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Cerebrovascular Accident

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1. 3 mechanisms of injury that occur in ischemic CVA: 1. local 18. Atherosclerosis: the most common form of vascular disease;
hypoxia associated with accumulation of lipids, fibrous tissue and
2. local hypoglycemia calcium deposits on arterial walls forming plaques that narrow
3. build-up of toxic metabolic waste the lumen, platelets aggregate around the platelets and
2. abulia: abnormal lack of ability to act or make decisions. The produce clots.
sever form is termed akinetic mutism 19. AVM bleeds are often less devastating, why?: The bleeds are
3. ACA supplies: the medial cerebral hemisphere (frontal and primarily into the malformation and only incidentally into the
parietal lobes) and subcortical structures (BG, anterior fornix adjacent brain
and anterior 4/5ths of corpus callosum) 20. basilar artery syndrome can be catestrophic because of::
4. acute signs and symptoms of stroke include:: -numbness bilateral pontine damage leading to Coma, locked-in
and/or weakness of the face, arm, or leg on ONE side syndrome, akinetic mutisms, or tetraplegia
-confusion and slurring of speech 21. Brunnstrom's Stages of Recovery Stage 1: Flaccidity, no
-visual disturbances in one or both eyes movement
-dizziness, gait disturbances, and/or balance/coordination 22. Brunnstrom's Stages of Recovery Stage 2: Min voluntary
dysfunction movement, spasticity begins to develop
-Severe headache (thunder) with no known cause
23. Brunnstrom's Stages of Recovery Stage 3: Voluntary control
5. Aerobic capacity after stroke: Reduced to 50-70% of movement synergies, spasticity peaks
Twice the O2 consumption seen in walking
24. Brunnstrom's Stages of Recovery Stage 4: Mastery of some
6. Agnosia: The inability to recognize familiar objects using one or movement combo outside of the synergies, spasticty begins to
more of the sensory modalities, while often retaining the ability decline
to recognize the same object using other sensory modalities
25. Brunnstrom's Stages of Recovery Stage 5: Difficult
7. Amaurosis Fugax is a frequent accompanying symptoms of: movemebt combo are learned, synergies lose their dominance
internal carotid artery syndrome
26. Brunnstrom's Stages of Recovery Stage 6: Disappearance of
8. Aneuryms acount for 90% of _______: SAH spasticity. coordinated joint movements
9. Aneurysm: Abnormal distension of blood vessels at 27. Brunnstrom's Stages of Recovery Stage 7: Normal movement
bifurcations caused by disease or weakening of the vessel
28. Central PCA syndromes include:: Thalamic pain syndrome
walls
Hemiballism
10. Aneurysm Tx.: Surgical clipping Contralateral hemiplegia from cerebral peduncle involvement
Endovascular coiling
29. Cerebellar hemorrhage: Results in ataxia and vestibulopathy
11. Anosognosia: Severe condition including denial, neglect and
30. Cerebrovascular disease: any disorder in which areas of the
lack of awareness of the presence or severity of one' s
brain transiently or permanently affected by ischemia or
paralysis.
hemorrhage; a disorder in which one or more blood vessels of
Lesion: non-dominant parietal lobe
the brain is/are impaired by a pathologic process
12. Anterior watershed zone: ACA meets MCA (leads to bilateral
31. Cognitive/behavior deficits in (L) CVA: Difficulty with
UE weakness)
processing info in sequential/linear manner
13. Apraxia: Inability to perform particular purposive actions, as a Described as: slower, negative, cautious, uncertain, depressed,
result of brain damage. anxious
14. Apraxia is most often seen in __________ hemisphere lesions. 32. Cognitive/behavior deficits in (R) CVA: Difficulty grasping the
While ataxia-like syndromes are more often seen in _________ whole idea or the overall organization of a pattern or activity
hemisphere lesions.: Left, right Described as: indifferent, quick, impulsive, euphoric, pt.
15. Are CVA's preventable?: Yes! 80% of CVA's are preventable overestimates their ability while minimizing their problems.
16. ___________________ are more common than _________________ in Major Issue: SAFETY!!
bowel and bladder dysfunctions: Constipation/impaction, 33. complete blockage of the internal carotid without adequate
incontinence collateral circulation will result in deficits in both _______ and
17. Ateriovenous malformation (AVM): Masses of abnormal blood ________: MCA and ACA
vessels which appear as a tangle of arteries and veins 34. Constructional Apraxia: Difficulty in recognizing parts to a
High pressure arteries connected to low pressure veins whole secondary to faulty spatial analysis & conceptualization
(instead of through capillaries) of the task.
35. CVA is defined as: a sudden loss of neurological function
resulting from interruption of blood flow to the brain; also
know as stroke/brain attack
36. damage or dying neurons release excessive amounts of 50. __________ given within 12 hours of ischemic CVA has been
_______: glutamate shown to decrease the mortality and morbidity in people
>65 years old: nimodepine (neuroprotective agent)
cells that normally take up this neuro-transmitter are 51. _____________ have a 30% higher incidence of CVA's and up to
compromising causing disturbance of energy 80% greater risk of developing a subsequent stroke: Men (in
metabolism(inability to produce ATP), facilitates entry of Ca2+ comparison to women)
into cells, activated catabolic enzymes that further degrade
the neural structures. this leads to an area of apoptosis and additionally, black men have 50% greater incidence than white
tissue death beyond infarction, usually within 3-4 hours men
(ischemic cascade)
52. Hemorragic CVA: Intracerebral (d/t HTN or cerebral amykiud
37. Depth and Distance Perception: Inaccurate judgment of angiopathy)
direction, distance and depth. SAH (d/t ruptured aneurysm or AVM)
Lesion: non-dominant occipital lobe
53. Hemorrhagic CVA have ________ survivability, but __________
38. Dressing Apraxia: Inability to dress oneself properly owing to functional recovery than ichemic strokes: poorer, better
a disorder in body scheme or spatial relations.
39. Dysarthria: Impairment of speech production due to secondary (Ischemic CVAs have better survivability but poorer functional
damage to CNS or PNS recovery)
Affects respirtation, phonation, articulation and resonance 54. How does recovery form a CVA occur?: Reduction of
40. Dysphagia: Deficits in swallowing due to lesions of CN IX and swelling or edema
X Existence of collateral blood flow
Causes delayed triggering of swallow reflex, decreases Neuroplasticity
pharyngeal peristalsis, decreased lingual control 55. how is the prognosis of thrombic CVA's compared to embolic
41. embolism: obstruction of blood flow secondary to a blood CVA's?: thrombic CVAs have a poorer prognosis
clot that is not inherent to the cerebral vascular system 56. Hyperreflexia, clonus, spasms, weakness, incoordination
42. Emotional liability: Unstable or changeable emotional state, fatigue, pain, are all indicative of ___________________: spacticity
characterized by a pathological rapid change from laughing to 57. Hypoperfusion: Results from systemic hypotension, leading to
weeping with only slight provocation decreased blood flow to the brain
43. Extension synergy LE: Hip extension, adduction*, IR 58. Hypoperfusion can lead to __________________: watershed lesions
Knee extension* where certain areas of the brain do not get sufficent blood
Ankle PF*/IV supply
Toe PF
59. Ideomotor vs Ideational apraxia: Ideomotor: Breakdown
44. Extension syngery UE: Scapular protraction between concept & performance; movement is not possible
Shoulder adduction*/IR upon command but occurs automatically.
Elbow extension
Forearm pronation* Ideational: Failure in the conceptualization of the task;
Wrist/finger flexion purposeful movement is not possible, either automatically or
45. Figure-Ground Discrimination: Inability to visually distinguish on command.
a figure from the background in which it is embedded. 60. if the dominant language hemisphere is affected in ACA
Lesion: non-dominant parietal lobe syndrome, what will you see?: the patient will have abuila
46. Finger Agnosia: Inability to identify the fingers of one's own and a reduction in the rate or complexity of language and
hand; correlates highly with poor dexterity speech
Lesion: parietal lobe of either hemisphere
47. Flexion synergy LE: Hip Flexion*/abd/ER non-dominant side = unilateral neglect
Knee flexion 61. In ACA syndrome, _______________________________ is affected by
Ankle DF/IV paresis and sensory loss: contralateral LE>UE
Toe DF 62. In an MCA occlusion, if the L hemisphere is involved (and it
48. Flexion synergy of UE: Scapular retraction/elevation is language dominant ) is will result in __________________. if the
Shoulder abduction/ER non-dominant (typically the R hemisphere) is involved,
Elbow flexion* especially the parietal lobe, it will result in _________________.:
Forearm supination global aphasia; perceptual deficits (anosognosia, unilateral
Wrist/finger flexion neglect, spatial disorganization)
49. Form Consistency: Inability to perceive or to attend to subtle
differences in form and shape.
Lesion: non-dominant parieto-temporo-occipital region
63. Incidence of Hemorragic CVA: Dramatically increases after 65 78. Oral Apraxia: Subtype of ideomotor apraxia in which
y/o and exponentially with increased age buccofacial muscles cannot produce purposeful movement.
Men > women 79. Pathogenesis of a hemorragic CVA: Hyalinization of blood
Black > white vessels (smooth muscle cells replaced by collagen. Changes
64. Intracerebral Hemorrhage (ICH): Typified by gradual and the permeability of the vessel wall which leads to hardening
steady evolution that occurs over minutes, hours, and days and calcification and therefore loss of elasticity)
(usually sudden onset)
Usually occurs during physical activity in the daytime Accumulation of fats and proteinaceous materal leading to
Severe headache, vomitting and seizures at onset vessel walls that are prone to leak and rupture
65. _________ is most commonly involved in embolic CVAs: MCA 80. PCA supplies:: occipital lobe, medial/inferior temporal lobe,
66. _________ is the primary arterial supply to the medulla and upper brainstem, midbrain, posterior diencephalon and
posterior-inferior cerebellum: vertebral artery thalamus
67. Lacunar CVA: Has characteristics of both ischemic and 81. Peripheral PCA syndromes include:: Transient global amnesia
hemorrhagic CVA Dyslexia without agraphia
Visual symptoms including visual agnosia, cortical blindness,
68. light alcohol consumption can decrease risk of CVA by
contralateral homoymous hemianopsia, prosopagnosia,
decreasing platelet aggregation: this is just a fun fact that i
topographic disorientation
feel is important for you to be reading right now.......go get a
drink......do it for your health. 82. Pontine hemorrhage: Tetraplegia and coma
Very poor prognosis
69. loss of blood flow to the brain leads to:: decreased o2 and
metabolites (glucose), resulting in neuronal dysfunction and 83. Position in space: Inability to perceive & to interpret spatial
cell death; stores of o2 and glucose are used within minutes concepts such as up, down, under, over, in, out, etc.
triggering the onset of neurologic deficits Lesion: non-dominant parietal lobe
84. Posterior watershed zone: PCA meets MCA (leads to cortical
without blood flow, there is also a toxic build-up of metabolic blindness and aphasia)
waste, resulting in additional damage. 85. Primary ICH: A spontaneous bleed due to microvascular
70. MCA occlusion is generally _____ more often than thrombic: disease associated with HTN and/or aging
embolic Rupture of microaneurysms that burst as a result of HTN
71. MCA occlusion results in: contralateral spastic paresis Small penetrating arteries are most involved
contralateral hemianesthesia 86. Prognosis of ICH: Good because lesions are characterized by
homonymous hemianopsia with impairment of conjugate gaze compression as opposed to tissue destruction. (although in
in the direction opposite the lesion general this type of stroke is very fatal becuase of the
72. MCA supplies:: the entire lateral surface of the brain (fronto- displacement of brain tissue and significant increase in HTN
temporo-parietal) as well as subcortical structures (BG and which can compress vital centers)
posterior internal capsules), corona radiata, globus pallidus, 87. Prosopagnosia: Inability to recognize familiar faces
caudate and putamen 88. Psychological problems are more severe with ______ CVA:
73. Medical Intervention of SAH/AVM: Surgery is Tx of choice Left
Lowering BP 89. Putaminal hemorrhage: Similar to MCA stroke but with greater
Treat cerebral edema alteration of consciousness
Anticonvulsants
90. Reflex sympathetic dystrophy (RSD): Also known as complex
74. Memory and representational deficits after stroke: Difficulty regional pain syndrome
describing details of imagined representations from long term Causes swelling and tenderness in the fingers, hands and
memory shoulder
75. most common form of cerebral emboli: cardiogenic; 91. Right CVAs result in __________ weakness and sensory loss.
fragments from a thrombus within the heart can dislodge and Left CVAs result in _________ weakness and sensory loss: left-
enters the cerebral circulation/75% of cardiac emboli lodge in sided, right-sided
the brain
92. Right-left discrimination: iInability to identify the R or L side of
76. Motor Neglect after stroke: Failure to move in contralesional one's own body or the examiner.
space despite awareness of stimulus there Lesion: parietal lobe of either hemisphere
Hemispace deficit =reference between right <-> left
93. Secondary complications of a SAH often prove _______: fatal
77. NIHS scale: An 11-item standardized assessment of neurologic
outcome and degree of recovery from stroke that is designed 2˚ complications include Vasospasm and inflammatory and
to be completed in 5-8 minutes fibrotic responses in the meninges
94. Secondary ICH occurs due to ______________________: trauma, 108. Thalamic hemorrhage: Results in contralateral hemiplegia with
impaire coagulation, toxic exposure disproportionately greater sensory loss
95. Sensory Neglect after stroke: Lack of awareness in 109. Thrombic ischemia: the development of existence of a blood
contralesional hemispace clot within the cerebral vascular system. This makes up 40% of
80% of Right CVA demonstrate visual neglect. CVS's and typically occurs in a vessel that is already partially
96. Severe aphasia of both production and comprehension occluded by atherosclerosis
resulting in poor reading and auditory comprehension, 110. Thrombic occlusion have the tendency to develop at sites
repetition, naming and writing. Speech is non-fluent. This is of turbulent flow. They are most common in:: internal carotid
known as:: global aphasia artery & vertebral artery
97. sever ischemia leads to necrosis of neurons and supporting Basilar artery & middle cerebral artery
cellular elements (glial cells). The ______________________ may 111. thrombolytic agents are given within _____ hours ofo nset to
remain viable for several hours from collateral arteries break up the thrombus to restore normal circulation.: 6; this
anastomosing with branches of the occluded vascular tree: helps increases chance of recovery and minimize disability
penumbra 112. Topographical Disorientation: Difficulty in understanding &
98. Simultanagnosia: Inability to percieve the hwole or the "big remembering the relationship of one location to another,
picture", only sees 1 element of an object at a time (decreased unable to trace path/route
visual span, tubular vision) Lesion: non-dominant occipito-parietal lobe
99. Somatognosia: Lack of awareness of the body strucutre and 113. True or false? Left-sided CVAs are more associated with
the relationship of body parts in oneself or in others aphasias and apraxia: True!
Difficulty performing transfers, following directions 114. true or false: MRI's are typically used for patients with a
100. Somatognosia is due to lesions in ______________________. pacemaker: false; MRI's CANNOT be performed if patient has
Unilateral neglect is due to lesions in _____________________: a pacemaker or any other implantable device
Dominant parietal lobe/posterior temporal lobe, non- 115. True or false? There is a significant chance of re-bleeding
dominant parietal-occipital area with mild/mod SAH: False! Mod/severe
101. Spacticity peaks in the Brunnstorm's stages of recovery 116. Unilateral neglect: Inability to register and to integrate stimuli
during stage ______________. It disappears at stage ___________: 3, and perceptions form one side of the body and the
6 environment
102. Spatial Memory Deficit: Impaired memory of location of 117. upper division MCA involvement of the dominant
objects/places (ie. Furniture in home) hemisphere results in _____________ aphasia. lower division
Lesion: non-dominant parietal lobe MCA occlusion of the dominant hemisphere result in
103. Spatial Relations Deficit: Inability to perceive the relationship ____________ aphasia: broca's, wernickes
of one object in space to another object, or to oneself. 118. Vertical Disorientation: Distorted perception of what is
Difficulty crossing midline. i.e. drawing a clock, setting a table vertical; causes imbalance & distorted midline orientation
Lesion: non-dominant parietal lobe Lesion: non-dominant parietal lobe
104. Subarachnoid Hemorrhage (SAH): Causes extreme elevations 119. Wallenberg's Syndrome: a vertebral artery syndromes
in ICP due to obstruction of CSF coupled with cerebral edema characterized by ipsilateral vertigo. nausea, nystagmus,
ipsilateral hoarseness and dysphagia, Horners syndrome,
Common sites: Anterior communicating artery, posterior ipsilateral ataxia, ipsilateral loss of facial sensation to pain and
communicating arter and middle cerebral artery temperature, ipsilateral loss of sensation on arm, trunk and leg,
105. surgical management of ischemic CVA: -carotid contralateral loss of pain and temperature
endarterectomy (treatment of choice for TIA) 120. What are contractures?: Shortening of muscles, tendons,
-posterior fossa decompression (secondary to cerebellar ligaments, joint capsule which leads to restricted ROM
edema)
121. what are the most common origins of emboli: A-fib and MI
106. Syndromes of lacunar CVA can be either of three things:
122. What is spasticity?: Lack of inhibition from higher levels
Pure motor (internal capsule-posterior limb)
causes an increase in stretch reflexes, exaggerated flexor
Facial weakness (internal capsule-anterior limb)
muscle response,
Pure sensory (posterolateral thalamus)
123. what is the danger of using anticoagulation therapy with
107. systemic cause of ischemia CVA: -low systemic perfusion
patients experiencing an ischemic CVA?: there is a risk of
secondary to cardiac failure or significant blood loss
conversion into a hemorrhagic CVA
-widespread hypo-perfusion and ischemia lead to anoxic brain
injury 124. what is the most common type of CVA?: ischemia (80%)
-neurological deficits are global and bilateral in nature 125. What is the most modifiable risk factor of a hemorragic
CVA?: Hypertension
126. What is the motor recovery progression after stroke: 139. Why do stroke patients have incoordination?: Cerebellar or
Initially flaccid BG involvement
Development of spasticity, hyperreflexia and synergies Proprioceptive losses
Spasticty and synergies decline and advanced movment motor weakness
patterns are possible Ataxia
127. What is the typical hemi arm posture?: Combination of Impaired stretch reflex response
flexion and extension patterns 140. Why is the cerebellum and brainstem a concern with
- Shoulder ADD (Extension) stroke?: Cerebellar edema may develop, resulting in death
- Elbow flexion (Flexion) from brainstem compression or herniation
- Forearm pronation (Extension)
- Wrist flexion (Flexion)
128. What is the typical hemi leg posture?: Combination of flexion
and extension patterns
- Hip flexion and adduction
- Knee extension
- Ankle plantarflexion
129. What type of stroke is caused by bleeding from an arterial
source into the brain parenchyma and is the most fatal?:
Intracerebral Hemorrhage
130. When does recovery from ICH occur?: When/if blood is
reabsorved before signficant tissue destruction occurs
131. Where do lacunar CVAs occur?: In the deep white matter of
the brain where tiny arterioles branch off of larger vessels &
are vulnerable to hypertensive hemorrhage or the vessel may
thicken or thrombose
132. which areas are most prone to anoxic brain injury?:
hippocampus (memory deficits)
purkinje fibers of the cerebellum (ataxia)
basal ganglia (incr. muscle tone)
133. which imaging intervention is most commonly used with
CVA patients?: CT scan
134. which of the following is the single most significant
controllable modifiable risk factor for CVA

A. Hypertension
B. adult onset diabetes (type2)
C. Cigarette smoking
D. Drug use: A. hypertension
135. while ischemia CVA is rarely fatal, _________________ is a
potential fatal sequela: cerebral edema (peaks in 3 to 4 days)
136. Why are AVMs a concern?: Due to the lack of capillary
communication, there is no O2 or glucose exchange in that
area
137. Why do contractures occur?: Lack of muscle opposition
Hypertonicity
Lack of normal positioning
138. Why do stroke pateints have paresis?: A decrease in the
number of functioning agnosti motor units
Recruitment order may be altered
Firing rates decrease
Denervation changes in corticospinal tract
Atrophy of muscle fibers

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