Stroke Syndromes Flashcards
Ischemic Stroke
Occlusion of a blood vessel; more common than hemorrhagic
*Thrombotic are most common
Hemorrhagic Stroke
Rupture of an aneurysm (Anterior communicating arteries)
- Produces crescent shaped CT image
- Will see severe headache, nuchal rigidity, and decreased consciousness
Lacunar infarct
Small infarcted area due to occlusion of small end artery
Watershed infarct
Occurs b/w distribution of two mjor arterie
TIA
Transient Ischemic Attack
Normal fnxn returns in 30mins-24hrs
*Assoc. w/ increased risk for stroke; possibly within hours
Ischemic cascade
Death of neuronal cells causes excess release of glutamate
=>Ca2+ into other cells causing their death as well
Pnumbra
Area surrounding center of infarction in which damage is not yet irreversible
Lesion of optic chiasm
Produces a bitemporal hemianopsia
Lesion central to optic chiasm
Produces homonymous hemianopsia
-(Optic tracct, lateral geniculate nucleus of thalamus, Area 17)
ICA Stroke
- May have amaurosis fugax due to occlusion of CRA
- Global aphasia
- Eye deviation to side of lesion
- Tongue deviation away from lesion
Contralateral:
Spastic paralysis w/ Babinski (Primary Motor Cortex)
Paralysis of lower face (UMNs of VII)
Loss of fine touch, vibration, conscious proprioception (SI)
-Pt. cannot localize pain either
Ipsilateral:
Vision loss
MCA stroke
-Global aphasia if on left
Contralateral:
Spastic paralysis (Lateral part of Area 4)
Loss of fine touch, vibration, conscious proprioception (Lateral part of Areas, 3,1,2)
No pain localization (Lateral part of Areas 3,1,2)
*All upper body > lower body
Ipsilateral: Eye deviation towards lesion Tongue deviation away from lesion Neglect `
ACA stroke
-Abulia, akinetic mutism, urinary incontinence
Contralateral:
Spastic paralysis w/ Babinski (Medial part of Area 4)
Loss of fine touch, vibration, conscious proprioception (Medial Areas 3,1,2)
No localization of pain (Medial Areas 3,1,2)
*Upper body > Lower body
PCA stroke
-Contralateral homonymous hemianopsia w/ macular sparing
- Memory deficits
- Due to damaged hippocampus
Abulia
Loss of ability to act voluntarily
Akinetic mutism
Decreased thought, movement, speech, emotion
Amaurosis fugax
Sudden transient loss of vision on one side due to occlusion of CRA
-TIA symptom
Stroke of lenticulo-striate branches
Supply genu and posterior limb of internal capsule (subcortical area)
Contralateral: Spastic paralysis w/ Babinski Loss of fine touch, vibration, conscious proprioception No ability to localize pain Lower facial paralysis
- damaged corticobulbar and corticospinal axons
- will not see any cortical signs
Thalamic strokes
- Involve penetrating branches of PCA
- Symptoms assoc. w/ branches involved
- Produces thalamic syndrome if VPL is involved
Weber’s Syndrome
Stroke of penetrating branches of PCA
-Affects basal area
Contralateral:
Spastic paralysis w/ Babinski (PLIC)
Lower facial paralysis
Ipsilateral:
Oculomotor opthalmoplegia
Oculomotor opthalmoplegia
Damage to CN III
- Lateral strabismus
- Ptosis
- Pupil dilation
Claude’s Syndrome
Stroke of PCA or basilar artery
-Affect tegmentum of midbrain
Contralateral:
Tremor (Red nucleus)
Ipsilateral:
(Oculomotor opthalmoplegia
Benedikt’s Syndrome
- Stroke of penetrating branches of basilar artery
- Involves basal and tegmental areas => combination of Weber’s and Claude’s syndromes
Rostral pons strokes (Basal)
-Pontine arteries
Contralateral:
Spastic paralyis w/ Babinski (corticospinal axons)
Lower face paralysis (corticobulbar axons)
Rostral pons stroke (Tegmentum)
-Pontine arteries
Contralateral:
Loss of fine touch, vibration, conscious proprioception (Medial lemniscus)
Ipsilateral:
Facial sensory loss (V axons)
*Corneal reflex in ipsilateral side would be lost
Caudal pons stroke (Basal)
-Pontine arteries
Contralateral:
Spastic paralysis w/ Babinski (corticospinal axons)
Lower face paralysis (possible; could also be total ipsilateral)
Caudal Pons Stroke (Tegmentum)
-Pontine arteries
Ipsilateral: Facial paralysis (VII nucleus/axons) Medial strabismus (VI nucleus/axons)
*Could be many other symptoms (medial lemniscus) but these 2 are DIAGNOSTIC
Locked-in syndrome
Bilateral syndrome of basal pons occurring after basilar artery stroke
-Entirely paralyzed except for vertical eye movement
(Vertical gaze center found in PAG)
*Pt not in full coma because RAS is intact
Wallenburg’s Syndrome
(Lateral medullary syndrome)
(PICA syndrome)
-Stroke involving branches of PICA
Contralateral:
Loss of pain and temp. sensation (Lateral spinothalamics)
Ipsilateral:
Loss of pain and temp. in face (Spinal tract/nucleus of V)
Vertigo, nystagmus, nausea, vomiting (Vestibular nuclei)
Ataxia (Inferior cerebellar peduncle)
Horner’s Syndrome (Sympathetic projections in lateral spinothalmic area)
Absent gag reflex, dysponia, dsypnea, dysphagia (Nucleus ambiguus)
Horner’s Syndrome
Damage to sympathetic axon on their way to the intermediolateral cell column @ T1-L2
1 Miosis
- Ptosis
- Anhydrosis
Medial medullary syndrome
-Stroke of medial medullary branches of vertebral artery
-Contralateral:
Loss of fine touch, vibration, conscious proprioception (medial lemniscus)
Spastic paralysis w/ babinski (pyramids)
Deviation of tongue to side of lesion (axon of CN XII)
Ipsilateral:
Possible atrophy and fasciculations (inferior cerebellar peduncle possible)
Spinal cord stroke
- Anterior/vertebral arteries
- Symptoms will be assoc. w/ pathways affected
- Presents w/ NO CORTICAL OR CN SIGNS
Corticobulbar tract
UMN innervation for cranial nerves
-Axons originate in cortex and terminate in motor nuclei of CNs
Dead Reds
Red stained neurons that are pathognomonic for ischemic stroke
