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Neuro Anatomy > CVA > Flashcards

CVA Flashcards

1
Q

TIA

A

Transient ischemic attack
Temporary interruption of blood supply to brain
Symptoms last for a few mins to hours but do not last longer than 24
No residual deficits
Precursor to susceptibility for CI or MI

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2
Q

HTN and CVA

A

-Reducing diastolic by 5-6mm Hg can reduce risk by up to 40%

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3
Q

Homocysteine

A

High plasma levels w/ low folate and B6 associated w/ increase risk of heart disease which may increase stroke risk

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4
Q

Cigarette smoking

A

Increase risk by 50%

Associated w/ number per day

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5
Q

Alcohol

A

Direct dose rln w/ stroke

3+/day increase risk by 45%

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6
Q

Causes of CVA

A

Cerebral infarction 70%(thrombus or embolus occlusion)

Hemorrhage’s 20%(subarachnoid, subdural, intracerebral)

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7
Q

Thrombus usually form

A

Branching or curves in arteries

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8
Q

A-fib

A

Believed to cause thrombus formation

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9
Q

Embolic infarction

A

(Thrombus, tissue, fat, air, bacteria or foreign bodies)
Results are more damaging as no time for collateral circulation to develop

Heart is most common source of embolic material (atherothrombic disease)

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10
Q

Artery to artery embolism

A

from atherothrombic lesion in carotid or verterobasilar

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11
Q

Formation of a thromboemboli begins

A

Distal vessels of the artery

Micro vascular occlusion that progressively increase in number and continue to impair blood flow

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12
Q

Astroglial swelling

A

Earliest cell changes noted w/ single artery occlusion

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13
Q

Functioning is impaired when

A

Blood flow falls below 20mL/100mg

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14
Q

Neuronal death occurs when

A

The brain relieves less than 8-10mL/100mg/min

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15
Q

Complete cerebral circulatory arrest results in

A

irreversible cellular damage with a core area
of focal infarction

Cells that have 80-100% ischemia will die in a few min b/c they cant produce ATP ->activation of Ca -> chain rxn to cell death

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16
Q

Area surrounding the core

A

Ischemic penumbra - receives collateral circulation but is not able to sustain fx

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17
Q

Secondary response to ischemic CVA

A

Decreased perfusion relative to O2 requirements
Areas of altered metabolism distant from site
Decline in O2 metabolism of unaffected side from acute to subacute (delay of corpus callosum fiber degeneration)

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18
Q

Glutamate and secondary damage

A

Normal: glutamate is an excitatory NT
released into the EC space and is quickly reabsorbed
• If the cells that normally uptake compromised, excess glutamate depolarizes the post synaptic cells
• excess glutamate allows the influx of Ca++ ions
into the cells which begins the process of cell death
• Catabolic enzymes are activated by the release of the Ca++ ions
and damage the cells that support the neurons (glial cells)

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19
Q

The hypoxia triggers

A

Neurotoxin release —> cell death

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20
Q

Middle cerebral artery syndrome

A

-Supplies most of the lateral cortex and also frontal, temporal, and parietal lobes
- Contralateral hemiplegia and hemianesthesia (sensory loss) with greater involvement of the face and upper extremity than the lower extremity because of the somatotopic
organization of the cortex

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21
Q

Middle cerebral artery syndrome

A

– If the dominant hemisphere (~left) is involved, global aphasia (Broca’s and Wernicke’s aphasia) (loss of fluency, ability to name objects, comprehend auditory information, and repeat language)

– If the non-dominant hemisphere (~right) is involved,
deficits in spatial awareness/attention will be present /(Contralateral body and space >ipsilateral body and space)

– Homonomous hemianopsia if involvement of optic
radiations

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22
Q

Anterior cerebral artery syndrome

A

Uncommon and often a result of an embolus

– Supplies the medial aspect of the cerebral hemisphere (frontal and parietal lobe)

– Results in contralateral hemiparesis and sensory loss with
greater involvement of the lower extremity than the
upper extremity and face because of the somatotopic
organization of the cortex

Collateral flow can compensate for the occlusion so
dysfunction can be minimal

– Primitive reflexes may be present (frontal release signs)

– Abulia (loss of desire to perform tasks or a delay in verbal and motor response if there is significant involvement of the frontal lobe (role in cognitive functioning and initiative)

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23
Q

Internal carotid artery syndrome

A

Supplies the MCA and the ACA

– Severity depends on the etiology, thrombus, or embolus of decreased blood flow

– If collateral circulation is present, the condition may be asymptomatic

– If collateral circulation is not present, extensive involvement resembling MCA and ACA manifestations may be present with possibility of coma and death

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24
Q

Posterior cerebral artery suplies

A

arises from terminal branches of the basilar artery and supplies the inferior and medial temporal lobes

– Also supplies the medial occipital cortex and most of the medial parietal cortex

– Also supplies a small portion of midbrain and most of the thalamus

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25
Q

Posterior cerebral artery occlusion-thalamic branches

A

Occlusion of the thalamic branches produces contralateral sensory loss

– Can also produce thalamic syndrome, which includes abnormal sensations of pain, temperature, touch and proprioception

– The pain can often be incapacitating (intractable and searing!)

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26
Q

PCA occluded at its origin

A

contralateral hemiplegia results from infarction of the cerebral peduncle in the midbrain (LCST in middle 1/3)

– Homonomous hemianopsia

– Cortical blindness (if PVC is involved)

– Cognitive dysfunction (memory loss) if hippocampus is involved

– Neglect can occur if significant portion of right parietal lobe is involved (non-dominant hemisphere (~right)-spatial attention/awareness)

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27
Q

Lucunar syndromes

A

Small vessel infarcts (aka lucanar infarcts because they resemble small lakes/cavities) occur in deep structures of the brain

– Small infarcts at the end of the arteries commonly found in the basal ganglia, internal capsule, and pons

Characteristic of ischemic cysts surrounded by astrocytotic gliosis (scarring of the support structures of the brain)

– Strongly associated with HTN and DM

– Signs are consistent with the neuroanatomic sites that are involved

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28
Q

Types of lucanar stroke

A

Pure motor lacunar stroke
– Posterior limb of the internal capsule, or anterior pons

Pure sensory lacunar stroke
– VPL of thalamus

Dysarthria-clumsy hand syndrome
– Base of pons, or genu of internal capsule
– Medial motor fibers controlling muscles for the face and the hand are primarily involved

– Syndrome characterized by difficulty with motor aspects of speech (dysarthria) and contralateral weakness (~clumsiness) of the hand

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29
Q

Diagnosing ischemic CVA

A
  • hx of neurological event - timing, pattern of onset, course
  • carotid artery and vertebral artery studies are performed using Doppler ultrasound to identify plaque accumulation
  • neuroimaging
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30
Q

Timing of embolic vs thrombosis

A

Embolic occur rapidly w/ no warning

Progressive suggest thrombosis

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31
Q

MRI

A

Allows ID w/in 2-6 hours

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32
Q

CT scan

A

Most convenient and readily available

  • confirm the dx and assist w/ thx (after 6-12 hours)
  • bleeding into the brain can be seen along w/ displacement of brain structures
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33
Q

PET scan

A

Detection of stroke earlier and w/ higher sensitivity

Eval the areas not immediately affected by infarct showing hypo metabolism and decreased blood flow

34
Q

Treatment of ischemic CVA

A

Acute tx: managing the stroke, preventing further embolic strokes

Blood flow and perfusion around the damaged area is the primary concern

Blood pressure should be normalized without compromising circulation

35
Q

Edema control

A

Small amounts can create pressure on brain stem/cerebellum —> respiratory arrest (most common cause of death)

36
Q

TPA

A

tissue plasminogen activator (TPA)

In emergent state, used to form plasmin which actively digests fibrin strands and is effective in dissolving the thrombus or blood clot responsible for the event

This will potentially save the penumbral neuronal tissue

37
Q

Mechanical Embolus Removal

A

device goes into a straight wire that turns in to
a cork screw when it comes out of the guide catheter that is screwed into the clot

A balloon is pumped proximal to the clot to prevent antegrade flow

Then the clot is pulled out

38
Q

Anticoagulation therapy

A

Once pt is stable (control BP over 140/90)

39
Q

Tx of ischemic CVA

A

Lipid Lowering Agents – Statin drugs

Surgical Intervention – Carotid endarterectomy

Neuro protection– Drugs that are aimed at decreasing the amount of cell death

Nerve Growth – Stem cells

Control of secondary symptoms

40
Q

Hemorrhage - single most modifiable risk factor

A

HTN

Chronic — fibrinoid necrosis in penetrating and subcortical ateryies —> weakening of walls —> formation of aneurysmal outpouching or microaneurysms

41
Q

Hemorrhage risk factors

A 
Excessive alcohol use
Long term anticoagulant therapy 
NSAIDS
Liver disease
Obesity 
Etc
42
Q

Intercerebral hemorrhagic syndromes

A 
Putamen
Thalamus
Cerebellum
Caudate
Internal capsule
Pons 
Lobes
43
Q

Intracerebral hemorrhage

A

Rupture in a blood vessel - most deadly of stroke subtypes

Due to abnormality of vessel structure/ changes brought about by HTN

Weakening of vessels

When the hemorrhage occurs it spreads along the path of least resistance which is usually along the fiber tracts of the white matter

Edema forms in the parenchyma

Neurologic symptoms occur gradually as there is expansion of the hematoma

44
Q

Intracranial hemorrhages

A

Most common

Spontaneous bleeding into surrounding brain tissue —> form a space occupying lesion

45
Q

Incidence of ICH

A

Increases dramatically over 65 years of age

More frequent in men

46
Q

intracerebral and HA

A

Present in 30-40% of cases associated w/ large superficial hemorrhage’s

Leaves cavity

47
Q

Putamen

A

50%-80% occur in the putamen

Contralateral sensorimotor deficit resulting from its proximity to the internal capsule

Oculomotor deficits common with pupillary abnormalities, visual field loss, and conjugate gaze deviation

Wernicke’s (receptive) aphasia with posterior putamen lesions
Abulia (lost motivation) and motor impersistence may be seen with anterior putamen lesions

48
Q

Thalamus

A

Sensory loss or dysthesias, possibly some motor deficits

Oculomotor dysfunction including gaze palsies, often with downward eye deviations and convergence spasm, or constriction meiosis

With dominant hemisphere involvement (~left), aphasia, disorientation, and memory disturbances can be seen

49
Q

Cerebellum

A

Ataxia is the hallmark sign

Nausea, vomiting, dizziness, nystagmus, vertigo

Brainstem signs such as facial paresis can be seen

Should be monitored carefully for compression in the region of the 4th ventricle which may cause life threatening changes

50
Q

Pons

A

Brainstem hemorrhages commonly arise in the middle pons

Coma, quadriplegia, unreactive pupils

51
Q

Caudate

A

Rupture into the ventricles

Headache, vomiting, LOC

Mimics subarachnoid hemorrhage

Internal capsule may be involved causing sensorimotor (sensory and motor) involvement

52
Q

Internal capsule

A

Presents as pure motor, pure sensory, or sensorimotor stroke with ataxia

53
Q

Lobar

A

Centered in the immediate subcortical white matter

Symptoms are lobe specific

54
Q

Subarachnoid hemorrhage

A

Can occur suddenly with a searing pain

Sometimes the headache will begin with exertion

Can be spontaneous, often seen in individuals who have normal BP

Occurs from bleeding into the subarachnoid space between the arachnoid and the pia which are continuous with the brain

55
Q

Subarachnoid hemorrhage can result from

A

Trauma, neoplasm, infections

Aneurysms and vascular abnormalities

56
Q

Types of subarachnoid hemorrhage

A
  • Barry aneurysm
  • venous malformations
  • AVM
  • cavernous malformation
57
Q

Barry aneurysm

A

Congenital abnormal dimension at bifurcation where the medial layer of vessel is weakest

90% SAH due to this

58
Q

Venous malformations

A

Veins, thickened and hyalinzed w/ minimal elastic tissue or smooth muscles

HA or focal neuro deficit

59
Q

AVM

A

Less than 3 cm in diameter more likely to bleed because pressure is higher

Seizures, HA, progressive focal neuro deficit

May have cognitive decline

60
Q

Cavernous malformations

A

Dilated endothelial lined fibrous tissue where no elastin is present in vessel walls

S/s depend on location - thrombus and scarring surround it

61
Q

SAH clinical manifestations

A 
HA
Nausea and vomiting
Syncope
Neck pain 
Coma 
Confusion 
Lethargy 
Seizures
62
Q

SAH dx

A

Up to 38% misdx —> viral meningitis, migraine/HA

CT

63
Q

SAH manage

A

Manage aneurysm
Evacuation of large hematoma and causative aneurysm
Manage vasospasm

64
Q

SAH prognosis

A

If hematoma is <3 cm - prognosis good

Mortality rate in >75 yr old - high

Few are able to live independently

65
Q

SAH are mostly often result of

A

tearing of the bridging veins between the brain surface and the dural sinus

Results in accumulation of blood in the dural space– If the volume is great enough—> space occupying lesion —> herniation of the cortex into adjoining spaces

66
Q

SAH dx tool or choice

A

non contrast enhanced CT

When the hematoma is dense, MRI may be useful

67
Q

Epidural hematoma

A

meningeal arteries run in the periosteal layer
of the dura —> torn during a traumatic skull injury
and bleeding occurs between the periosteum
and the skull —> Damage from compression

medical emergency and the hematoma must be evacuated because of the potential for extensive pooling of the blood

68
Q

Dx hemorrhagic CVA - CT

A

specific area can be ID and the amount of blood present

immediately in individuals suspected of having ICH

69
Q

Dx of hemorrhagic CVA - MRI

A

multiplanar views and can discriminate subtle changes and rapidly flowing blood

Limited usefulness in the first 24 hours

70
Q

Prothrombin time, partial thromboplastin time, and platelet count

A

Performed to rule out a bleeding disorder

In all individuals

71
Q

Coagulation factor deficits

A

Detected by eval of liver enzymes

72
Q

Differential Dx

A 
Ischemic stroke
Migraines
Tumor
Seizures
Abscess
HTN 
Encephalopathy
73
Q

Intracerebral hemorrhage: manage

A

Reduction of elevated BP w/ rapid acting antihypertensive meds

Control ICP, edema

Vit K can be useful to correct elevated PPT

Supportive care

Cardiac monitoring

74
Q

Intracerebral hemorrhage - most important predictor of mortality

A

Hemorrhage size

Individuals with coma or wide spectrum neurological deficits tend to do poorly compared to alert patients with focal neurological involvement

75
Q

General manifestations of CVA

A

Hemiplegia:

Motor control deficits 
Strength deficits
Muscle tone changes
Sensory changes
Perceptual deficits
Emotional (liability or dysregulation syndrome, apathy, euphoria, depression)
Balance deficits
Speech deficits (wernicke’s and broca’s)
Visual field deficits
Mental and intellectual impairment
76
Q

CVA behavior changes - left hemisphere damage

A

right hemiplegia

presents with difficulties in communication and in processing information in a sequential manner

anxious, cautious, and disorganized

tend to be realistic about their deficits

77
Q

CVA behavior changes - right hemisphere damage

A

left hemiplegia

presents with difficulty with spatial perceptual tasks, they are quick and impulsive

They overestimate their abilities and are at a much greater risk for safety

Cannot attend in a crowded environment

78
Q

Primary complications of CVA

A

Seizures

Respiratory involvement due to paralysis of the thorax

Trauma from falls

Thrombophlebitis, and vascular changes are aggravated by nactivity

Choking secondary to feeding and swallowing issues

79
Q

Secondary complications of CVA

A

Pain
CRPS (Complex Regional Pain Syndrome)

Shoulder - Hand syndrome (Begins with tenderness and swelling of the hand and diffuse aching pain from altered sensitivity in the arm - Pain interferes with movement re-education)

Edema Primarily in the hand and foot

Shoulder subluxation

80
Q

Management active rehab

A

Once medical status has stabilized, return to optimal function
Management of Tone/Spasticity

Management of motor control, force production, reaction time, speed of movement, and endurance

Management of sensory deficits

Bed mobility training

Transfer training

Gait training

Balance training

Wheelchair mobility training

Cognitive and Behavioral training

81
Q

CVA general prognosis

A

Most recovery occurs in first 6 months

Failure to recover grip before 24 days is correlated with no recovery of arm function at 3 months

No arm movement accompanied with loss of LE motor control is associated with poor outcomes

82
Q

Vascular disorders of spinal cord

A

Rare
Infarction can be a result of any of the same conditions as they occur in Brian

Some symptoms appear to be LMN affecting at level of anterior horn cell

(Vascular malformations, transverse myelitis, MS, degenerative disorders)

Necrosis at several levels = sensorimotor loss and pain

Lesion may involve central structures or nerve roots

Clinical manifestation depend on level of SC affected and specific structure affected

Neuro Anatomy (22 decks)

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