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Neuro Mod 2 Flashcards

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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
If MCA has infarct of superior branches (lateral frontal/parietal lobes) what is result?
Global/Broca's aphasia & most classic MCA signs/symptoms
26
If MCA has infarct of inferior branches (lateral temporal and inferior parietal lobes) what is result?
Wernicke's and visual hemianopsia
27
What are the motor changes with MCA infarct? (3)
contralateral hemiparesis or hemiplegia (area 4 and 6) conjugate gaze (horizontal) Apraxia (inability to perform purposeful voluntary movement)
28
What two body locations are affected in MCA infarct with contralateral hemplegia?
lower face/trunk and UE | LE is spared
29
What happens with conjugate gaze in MCA infarct? (2)
eyes deviate toward side of lesion | normal: area 8 provides conjugate gaze toward opposite side (CN6 an CN3 control)
30
What is the apraxia that occurs with MCA infarct?
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)
31
What sensory changes are seen with MCA infarct?
``` 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) ```
32
What are the potential behavioral/personalities changes with MCA infarct?
apathy, poor motivation perseverance social inappropriateness
33
What is result of dominant hemisphere loss with MCA infarction?
Apraxia | Language/communication loss - aphasia (Broca's aphasia, Wernicke's aphasia, global aphasia)
34
What is Broca's aphasia?
comprehend but cant speak area 44, 45
35
What is Wernicke's aphasia
speak but cant comprehend - word salad area 22
36
What is global aphasia?
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
37
What defects result in non-dominant hemisphere loss with MCA infarction?
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
38
What is dressing apraxia?
not actual motor are but occurs because of inability to connect motor to purpose/meaning
39
what is motor dysprosodia?
difficulty of speech in producing the normal pitch rhythm and variation of stress/tone (musical aspects of speech)
40
What is sensory dysprosodia?
difficulty of speech in interpreting the normal pitch, rhythm, and variation of stress/tone in speech (musical aspects of speech)
41
What is the confusion seen in non-dominant hemisphere loss with MCA infarction?
non-dominant hemisphere plays a role in familiarity, memory of environment/people, distinguishing stimuli, lost in familiar surroundings, recognizing people
42
What does the PCA (posterior cerebral artery) supply?
occipital lobe | inferior regions of temporal lobe
43
What is extinction?
inability to focus of 2 stimuli - usually cant focus on physical left side of stimuli
44
What is result in infarction of PCA?
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
What is visual agnosia?
inability to recognize an object by sight | lesion in secondary visual cortex of occipital lobe (areas 18,19)
46
What is prosopagnosia?
difficulty recognizing familiar faces | occipital lobe secondary area, association areas temporal/parietal lobes
47
Alexia?
cannot read
48
What regions do the perforating arteries occur in?
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
Acute Concussion
transient impairment of neurologic function that resolves spontaneously
50
Clinical symptoms of Acute concussion?
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
What is seen in neurological imaging for acute concussion?
no structural abnormalities are demonstrated in standard neurological imaging studies
52
Current pathophy on concussions?
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
What are the common physical symptoms of concussion?
``` 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
What are the thinking/remembering symptoms of concussion?
difficulty thinking clearly, feeling slowed down, difficulty concentrating, difficulty remembering new information
55
What are the current consensus guideline for same day RTP?
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
Post same day RTP criteria at rest?
asymptomatic complete neuro eval - return to baseline IMPACT scores return to baseline
57
Post same day RTP criteria during exertion (includes both physical and cognitive)
asymptomatic complete neuro eval - return to baseline progressive physical exercise testing - recommend before RTP clearance aerobic and resistance exercise progression tests
58
What are pre and post injury IMPACT scores?
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
What are some possible complications of a concussion?
``` 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
What is post concussion syndrome?
recovery/symptoms persist >3months longer recovery =considered more severe concussion increased risk of other concussion complications
61
What is second impact syndrome?
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
What is chronic traumatic encephalopathy?
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
What are mild cognitive impairments seen possible complications of concussion?
similar onset later in life pattern to chronic traumatic encephalopathy multiple concussions increase the risk
64
Epidemiology for TBI
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
What are the 2 classification systems utilized in assessment of TBI?
Glasgow Coma Scale | The Ranchos Los Amigos Scale
66
What is the Glasgow Coma Scale?
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
What are the mild, moderate and severe ranges for the Glasgow Coma scale?
mild 13-15 moderate 9-12 severe 3-8
68
What is the Ranchos Los Amigos Scale?
measures the levels of awareness, cognition. behavior and interactions with the environment eight levels of classification
69
Ranges for the Ranchos Los Amigos Scale?
level 1-unresponsive | level 8 purposeful and appropriate responses
70
What are the mechanisms of injury for TBI? (4)
alcohol often involved MVA - leading cause Falls - second most leading cause - elderly pop at risk firearms
71
3 types of brain damage associated with TBI?
compressive tensile shearing
72
What are the 3 physical categories of mechanism of injury for TBI?
impact loading impulsive loading static or quasi-static loading
73
What are impact, static and impulsive loading?
(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
What are some types of primary injury for TBI?
``` skull fracture intracranial hemorrhage coup and contrecoup contusions diffuse axonal injury auditory/vestibular dysfunction penetrating injury - gunshot or missile objects ```
75
What is an intracranial hemorrhage?
vascular rupture
76
What are the different potential regions of vascular disruption?
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
What are coup and contrecoup contusions?
combination of vascular and tissue damage | shaken baby syndrome
78
What are the individual definitions of coup and countrecoup?
2. coup = injury at site of direct impact 3. 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
What is diffuse axonal injury
extensive tensile damage to the white matter of the brain | axons literally stretched and damaged - cant function
80
What are the 3 grades of axonal damage with TBI?
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
What can lead to auditory/vestibular dysfunction in TBI?
damage in temporal bone area may lead to fracture or impact damage
82
What is the 3 physiological processed that occur with secondary injury in TBI?
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
What is amyloid angiopathy?
amyloid deposition in the walls of the small to medium sized cortical and leptomeningeal arteries potential ischemia/hemorrhage in affected areas
84
What are neurofibrillary tangles?
intracellular protein deposits that cause disruption of the normal cytoskeletal architecture with subsequent neuronal cell death
85
What are neuritic plaques?
spherical accumulation of amyloid (fibrous protein) surrounded by degenerating or dystrophic nerve endings (neuritis)
86
What are the classis pathological findings in AD?
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
What is the cellular pathology of AD?
loss and shrinkage of neurons | loss of dendrite size and synapses thought to be primary functional CNS loss
88
In most cases of AD every part of the cerebral cortex is involved except what?
occipital pole is often spared
89
What are the symptoms of moderate/severe TBI?
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
What are the symptoms of mild TBI?
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
What can ICP lead to in second injury of TBI?
cerebral hypoxia, ischemia and edema hydrocephalus brain herniation - various types depending on the structure involved
92
How do cytokines lead to further CNS cellular damage in second injury of TBI?
contribute to inflammatory cascades leading to cell death
93
How does the parasympathetic lead to further CNS cellular damage in second injury of TBI?
behavior suppression/LOC from parasympathetic influence brainstem
94
How does the sympathetic lead to further CNS cellular damage in second injury of TBI?
increase in cell metabolism from excessive sympathetic release leads to further cell death
95
What is the result of excitatory neurotransmitter release from damaged neurons in second injury of TBI?
inflammation, swelling altered neuronal cell membrane function cell death

Patho- Neuro (5 decks)

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