Cerebral and Lacunar Strokes B&B Flashcards
what are the etiologies of strokes (2)? what is the best first test for diagnosis?
- 80% ischemic - thrombosis, embolism, hypoperfusion —> symptom onset over hours
- 20% hemorrhagic —> sudden onset
first test: non-contrast CT of head
you suspect your patient is having a stroke - what is the first test you should run?
non-contrast CT of head
what part of the body will display symptoms from stroke of the ACA vs MCA vs PCA? (think of the homunculus)
ACA: lower limb (supplies superior overlying strip of the cortex and the medial sides of the hemispheres)
MCA: upper limb, face (supplies most of cerebrum, lateral portion)
PCA: vision (supplies occipital lobe)
how do MCA strokes present? (4)
most common site of stroke
- contralateral motor/sensory symptoms
- arms (>legs) + face (think of homunculus)
- spastic (UMN) paralysis
4a. left sided - aphasia (speech center is L in most patients)
4b. right sided - hemineglect
what is the most common site of stroke, and how does it present?
middle cerebral artery (MCA)
- contralateral motor/sensory symptoms
- arms (>legs) + face (think of homunculus)
- spastic (UMN) paralysis
4a. left sided - aphasia (speech center is L in most patients)
4b. right sided - hemineglect
Pt is 75yo M presenting with acute onset of loss of movement in his R arm and drooping of the R face with drooling from the corner of his mouth. Pt has difficulty speaking.
What is most likely going on? Be exact.
stroke of L MCA (MCA = most common site of stroke)
- contralateral motor/sensory symptoms
- arms (>legs) + face (think of homunculus)
- spastic (UMN) paralysis
4a. left sided - aphasia (speech center is L in most patients)
4b. right sided - hemineglect
how will MCA stroke affect facial function?
recall upper face has dual innervation by R and L UMN - unaffected by unilateral MCA stroke
lower face has single UMN supply from contralateral motor cortex fibers running in corticobulbar tract - MCA stroke will cause UMN damage (spastic paralysis)
how does ACA stroke present?
ACA (anterior cerebral artery) supplies medial cortex (midline portion) —> causes symptoms in lower extremities (think of homunculus with legs hanging over the edge)
legs > arms
Pt is 75yo M presenting with acute weakness in his R hip and leg. PE reveals decreased sensation to pinprick and vibration in his R leg. What is the most likely diagnosis? Be exact.
stroke of L ACA (anterior cerebral artery)
ACA (anterior cerebral artery) supplies medial cortex (midline portion) —> causes symptoms in contralateral lower extremities (think of homunculus with legs hanging over the edge)
how does a PCA stroke present? (3)
recall PCA (posterior cerebral artery) supplies posterior brain (duh!) and therefore visual cortex
- visual hallucinations
- visual agnosia
- contralateral hemianopia with macular sparing (dual innervation by PCA + MCA)
Pt is 80yo M presenting with acute visual loss on the R side. His wife reports he is seeing people not in the room. PE is negative for motor or sensory deficits. Visual exam shows loss of the L medial and R lateral fields with macular sparing. What is the diagnosis? Be exact.
stroke of L PCA (posterior cerebral artery)
recall PCA (posterior cerebral artery) supplies posterior brain (duh!) and therefore visual cortex
- visual hallucinations
- visual agnosia
- contralateral hemianopia with macular sparing (dual innervation by MCA + PCA)
explain why PCA strokes spare the macula
macula: central, high-resolution vision (reading)
has dual blood supply from middle (MCA) and posterior (PCA) cerebral arteries
PCA strokes (affecting occipital lobe) often spare the macula
stroke of which artery can present with thalamic syndrome? how will this present?
posterior cerebral artery (PCA) strokes
—> contralateral total sensory loss of face, arms, legs + proprioception deficit [recall thalamus is sensory relay]
but NO motor deficits
may result in chronic pain on contralateral (affected) side
what are 3 possible causes of hypoxic encephalopathy?
- shock
- anemia
- repeated hypoglycemia
loss of consciousness can occur in <10 seconds, permanent damage <4 mins (no glycogen storage in neurons!), can result in coma/ vegetative state
which 2 populations of neurons are highly susceptible to hypoxic encephalopathy?
- pyramidal cells of hippocampus
- Purkinje cells of cerebellum
hypoxic encephalopathy can be caused by shock, anemia, repeated hypoglycemia