2. Vascular Neurology Flashcards
ABCD2 score is used for?
Identification of risk factors that predict stroke after TIA.
ABCD2 score points?
Age of 60 years or more (1 point).
Initial BP: SBP ≥ 140 or DBP ≥ 90 (1 point).
Clinical symptoms:
1 point for speech impairment without weakness.
2 points for unilateral weakness.
Duration of symptoms:
0 points for < 10 minutes.
1 point for 10 to 59 minutes.
2 points for 60 minutes or more).
Diabetes (1 point).
Stroke risk after low risk TIA based on ABCD2 score?
0-3 points: Low Risk.
2-Day Stroke Risk: 1.0%
7-Day Stroke Risk: 1.2%
90-Day Stroke Risk: 3.1%
Stroke risk after moderate risk TIA based on ABCD2 score?
4-5 points: Moderate Risk.
2-Day Stroke Risk: 4.1%
7-Day Stroke Risk: 5.9%
90-Day Stroke Risk: 9.8%
Stroke risk after high risk TIA based on ABCD2 score?
6-7 points: High Risk.
2-Day Stroke Risk: 8.1%
7-Day Stroke Risk: 11.7%
90-Day Stroke Risk: 17.8%
Picture? And presentation?
Restricted diffusion in the pons and the cerebellum.
Quadriplegia and impaired horizontal gaze - locked-in syndrome.
Vertical gaze impairment lesion localization?
Midbrain lesions.
Maximum NIHSS score?
42
tPA/Alteplase dose?
The dose is 0.9 mg/kg, with a 10% bolus and the rest over 1 hour, with a maximum dose of 90 mg.
tPA trial for the 3-hour window?
FDA approved on the basis of the National Institute of Neurological Disorders and Stroke (NINDS) tPA trial.
Published 1995.
tPA trial for the 4.5-hour window?
The European Cooperative Acute Stroke Study 3 (ECASS3), intravenous tPA is safe and beneficial up to 4.5 hours after the onset of symptoms.
Locked-in syndrome?
Caused by a basilar occlusion.
Bilateral infarcts at the base of the pons, affecting the long tracts but preserving the reticular activating system.
Patients are awake, consciousness is preserved, and they can blink and move their eyes vertically; however, they are quadriplegic, unable to speak, and with impairment of horizontal eye movements.
Top of the basilar syndrome?
Infarcts of various structures including the midbrain, thalamus, and temporal and occipital lobes.
The manifestations are complex and varied, including combinations of behavioral abnormalities, alteration of consciousness, pupillary manifestations, disorders of ocular movements, visual field defects, and motor and/or sensory deficits.
Venous sinus thrombosis clinical presentation?
Headache in about 90% of cases in adults.
Seizures in 40% of patients (higher than arterial strokes).
Increased ICP - due to occlusion of venous drainage, hemorrhagic infarct and edema.
Diplopia due to 6th CN palsy - nonlocalizing and may be a manifestation of increased ICP.
Focal neurologic findings depending on the area affected along the thrombosed venous sinus.
> Thrombosis of the deep venous system may lead to deep venous infarcts, including bilateral thalamic infarcts.
> Superior sagittal sinus thrombosis can lead to infarcts in the parasagittal cortex bilaterally along the sinus.
Picture? Vessel occluded?
Wallenberg’s or lateral medullary syndrome - right lateral medulla and cerebellum infarct.
Caused by occlusion of the PICA, and is often associated with occlusion of the vertebral artery.
Wallenberg’s or lateral medullary syndrome involved structures and manifestations?
• Vestibular nuclei, causing vertigo, nystagmus, nausea, and vomiting.
• Descending tract and nucleus of the 5th CN, producing impaired sensation on the ipsilateral hemiface.
• Spinothalamic tract, producing loss of sensation to pain and temperature in the contralateral hemibody.
• Sympathetic tract, manifesting with ipsilateral Horner’s syndrome with ptosis, miosis, and anhidrosis.
• Fibers of the 9th and 10th CN, presenting with hoarseness, dysphagia, ipsilateral paralysis of the palate and vocal cord, and decreased gag reflex.
• Cerebellum and cerebellar tracts, causing ipsilateral ataxia and lateropulsion.
• Nucleus of the tractus solitarius, causing loss of taste.
Patients may present with combinations of these manifestations and not always with a complete syndrome.
Hiccups is typically seen in this syndrome, but may not be explained by a lesion to a specific structure in the brainstem.
Vertebral artery dissection? Most common site of dissection?
Can cause lateral medullary syndrome.
The most common site of a vertebral dissection is at the level of C1-C2, where the artery is mobile as it is leaving the transverse foramina to enter the cranium.
Vertebral artery dissection? Imaging modalities?
Catheter angiogram - gold standard, will demonstrate the narrowing of the vessel, the extension of the dissection with an intimal flap, or double lumen. Potential risk of causing or worsening an existing dissection.
CTA and MRA with contrast have replaced a catheter angiogram for the diagnosis of dissection of the cervical arteries.
MRA with a time-of-flight sequence: assess the flow at the site of the dissection; however, it does not provide information about the vessel wall.
MRI with fat-suppression technique: assess the vessel wall and surrounding tissues, and very useful in nonocclusive dissections, when conventional angiogram will not give information about the vessel wall.
NINDS trial stats?
Symptomatic ICH occurred in 6.4% of the tPA group, compared with 0.6% in placebo group.
tPA group had improved clinical outcomes and were at least 30% more likely to have minimal or no disability at 3 months.
The mortality at 3 months was 17% in the tPA group and 21% in the placebo group.
The earlier the administration, the better the prognosis and the lower the risk of hemorrhage.
ECASS3: tPA between 3 and 4.5 hours additional exclusion criteria?
NIHSS >25.
Age >80.
History of both stroke and diabetes.
Any anticoagulant use, regardless of prothrombin time or INR.
Amaurosis fugax?
Transient monocular blindness.
Painless visual loss: a “shade” or “curtain” moving in the vertical plane, with a rapid onset and brief duration of a few minutes.
Vision is most commonly recovered completely.
However, the presentation of amaurosis fugax in a patient with an underlying ICA stenosis, may herald the occurrence of a stroke.
Amaurosis fugax causes?
Atherosclerotic stenosis of the ipsilateral ICA.
Transient occlusion of the retinal or ophthalmic arteries (the retinal artery originates from the ophthalmic artery, which is a branch of the ICA).
Other rate causes include giant cell arteritis, and embolism from other source.
Differentiate AICA from PICA strokes?
anterior inferior cerebellar artery
1- Ipsilateral deafness occurs with AICA infarcts.
(Hearing loss attributed to involvement of the lateral pontomedullary tegmentum.
Audiologic evaluations have also suggested an inner ear and cochlear injury, which could be explained by involvement of the labyrinthine artery, which is a branch of the AICA).
2- By imaging, AICA infarcts affect the cerebellum more ventrally as compared with PICA infarcts.
Picture? Mechanism?
Bilateral thalamic infarction, which can be seen with occlusion of the artery of Percheron.
The P1 segment of the PCA gives rise to interpeduncular branches that will provide vascularization to the medial thalamus. Most frequently, these branches arise from each PCA separately and will give perfusion to the thalamus on their respective side. In some cases, a single artery called the artery of Percheron will arise from the P1 segment on one side and will supply the medial thalami bilaterally. This is a normal variant. If an occlusion of the artery of Percheron occurs, the result will be an infarct in the medial thalamic structures bilaterally.
Thrombosis of the deep venous structures may produce venous infarcts in the thalamus, but this is not seen with superior sagittal sinus thrombosis.
The recurrent artery of Heubner? Origin? Supplies?
A branch of the ACA - largest deep penetrating branch.
Supplies the anterior limb of the internal capsule, the inferior part of the head of the caudate, and the anterior part of the globus pallidus.
The pericallosal artery origin?
One of the subdivisions of the ACA, running along the corpus callosum.
Lacunar stroke? Mechanism? Risk factors?
Occurs from occlusion of a small penetrating artery, as a consequence of chronic hypertension.
Diabetes and hyperlipidemia also play a role but to a lesser degree.
These small vessels develop lipohyalinosis with vessel wall degeneration and luminal occlusion.
Atherosclerosis of the parent vessel may occlude the opening of these small penetrating branches, or predispose to the entry of embolic material that will occlude them.
Lacunar infarcts? Locations?
Putamen.
Caudate nuclei.
Thalamus.
Basis pontis.
Internal capsule.
Deep hemispheric white matter.
Lacunar stroke syndromes?
• Pure motor, usually involving face, arm, and leg equally, and the most frequent location is in the territory of the lenticulostriate branches, affecting the posterior limb of the internal capsule, but has also been described with lacunes in the ventral pons.
• Pure sensory, with hemisensory deficit involving the contralateral face, arm, trunk, and leg from a lacune in the thalamus.
• Clumsy-hand dysarthria occurs more frequently from a lacune in the paramedian pons contralateral to the clumsy hand, but it may also occur from a lacune in the posterior limb of the internal capsule.
• Ataxic hemiparesis, in which the ataxia is on the same side of the weakness, but out of proportion to the weakness, and this occurs from lacunes in the pons, midbrain, internal capsule, or parietal white matter.
Lacunar stroke “stuttering”?
The clinical manifestations of lacunar infarcts may have a sudden onset; however, it is not infrequent to see a stepwise “stuttering” progression of the neurologic deficits over minutes, and sometimes over hours to even days.
Lenticulostriate branches origin? Supplies?
Arise from the trunk of the MCA before its bifurcation
Provide vascular supply to the putamen, part of the head and body of the caudate nucleus, the outer globus pallidus, the posterior limb of the internal capsule, and the corona radiata.
Superior division of MCA stroke? Presentation?
Hemiparesis affecting mainly arm and face, probably from ischemia to the lateral hemispheric surface.
Eye deviation occurs from unopposed action originating from the other frontal eye fields.
Broca’s or motor aphasia.
Aphasia types in MCA and MCA branches strokes?
Broca’s or motor aphasia occurs from ischemia in the territory of the superior division of the MCA affecting the dominant inferior frontal gyrus.
Ischemia in the territory of the inferior division of the MCA in the dominant hemisphere will cause Wernicke’s aphasia.
A left MCA trunk occlusion will likely produce a global aphasia (will also produce ischemia in the lenticulostriate arteries’ territory presenting with hemiparesis or hemiplegia affecting face, arm, and leg).
An infarct of the lenticulostriate branches will not present with cortical findings such as aphasia.
ACA branches and supply?
ACA supplies the anterior three-quarters of the medial surface of the frontal lobe.
Deep penetrating branches originate from the ACA (proximal and distal to the Acomm), and the recurrent artery of Heubner is the largest of these deep branches.
These penetrating vessels supply the anterior limb of the internal capsule, the inferior part of the head of the caudate nucleus, and the anterior part of the globus pallidus.
ACA stroke presentation?
Given that both ACAs communicate via the Acomm, an occlusion proximal to the Acomm may not produce significant clinical manifestations in the setting of a normal complete circle of Willis.
An infarction occurring from an ACA occlusion distal to the Acomm presents with:
1- Contralateral sensorimotor deficits of the lower extremity, sparing the arm and face.
2- Urinary incontinence due to involvement of the medial micturition center in the paracentral lobule.
3- Deviation of the eyes to side of the lesion.
4- Paratonic rigidity occur sometimes.
An anterior communicating artery occlusion significance?
Does not produce clinical manifestations in patients with otherwise normal perfusion dynamics.
The vascular supply of the thalamus?
Originates mainly from the posterior circulation through four major arteries:
- The tuberothalamic artery: (aka polar artery) originates from the Pcomm and supplies the anterior portion of the thalamus, especially the ventral anterior nucleus.
- The thalamoperforating or paramedian artery originates from P1/PCA and supplies the medial aspect of the thalamus, especially the dorsomedial nucleus.
- The thalamogeniculate artery originates from P2/PCA and supplies the lateral aspect of the thalamus, including the ventral lateral group of nuclei.
- The posterior choroidal artery arises from P2/PCA and provides vascularization to the posterior aspect of the thalamus, where the pulvinar is located.
Picture? Artery involved?
Superior cerebellar artery (SCA) stroke - right cerebellar hemisphere superiorly. CT scan at the level of the midbrain.
Vascular supply of cerebellum and brainstem in general?
The SCA supplies most of the superior half of the cerebellar hemisphere, including the superior vermis, the superior cerebellar peduncle, and part of the upper lateral pons.
The anterior inferior cerebellar artery (AICA) supplies the inferolateral pons, middle cerebellar peduncle, and a strip of the ventral cerebellum between the posterior inferior cerebellar and superior cerebellar territories.
The posterior inferior cerebellar artery (PICA) supplies the lateral medulla, most of the inferior half of the cerebellum and the inferior vermis.
The inferior division of the MCA? Structures supplied? Stroke presentation?
Supplies the inferior parietal and lateral temporal lobe regions.
Stroke syndrome:
1- Wernicke’s (receptive) aphasia, in which the patient may speak fluently but does not make sense, and is not able to understand spoken language or follow commands. This occurs from ischemia of the posterior aspect of the superior temporal gyrus.
2- Agitation and confusion.
3- Cortical sensory deficits in the face and arm.
4- Visual defects in the contralateral hemifield.
Picture?
MRA: absence of basilar artery, probably from an occlusion.
What basilar occlusion can cause?
- Pontine infarct and will possibly result in a locked-in syndrome.
- Possibly could cause extensive brainstem infarction resulting in brain death.
Basilar occlusion mechanism?
- Local thrombosis of the basilar artery itself.
- Thrombosis of both vertebral arteries.
- Thrombosis of a single vertebral artery when it is the dominant vessel.
- Embolism can occur as well, frequently lodging distally in the vessel.
Parinaud’s syndrome? Clinical findings? Lesion location?
Characterized by:
- Supranuclear paralysis of eye elevation.
- Defect in convergence.
- Convergence-retraction nystagmus.
- Light-near dissociation.
- Lid retraction.
- Skew deviation of the eyes.
The lesion is localized in the dorsal midbrain and is classically seen with pineal tumors compressing the quadrigeminal plate; however, it can occur from midbrain infarcts.
Picture?
Absence of the ICA on the left side. The left MCA is still partially seen and is being supplied via the anterior communicating artery.
The anterior choroidal artery? Origin? Supplies?
Arises from the ICA just above the origin of the Pcomm (or supraclinoid ICA segment).
Supplies the internal segment of the globus pallidus, part of the posterior limb of the internal capsule, and part of the geniculocalcarine tract.
As it penetrates the temporal horn of the lateral ventricle, it supplies the choroid plexus and then joins the posterior choroidal artery from the posterior circulation.
Picture?
Occlusion of the main trunk of the left MCA, which is not filling with contrast beyond the occluded segment.
The ICA is visualized up to its terminus. The ACA is also visualized and the A1 segment is patent.
ACA segments?
A1 segment: extends from the ICA terminus to the Acomm artery.
A2 segment: extends from the Acomm artery to the bifurcation into pericallosal and callosomarginal arteries.
A3 segment: includes the distal branches after this bifurcation.
Picture? Mechanism?
Watershed infarction, between the superficial and deep territories of the MCA.
Occur when there is reduction of blood supply between two vascular territories; this region being susceptible to ischemia.
This reduction of blood flow can occur in the setting of systemic hypotension, especially with an underlying stenosis proximal to both territories, ie carotid stenosis.
Picture?
Hyperdense left MCA sign.
Hyperdense left MCA sign? Specificity? Sensitivity? Mimics?
loss of the insular ribbon, attenuation of the lentiform nucleus, and hemispheric sulcal effacement.
In a patient with a presumed stroke, the hyperdense MCA sign has good specificity and positive predictive value for atheroembolic occlusions of the affected vessel, and it is associated with poor prognosis.
This sign lacks sensitivity but is helpful when a strong clinical suspicion exists.
Mimics of hyperdense MCA sign, aka pseudohyperdense sign, include vascular calcification, increased hematocrit, and intravenous contrast.
Early signs (within 6 hours) of ischemic stroke on CT scan?
Hyperdense left MCA sign.
Loss of the insular ribbon.
Attenuation of the lentiform nucleus.
Hemispheric sulcal effacement.
“Person-in-a-barrel” syndrome?
Occurs in severe cases of bilateral watershed infarcts, in which the patient can only move the distal part of the extremities.
Watershed infarcts manifest clinically with proximal weakness, affecting the proximal upper and proximal lower extremities, with weakness at the shoulder and at the hip. This occurs because the watershed regions correlate with the homuncular representation of the proximal limbs and trunk.
Medial medullary syndrome?
Caused by occlusion of the vertebral artery or one of its medial branches.
Infarct affecting the pyramid, medial lemniscus, and emerging hypoglossal fibers.
- Contralateral arm and leg weakness sparing the face (from corticospinal tract involvement prior to its decussation).
- Contralateral loss of sensation to position and vibration.
- Ipsilateral tongue weakness.
Giant cell arteritis?
Older adults, typically > 50 years of age.
Inflammation of the temporal artery predominantly but may also affect other branches of the ECA.
Headaches, associated with generalized constitutional symptoms, jaw claudication, and tenderness of the scalp around the temporal artery.
May overlap with polymyalgia rheumatica, and patients will also present with proximal muscle pain and achiness.
Labs: leukocytosis and very elevated sedimentation rates and C-reactive protein levels.
The diagnosis is based on a biopsy of the temporal artery demonstrating granulomatous inflammation.
Blindness may occur from ocular ischemia, and these patients should be treated ASAP with steroids while arranging for a temporal artery biopsy.
Millard–Gubler syndrome?
The lesion is localized in the pons and affects the corticospinal tract before its decussation (which occurs at the level of the pyramids), as well as the VII cranial nerve nucleus and/or fibers.
Manifested by contralateral hemiplegia with ipsilateral facial palsy.
> > When there is also conjugate gaze paralysis toward the side of the brainstem lesion, it is called Foville syndrome.
Intracranial aneurysms etiology?
Most often acquired and sporadic.
In associations with various conditions:
1- AVMs.
2- AD polycystic kidney disease.
3- Aortic coarctation.
4- Fibromuscular dysplasia.
5- Marfan’s syndrome.
6- Ehlers–Danlos syndrome.
Can also be familial. Screening with CTA or MRA is recommended in patients with two or more family members with an intracranial aneurysm or history of SAH.
Factors associated with increased risk of cerebral aneurysmal rupture and SAH?
1- Size: higher with diameters of 7 mm or higher, and the risk rises with increasing size.
2- Aneurysmal growth: growing aneurysm on imaging, or new symptoms from aneurysm growth (new cranial nerve palsy or mass effect).
3- Aneurysm location: posterior circulation aneurysms are at higher risk for rupture as compared to anterior circulation aneurysms.
4- Smoking.
5- Uncontrolled hypertension.
6- Patients with previous aneurysmal rupture are at higher risk for SAH.
Treatment of unruptured aneurysms?
Conservatively (imaging surveillance and observation) in patients with low risk of aneurysmal rupture).
Endovascular treatment (coiling).
Surgical treatment (clipping).
> > In selected aneurysms, endovascular coil embolization is associated with reduced procedural morbidity and mortality as compared to surgical clipping; however, the recurrence risk may be higher.
Occipital/PCA strokes in the dominant hemisphere manifestations?
- Homonymous hemianopia in the contralateral side. Typically, spares central vision because of collateral blood supply to macular cortical representation.
- Alexia (inability to read).
- Anomia.
- Achromatopsia (color anomia).
- Classical alexia without agraphia (with left occipital infarcts involving the splenium of the corpus callosum): patient cannot see what is placed in the right visual hemifield, and whatever can be seen in the left visual hemifield will be represented in the right occipital cortex, but due to corpus callosum involvement this information cannot be connected with language centers in the left hemisphere.
Benedikt’s syndrome?
Infarction in the right mesencephalic tegmentum in its ventral portion, involving the ventral part of the red nucleus, the brachium conjunctivum, and the fascicle of the third cranial nerve.
Ipsilateral third nerve palsy with contralateral involuntary movements such as tremor and choreoathetosis.
Results of the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial?
Randomized patients with a recent TIA or stroke with a 50% to 99% stenosis of a major intracranial artery to warfarin or aspirin.
The primary end point was ischemic stroke, intracranial hemorrhage (ICH), or death from vascular causes other than stroke.
Concluded that warfarin was associated with higher rates of adverse events and provided no benefit over aspirin.
Warfarin INR target?
Between 2.0 and 3.0, except in the setting of mechanical valves, in which the target INR is 2.5 to 3.5.
Gaze deviation with stroke?
MCA stroke: the frontal eye fields may be involved, and patients will have gaze deviation toward the hemisphere involved. This occurs because the contralateral frontal eye fields will be unopposed, “pushing” the eyes to the side of the infarct.
Pontine stroke: eyes deviate toward the hemiparetic side.
The Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial?
Studied the effect of atorvastatin 80 mg daily in patients with a recent (within 6 months) TIA or stroke, with LDL between 100 and 190 mg/dL.
The conclusion was that 80 mg of atorvastatin daily reduces the overall incidence of strokes and cardiovascular events.
SAMMPRIS (Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis) trial?
Compared best medical therapy versus intracranial stenting in patients with intracranial stenosis (70% to 99% stenosis) and recent stroke or TIA, demonstrating that medical therapy is superior.
The rate of early stroke was high in the stent group, and lower than expected in the medical therapy group.
Medical management in the study included aspirin 325 mg daily and clopidogrel 75 mg daily for 90 days, optimal management of risk factors (target systolic BP <140 mm Hg, and <130 mm Hg in diabetics, and target LDL <70 mg/dL), and lifestyle modifications.
Alberta Stroke Program Early CT Score (ASPECTS)?
A grading system to assess early ischemic changes in patients with acute ischemic strokes of the anterior circulation.
Two axial cuts are obtained on the CT, one at the level of the basal ganglia and thalamus, and another more cranial cut where these structures are not appreciated.
10 regions of interest, of which 4 are deep and defined as the caudate, the internal capsule, the lentiform nucleus, and the insular region, and 6 regions are cortical. These regions are assigned a point, which is subtracted if there is early ischemic change in that specific region.
A normal looking CT scan will obtain a maximum of 10 points, and a score of 0 is consistent with diffuse ischemic injury of the entire MCA territory.
An ASPECTS score of 7 or less correlates with increased dependence and death.
Segments of the ICA? by Bouthillier et al.
- The cervical (C1) segment: begins at the level of the CCA and ending where the ICA enters the carotid canal in the petrous bone. It has no branches.
- The petrous (C2) segment: runs within the carotid canal in the petrous bone. Vidian and caroticotympanic branches arise from this segment.
- The lacerum (C3) segment: runs between where the carotid canal ends and the superior margin of the petrolingual ligament (this ligament runs between the lingula of the sphenoid bone and the petrous apex and is a continuation of the periosteum of the carotid canal).
- The cavernous (C4) segment: begins at the superior margin of the petrolingual ligament, runs within the cavernous sinus, and ends at the proximal dural ring formed by the junction of the medial and inferior periosteum of the anterior clinoid process. Meningohypophyseal trunk, inferolateral trunk, and capsular arteries arise from this segment.
- The clinoid (C5) segment: runs between the proximal dural ring and the distal dural ring where the ICA becomes intradural. Small segment - no branches.
- The ophthalmic (C6) segment: begins at the distal dural ring ending proximal to the origin of the Pcomm artery. Gives two major branches, the ophthalmic artery and the superior hypophyseal artery.
- The communicating (C7) segment: begins proximal to the origin of the Pcomm artery extending to the ICA bifurcation. Gives off the Pcomm artery and the anterior choroidal artery.
A more simple and practical classification divides the internal carotid into?
- Cervical segment.
- Petrous segment.
- Cavernous segment.
- Supraclinoid segment.
Symptomatic carotid stenosis treatment according to the North American Symptomatic Carotid Endarterectomy Trial (NASCET)?
Symptomatic carotid stenosis of 70% to 99% should be revascularized - the 2-year ipsilateral stroke rate was 26% with medical treatment versus 9% with CEA.
Symptomatic stenosis of 50% to 69% may also benefit from CEA, with greater impact in men versus women, in those with previous strokes versus TIAs, and with hemispheric versus retinal symptoms.
Stenosis of less than 50% or carotid occlusions, there is no evidence to support that surgical treatment is better than medical therapy. The treatment should be medical management.
Asymptomatic carotid disease treatment? Trials?
CEA has proven benefits over medical treatment in patients with more than 60% stenosis as demonstrated in the Asymptomatic Carotid Atherosclerosis Study (ACAS), and in the Asymptomatic Carotid Surgery Trial (ACST), however, the numbers needed to treat were high, and the benefit may not be significant in the real world, depending also on the experience of the surgeon.
In ACAS, the absolute risk reduction was 1.2% per year with a number needed to treat of 85 favoring the surgical group.
In ACST, the absolute risk reduction was 1.1% with a number needed to treat of 93 favoring surgery over medical therapy.
Risk of stroke after TIA?
Around 10% to 15% of patients who suffer a TIA will have a stroke within 3 months, and the risk is higher soon after the TIA, with 50% of the strokes occurring within 48 hours.
Guidelines recommend the following workup for TIAs:
- Neuroimaging within 24 hours, preferably an MRI with DWI.
- Noninvasive vascular imaging of the extracranial arteries.
- Noninvasive imaging of the intracranial vasculature if it is considered that this will alter management.
- Patients should be evaluated as soon as possible.
Picture? Mechanism?
Deep intracerebral hemorrhage, most likely caused by hypertension.
This occurs from rupture of deep perforating arteries, which suffer changes caused by chronic hypertension, leading to lipohyalinosis, making these vessels susceptible to sudden closure (causing lacunar infarctions) or rupture (causing hemorrhage).
Hemorrhages showing a fluid–fluid level?
Anticoagulation associated hemorrhage.
Intracerebral hemorrhage (ICH) accounts for approximately —-%? of all strokes.
10%.
The most common 2 causes of spontaneous ICH?
Hypertension, most common, 75% of cases.
Followed by cerebral amyloid angiopathy.
Hypertensive ICH most common locations?
Commonly originates in deep subcortical structures such as:
- Putamen.
- Caudate.
- Thalamus.
As well as in:
- Pons.
- Cerebellum.
- Periventricular deep white matter.
Charcot Bouchard microaneurysms have been classically associated with?
Hypertensive ICH; however, they are not found consistently and are described only in a small number of patients.
Cerebral amyloid angiopathy pathogenesis?
Results from the deposition of amyloid protein (congophilic material) in the media and adventitia of cerebral vessels, especially in cortical and leptomeningeal vessels.
This process is associated with cortical and lobar hemorrhages, which may be recurrent.
Since the angiopathy is diffuse, there are recurrent and multiple hemorrhages, and commonly MRI with gradient echo sequences will show multiple small areas of hypointensity suggesting prior hemosiderin deposition from prior microhemorrhages.
Moyamoya disease? Pathogenesis?
Noninflammatory, nonatherosclerotic vasculopathy that affects the intracranial circulation, leading to arterial occlusions and prominent arterial collateral circulation.
Moyamoya disease? Presentation?
It presents most commonly in children and adolescents, with a second peak in the fourth decade of life, but with a much lower frequency.
Clinical manifestations include TIAs and strokes, as well as ICHs.
In childhood the presentation is predominantly ischemic, with strokes and TIAs, which may be precipitated by hyperventilation.
In adults, the presentation is most frequently ICH.
Other manifestations include headaches, seizures, movement disorders, and cognitive deterioration.
The diagnosis of moyamoya disease? Imaging? Histopathology?
Based on the angiographic findings, characterized by progressive bilateral stenosis of the distal ICAs, extending to proximal ACAs and MCAs, and the development of extensive collateral circulation at the base of the brain, with the “puff of smoke” appearance.
Histopathologically, there is intimal thickening by fibrous tissue of the affected arteries, with no inflammatory cells or atheromas.
Treatments of Moyamoya disease?
There is no curative treatment for this condition. Revascularization procedures may improve perfusion, angiographic appearance, and ischemic manifestations; however, they may not impact the frequency of hemorrhagic events.
Medications such as antiplatelets, vasodilators, calcium-channel blockers, and steroids have been used with equivocal results.
Anticoagulation is not helpful and usually avoided given the hemorrhagic complications.
Picture?
Amyloid angiopathy - multiple small rounded areas of gradient echo susceptibility throughout the brain, representing microhemorrhages with hemosiderin deposition.
Amyloid angiopathy Histopathology?
Histologically, there is deposition of Congo-red positive amyloid material in the media and adventitia of small- and medium-sized vessels. This causes weakening of the vessel walls.
Genetics associations with amyloid angiopathy?
There are associations of amyloid angiopathy with apolipoprotein E4 and E2, as well as with Alzheimer’s disease.
Dejerine–Roussy syndrome?
Caused by a thalamic infarct, in which the lesion affects the sensory relay nuclei.
Present with severe deep and cutaneous sensory loss of the contralateral hemibody, usually the entire hemibody and up to the midline. In some cases, there may be dissociation of sensory loss, often affecting position sense more than other sensory functions.
With time, some sensation returns, but the patient may develop severe pain, allodynia, and paresthesias of the affected body part.
The anterior and the posterior choroidal arteries origins?
The anterior choroidal arteries arise from the anterior circulation, more specifically from the ICA slightly distal to the origin of the Pcomm artery.
The posterior choroidal arteries arise from the posterior circulation, more specifically from the PCAs.
The vertebral artery origin?
The vertebral arteries originate from the subclavian arteries on their respective sides.
The vertebral artery segments? Vascular supply in general?
V1 segment: extends from the subclavian artery to the transverse foramen of C5-C6.
V2 segment: runs within the transverse foramina of the cervical vertebra from C5-C6 to C2.
V3 segment: extends from the transverse foramen of C2 and turns posterolaterally around the arch of C1, between the atlas and the occiput. It is extracranial.
V4 segment: begins where the vertebral artery enters the dura at the foramen magnum and joins the contralateral vertebral artery to form the basilar artery. Gives off the PICA and the ASA. Both vertebral arteries will join to form the basilar artery.
The posterior circulation provides the vascular supply to the brainstem, cerebellum, the thalamus, and the occipital lobes.
Picture?
Hemorrhagic infarct from left transverse sinus thrombosis.
CVST associated infarct pathogenesis?
Occlusion of the venous sinuses will lead to venous infarction and localized edema. The affected tissue becomes engorged, swollen, and the parenchyma will suffer ischemia, leading to infarct and hemorrhage, which is also influenced by the impaired venous drainage.
Given the occlusion of venous drainage and in the setting of parenchymal edema, the content of the intracranial volume will tend to rise, leading to intracranial hypertension.
Picture?
Left transverse sinus thrombosis.
Cerebral venous sinuses illustration?
Picture?
A blood vessel with a thick wall, which contains a basophilic granular material. This pathologic finding is characteristic of CADASIL.
Picture?
Cavernous malformation - typical “popcorn-like” appearance, with a dark rim on T2 consistent with hemosiderin.
Picture?
Spinal dural arteriovenous fistula (DAVF) - a lesion with T2 hyperintensity in the spinal cord, with perimedullary flow voids.
Picture?
ICH in the right anterior temporal lobe.
Hemorrhage is approximately 1 week old. Early subacute.
ICH timing table?
