Cerebrovascular Disease Flashcards
ischemia vs hemorrhage
ischemia=no blood flow (more common), vs. hemorrhage=ICH, SAH
-byproducts of CV dz manifest as sudden, focal neurological deficits related to specific vascular territories of the CNS
causes of impairment or LOC
- global deficit
- usually d/t cerebral hypoperfusions, vasovagal syncope, or toximetabolic d/o
TIA
- transient ischemic attack
- sudden focal neurological deficits which completely resolve within 24hrs
- serious warning of high stroke risk
STROKE
- refers to a sudden focal neurological deficit which does NOT completely resolve within 24hr
- may variable improve over several weeks to months
- most often caused by ISCHEMIC infarction
- pts with suspected acute stroke should initially receive a head CT sans contrast to rule out hemorrhage
RF for atherosclerosis (which most pts with CV dz have)
- HTN/HL
- heart dz
- DM
- smoking
- FHx of vascular dz
- minor: obesity, lack of exercise, xs EtOH consumption
Atherosclerotic changes
- predominate at bifurcation pts of large, major cervical and intracranial arteries
- d/t turbulent blood flow at these sites
intravascular atheromas or arterial plaques
- over years develop from subintimal lipid deposition, smooth muscle proliferation, and fibrosis.
- enlarging ones may narrow or occlude an artery or may ulcerate
- ulceration disrupts intima, coagulation process initiated
once coagulation process initiated:
-leads to local occlusion (thrombosis) or distal propagation (embolization) of blood clot, platelets, fibrin, cholesterol, or calcified elements (emboli)
What are the two basic mechanisms of ischemic infarction?
- local arterial THROMBOSIS of an atheroma (form in vessel at site)
- EMBOLIC arterial occlusions from proximal sources (travel to site)
collateral blood flow
-enhanced by congenitally complete CoW at base of brain
cool branches of external carotid artery
-can supply blood in reverse direction through the ophthalmic artery to the CoW
cool vertebrobasilar
VB flow ending in PCA may continue through patent posterior communicating branches of the CoW and supple MCA and ACA
microscopically within 12-36 hours of clinical stroke
- ischemic neurons shrink and appear eosinophilic (“pink neurons”)
- days later: macrophages scavenge necrotic debris and cyst formation occurs with astrocytes at the periphery of the infarction.
perforator or lenticulostriate arteries
- arise abruptly from BASILAR artery and proximal ACA, MCA
- supply deeper structures with significant functions (basal ganglia, internal capsule, thalamus, corona radiata)
What deeper structures are vascularized by the perforator or lenticulostriate arteries
- BASAL GANGLIA
- internal capsule
- thalamus
- corona radiata
lacunar infarcts
small artery occlusions caused by THROMBOSIS (form in vessel at site)
general path of TIA
- an embolus from an arterial of cardiac source obstructs a branch of an internal carotid or vertebrobasilar artery
- clinical deficit depends on location of ischemic area
- deficit resolves quickly as embolus fragments or disintegrates=re-establish flow before permanent damage is done
amaurosis fugax (monocular blindness)
- is a type of carotid territory TIA involving ophthalmic artery or its retinal branches
- pt says: “lowered dark shade” in one eye which gradually lightens up
what can carotid TIAs do?
-causes hemispheral ischemia leading to hemiparesis or aphasia
vertebrobasilar territory TIAs
-cause ischemia of: brainstem, cerebellum, or visual (occipital) cortex, producing symptoms of ataxia, homonymous hemianopsia, or hemiparesis associated with “crossed” brain stem syndromes
completed ischemic infarction
- certain stroke syndromes suggest occlusion of larger arteries or branches
1a. precentral MCA: hemiparesis with greater weakness of face and upper limb
1b. postcentral MCA: sensory deficits limited to face and upper limb
2a. precentral ACA: hemiparesis with greater weakness of lower limb
2b. postcentral ACA: sensory deficits limited to lower limb
crossed brainstem syndromes
- Weber and Wallenberg
- occur with occlusion of large vertebrobasilar arterial branches
Lacunar syndromes
-pure motor hemiplegia, ataxic-hemiparesis, clumsy hand-dysarthria=lacunar syndromes from tiny infarcts in the internal capsule, corona radiata, or basilar pons
pure sensory stroke
-a lacunar syndrome from a small vessel occlusion involving the thalamus
What about the heart?
It can be a source of emboli causing TIAs or ischemic infarction in large artery territories
Where can emboli arise from with the heart? (echo helps determine cardiac sources)
- f/m endocardial clot associated with an acute MI
- f/m poorly contracting LV
- f/m LA clot created d/r afib
- infected/septic emboli from endocarditis
venous clots
-in adults with PFO, can pass from R–>LA into cerebral circulation
arterial lesions
usually consist of atherosclerotic plaques or stenoses which locally thrombose or embolize distally (lacunar infarctions from small vessel atherosclerotic occlusions are thrombotic in nature)
hypercoaguable states (hereditary or acquired)
- can cause occlusions of large and small arteries in addition to cortical veins
- ex: sickle cell anemia, polycythemia vera, antiphospholipid antibody syndrome.
non-atherosclerotic arterial lesions (rare)
- traumatic or spontaneous arterial dissections
- inflammation (vasculitis)
- degenerative occlusive disease (fibromuscular dysplasia)
how can carotid TIAs be evaluated?
- with ultrasound imaging of the cervical internal carotid artery
- also: MRA, CTA, or move invasive catheter angiography
Who benefits from carotid endarterectomy (surgical removal of atheromatous plaque)?
-pts w/ symptomatic atheromatous lesions of 70-99% stenosis at the origin of the internal carotid artery
(smaller risk reduction in symptomatic 50-69% and asymptomatic 60-99%)
What percent stenotic lesion precludes surgery
complete or 100% stenotic lesions (at origin of internal carotid artery) since its thrombotic occlusion extends from the neck to the base of the skull
what are other neurointerventional procedures to tx cervical internal carotid stenotic dz?
arterial stenting and angioplasty via intravascular catheters.
What are the benefits of warfarin therapy?
helps reduce the stroke risk in pts with chronic afib (target INR 2.5) <>
tx for non-afib TIA pts?
stroke reduction with antiplatelet drugs such as:
- ASA 50-325mg daily
- Clopidogrel (Plavix) 75mg daily
- ASA 25mg/Dipyridamole 200mg
- Statins (reduce r/o stroke even sans HL)
Treatment of ischemic infarction
-iv tPA (tissue plasminogen activator)-thrombolytic administered within THREE HOURS of stroke onset
What are conditions that prohibit tPA?
- rapidly improving (TIA) or post-ictal deficits (sz)
- presence of hemorrhage (inc bleed risk) on CT
- uncontrollable HTN
- extreme hypo- or hyperglycemia
- concurrent use of warfarin (inc bleed risk)
- inc bleeding risk f/m recent sx or invasive procedures
What is the greatest risk of using tPA?
(potentially fatal) intracranial hemorrhage
What if ischemic stroke pt cannot receive tPA?
-brain CT or MRI scans help indicate whether a LARGE artery occlusion occurred in which case embolic sources must be investigated for possible need for warfarin, carotid endarterectomy, or interventional procedures (vs. small guy use anti-platelet drugs and medical therapy)
hyperglycemia during an acute ischemic infarction
- associated with poorer prognosis
- preferred initial iv fluid: saline sans dextrose
- insulin may be need to ensure nml glucose levels
besides glucose levels what else needs to be closely monitored?
BP
indications for warfarin therapy
- pts with afib
- ischemic infarction related to: antiphospholipid syndrome, arterial dissection, cerebral venous thrombosis
when warfarin is not indicated what is used
antiplatelet medication
When a pt with a recent cerebral infarction develops impaired consciousness in the absence of hypoglycemia what must be considered?
increased ICP
- in 3-5d of an extensive cerebral infarction brain edema can develop
- even earlier, hemorrhagic transformation of an initially ischemic infarct can occur
what is the relationship between mechanical hyperventilation and inc ICP?
if an obtunded pt requires tracheal intubation for airway protection, mechanical hyperventilation to a pCO2 of 30-35mmHg helps reduce inc ICP
-hypocapnia induces cerebral vasoconstriction which reduces cerebral blood volume
besides mechanical hyperventilation what is another means of reducing elevated ICP
iv mannitol; 0.25gm/kg every 6h if serum osm < 310
-corticosteroids DO NOT reduce inc ICP from ischemic infarction or hemorrhage, but do counteract the elevated ICP from tumor or infection
what happens when there is a sudden rupture of arterial blood into the brain parenchyma?
since arterial bp normally exceeds ICP, there will be an abrupt increase in ICP causing severe HA, impairment or LOC and a focal neurological deficit-dependent on the location of the bleeding
what happens when ICP increases and the edema around the hematoma worsens
there is potentially fatal shifting or herniation of the brain and perfusion around the area of the hematoma is impaired
deeply located vs. superficial hemorrhage
- deeply located: suggest HTN as cause
- superficial, at the poles of the frontal, temporal, or occipital lobes: head trauma
pathologically how does a cerebral hemorrhage appear?
dark red clot with surrounding edema and occasional dissection into the ventricular system if the bleeding is deep and extensive
Subdural hematoma path in elderly
- mild head trauma may tear taut bridging cortical veins which empty into larger venous sinuses
- venous bleeding accumulates in subdural space
- progressive expansion may impair cognition and consciousness, and create focal neurological deficits
how are most cerebral hemorrhages readily seen?
noncontrasted CT brain scan
why is it indicated to screen the urine for illicit drugs?
cocaine or other sympathomimetic drugs which abruptly increase bp may also cause cerebral hemorrhage
What is the most common cause of cerebral hemorrhage
HTN!!
- the weakened walls of small lenticulostriate arteries rupture, bleeding most often into the striatum (putamen and caudate) and thalamus <>
- tx: control bp and increased ICP
What appears white on CT?
acute blood appears dense or “white” on CT, as do calcified structures such as the skull
What is cerebral amyloid angiopathy
- leads to recurrent lobar hemorrhages usually in the posterior cerebral hemispheres
- hereditary condition where arterial walls are weakened by amyloid deposits
which congenital vascular abnormality carries a r/o rupture and hemorrhage?
AVMS (abnml connection of cerebral a to v, sans intervening capillary bed which enlarge over time)
-can be visualized on a brain MRI scan
ischemic infarcts and cerebral hemorrhages
- cerebral hemorrhages may occur within brain tumors or ischemic infarcts
- damaged, ischemic endothelium may leak or ooze blood if reperfusion occurs in an ischemic infarction
what is the m/c c/o bleeding into the subarachnoid space
TRAUMA (in the absence of trauma, a ruptured congenital berry aneurysm)
congenital berry or saccular aneurysms
- arise in the CoW at the base of the brain, especially anteriorly
- berry enlarge overtime with greater risk of rupture beyond 7-10 mm in size
- some pts have a sentinel HA or “warning leak” from a mild to moderate amount of bleeding
why is SAH the WHOML
- d/t increased ICP and meningeal irritation by the blood
- also: nuchal rigidity and meningeal signs
- n/v/impaired consciousness
- no localizing neuro signs since hemorrhage doesnt involve brain parenchyma itself
third cranial (oculomotor) nerve palsy
-this suggests that the berry aneurysm is near the posterior communicating artery
if a pt is suspected of having SAH from aneurysmal rupture what test should they have done?
noncontrasted CT brain scan-which often shows blood in cisterns and sulci around the base of the brain
-If the CT brain scan appears nml, LP is necessary to exclude small volume of subarachnoid blood
Xanthochromia
-yellow coloration of CSF indicating breakdown of blood within the CSF prior to the LP; blood constant from tube to tube (vs traumatic LP blood amt decreases)
What can be used to locate an aneurysm
emergent angiography, preferably conventional catheter angiography for optimal imaging
what can help prevent some future rebleeding
neck of the berry aneurysm should be surgically clipped OR an intravascular catheter may be used to occlude the aneurysm with metallic coils
whats a serious complication of SAH
cerebral vasospasm-reduced blood flow from cerebral vasospasm creates ischemic infarctions and is more likely after a large volume SAH
How do you minimize cerebral vasospasm postoperatively
Triple H therapy:
- HTN-induced vasopressor medication
- hypervolemia-generous iv hydration
- hemodilution (phlebotomy to remove blood)
also. ..oral nimodipine (CCB) improves pt outcome; neuroprotective
CUBS and BEAMS
CUBS: crescent, subdural, bridging veins
BEAM: epidural, MMA, lucid
presentation within 3.5-4 hours of symptom onset and no contraindications
iv alteplase
stroke with no prior antiplatelet therapy
ASA
stroke on ASA therapy
ASA + dipyridamole OR Clopidogrel
stroke on ASA therapy and pt with intracranial large artery atherosclerosis
ASA + Clopidogrel
stroke with evidence of afib
long-term anticoagulation (warfarin, dabigatran, rivaroxaban)
amaurosis fugax
- painless, rapid, transient monocular vision loss
- curtain descending over the visual field
- mc etiology: retinal ischemia d/t atherosclerotic emboli originating from ipsi carotid artery
- pts with vascular rf should receive duplex US of the neck
lacunar stroke of posterolateral thalamus
- sudden onset contra sensory loss involving all sensory modalities (pure sensory stroke)
- wk to mo later pt can develop thalamic pain syndrome=paroxysmal burning pain over affected area that is exacerbated by light touch
basal ganglia (putamen)
- common site of hypertensive intraparenchymal brain hemorrhage
- internal capsule that lies adjacent to the putamen is almost always involved=contra hemiparesis, contra sensory loss, conjugate gaze deviation toward the side of lesion (gaze palsy)
cerebellum hemorrhage
- usually NO hemiparesis
- facial weakness
- ataxia and nystagmus
- occipital HA and neck stiffness
Thalamus
- contra hemiparesis and hemisensory loss
- nonreactive miotic pupils
- upgaze palsy
- eyes deviate toward hemiparesis
central lobe
- contra hemiparesis (Frontal lobe)
- contra hemisensory loss (parietal lobe)
- homonymous hemianopsia (occipital lobe)
- eyes deviate away from hemiparesis
- high incidence of seizures
pons
- deep coma and total paralysis within minutes
- pinpoint reactive pupils
anterior cord syndrome
- 2/2 injury to the anterior spinal artery affecting ant 2/3 of the spinal cord
- neurological findings:
- –b/l hemiparesis: lateral corticospinal tract at level of cord injury and below
- –diminished b/l pain and temp sensation (1-2 levels below cord injury)
- –intact b/l proprioception, vibe sense, and light touch (dorsal column gets blood from post spinal arteries)
parietal lobar hemorrhage
-amyloid angiopathy is most common cause of spontaneous lobar hemorrhage, especially in pts >60
what should be done before thrombolytic therapy (iv alteplase) is given
-noncontrast head CT to rule out hemorrhagic stroke and screen for other contraindications to therapy
nontraumatic SAH
- most commonly d/t ruptured saccular berry aneurysm
- CT without contrast shows acute hemorrhage surrounding brainstem and basal cisterns
- negative head CT? undergo LP-high opening pressure and xanthochromia
what should be done with pts with a confirmed diagnosis
-further evaluate with cerebral angiography and tx with craniotomy with aneurysm clipping OR endovascular methods (coiling/stenting of aneurysm)
spontaneous deep intracerebral hemorrhage
- typically caused by hypertensive vasculopathy involving penetrating branches of the major cerebral arteries
- chronic HTN leads to formation of charcot-bouchard aneurysms which may rupture and bleed within the deep brain structures
- common locations include: basal ganglia (putamen), cerebellar nuclei, thalamus, pons
putaminal hemorrhage
- contra hemiparesis
- contra sensory loss d/t injury of the adjacent internal capsule
central retinal artery occlusion
- monocular painless acute vision loss
- most commonly caused by an embolized atherosclerotic plaque form the ipsi carotid artery
- w/u includes noninvasive imaging of the carotids to evaluate for stenosis
diabetic ophthalmoplegia
- most common cause of CN3 palsy in adults is ischemic neuropathy d/t poorly controlled DM
- paralysis of levator muscle and 4EOMs with preserved pupillary response
- cp: ptosis, down and out gaze, diplopia, nml pupillary resp
neurologic complications of infective endocarditis
- embolic stroke
- cerebral hemorrhage
- brain abscess
- acute encephalopathy or meningoencephalitis
lesion of posterior limb of internal capsule (lacunar infarct)
- acute unilat motor impairment (pure motor hemiparesis)
- no sensory or cortical deficits
- no visual field abnormalities
- assoc most commonly with chronic HTN which leads to arteriolar sclerosis and occlusion of deep penetrating branches of major cerebral arteries
MCA occlusion lesion
- contra somatosensory and motor deficit (face, arm, leg)
- conjugate eye deviation toward side of infarct
- homonymous hemianopia
- aphasia (dominant hemisphere)
- hemineglect (nondominant hemisphere)
ACA occlusion lesion
- contra somtosensory and motor deficit, predominantly in LE
- abulia (lack of will or initiative)
- dyspraxia, emotional disturbances, urinary incontinence
Vertebrobasilar system lesion (supplying the brainstem)
- alternate syndrome with contra hemiplegia and ipsi CN involvement
- possible ataxia
