
Q

Circle of Willis receives blood from where?

A

ICA (internal carotid), and VA (vertebral arteries/basilar arteries)

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17
Q

Function of the circle of willis?

A

origin of major blood vessels of the brain
anastomosis pathways
small perforating arteries - a group that contribute to blood supply to the subcortical regions of the brain

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18
Q

What are the subcortical regions of the brain supplied by the small perforating arteries of the circle of willis?

A

diencephalon (thalamus, hypothalamus, subthalamus)
internal capsule - pathway of myelinated axons leaving and entering the cerebral cortex, located between thalamus and basal ganglia
limbic structures (amygdale, hippocampus)
pons

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19
Q

What does the anterior cerebral artery supply?

A

medial (sagittal) regions of each hemisphere - motor and sensory areas - lower body (distribution can be observed in homunculus diagram)
small perforating arteries - portions of sub-cortical structures (internal capsule and basal ganglia)

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20
Q

What happens with motor function if infarction of ACA?

A

lower extremity contralateral hemiparesis (motor loss)
urinary incontinence
possible motor disorders associated with basal ganglia (parkinsons patterns)

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21
Q

What happens with sensory function if infarction of ACA? (2)

A

lower extremity contralateral hemiparaesthesia (abnormal sensation)
hemianesthesia (loss of sensation)

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22
Q

What happens with the behavioral/personality changes (pre-frontal lobe involvement) if infarction of ACA? (3)

A

apathy, poor motivation
perseverance
social inappropriateness

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23
Q

What happens with the akinetic mutism (bilateral damage to frontal lobe) if infarction of ACA?

A

conscious alert pt who retains ability to move/speak but fails to do so
akinesia - lack of movement
mutism - lack of speech
damaged pathways inhibit motivation/increase apathy cause passiveness to interact or respond

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24
Q

What does the middle cerebral artery supply?

A

lateral aspect of each hemisphere (frontal, parietal and temporal lobes)
motor and sensory areas - face, UE and trunk
association areas
prefrontal lobe
MCA supplies portion of optic tract

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25
Q

If MCA has infarct of superior branches (lateral frontal/parietal lobes) what is result?

A

Global/Broca’s aphasia & most classic MCA signs/symptoms

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26
Q

If MCA has infarct of inferior branches (lateral temporal and inferior parietal lobes) what is result?

A

Wernicke’s and visual hemianopsia

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27
Q

What are the motor changes with MCA infarct? (3)

A

contralateral hemiparesis or hemiplegia (area 4 and 6)
conjugate gaze (horizontal)
Apraxia (inability to perform purposeful voluntary movement)

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28
Q

What two body locations are affected in MCA infarct with contralateral hemplegia?

A

lower face/trunk and UE

LE is spared

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29
Q

What happens with conjugate gaze in MCA infarct? (2)

A

eyes deviate toward side of lesion

normal: area 8 provides conjugate gaze toward opposite side (CN6 an CN3 control)

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30
Q

What is the apraxia that occurs with MCA infarct?

A

most common with dominant but may see in non-dominant infarction
pre-motor, motor and sensory association areas
UE apraxia
sensory apraxia (ideational apraxia, conceptual apraxia)

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31
Q

What sensory changes are seen with MCA infarct?

A 
contralateral hemiparaesthesia (abnormal sensation) or hemianesthesia (loss of sensation) - lower face/trunk and UE, LE is spared
Contralateral astereoagnosis -tactile agnosis - inability to judge interpret object by touch
other sensory loss - visual - hemianopia - 1/2 of visual field loss, MCA supplies portion of optic tract - auditory or smell (temporal lobe areas)
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32
Q

What are the potential behavioral/personalities changes with MCA infarct?

A

apathy, poor motivation
perseverance
social inappropriateness

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33
Q

What is result of dominant hemisphere loss with MCA infarction?

A

Apraxia

Language/communication loss - aphasia (Broca’s aphasia, Wernicke’s aphasia, global aphasia)

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34
Q

What is Broca’s aphasia?

A

comprehend but cant speak area 44, 45

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35
Q

What is Wernicke’s aphasia

A

speak but cant comprehend - word salad area 22

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36
Q

What is global aphasia?

A

sensory and motor language loss
combination of fluent (sensory) and non-fluent (motor) aphasia
global damage to dominant hemisphere (massive MCA infarct)-involve both parietal/temporal and frontal lobes

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37
Q

What defects result in non-dominant hemisphere loss with MCA infarction?

A

anosognosia - neglect, denial of injury, wont turn head to contralateral side
construct apraxia - cant draw a clock
dressing apraxia
language/communication loss-dsyprosodia (motor and sensory)
confusion
extinction
unintentional fabrication of information - lack of ability to recognize errors or from memory loss

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38
Q

What is dressing apraxia?

A

not actual motor are but occurs because of inability to connect motor to purpose/meaning

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39
Q

what is motor dysprosodia?

A

difficulty of speech in producing the normal pitch rhythm and variation of stress/tone (musical aspects of speech)

40
Q

What is sensory dysprosodia?

A

difficulty of speech in interpreting the normal pitch, rhythm, and variation of stress/tone in speech (musical aspects of speech)

41
Q

What is the confusion seen in non-dominant hemisphere loss with MCA infarction?

A

non-dominant hemisphere plays a role in familiarity, memory of environment/people, distinguishing stimuli,
lost in familiar surroundings, recognizing people

42
Q

What does the PCA (posterior cerebral artery) supply?

A

occipital lobe

inferior regions of temporal lobe

43
Q

What is extinction?

A

inability to focus of 2 stimuli - usually cant focus on physical left side of stimuli

44
Q

What is result in infarction of PCA?

A

primary area (17) visual changes - blindness
visual association areas (18,19) (visual agnosia, prosopagnosia, alexia)
possible memory impairments (temporal lobe involvement)
small branches of PCA supply some of thalamus and midbrain - potential for sensory or motor symptoms in addition to visual chgs

45
Q

What is visual agnosia?

A

inability to recognize an object by sight

lesion in secondary visual cortex of occipital lobe (areas 18,19)

46
Q

What is prosopagnosia?

A

difficulty recognizing familiar faces

occipital lobe secondary area, association areas temporal/parietal lobes

47
Q

Alexia?

A

cannot read

48
Q

What regions do the perforating arteries occur in?

A

sub cortical regions
diencephalon (thalamus, hypothalamus, subthalamus)
internal capsule - pathway of myelinated axons leaving and entering the cerebral cortex, located between the thalamus and basal ganglia
limbic structures
pons
cerebellum

49
Q

Acute Concussion

A

transient impairment of neurologic function that resolves spontaneously

50
Q

Clinical symptoms of Acute concussion?

A

may or may not involve loss of consciousness
concussion symptoms usually resolve in predictable sequential pattern - small percentage of concussion symptoms do not resolve in typical time frame

51
Q

What is seen in neurological imaging for acute concussion?

A

no structural abnormalities are demonstrated in standard neurological imaging studies

52
Q

Current pathophy on concussions?

A

absence of gross CNS damage - result in functional loss not structural damage
metabolic changes- alterations in intracellular/extracellular glutamate, K and Ca
cerebral blood flow mismatch - relative decrease in cerebral blood flow to meet the altered metabolic demands of the involved neurons
transient microscopic damage to individual neurons - effects of the mechanical forces of the cell

53
Q

What are the common physical symptoms of concussion?

A 
H/A
fuzzy of blurry vision
nausea or vomiting (early on)
dizziness
sensitivity to noise or light
balance problems
feeling tired, having no energy
convulsions
LOC
54
Q

What are the thinking/remembering symptoms of concussion?

A

difficulty thinking clearly, feeling slowed down, difficulty concentrating, difficulty remembering new information

55
Q

What are the current consensus guideline for same day RTP?

A

NO same day RTP if dx of concussion is determined/suspected
regardless if acute symptoms resolve
DONT shake it off and send the kid back in

56
Q

Post same day RTP criteria at rest?

A

asymptomatic
complete neuro eval - return to baseline
IMPACT scores return to baseline

57
Q

Post same day RTP criteria during exertion (includes both physical and cognitive)

A

asymptomatic
complete neuro eval - return to baseline
progressive physical exercise testing - recommend before RTP clearance
aerobic and resistance exercise progression tests

58
Q

What are pre and post injury IMPACT scores?

A

standardized testing tool to compare pre and post injury status
requires training to properly evaluate/analyze the results
assists in establishing return to baseline status

59
Q

What are some possible complications of a concussion?

A 
post-concussion syndrome
post-concussion seizures
second impact syndrome
chronic traumatic encephalopathy
depression - multiple concussions increase risk for post-concussion depression
mild cognitive impairments
60
Q

What is post concussion syndrome?

A

recovery/symptoms persist >3months
longer recovery =considered more severe concussion
increased risk of other concussion complications

61
Q

What is second impact syndrome?

A

if athlete still symptomatic and allowed RTP then increase risk of second impact syndrome
bleeding risk associated with second injury -increased intracranial pressure d/t hematoma
brain injury from increased intracranial pressure

62
Q

What is chronic traumatic encephalopathy?

A

progressive neurodegenerative pathology associated with any form of repeated brain trauma
progress decline of memory, cognitive function, mood, behavior, etc
symptoms may not manifest until long after sport participation (>40-50yo)

63
Q

What are mild cognitive impairments seen possible complications of concussion?

A

similar onset later in life pattern to chronic traumatic encephalopathy
multiple concussions increase the risk

64
Q

Epidemiology for TBI

A

a. Major cause of death in ages < 45
• Highest of TBI mortality in 15 – 24 yrs of age
• MVA associated with TBI is leading cause of death in 20-24 yr olds

b. Highest risk of TBI
• Ages 15 -30
(i) High risk behavior accidents associated with late teens/early twenties
• Male > Female
(i) Males/female incidence of TBI = 2:1
(ii) Male/female mortality rate of TBI = 3.4:1
(iii) Male/female firearms associated risk of TBI = 6:1
(iv) Male/female MVA (motor vehicle accident) = 2.4:1

65
Q

What are the 2 classification systems utilized in assessment of TBI?

A

Glasgow Coma Scale

The Ranchos Los Amigos Scale

66
Q

What is the Glasgow Coma Scale?

A

defines the severity of a TBI (within 48 hours of injury)
is based on 15 pt scale for estimating and categorizing the outcomes of brain injury on the basis of overall social capability or dependence on others

67
Q

What are the mild, moderate and severe ranges for the Glasgow Coma scale?

A

mild 13-15
moderate 9-12
severe 3-8

68
Q

What is the Ranchos Los Amigos Scale?

A

measures the levels of awareness, cognition. behavior and interactions with the environment
eight levels of classification

69
Q

Ranges for the Ranchos Los Amigos Scale?

A

level 1-unresponsive

level 8 purposeful and appropriate responses

70
Q

What are the mechanisms of injury for TBI? (4)

A

alcohol often involved
MVA - leading cause
Falls - second most leading cause - elderly pop at risk
firearms

71
Q

3 types of brain damage associated with TBI?

A

compressive
tensile
shearing

72
Q

What are the 3 physical categories of mechanism of injury for TBI?

A

impact loading
impulsive loading
static or quasi-static loading

73
Q

What are impact, static and impulsive loading?

A

(i) Impact loading
1. head collides with object; speed is contributing factor

(ii) Impulsive loading
1. sudden acceleration/deceleration motion without significant physical contact

(iii) Static or quasi-static loading
1. mechanical loading on brain but speed isn’t a factor

74
Q

What are some types of primary injury for TBI?

A 
skull fracture 
intracranial hemorrhage
coup and contrecoup contusions
diffuse axonal injury
auditory/vestibular dysfunction
penetrating injury - gunshot or missile objects
75
Q

What is an intracranial hemorrhage?

A

vascular rupture

76
Q

What are the different potential regions of vascular disruption?

A

epidural - meningeal arteries, dural arteries/vein, diploic veins from skull bone marrow
subdural - associated with high mortality (60-80%)
subarachnoid hemorrhage - damage causes release of blood into CSF
intracerebral hemorrhage - blood vessels within CNS tissue

77
Q

What are coup and contrecoup contusions?

A

combination of vascular and tissue damage

shaken baby syndrome

78
Q

What are the individual definitions of coup and countrecoup?

A
  1. coup = injury at site of direct impact
  2. contrecoup = injury at site opposite of direct impact
    a. contrecoup damage is most likely from inertia of impact causing collapse or secondary impact injury
79
Q

What is diffuse axonal injury

A

extensive tensile damage to the white matter of the brain

axons literally stretched and damaged - cant function

80
Q

What are the 3 grades of axonal damage with TBI?

A

Grade 1- parasagittal white matter of the cerebral hemispheres
grade 2 - grade 1 + corpus callosum damage
grade 3 - grade 2 + along with a focal lesion in the cerebral peduncle

81
Q

What can lead to auditory/vestibular dysfunction in TBI?

A

damage in temporal bone area may lead to fracture or impact damage

82
Q

What is the 3 physiological processed that occur with secondary injury in TBI?

A
  1. excitatory neurotransmitter (amino acids) release from damaged neurons
  2. excessive sympathetic, parasympathetic, cytokines all lead to further CNS cellular damage
  3. elevated intracranial pressure (ICP)
83
Q

What is amyloid angiopathy?

A

amyloid deposition in the walls of the small to medium sized cortical and leptomeningeal arteries
potential ischemia/hemorrhage in affected areas

84
Q

What are neurofibrillary tangles?

A

intracellular protein deposits that cause disruption of the normal cytoskeletal architecture with subsequent neuronal cell death

85
Q

What are neuritic plaques?

A

spherical accumulation of amyloid (fibrous protein) surrounded by degenerating or dystrophic nerve endings (neuritis)

86
Q

What are the classis pathological findings in AD?

A

Neuritic plaques and neurofibrillary tangles - these are not unique to AD but consistent, found in other degenerative diseases as well as normal findings
amyloid angiopathy

87
Q

What is the cellular pathology of AD?

A

loss and shrinkage of neurons

loss of dendrite size and synapses thought to be primary functional CNS loss

88
Q

In most cases of AD every part of the cerebral cortex is involved except what?

A

occipital pole is often spared

89
Q

What are the symptoms of moderate/severe TBI?

A

may or may not lose consciousness
progressive/persistent H/A, repeated vomiting or nausea, convulsions or seizures, an inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination and increased confusion, restlessness or agitation

90
Q

What are the symptoms of mild TBI?

A

may or may not lose consciousness
H/A confusion, lightheadedness, dizziness, blurred vision changes, ringing in the ears, altered taste, fatigue/lethargy, altered sleep patterns, behavioral/mood changes, and trouble with memory, concentration, attention or thinking

91
Q

What can ICP lead to in second injury of TBI?

A

cerebral hypoxia, ischemia and edema
hydrocephalus
brain herniation - various types depending on the structure involved

92
Q

How do cytokines lead to further CNS cellular damage in second injury of TBI?

A

contribute to inflammatory cascades leading to cell death

93
Q

How does the parasympathetic lead to further CNS cellular damage in second injury of TBI?

A

behavior suppression/LOC from parasympathetic influence brainstem

94
Q

How does the sympathetic lead to further CNS cellular damage in second injury of TBI?

A

increase in cell metabolism from excessive sympathetic release leads to further cell death

95
Q

What is the result of excitatory neurotransmitter release from damaged neurons in second injury of TBI?

A

inflammation, swelling
altered neuronal cell membrane function
cell death

Patho- Neuro (5 decks)

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