Flashcards in CN LANGE - Stroke I Deck (96):
The incidence of stroke increases with age, with approximately ... of all strokes occurring in those older than 65yrs.
Stroke is a syndrome characterized by ...?
1. Sudden onset.
2. Focal involvement of the CNS.
3. Lack of rapid resolution.
4. Vascular cause.
Well-documented risk factors for stroke - Nonmodifiable risk factors:
1. Incr. age.
2. Male sex.
3. Low birth weight.
4. African American ethnicity.
5. Family history of stroke.
Well-documented risk factors for stroke - Modifiable risk factors - Vascular:
3. Asymptomatic carotid stenosis (>60% diameter).
4. Peripheral artery disease.
Risk factors for stroke - Modifiable - Cardiac:
Risk factors for stroke - Modifiable - Endocrine:
2. Postmenopausal hormone therapy (estrogen +/- progesterone).
Risk factors for stroke - Modifiable - Metabolic:
1. Dyslipidemia -->High total cholesterol (top 20%), low HDL cholesterol (
Risk factors for stroke - Modifiable - Hematologic:
Stroke in evolution or progressing stroke:
A stroke that is actively progressing as a direct consequence of the underlying vascular disorder (but not because of associated cerebral edema) or has done so in recent minutes --> Termed Stroke in evolution or progressing stroke.
Focal involvement - Hemorrhage produces a less predictable pattern:
Complications such as:
1. Incr. ICP.
2. Cerebral edema.
3. Compression of brain tissue and blood vessels.
4. Dispersion of blood through the subarachnoid space or cerebral ventricles can impair brain function at sites REMOTE from the hemorrhage.
The anterior circulation supplies most of the ...?
2. Subcortical white matter.
3. Basal ganglia.
4. Internal capsule.
The anterior circulation consists of ...?
The internal carotid artery and its branches:
1. Anterior choroidal.
2. Anterior cerebral.
3. Middle cerebral.
--> The middle cerebral artery in turn gives rise to deep, penetrating lenticulostriate branches.
Anterior circulation strokes are commonly associated with symptoms and signs that indicate:
Anterior circulation strokes also often produce:
2. Hemisensory disturbances.
3. Visual field defects.
--> But these can occur with posterior circulation strokes as well.
The posterior circulation supplies:
1. The brainstem.
4. Portions of the occipital and temporal lobes.
The posterior circulation consists of:
1. Paired vertebral arteries.
2. The basilar artery and their branches:
c. Superior cerebellar.
The PCA also gives off ...?
Thalamoperforate and thalamogeniculate branches.
Posterior circulation strokes produce symptoms and signs of:
Brainstem or cerebellar dysfunction, or BOTH:
2. Drop attacks (sudden collapse WITHOUT loss of consciousness).
5. CN palsies.
7. Crossed sensorimotor deficits --> Affect the face on one side of the body and the limbs on the other.
Posterior circulation stroke may also cause:
2. Hemisensory disturbances.
3. Visual field deficits.
--> Can also occur with anterior circulation strokes.
Territories of the principal cerebral arteries - Anterior choroidal:
2. Globus pallidus.
3. Lower internal capsule.
Territories of the principal cerebral arteries - Anterior cerebral:
1. Medial frontal and parietal cortex + subjacent white matter.
2. Anterior corpus callosum.
Territories of the principal cerebral arteries - MCA:
LATERAL frontal, parietal, occipital, and temporal cortex + subjacent white matter.
Territories of the principal cerebral arteries - Lenticulostriate branches:
1. Caudate nucleus.
3. Upper internal capsule.
Territory of PICA:
2. Lower cerebellum.
Territory of AICA:
1. Lower + Middle pons.
2. Anterior cerebellum.
Territory of superior cerebellar artery:
1. Upper pons.
2. Lower midbrain.
3. Upper cerebellum.
Territory of PCA:
1. Medial occipital + temporal cortex + subjacent white matter.
2. Posterior corpus callosum.
3. Upper midbrain.
Territory of thalamoperforate branches:
Territory of thalamogeniculate branches:
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Headache:
A --> 25%.
P --> 3%.
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Altered consciousness:
A --> 5%.
P --> 16%.
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Aphasia:
A --> 20%.
P --> 0%.
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Visual field defect:
A --> 14%.
P --> 22%.
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Diplopia:
A --> 0%.
P --> 7%.
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Vertigo:
A --> 0%.
P --> 48%.
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Dysarthria:
A --> 3%.
P --> 11%.
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Drop attacks:
A --> 0%.
P --> 16%.
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Hemi- or monoparesis:
A --> 38%.
P --> 12%.
Symptoms/Signs (S/S) of anterior vs posterior circulation ischemia - Hemisensory deficit:
A --> 33%.
P --> 9%.
Although TIAs do NOT themselves produce lasting neurologic dysfunction, they are important to recognize because ...?
Approx. 1/3 of patients with TIAs will go on to have a stroke within 5years --> This risk may be reduced with treatment.
What other thing can produce FOCAL + CENTRAL neurologic deficits that begin abruptly and last for at least 24h?
1. Hypoglycemia + other metabolic disturbances.
--> The term stroke is used only when such events are caused by vascular disease.
Among ischemic strokes (90%):
50% --> Attributed to cardiac embolism.
25% --> Large artery occlusion.
10% --> Small artery occlusion.
--> The remaining = cryptogenic.
Stroke - Blood flow to the ischemic core is typically ...?
Less than 20% of normal.
Severe ischemia produces ...?
SELECTIVE neuronal necrosis, in which most or all neurons die BUT glia + vascular cells are preserved.
Complete, permanent ischemia, such as occurs in stroke WITHOUT reperfusion, causes ...?
PANNECROSIS --> Affecting ALL cell types --> Chronic cavitary lesions.
Where ischemia is incomplete (20-40%) - as in the ischemic borderzone or penumbra - Cell damage is potentially ...?
Reversible and cell survival may be prolonged.
Death of penumbral tissue is associated with worse or better clinical outcome?
WORSE clinical outcome.
Brain edema is another determinant of stroke outcome - VASOGENIC Edema is usually maximal approx. when?
2 to 3 days after stroke --> May be sufficiently severe that it produces a mass effect that causes herniation (displacement of brain tissue between intracranial compartments) and death.
Emboli in the posterior cerebral circulation usually lodge where ...?
At the apex of the basilar artery or in the posterior cerebral arteries.
Embolic strokes often produce neurologic deficits that are maximal when?
Hemorrhage may interfere with cerebral function through a variety of mechanisms, including:
1. Destruction or compression of brain tissue.
2. Compression of vascular structures.
All intracranial hemorrhage is caused by arterial bleeding EXCEPT:
IntraCEREBRAL hemorrhage causes symptoms by ...?
DESTROYING or COMPRESSING brain tissue.
Unlike ischemic strokes, intracranial hemorrhage tends to cause ...?
1. More severe HEADACHE.
2. DEPRESSION OF CONSCIOUSNESS.
==> As well as neurologic deficits that do NOT correspond to the distribution of any single vessel.
SAH - Leads to cerebral dysfunction due to:
1. Incr. ICP.
2. Resulting hypoperfusion.
3. Direct destruction of tissues.
4. Toxic constituents of subarachnoid blood.
SAH may be complicated by ...?
1. Vasospasm (leading to ischemia).
3. Extension of blood into brain tissue (producing an intracerebral hematoma).
SAH typically presents with ... rather than ... .
Headache rather than focal neurologic deficits.
Focal cerebral ischemia - Pathophysiology is complex as it involves a process that evolves over time, affects the brain nonuniformly, and targets multiple cell types. Mention the major injury mechanisms:
1. Energy failure.
2. Ion gradients.
3. Calcium dysregulation.
5. Oxidative and nitrosative injury.
6. Cell death cascades.
Focal cerebral ischemia - Ion gradients:
1. K leaks from cells --> Depolarizes adjacent cells --> Activating voltage-gated ion channels + neurotransmitter release.
2. Extracellular K and neurotransmitter glutamate trigger cortical spreading depression --> Leading to further neuron + astrocyte depolarization.
--> This consumes additional energy and may extend the infarct.
Focal cerebral ischemia - Calcium dysregulation:
1. Ischemic elevation of extracellular K causes membrane depolarization and triggers Ca entry.
2. Catabolic proteases, lipases, and nucleases are activated.
3. Mitochondrial function is compromised --> Cell death pathways are mobilized.
Focal cerebral ischemia - Excitotoxicity:
Refers to the neurotoxic effects of excitatory neurotransmitters, especially glutamate.
--> Ischemia promotes excitotoxicity by:
1. Stimulating neuronal glutamate release.
2. Reversing astrocytic glutamate uptake.
3. Activating glutamate receptor-coupled ion channels.
--> Ca-influx through these channels contributes to Ca dysregulation and activates neuronal NO synthase --> Generating potentially neurotoxic NO.
Focal cerebral ischemia - Oxidative and nitrosative injury:
1. Inhibition of mt enzymes.
2. DNA damage.
3. Activation of ion channels.
4. Covalent modification of proteins.
5. Triggering cell death pathways.
Focal cerebral ischemia - Inflammation - Although the early inflammatory response exacerbates injury, subsequent inflammatory events ...?
May be NEUROPROTECTIVE or contribute to repair.
The first line of defense against ischemia is collateral circulation. Collateral circulation in bilateral vertebral artery occlusion?
The first line of defense against ischemia is collateral circulation. Collateral circulation in common carotid artery occlusion:
Contralateral common carotid artery via ipsilateral external carotid artery or vertebral artery via ipsilateral occipital artery.
The first line of defense against ischemia is collateral circulation. Collateral circulation in internal carotid artery occlusion:
Ipsilateral external carotid artery via ophthalmic artery or circe of Willis.
The first line of defense against ischemia is collateral circulation. Collateral circulation in middle cerebral artery occlusion:
Ipsilateral anterior or posterior cerebral artery via leptomeningeal anastomoses.
Focal cerebral ischemia - Survival and repair mechanisms:
1. Collateral circulation.
2. Inhibitory neurotransmitters.
3. Transcriptional hypoxia response.
6. Ischemic tolerance.
7. Repair mechanisms.
Focal cerebral ischemia - Survival and repair mechanisms - Neurogenesis:
Cerebral ischemia stimulates neurogenesis + some new neurons migrate to ischemic brain regions.
--> Here they may promote survival and repair by releasing GFs, suppressing inflammation, or other effects.
Focal cerebral ischemia - Survival and repair mechanisms - Ischemic tolerance:
1. Ischemia may provide PARADOXICAL protection against subsequent ischemia.
2. Mild ischemia PRECONDITIONS brain tissue and confers relative ischemia resistance.
--> Ischemic tolerance involves extensive changes in gene expression and numerous molecular mediators.
Focal cerebral ischemia - Repair mechanisms:
1. Most patients recover to some extent after stroke, reflecting a capacity for spontaneous postischemic repair and the brain's innate plasticity.
2. Plastic changes occur in the peri-infarct region + at REMOTE sites such as the CONTRALATERAL hemisphere.
--> Include changes in gene expression, incr. neuronal excitability, axonal sprouting, synaptogenesis, somatotopic reorganization, and formation of new neuronal circuits.
Pathology - Large artery occlusion - On GROSS inspection:
A recent infarct from large artery occlusion is a swollen, softened area of brain that usually affects BOTH gray and white matter.
Pathology - Large artery occlusion - Microscopy:
1. Acute ischemic changes in neurons (shrinkage, microvacuolization, dark staining).
2. Destruction of glial cells.
3. Necrosis of small blood vessels.
4. Disruption of nerve axons and myelin.
5. Accumulation of interstitial fluid.
6. Perivascular hemorrhages may be observed.
Pathology - Large artery occlusion - Depending on the interval between infarction and death, cerebral edema may also be present - Maximal when?
During the first 4-5 days after stroke and can cause herniation of the cingulate gyrus across the midline or of the temporal lobe below the tentorium.
Pathology - Small artery occlusion - Gross:
1. Lacunes, or small cavities up to 15mm in diameter usually located in subcortical white (eg internal capsule) or deep gray (eg basal ganglia or thalamus) matter.
2. White matter (including periventricular) lesions showing punctate or confluent myelin refraction, gliosis, and axonal loss
Pathology - Small artery occlusion - Microscopy:
2. Lipohyalinosis (collagenous thickening and inflammation of the vessel wall).
3. Fibrinoid necrosis (vessel-wall destruction with perivascular inflammation.
Clinical-anatomic correlation - The anterior cerebral artery supplies the ...?
1. Parasagittal cerebral cortex --> Portions of motor + sensory cortex related to the contralateral LEG.
2. The so-called bladder inhibitory or micturition center.
3. Anterior corpus callosum.
Anterior cerebral artery stroke - Clinical syndrome:
1. Contralateral paralysis + sensory loss exclusively or primarily affecting the LEG.
2. There may also be abulia (apathy), disconnection syndromes such as the alien hand (involuntary performance of complex motor activity), transcortical expressive aphasia, and urinary incontinence.
MCA - Cortical branches include the superior division, which supplies:
1. The motor and sensory representation of the face, hand, and arm.
2. Broca area of the dominant hemisphere.
MCA - Inferior division supplies:
1. The visual radiations.
2. Visual cortex related to macular vision.
3. Wernicke area of the dominant hemisphere.
MCA - Lenticulostriate branches:
From the most proximal portion (stem) of the MCA --> Supply the basal ganglia + motor fibers to the face, hand, arm, and leg as they descend in the genu and the posterior limb of the internal capsule.
MCA - Superior division stroke:
1. Contralateral hemiparesis that affects the face, hand, and arm but spares the leg.
2. Contralateral hemisensory deficit in the same distribution.
3. No homonymous hemianopia.
--> If the dominant hemisphere is involved --> Broca aphasia.
MCA - Inferior division stroke:
1. Contralateral homonymous hemianopia that may be denser INFERIORLY.
2. Impaired cortical sensory functions (eg graphesthesia and stereognosis) on the contralateral side of the body.
3. Disorders of spatial thought (eg anosognosia, neglect of the contralateral limbs and contralateral side of the external space, dressing apraxia, and constructional apraxia).
4. If the dominant hemisphere is involved --> Wernicke aphasia.
MCA - Inferior division stroke - NON dominant hemisphere:
An acute confusional state may occur.
MCA - Occlusion at the bifurcation or trifurcation of the MCA:
Combines features of superior + inferior division stroke:
1. Contralateral hemiparesis + hemisensory deificit involving the face and arm more than leg.
2. Homonymous hemianopia.
3. If the dominant hemisphere is affected --> Global combined aphasia.
MCA - Occlusion of the stem of the MCA:
Proximal to the origin of the lenticulostriate branches --> Clinical syndrome similar to that seen after occlusion at the trifurcation.
--> In addition: Involvement of the internal capsule causes paralysis of the contralateral leg, so hemiplegia and sensory loss affect face, hand, arm, and leg.
In addition to anterior and middle cerebral arteries, the ICA also gives rise to the ...?
Ophthalmic artery, which supplies the retina.
1. May be ASYMPTOMATIC or cause strokes of highly variable severity - depending on the adequacy of collateral circulation.
2. Symptomatic occlusion results in a syndrome similar to that of MCA (contra hemiplegia, hemisensory deficit, and homonymous hemianopia, + aphasia if dominant is involved).
3. Monocular blindness is also common.
The paired PCAs arise from the tip of the basilar artery in most cases and supply:
1. The occipital cortex.
2. Medial temporal lobes.
3. Posterior corpus callosum.
5. Rostral midbrain.
PCA - Emboli in the basilar artery tend to lodge at ...?
Its apex and occlude one or both PCAs.
--> Subsequent fragmentation can produce asymmetric or patchy PCA infarction.
PCA occlusion produces:
1. Homonymous hemianopia affecting the contralateral visual field, except that macular vision may be spared.
2. In contrast to visual field defects from MCA infarction --> Those caused by PCA occlusion may be denser SUPERIORLY.
PCA occlusion - With occlusion near the origin of the PCA at the level of the midbrain, what may occur?
Ocular abnormalities may occur, including:
1. Vertical gaze palsy.
2. III nerve palsy.
4. Vertical skew deviation of the eyes.
PCA occlusion - Involvement of the occipital lobe of the dominant hemisphere may cause:
1. Anomic aphasia --> Difficulty in naming objects.
2. Alexia without agraphia.
3. Visual agnosia.
Visual agnosia is ...?
Failure to identify objects presented in the LEFT side of the visual field, caused by a lesion of the CORPUS CALLOSUM that disconnects the right visual cortex from language areas of the left hemisphere.
BILATERAL PCA infarction may result in:
1. Cortical blindness.
2. Memory impairment (from temporal lobe involvement).
3. Inability to recognize familial faces (prosopagnosia).
4. As well as a variety of exotic visual and behavioral syndromes.