Stroke

Vascular Anatomy

100

Name 4 of the 7 segments of the internal carotid artery

Cervical segment petrous segment lacerum portion cavernous segment clinoid segment Ophthalmic portion Communicating portion OPAAM (ophthalmic, anterior choroidal, anterior cerebral, middle cerebral).

200

Describe/draw the posterior circulation and its connection with the anterior circulation; discuss the territory covered by the PCA.

PCA- curves back after arising from the top of the basilar and sends branches over the inferior and medial temporal lobes and over the medial occipital cortex; inferior an dmedial temporal and occipital cortex; thalamus/internal capsule/midbrain (thalmoperforating arteries (P1)thalmogeniculate (P2) and posterior choroidal arteries).

300

Name the origin/describe the course of the anterior choroidal artery and the anatomic structures it supplies.

ICA-long aubarachnoid course, enters the temporal horn of lateral ventricle through choroidal fissure to supply: Hippocampus, amygdala, optic tract, LGN, Meyer's loop, globus pallidus, choroid plexus, internal capsule (ventrolateral portion of the PLIC and part of the genu).

400

Discuss the blood supply to the cerebellum.

pg. 712 PICA-supplies the lateral medulla, inferior half of the cerebellum and the inferior vermis. AICA- inferior lateral pons, the middle cerebellar peduncle, a strip of the ventral (anterior) cerebellum between the PICA and SCA territories (flocculus). SCA- upper lateral pons, superior cerebellar peduncle, superior half of the cerebellar hemisphere (deep cerebellar nuclei and superior vermis).

500

Name the 4 types of vascular malformations. Define an AVM and its four anatomical components and where the majority occur with the annual rupture rate.

Venous angiomas (DVA), cavernous malformations, capillary telangiectasias, arteriovenous malformations (AVM)s. AVM is a sructure made of arteries and veins without capillaries in between. Feeding arteries, nidus (coiled/tortuous vessels), draining veins, surrounding parenchyma. Most commonly found ~90% supratentorial and 50% are in the watershed zones; 3% annual rupture rate.

Thalamus/Lacunar Infarcts

100

Discuss the pattern of weakness and the localizations of pure motor hemiparasis or dysarthria hemiparesis.

Weakness same in face/arm/leg 1. Posterior limb of the internal capsule. 2. Ventral pons. 3. Corona radiata. 4. Cerebral peduncle.

200

Discuss the clinical syndrome affecting the anterior thalamus including its arterial supply including origin.

Clinical syndrome: abulia, apathy, aphasia, and affect (neuropsychological) changes, fluctuating levels of consciousness; involvement of the polar/tubero-thalamic artery from PCOMM.

300

Discuss the clinical syndrome of an infarct involving the paramedian arteries (including the origin) supplying the thalamus.

PCA-P1 segment Paramedian- posterior/thalamoperforating arteries: altered mental status/changes in consciousness>>confusion, agitation/aggression +/- memory disruption-similar to thiamine deficiency Korsacoff syndrome-destroys the medial dorsal thalamic nuclei(thalamic dementia)-associated behavioral abnormalities; vertical gaze abnormalities (involvement of the interpeduncular arteries P1 (medial to paramedian artery)>>involvement of the midbrain/septal nuclei TGA

400

Discuss the localization of pure sensory stroke and sensorimotor strokes with the involved anatomical structures including blood supply.

VPL +/- posterior limb of the internal capsule;VPL (thalamoperforator branches of the PCA) +/- lenticulostriate arteries.

500

Discuss the clinical syndrome of an infarct involving the posterolateral thalamus and the involved vessel. Discuss the clinical syndrome of an infarct involving the dorsal region to the thalamus and the involved vessel.

Postero/inferolateral thalamogeniculate artery: Pure sensory stroke (VPM/VPL), sensorimotor stroke (ataxia (VL)/hemiparesis), Dejerine-Roussey syndrome (sensory loss, paresis, post lesion pain). Dorsal-posterior choroidal (P2): visual field deficit: homonomous quadrantinopsia or homonomous horizontal sectoranopia; pulvinar involvement-thalamic aphasia-dysprosody, dysarthria, selective impairment in semantic memory; hyperkinetic movements

Brainstem

100

Name a midbrain syndrome (vascular supply)-describe its anatomical clinical features.

Weber's: PCA/top of the basilar. Ipsilateral 3rd nerve palsy, contralateral hemiparesis. Claude's: PCA/top of the basilar. Ipsilateral 3rd nerve palsy, contralateral ataxia. Benedickt's: PCA/top of the basilar. Both.

200

Name a pontine syndrome its vascular supply and anatomical/clinical features.

Millard-Gubler Syndrome (Hemiparesis Alterans)- ipsilateral lateral rectus palsy, ipsilateral peripheral 7th nerve palsy, contralateral facial sparing hemiparesis. Locked-in Syndrome-ventral pontine lesions- (blink and move eyes vertically) LIPS-lateral inferior pontine syndrome (AICA)- decreased facial sensation, ipsilateral facial paralysis, nystagmus, vomiting, vertigo, ear deafness, PPRF (gaze paresis to the side of the lesion), decreased pain/temp contralateral body, ipsilateral ataxia. MIPS-medial inferior pontine syndrome (Foville syndrome)-paramedian branches of basilar or proximal AICA, similar to medial medullary (CN VI instead of XII).

300

Name both medullary syndromes with vascular supply and describe anatomical/clinical features.

Medial medullary syndrome: Paramedian branches of the vertebral and anterior spinal arteries. Contralateral arm/leg weakness, contralateral decreased position and vibration sense, ipsilateral tongue weakness. Lateral medullary syndrome: Vertebral artery often PICA. Ipsilateral ataxia, vertigo, nystagmus/nausea, ipsilateral facial decrease to pain/temperature, contralateral hemi-body decrease to pain/temperature, ipsilateral Horner's syndrome, hoarseness/dysphagia, ipsilateral decreased taste.

400

Discuss right-way and wrong-way eyes and associated lesions.

1. Right-way eyes caused i.e. cortical lesion affecting corticospinal pathways and frontal eye fields. 2. Wrong-way eyes caused i.e. by a left pontine lesion affecting corticospinal pathways and the PPRF; lesions in the thalamic region (coma).

500

Case 14.6. pp: 675 Wrong-way eyes, limited upgaze, decreased responsiveness and hemiparesis.

Discussion: Dx: evolving basilar artery thrombosis. Highlight key symptoms/signs; explain PE findings: waxing/waning course, blurred vision (occipial lobes/diplopia), alternating right/left/right hemiparesis with b/l Babinski; wrong-way eyes, limited upgaze, impaired consciousness, (shivering, headache, nausea, dysarthria-pontine lesions).

Hemorrhage/Veins/tPA

100

What is the most common site of intracerebral hemorrhage (most common site of hypertensive hemorrhage) and its main blood supply?

Putamen- lenticulostriate arteries; anterior choroidal artery.

200

Discuss/draw the venous drainage of the brain. Include superficial/deep draining veins and sinuses. Name the two fairly constant cortical veins and their drainage.

Superficial veins drain mainly into the superior sagittal sinus and the cavernous sinus. The superior sagittal sinus drains the into the two transverse> sigmoid sinus>IJ. The cavernous sinus drains via the superior petrosal>transverse sinus, inferior petrosal into the internal jugular veins. Deep veins drain into the internal cerebral and basal vein of Rosenthal> great vein of Galan which is then joined by the inferior sagittal sinus to form the straight sinus. The confluence of sinuses (torcular) where the superior sagittal, straight sinues and occipital sinuses drain into the transverse sinuses. The inferior anastomotic vein of Labbe>transverse sinus, the superior anastomotic vein of Trolard>superior sagittal sinus.

300

Discuss the clinical syndromes associated with each of the following sinus thrombosis by location. 1. Cavernous Sinus Thrombosis. 2. Transverse Sinus Thrombosis i.e. Gradnigo syndrome. 3. Sagittal Sinus thrombosis.

1.Papilledema, proptosis and painful ophthalmoplegia. 2. CNVI palsy and facial pain (CNV involvement). 3. Paraparesis, seizures or AMS; can cause increased ICP with increased incidence during pregnancy and post-partum period.

400

Discuss the causes of non-traumatic subarachnoid hemorrhage, risk factors and common locations of aneurysms. Briefly discuss known complications with therapies and prognosis.

(75-80%) ruptured arterial aneurysm, (4-5%) bleeding AVM, other. Risk factors: athersclerotic disease, congenital anomalies in cerebral blood vessels, polycystic kidneydisease, connective tissue disorders. Locations (saccular/berry aneurysms):arterial branch points from the circle of Willis. (ACOMM 30%, PCOMM 25%, MCA 20%, vertebrobasilar systme 15%). Complications: hydrocephalus, seizures, vasospasm, rebleeding and hyponatremia. Vasospasm: occurs ~1 week post-bleed; treated with triple H therapy (hypertension, hypervolemia and hemodilution) and nimodipine. Prognosis: (15% dies immediately, 25% at day 1 and 60% at 6 months) ~24% die within 24 hours, 60% die at 6 months

500

Name the indication for IV tPA, dosing/administration. Name contraindications to I.V. tPA. What is the risk of hemorrhage (overall/intracranial/fatal)?

Indicated for acute stroke patients presenting within 3 hours of symptom onset; 4.5 hours in some cases. .9mg/kg with 10% given over 1 minute and the rest over 1 hour. Contraindications: 1.Spontaneous clearing of neurological signs. 2. Seizure at onset of symptoms. 3. h/ prior ICH or train tumor. 4. Head trauma, I or prior ischemic infarction in prior 3 months). 5. GI/GU hemorrhage in the previsous 3 weeks. 6. Major surgery in the previous 2 weeks. 7. Arterial puncture at a non-compressible site in the previous 1 week. 8. Uncontrolled HTN at the time of treatment (BP>185/110). 9. INR >1.7 or known bleeding diathesis. 10. Heparin in the preceding 48 hours, abnormal. 11. Platelet count <100,000. Blood glucose <50 or >400 mg/dL. 13. CT with infarction hypodensity >1/3 cerebral hemisphere. Risk hemorrhage overall 11%, ICH 6%, fatal hemorrhage 3%.

Landmark Studies

100

What trial found that despite an increased incidence of symptomatic intracerebral hemorrhage, treatment with intravenous t-PA within three hours of the onset of ischemic stroke improved clinical outcome at three months? What trial tested/extended tPA administered in patients with acute ischemic stroke from time window of 3 to 4.5 hours after the onset of stroke symptoms?

NINDS tPA-stroke study (National Institute of Neorological disorders and Stroke) ECASSIII- European Cooperative Acute Stroke Study

200

What trial showed both absolute and relative risk reduction over 5 years of carotid endarterectomy in asymptomatic patients with 60-99% stenosis? What trial showed benefit of carotid endarterectomy in symptomatic patients with 50-99%?

ACAS (Asymptomatic Carotid Atherosclerosis Study) NASCET (North American Symptomatic Carotid Endarterectomy Trial)

300

What trial found warfarin was associated with significantly higher rates of adverse events and provided no benefit over aspirin? Aspirin should be used in preference to warfarin for patients with intracranial arterial stenosis?

WASID (Warfarin vs. Aspirin for Symptomatic Intracranial Arterial Stenosis)

400

What international, phase III, randomized, controlled trial tested rapid blood pressure lowering (target systolic blood pressure <140 mm Hg) versus a more liberal target of systolic blood pressure (SBP) <180 mm Hg for seven days in patients with intracerebral hemorrhage (ICH)? What were the findings? What is the ongoing American analog?

INTERACT II (Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial). INTERACT2 data support a more aggressive goal of SBP<140 mm Hg for seven days in spontaneous ICH patients. The ATACH II trial, which is a North American analog to INTERACT2 randomizes patients to a SBP goal of <140 versus <180 mm Hg using intravenous nicardipine as the blood pressure lowering agent. It is hoped that this trial, which is expected to be completed in 2016, will corroborate the results of INTERACT2.

500

What trial found that among patients with TIA or minor stroke who can be treated within 24 hours after the onset of symptoms, the combination of clopidogrel and aspirin is superior to aspirin alone for reducing the risk of stroke in the first 90 days and does not increase the risk of hemorrhage? What trial found that adding aspirin to clopidogrel in high-risk patients with recent ischaemic stroke or transient ischaemic attack is associated with a non-significant difference in reducing major vascular events, with an increased risk of lifethreatening or major bleeding is increased by the addition of aspirin?

CHANCE trial (Clopidogrel in High-Risk Patients with Acute Nondisabling Cerebrovascular Events Trial). MATCH-(Management of Atherothrombosis with Clopidogrel in High-risk patients).