Cerebral vasculature and stroke Flashcards Preview

Boards deck 1 > Cerebral vasculature and stroke > Flashcards

Flashcards in Cerebral vasculature and stroke Deck (18):

Draw Circle of Willis

see pg 458


What kind of brain damage may be seen in severe hypotension?

damage to the watershed areas of the brain.
upper leg and upper arm weakness as well as defects in higher order visual processing


How does therapeutic hyperventilation work? For what brain problem is it useful? Explain the underlying physiology.

brain perfusion is driven primarily by CO2 concentration and relies on tight autoregulation.
Therapeutic hyperventilation is useful in cases of acute cerebral edema. Hyperventilation decreases the CO2 concentration in the brain, which reduces brain perfusion via vasoconstriction. Reduced perfusion decreases intracranial pressure.


Does oxygen play a role in autoregulation of brain perfusion? When does CO2 stop influencing cerebral blood flow?

Only marginally: hypoxemia increases cerebral pressure only when PO2 is less than 50 mmHg.
Increasing CO2 causes increased brain bloodflow until it plateaus at 90 mmHg.


What anatomical areas may be affected by an MCA stroke?

motor cortex, sensory cortex, Broca's area in the frontal lobe and Wernicke's area in the temportal lobe


What are the clinical findings that may be associated with an MCA stroke?

contralateral paralysis of the upper limb and face
contralateral sensation loss of upper AND lower limbs, and face
aphasia if dominant hemisphere. Hemineglect if nondominant (usually right) hemisphere).


What areas may be lesioned in an ACA stroke? Clinical findings?

motor cortex: lower limb
sensory cortex: lower limb
causes contralateral lower limb paralysis and loss of sensation.


What areas might be lesioned in a lenticulostriate stroke? clinical findings? important causes?

striatum and internal capsule may be injured.
this causes contralateral hemiparesis or hemiplegia
Note that this is a common location of lacunar infarcts secondary to un-managed HTN


What structures might be damaged in an ASA lesion? What are the clinical manifestations? Include contralatera/ipsilateral.

lateral corticospinal tract, medial lemniscus, and caudal medulla, esp. the hypoglossal nerve.
Lateral CST lesions will cause contralateral hemiparesis of upper and lower limbs.
medial lemniscus lesions will cause problems with contralateral proprioception (among other things, I would imagine)
hypoglossal nerve problems will cause IPSILATERAL hypoglossal dysfunction.


What is medial medullary syndrome?

syndrome caused by infarct of the paramedian branchesof the ASA and vertebral arteries. basically what I describe as an ASA stroke.


What structures might be damaged by a PICA lesion?

lateral medulla: vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguus, sympathetics, and inferior cerebellar peduncle.


What are the clinical manifestations of a PICA lesion?

vomiting, vertigo, nystagmus; decreased pain and temperature sensation from ipsilateral face and contralateral body, dysphagia and hoarseness, decreased gag reflex, ipsilateral horner syndrome, ataxia. These nucleus ambiguus effects are specific to PICA lesions
causes lateral medullary syndrome


What are the clinical manifestations of an AICA lesion?

lateral pons: cranial nerve nuclei: vestibular nuclei, facial nucleus, spinal trigeminal nucleus, cochlear nuclei, sympathetics.
also causes middle and infereior cerebellar peduncle dysfunction


Clinical manifestations of AICA lesions

vomiting, vertigo, nystagmus. paralysis of the face (important!). decr. lacrimation, salivation. decreased tased from anterior 2/3 of tongue. decreased corneal reflex (which requires CN7). Face has decreased pain and temp sensation. ipisilateral hearing loss. ipsilateral horner syndrome.
the middle and inferior peduncle dysfunction causes ataxia
remeber, facial nucleus effects are specific to AICA


What do lesions to the basilar artery do? Clinical manifestations?

affect the pons, medulla, lower midbrain, corticospinal, and corticobulbar tracts. Also the ocular cranial nerve nuclei and the PPRF.
this means the pt will have preserved consciousness with blinking, quadriplegia, loss of voluntary facial, mouth, and tongue movements.


What are common lesions to the AComm? Clinical effects?

These tend to be ANEURYSMS, NOT strokes, though aneurysms can lead to stroke. Saccular aneurysms can impinge cranial nerves and cause visual field defects


What are common lesions to the PComm? clinical effects?

this is a common site of saccular aneurysms
it causes CN III palsy: eye is down and out with ptosis and pupil dilation.


Lesions to the PCA and clinical effects

occipital cortex and visual cortex lesions.
causes contralateral homonymous hemionopsia.

Decks in Boards deck 1 Class (67):