2 - Stroke Syndromes Flashcards
Cerebral Perfusion Pressure (CPP)
Clinical presentation of High and Low CPP?
What occurs to the graph of Brain Blood Flow vs MAP in chronic hypertension?
Gradient that cuases blood to flow to the brain
CPP = Mean Arterial Pressure (MAP) - Intracranial Pressure (ICP)
High - Hypertensive, encephalopathy, cerebral edema
Low - Foca/global ischemia
Shifted right w/higher MAP
Ischemic Stroke
Two Types: Embolic / Thrombotic
tPA Drug?
Loss of blood supply to certain regions of the brain that leads to local infarction (death) of tissue– %85 of ALL strokes
Embolic Stroke: Masses (emboli) formed elsewhere in the ciruclatory system travel and blood vessels of smaller diameter
Thrombotic: Build-up of athersclerotic plaques with the vessel, resulting in gradual vessel occlusion (Most common stroke syndrome)
Tissue Plasminogen Activator (tPA) - Breaks up clots, effectively diminished > 3 hrs; increased risk of Hemorrhagic Stroke
Hemorrhagic Stroke
Two Types: Intraerebral (ICH), Subarachnoid (SAH)
Blood vessel rupture leads to bleeding
Rupture of aneurysm
Can lead to herniation, and death–clinical emergency
Intracerebral (ICH) - internal bleeding in the brain
Subarachnoid (SAH) - rupture of surface blood vessel leads to buildup of blood and increased pressure in subarachnoid space - “Thunderclap Headache, worst headach of my life”
Pathogenic Events in Focal Cerebral Ischemia:
Minutes
Hours
Days
What is the clinical implication of this?
Minutes:
Anoxic Depolarization (AD), neurons depolarizing; Ischemic Core will die within minutes
Excitotoxicity - Glutamate and calcium overload
Hours:
Peri-infarct Depolarization (PIDs), Inflammation
Days:
Apoptosis
Major damage can be prevented from face re-prefusion (quick action)
Ischemic Core vs Penumbra
Ischemic Core - Acute Neuronal Damage and Death; spread of Anoxic Depolarization
Penumbra - Peri-infarct Depolarizations; area surrounding Ischemic Core
*Depolarizations become shorter as we move from core
Clinical: Imaging of Stroke
Non-Contrast
CT
Diffusion Weighted MRI
Histological Sign
Non-contrast CT must be performed to rule out hemorrhage prior to tPA administration
- - -
CT Scans: Widely available, rapid results
Diffusion-weighted MRI scans: Much more accurate than CT, but availability/cost may be prohibitive
Histological: Eosinophilic (red) neurons; visible 4-12 hours after Ischemic Stroke
Stroke Terminology: Penumbra
Area immediately surrounidng the dead core that is potentially salvagebale, but will become infarcted with inadequate intervention
Result of glutamate excitotoxicity from dying neurons and continued hypoxia (ischemic cascade)
Clinical: Transient Ischemic Attack (TIA)
Acute episode typically resolved in 30 min - 24 hrs
TIAs are critically important to recognize, diagnose and treat, despite the restoration of function, because it is highly predictive of major stroke (often within days of the TIA)
Clinical: Cortical Strokes (“Large Vessel Strokes”)
Amaurosis Fugax?
Contra/Ipsi/Global Symptoms?
Stroke of major cortical artery territory
Internal Carotid (ICA) major branches are ACA + MCA; so symptoms can be very diverse
- - -
Amaurosis Fugax - Occlusion of Central Retinal Artery (br. of Opthalmic); transient, unilateral loss of vision; TIAs of the ICA can trigger this condition
Contra - Spastic Limb Paresis (B.A. 4), Loss of pain/proprio/touch (B.A. 3, 1, 2), Lower Facial Paralysis (UMN of CN VII); Babinski–Primary Motor/Somatosensory
Ipsilatera - Loss of Vision (Opthalmic A. -> Central Retinal A.)
Global - [Dominant Hemisphere] Language (Broca/Wernicke), [Non-Dominant] Neglect
Clinical: Middle Cerebral Artery Stroke
Signs/Symptoms
“Upper > Lower”
Most common cerebral artery infarct (biggest territory); 3 general regions (Superior, Inferior, Deep Territory)
Signs:
- Two Possibilities
A. [Dominant Hemisphere] Global Aphasia,
B. [Non-Dominant] Neglect
- Tongue deviate away from the site of lesion
Clinical: Anterior Cerebral Artery Stroke
Lower>Upper
Signs/Symptoms:
- Presents as UMN type weakness
- Contralateral leg more than arm/face
- Medial Frontal Lobe effects (albulia (lazy), akinetic mutism, urinary incontinence)
Clinical: Posterior Cerebral Artery Stroke
Symptoms:
- Contralateral Homonymous Hemianopsia (loss of 1/2 of visual field) with macular sparing
- Memory deficits (hippocampus)
- Alexia without agraphia (splenium of Cerebral Cortex)
***Hippocampus vulnerable to ischemic hypoxia, esp. pyramidal excitatory***
Clinical: Subcortical Strokes - Penetrating Branches of Middle Cerebral Artery (Lateral Striate Arteries) (“Small Vessel Strokes”)
Lenticuloostriate Arteries of the MCA (lateral striate branches) supply genu (corticobulbar) and posterior limb (motor/somatosensory radiation) of the Internal Capsule (IC)
Similar to Cortical Stroke:
Contralateral: Babinkski, loss of fine touch, inability to localize pain, facial paralysis
***There will NOT be cortical signs (Aphasia, Neglect, etc)***
Test CN VII and XII
Clinical: Thalmic Strokes
Contralateral Homonymous Hemianopsia
Posterior Cerebral Artery (PCA), the Posterior Communicating Artery, and the Anterior Choroidal Artery primary supply to Thalamus
Symptoms can be varied
Contralateral Homonymous Hemianopsia - only see 1/2 visual world (R or L); involving LGN
Thalamic Syndrome (Dejerine-Roussy Syndrome) - Extreme contralateral pain
Clinical: Midbrain Stroke
Weber’s Syndrome
Claude’s Syndrome
Benedikt’s Syndrome
NO Cortical or Visual field deficits
Lateral nature of facial sensation:
Cortex = contralateral numbness, Brainstem = Ipsilateral numbness
Weber’s Syndrome: Penetrating branches of the PCA (basal midbrain, crus cerebri, substantia nigra, exiting CN III fibers)
Claude’s Syndrome: PCA/basilar artery (tegmentum); Diplopia, ptosis, lateral strabismus–also upper limb tremor (Red Nucleus)
Benedikt’s Syndrome: Penetrating branches of the baslar artery (basal and tegmental midbrain)
