Lecture: CVA Syndromes Flashcards
CVA syndromes
- MCA
- ACA
- PCA
- IC
- Vertebral
- Basilar
- Cerebellar
Anterior Cerebral Artery Syndrome***
Supplies: medial cerebral hemisphere (frontal & parietal lobes) & subcortical structures
If the dominant language hemisphere is affected, ABULIA and a reduction in the rate or complexity of language & speech results. The severe
form of abulia is termed AKINETIC MUTISM
- Contralateral LE > UE* affected by paresis and sensory loss
- Memory and behavioral impairments
- Non-dominant side damage : unilateral neglect
Middle Cerebral Artery Occlusion***
- Generally embolic more often than thrombic!
- Most often occluded artery as a result of vascular disease
- Supplies the entire lateral surface/cerebral hemisphere of the brain (fronto-temporo-parietal)
Results in
• Contralateral spastic hemiparesis
• Contralateral hemianesthesia
• Homonymous hemianopsia with impairment of conjugate gaze in the direction opposite the lesion
Homonymous Hemianopsia
Loss of the temporal visual field from one eye & the nasal visual field of the other eye.
• R occipital lobe damage -> loss of L visual field
• L occipital lobe damage -> loss of R visual field
MCA Occlusion: effect on hemispheres
- If the (L) hemisphere is involved (and is language dominant) -> global aphasia (Severe aphasia of both production & comprehension, Poor reading & auditory comprehension, repetition, naming, & writing)
- If the non-dominant (typically (R) side) hemisphere is affected, esp. in the parietal lobe, it will result in perceptual deficits
MCA upper division occlusion
Upper division MCA involvement of dominant/L hemisphere of frontal lobe-> Broca’s aphasia (Awkward articulations, restricted vocabulary, restriction to simple
grammatical forms, Comprehension is intact, Reading is less impaired than speech & writing.
“D—d—d—dg, eh, no…d-d… darn…p-p-pet”
Lower Division MCA Occlusion
auditory association complex of lateral temporal lobe
-> Wernicke’s aphasia (Loss of auditory comprehension, poor command following, Loss of ability to read & write,Fluent speech but lack content or meaning.)
Question: “How are you today?”
Answer: “When? Easy for my river runs purple boxes wizzel abata Hon when goobles come.”
Conduction Aphasia
Results from interruption in connections between Broca’s &Wernicke’s areas
• Presents like Wernicke’s aphasia, but with good comprehension & understands your commands
• Poor repetition, naming, & writing
Internal Carotid Artery Syndrome
due to hypoperfusion, embolus or thrombus
Amaurosis Fugax (Transient monocular blindness) is a frequent accompanying symptom
• Temporary fading of vision or blindness
• Due to ↓ blood supply from the ICA to the opthalmic artery
Supplies both MCA & ACA
• Complete blockage without adequate collateral circulation will result in deficits in both MCA & ACA!
Significant edema is common w/ possible uncal herniation, coma, &death
Posterior Cerebral Artery Syndrome : Supplies and branches
Supplies: occipital lobe, medial/inferior temporal lobe, upper brainstem, midbrain, posterior diencephalon, & thalamus
Two branches:
• Central vs. Peripheral Branch
Central PCA Syndromes (good way to remember is THC)
Thalamic Pain Syndrome- a lot of pain from stimulus that is usually not painful, happens post 1 month hemisensory loss recovery
Hemiballismus- Movement disorder typified by flinging, flailing movements of one extremity
Contralateral hemiplegia from cerebral peduncle involvement (if accompanied by CNIII palsy, then Weber’s Syndrome)
Peripheral PCA Syndromes
Transient Global Amnesia (TGA)
• hippocampal lesion
Dyslexia w/o agraphia; color naming & discrimination problems
Visual symptoms - occipital lobe lesions ( Remember, hemianopsia, prosopagniosa, topographic disorientation has something to do with vision)
Cerebellar lesion symptoms
Superior Cerebellar artery-vestibular
Inferior Cerebellar artery- face,dysphagia
Direction-changing nystagmus
• Nystagmus: rapid involuntary rhythmic eye movement with the eyes moving quickly in one direction (quick phase), and then slowly in the other (slow phase).
- Dizziness
- Nausea/Vomiting
- Ipsilateral ataxia
Sensory changes: decreased light touch, vibration, position sense
UE more impacted than LE
Anterior Inferior Cerebellar Artery (AICA) syndrome
Lateral Pontine Syndrome
Vestibular: sudden onset vertigo, vomiting, nystagmus
Motor: ipsilateral ataxia, falling to ipsilateral side, ipsilateral face paralysis
Sensory: ipsilateral loss of facial sensation, ipsilateral hearing loss and tinnitus, contralateral loss of pain and temperature
Basilar Artery Syndrome
Supplies: Pons, portions of the
midbrain, cerebellum and diencephalon
CN 4-8
• Can be catastrophic because of (B) pontine damage
- Coma
- Locked in syndrome- paralysis except for eyes
- Akinetic mutism
Tetraplegia (bilateral corticospinal tract lesions)
Poor prognosis
Vertebral Artery Syndrome
VA is the primary arterial supply to the medulla & posterior-inferior cerebellum, CN 9-12
Most commonly occluded by atherosclerosis, but is susceptible to trauma, such as MVA or inappropriate extension - rotation manipulations!
Posterior Inferior Cerebellar Artery (PICA) Syndrome AKA
Wallenberg’s (Lateral Medullary) Syndrome
Lateral Medullary Syndrome = Wallenberg Syndrome = PICA Syndrome
Vestibular: Nystagmus, nausea/vomiting, vertigo
Motor: ipsilateral UE/LE ataxia, gait ataxia, dysphagia, dysarthria
Sensory: contralateral loss of pain and temperature of the body, ipsilateral loss of pain and temperature of the face, ipsilateral Horner’s syndrome
Ischemic vs Hemorrhagic CVA recoveries
Ischemic CVAs
• Better survivability, but poorer functional recovery
Hemorrhagic CVAs
• poorer survivability, but better functional recovery
Factors of recovery
- Reduction of swelling or edema
- Existence of collateral blood flow
- Neuroplasticity
Hemorrhagic CVA types and causes
Most common types are
• Intracerebral Hemorrhage (ICH) due to HTN or cerebral amyloid angiopathy (CAA- natural protein from aging)
• SAH due to ruptured aneurysm or AVM
Other causes: • Hyper-anticoagulation • Hemorrhage from brain tumor • Trauma (such as TBI) - ETOH
Hemorrhagic CVA syndromes (CPPT or Cool PowerPoinT)
Putaminal Hemorrhage
• Similar to MCA stroke, but with greater alteration of consciousness
Thalamic Hemorrhage
• Results in contralateral hemiplegia with disproportionately greater sensory loss!
Cerebellar Hemorrhage
• Results in ataxia and vestibulopathy
Pontine Hemorrhage
Offers the poorest prognosis
• Tetraplegia and coma
Intracerebral Hemorrhage (ICH)- evolution symptoms the two types Prognosis
gradual & steady evolution! that occurs over minutes,
hours and days, some are sudden onset
severe HA, vomiting and seizures at onset
Primary ICH
• A spontaneous bleed, and is usually due to microvascular disease associated with HTN and/or aging
• Small penetrating arteries are the most frequently involved
Secondary ICH Occurs due • Trauma • Impaired coagulation • Toxic exposure
Intracerebral Hemorrhage (ICH)-
Prognosis
Most fatal of all CVA subtypes
Prognosis for recovery from ICH is greater because lesions are characterized by compression as opposed to tissue destruction
The expanding lesion causes significant ↑ in HTN, and can be fatal due to the compression of vital centers
Medical Intervention for ICH
- Lowering of BP into the normal range via anti-hypertensive medications
- Treatment of cerebral edema - steroids, mannitol
- Anticonvulsants if seizures are present
SAH-
where
Most common sites
Most common cause
subarachnoid space between the arachnoid & the
pia mater
Most common sites • Anterior communicating artery • Posterior communicating artery • Middle cerebral artery -bones of the orbit and posterior fossa
Aneurysms
Other causes: vascular malformations, trauma, infection
Aneurysm: Surgical Interventions
Surgical Clipping- Craniotomy & clipping at “neck”
Endovascular Coiling
• Catheter up femoral artery - aorta - aneurysm
• Platinum coils - thrombotic reaction - blocks flow & prevents rupture
Dangers of SAH
Susceptibility to re-rupture
• Obstruction of the SA space which can lead to hydrocephalus due to CSF blockage
Blood in SA space may lead to:
• Vasospasm: resulting in ischemic infarction of the adjacent vessels
• Inflammatory and fibrotic responses in the meninges
• These secondary complications often prove fatal
SAH severity levels
- Mild is often associated with stiff neck, mild HA, and confusion lasting for weeks
- Moderate is associated with mild coma, moderate to severe HA
- Severe can be fatal, and is associated with severe HA, decerebrate rigidity and deep coma
Risk of re bleeding in mod and severe lvls
Arteriovenous Malformation (AVM) Process symptoms cause hemorrhages location prognosis
Is the result of abnormal fetal development
High pressure arteries connect directly to low pressure veins instead of through capillaries.
Lack of O2 or glucose -> tiny hemorrhages presenting as HA
focal deficits may occur as a result of shunting away of
blood from healthy brain into the fistula (cerebral steal syndrome)
Arteriovenous Malformation (AVM)
hemorrhages location
prognosis
Hemorrhages can be parenchymal or subarachnoid
Prognosis is good, surviving the 1st bleed
cerebral steal syndrome
Arteriovenous Malformation causing focal deficits may occur as a result of shunting away of
blood from healthy brain into the fistula
(cerebral steal syndrome)
AVM: Treatments
- Radiation - indicated for very small & deep AVM’s
- Embolization - indicated for larger AVM’s. Angiogram then coils, balloons, etc.
- Surgery - total cure. complete resection, thus disallowing them from ever recurring again.
Medical Intervention for SAH/AVM
Surgery is the treatment of choice
• Craniotomy and evacuation
• Craniectomy and evacuation if ICP is abnormally high
Lacunar CVA
Location
Syndromes
Occurs in the deep white matter of the brain
Syndromes tend to be either
• Pure motor (internal capsule-posterior limb)
• Facial weakness (internal capsule-anterior limb)
• Pure sensory (posterolateral thalamus)
