Quiz: Cerebrovascular disorders (Im not sure if this is fair game for a test) Flashcards

1
Q

Thrombosis

A

Blood clot that forms in a vein, stagnent
* leads to ischemic stroke

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2
Q

Embolic occlusion

A

Moving clot, obstruction of an artery, heart most common source (think arrythmias)
* this is an embolism
* Leads to ischemic stroke

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3
Q

What is the most common site of atherosclerosis and atherothrombosis leading to a stroke?

A

Proximal ICA
* I think it has to do w/ where it branches off the aortia
* most common place for ischmic stroke because the heart will throw a clot (look at the anatomy)

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4
Q

Secondary vascular responses that occur w/ ischemic stroke
* Further microvascular occlusions increase and continue to impair blood flow
* Cell death can occur in any CNS injury
* W/ astrocyte (in the brain) swelling, can lead to occlusion of a single artery in the brain
* Narrowing of lumina of microvessels

A
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5
Q

What is parenchyma?
* What happens if its blood supply is temporarily disrupted?

A

Tissue of the brain
* highly vulnerable to an interruption in its blood supply

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6
Q

When the cerebral BF falls below _ neuronal fucntioning is impaired (said we didnt have to know these #’s)
* neuronal death, or infarction, occurs when cerebral BF is less than _ to _

A

20 mL / 100 mg of tissue

8 to 10 mL / 100 mg/min

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7
Q

What is an ischemic core?

A

Frequently, in an acute infarction, a portion of the affected brain receives no blood, and is not salvageable, this is the ischemic core.

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8
Q

Hypoxic changes = hypoxic ischemia

A
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9
Q
A
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10
Q

syndrome = a group of pathologies that share common charcteristics - enough for it to be one classification/group

A
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11
Q

When the blockage is in the more proximal component of the artery, the resulting area of hypoxia is greater than if the clot is lodged in a more distal part of the artery

Because of the collatearl circulation provided by the circle of willis, some areas of the brain are supplied by more than one artery. When one artery is blocked circulation is provided to the tissues through the blood supply of other arteries

A
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12
Q

What does the MCA supply? (3)
* Where does it stem from?

A

1) Basal ganglia
2) Internal capsule
3) Lateral hemisphere

Stems from the ICA

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13
Q

What is the most common place in the body to have a stroke?

A

MCA

I think this is because strokes most commonly form in the ICA (because anatomy) and get caught in the MCA (because the MCA connects directly to the ICA)

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14
Q

Deficits observed w/ MCA occlusion:
* whats more involved LE or UE

A

1) Contralateral spastic hemiparesis and sensory loss of the face, UE, and LE - HOWEVER, THE FACE AND UE ARE MORE INVOLVED THAN LE

2) difficulty speaking

3) Perceptual deficits (unilateral neglect, anasognosia, apraxia, and spatial disorganization) - more common w/ R hemisphere damage

Homonymous hemianopsia is also a common finding

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15
Q

What does the ACA supply? (3)
* What does it stem from?
* potentially deficits?
* UE or LE more impacted?

A

Supplies the frontal lobe, parietal lobe, part of the internal capsule (deep)

Stems from the ICA

Deficits: contralateral hemiparesis and sensory loss with greater involvement of the LE than the UE because the somatotopic organization of the medial aspect of the cortex includes the functional area for the LE

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16
Q

Internal carotid artery syndrome:

What is supplied by ICA (3)
* possible deficits

A

Supplies:
* MCA
* ACA
* Anterior choroidal arteries - these supply the ventricles

Possible deficits
* Produce massive infarction in the region of the brain supplied by the MCA - because ACA has more collateralization due to the circle of willis
* If collateral circulation to the ACA from the circle of willis is absent, extensive cerebral infarction in the areas of both the ACA and MCA can occur. Significant edema is common with possible uncal herniation, coma, and death (mass effect)
* S/s of both ACA and MCA can be seen

With competent circle of willis, occlusion can be asymptomatic

17
Q

Why is the ACA less impacted than the MCA in internal carotid artery syndrome (ICA occluded)

A

We see MCA deficits because it is not part of the circle of willis. The ACA is part of the circle of willis so we will see that collaterilization keeping it alive. So deficits are in an MCA pattern, not a ACA
* however, if the circle of willis is incompenent well see ACA damage along w/ MCA damage

18
Q

Posterior cerebral artery syndrome:
* what does the PCA supply?
* Stems from
* Possible deficits

A

PCA supplies:
* Midbrain
* Occipital lobe
* Temporal lobe

Stems from basilar artery - so ICA damage won’t really affect here

Possible deficits:
* Contralateral sensory loss or central poststroke thalamic pain - thalamic pain is rare stroke is typically painless - this is intense pain throughout extremities
* Homonymous hemianopsia, visual agnosia (difficulty using vision to recognize objects), prosopagnosia, or, if bilateral, corticl blindness
* Amnesia - because of the memory portion of the temporal
* Cognitive dysfunction, neglect, aphasia
* Wide variety of effects in subthalamic structures involved
* Contralateral hemiplegia/paresis

19
Q

Vertebral and posterior inferior cerebellar artery syndrome (PICA)
* Blood supply to the brainstem, medulla, and cerebellum is provided by the vertebral and posterior cerebrellar arteries
* Wallenberg syndrome is releated to the lateral medulla and the posterioinferior cerebllum and is characterized by vertigo, nausea, hoarseness, and dysphagia (dfficutly swalling)
* Edema associated w/ cerebllar infarction (anything that causes swelling in the cerebellum) can cause sudden respiratory arrest from high intracranial pressure (ICP) in the posterio fossa. Gait unsteadiness, dizziness, nausea, and vomiting may be the only early symptoms

this is considered a serious infarct. Its impacting the brainstem which does vegetative functions.
* no collaterilzation here as well

20
Q

Basilar artery syndrome:
* ischemia as a result of occlusion of the basilar artery can affect the brainstem, including the corticospinal tracts, corticobulbar tracts, medial and superior cerebellar peduncles, spinothalamic tracts, and cranial nerve nuclei
* if the basilar artery is occluded are symptoms unilateral or bilateral?

A

Symptoms are bilateral because it supplies bilaterally - because it supplies entire brainstem
* however, when a branch of the basilar artery is occluded, the symptoms are unilateral, involving the sensory and motor aspects of the cranial nerves

21
Q

Superior cerebllar artery syndrome:
* Occlusion of the superior cerebllar artery results in severe ipsilatearal cerebellar ataxia (poor motor coordination), nausea and vomiting, and dysarthria, or slurring of speech
* Scanning speech, a drawn-out and monotone speech pattern, reflects damage to the cerebellym. Loss of pain and temperature in the contralateral extremitites, torso, and face occurs
* Dysmetria, characterized by the inability to place the extremity at a precise point in space, is common, affecting the ipsilateral upper extremity

rememebr cerebellum has speech functions as well

key is the deficits are ipsilateral because cerebllar tractions don’t decussate

22
Q

Lacunar syndrome
* what is it?
* deficits

A

Deep in white matter, small subcortical lesions

Possible deficits: - varity because of how deep these are
* Dysarthria / clumsy hand syndrome
* Ataxic hemiparesis
* Sensory / motor
* Dystonia / involuntary movements (choreoathetosis, hemiballismus)

23
Q

Vertebrobasilar artery syndrome
* so impacts all those arteries in the back
* Possible deficits - occlusions of the vertebrobasilar system can produce a wide variety of symptoms with both upsualteartl and contralateral signs because some of the tracts in the brainstem will have cross while others have not
* what syndrome can it cause?

A

can cause lcoked in syndrome: acute hemiparesis rapidly progressing to tetraplegia and lower bulbar paralysis - the pt cannot move or speak but remains alert and oriented. Horizontal eye movements are impaired but verticle eye movements and blinking remain intact

24
Q

which artery causes locked in syndrome

A

vertebrobasilar

25
Q

medical amangement for strokes
* diagnosis - timing, pattern of onset, course
* how fast does an embolic stroke come on?
* How does a thrombosis stroke come on?

A

Embolic strokes come on rapdily w/o a warning (remember, an embolism causes an immidate blockage - this makes sense)

Thrombosis - more progressive, uneven onset. I think this is just thrombus froming and slowly blocking the artery

26
Q

The national institutes of health stroke scale is a valuable clinical tool for assessing stroke severity, and is recommended for use in emergency departments
* The scale includes 15 items for inital and serial examination of impairments following acute stroke
* A higher or lower number on the NIHSS indicates a more severe stroke?

A

Higher # = more severe stroke

27
Q

What is the first imaging done for a stroke?
* what does it help us determine?

A

Ct scan
* acute phase of stroke
* most radily available
* should be performed within 25 minutes of pts arrival
* Helps us determine if its an ischemic or hemorrhagic stroke

28
Q

MRI: imaging for stroke
* increased senstivity, contraindicated w/ pacemakers
* Ifdentifies ischemic event within 2-6 hours of onset

Other imaging:
* Angiography, ultrasround, PET

29
Q

:

Pharmacotherapy - spasticity

Contraverisal because these medications side effects are hard to tolerate - so do we use it or not use it - does benefit outweight the risk? - side effects are extreme fatigue and drowsiness - because these drugs are made to calm down the body and effect is systemic w/ these oral drugs - can’t target it

Common SEs: fatigue, drowsiness

Oral: Baclofen and benzodiazepines work at the level of the spinal cord; dantrolene works on muscle fibers itself

Botulinum toxin (BOTOX) - decrease diring of specific muscles
* Choosing the appropriate muscle or group of muscles is critical for successful outcomes. The effects of botulinum toxin are temporary, usually lasting for approximately 3-6 months

remember, sometimes we don’t want to treat spasticity because if its in the LE’s it might actually benefit their function

30
Q

Subarachnoid hemorrhage:
* how does it begin?
* What layers is this blood between
* what leads to them typically?

A

Begins w/ the sudden onset of a severe HA that reaches maximal intensity in seconds (thunderclao HA); sometimes the HA begins w/ exertion (because remember, the vessel is litteraly bursting)

Blood in the subarachnoid space between the arachnoid and the pia

Spontaneous, is often seen in normotensive persons, and results in searing pain that pt describes as the worst HA of my life

Aneurysms and vascular malformations are responsible for most SAHs

Risk factors for sah include smoking, excessive alc, and hypertension

31
Q

Types of aneyrusms

Berry aneurysm is a congential abnormal distenion of a local vessel that occurs at a bifurcation

Venous malformations are composed entirely of veins which are usually thickened and hyalinized, with minimal elastic tissue or smooth muscle

arteriovenous malformation (AVM) is characterized bu direct artery to vein communication w/o an intervening capillary bed
* brain parenchyma is found wihtin the AVM
* abnormal feltal development

32
Q

Clinicl manifestions of hemmorhage
* HA
* Common associated symptoms at the time of the rupture include nausea and vomiting, syncope, neck pain, coma, confusion, lethargy, seizures

33
Q

medical management of hemorrhage

Diagnosis
* can be initally misdiagnosed - meningitits, migraine
* CT scan

Tx:
* neurosurgical consult
* treatment of individualus with SAH involves the prevention and amangement of the relatively common secondary complications of SAH: rebleeding, vasospasm, hydrocephalus, hyponatremia, and seizures

Prognosis
* high mortality rate in elderly
* Poor functional outcomes
* Best in early aggresive tx
* Less than 3cm = good prognosis

34
Q

Subdural hemorrgage:
* subdrural hemorrhage or hematoma - most often the result of tearing of the bridging veins between the brain surface and dural sinus
* Falls
* Fragility of bridging veins and cerebral atrophy
* Anticoagulant therapy is a risk factor

35
Q

this is showing a midline shift of brain (hematomas shown as well)

Brain is also being herniated through the formaen magnum

36
Q

hematoma hernaited brain down through the foramen magnum

37
Q

Ischemic: better change of survival
* more likely to have perm disability

Hemorrgaic: worse chance of survivial
* with survival better chance of recovery