Vertebrobasilar Stroke Syndromes B&B Flashcards
describe the blood supply of the brainstem (be specific)
midbrain: posterior cerebral artery (lateral + midbrain)
pons: anterior inferior cerebellar artery (AICA) (lateral) + basilar (medial)
medulla: posterior inferior cerebellar artery (PICA) (lateral) + anterior spinal artery (ASA) (medial)
[just for note, recall that the cranial nerves divisible by 12 are found in the midline, all others are lateral!)
fill in the blank regarding the blood supply of the brainstem:
lateral midbrain:
medial midbrain:
lateral pons:
medial pons:
lateral medulla:
medial medulla:
midbrain: posterior cerebral artery (lateral + midbrain)
lateral pons: anterior inferior cerebellar artery (AICA)
medial pons: basilar
lateral medulla: posterior inferior cerebellar artery (PICA)
medial medulla: anterior spinal artery (ASA)
[just for note, recall that the cranial nerves divisible by 12 are found in the midline, all others are lateral!)
what is the rarest type of cerebellar stroke, and how does it present?
SCA (superior cerebellar artery) stroke: present with ipsilateral cerebellar ataxias
—> dysmetria (failed finger to nose)
—> dysdiadochokinesia (can’t flip hand quickly)
—> N/V
[note in reality SCA strokes are rarely confined to the cerebellum]
how does a basilar artery stroke present?
locked-in syndrome: bilateral paralysis (quadriplegia) but can blink (upper brainstem intact)
this is due to stroke affecting the ventral pons —> loss of bilateral corticospinal and corticobulbar tracts
what is the cause of locked-in syndrome?
basilar artery stroke
locked-in syndrome: bilateral paralysis (quadriplegia) but can blink (upper brainstem intact)
this is due to stroke affecting the ventral pons —> loss of bilateral corticospinal and corticobulbar tracts
contrast locked-in syndrome with vegetative state
locked-in syndrome: due to basilar artery stroke damaging ventral pons (loss of bilateral corticospinal + corticobulbar tracts) —> bilateral paralysis (quadriplegia) but ability to blink (upper brainstem intact)
vegetative state: motor function intact, but cortical dysfunction (can’t process the world around them)
what is the cause and presentation of central pontine myelinolysis?
aka “osmotic demyelination syndrome”: demyelination of central pontine axons due to lesion at the base of the pons —> loss of bilateral corticospinal + corticobulbar tracts —> bilateral paralysis (quadriplegia)
caused by over-correction of low sodium (Na+ is increased too quickly)
what is “top of the basilar syndrome”? what is the usual cause?
very rare occlusion of upper basilar artery (usually embolic)
presents with changes in consciousness (coma) + visual symptoms (hallucinations, blindness)
usually no significant motor loss
how does “top of the basilar syndrome” present?
very rare occlusion of upper basilar artery (usually embolic)
presents with changes in consciousness (coma) + visual symptoms (hallucinations, blindness) + eye problems (CN III palsies, loss of vertical gaze, convergence problems)
usually no significant motor loss
On rounds, you encounter a patient in the ICU who is currently in a coma. When awake, they experienced hallucinations, blindness, and loss of vertical gaze. However, motor function tested normally. What might be going on?
Top of the Basilar Syndrome: very rare occlusion of upper basilar artery (usually embolic)
presents with changes in consciousness (coma) + visual symptoms (hallucinations, blindness, CN III palsies)
usually no significant motor loss
how does an AICA stroke present? What area of the brainstem is affected? (7)
lateral pontine syndrome —> loss of:
- vestibular nuclei - nystagmus, vertigo, N/V
- spinothalamic tract - contralateral pain/temp loss
- spinal V nucleus - ipsilateral facial pain/temp loss
- sympathetic tract - Horner’s syndrome
- facial nucleus - ipsilateral facial droop, loss of corneal reflex
- cochlear nuclei - deafness
- CN VII - loss of anterior taste
[recall that cranial nerves NOT divisible by 12 run through the lateral brainstem!]
what are the 3 key features of Horner’s syndrome?
- miosis = small pupil
- ptosis = drooping eyelid
- anhidrosis = lack of sweat (usually can’t detect clinically)
remember sympathetic tracts run from hypothalamus —> through lateral brainstem —> exit T1 —> travel up to face/eyes via cervical ganglion
how does an PICA stroke present? What area of the brainstem is affected?
lateral medullary syndrome, aka Wallenberg’s —> loss of:
- vestibular nuclei - nystagmus, vertigo, N/V
- sympathetic tract - Horner’s
- spinothalamic tract - contralateral pain/temp loss
- spinal V nucleus - ipsilateral facial pain/temp loss
- nucleus ambiguus (IX, X) - hoarseness, dysphagia, weak gag reflex (unique to this syndrome)
Wallenberg Syndrome
lateral medullary syndrome caused by PICA stroke, aka Wallenberg’s —> loss of:
- vestibular nuclei - nystagmus, vertigo, N/V
- sympathetic tract - Horner’s
- spinothalamic tract - contralateral pain/temp loss
- spinal V nucleus - ipsilateral facial pain/temp loss
- nucleus ambiguus (IX, X) - hoarseness, dysphagia, weak gag reflex (unique to this syndrome)
[Take an M for Medulla and flip it LATERALLY to get a W for Wallenberg!]
how does a stroke of the anterior spinal artery (ASA) present at the level of the medulla vs spinal cord?
affects midline structures
spinal cord: loss of ALL but posterior columns - only vibration/proprioception intact, paralysis below lesion
medulla: medial medullary syndrome - loss of corticospinal + medial lemniscus + CN 12 —> contralateral hemiparesis, contralateral loss of prop/vibration, flaccid paralysis of tongue (lick the lesion)
