Transient ischemic atack

Clinical picture of TIA

Neurologic deficits are completelly and spontaneously reversible in less than 24 hours– No signs on CT

TIA is usually characterized by focal neurological symptoms.

There are 2 main groups of TIA’s symptoms:– General - usually manifest as headache, dizziness,

short loss of consciousness – Focal symptoms depend on the vessel territory

TIAs in carotid distribution

subjective sensory disorders motor disorders transient aphasia blindness or reduction of vision Focal Jackson motor or sensory

epileptic attacks

TIAs in vertebrobasilar distribution 70 % of all TIAs Vestibular syndrome Brainstem – cerebellum syndrome Paresis of oculomotor muscles Bulbar syndrome Alternate syndromes Cortical vision disorders Atonic – adynamic syndrome - “drop –

attacks “ Paroxysmal hypersomnic and katalepsic

syndromes temporal epilepsy

Diagnostic tests in stroke

Diagnosis-Critical Pathway

Initial– ECG, Cardiac Enzymes– Haemogram (blood cell count) – Coagulation tests – NIR;

For etiologic diagnosis: genetic conditions - test for C protein, S protein, factor V, factor VIII, fibrinogen, etc

– Blood proteins; electrophoresis – glucose, Renal function studies, +/- drug

screen,

Diagnostic Tests

Noncontrast CT of head– Differentiate hemorrhage vs ischemia

MOST ischemic strokes are negative by CT for at least 6 hrs

– Hypodensity indicating infarct seen 24-48 hrs Can identify hemorrhage greater than 1cm, and

95% of SAH If CT is negative, but still considering SAH may

do lumbar punction

Diagnostic Tests

Depending on circumstances, other helpful tests– Echocardiogram – identifies mural thrombus,

tumor, valvular vegetations in suspected cardioembolic stroke

Transesophagian ecocardiography to see atria– Echography of arteries in the neck (Doppler,

duplex) finds out the absence or presence of stenosis and

occlusions of magistral arteries of head and neck. Dissection Degree of obstruction of the blood vessel Type of plaques, risk of emboli formation

Diagnostic Tests

– Angiography – “gold standard” identifies occlusion or stenosis of large and small vessels of head/neck, dissections and aneurysms

Usefull especially in hemorrhage before surgical intervantion

Angio CT, MRA scan – identifies large vessel occlusions – may replace angiography in the future

– MRI scan – identifies posterior circulation strokes better and ischemic strokes earlier than CT

Emergent MRI- considered for suspected brainstem lesion or dural sinus thrombosis

MRI techniques for recent ischemic stroke: diffusion and perfusion techniques allow rapid confirmation in vue of thrombolysis

Treatment of ischaemic stroke

Ischemic Stroke Management General Management

– General support measures IV, oxygen, monitor, elevate head of bed slightly Treat dehydration and hypotension Avoid overhydration – cerebral edema Avoid IVF with glucose – except if hypoglycemic Fever – worsens neurologic deficits

Hypertension– Treatment indicated for SBP > 220 mm Hg or mean

arterial pressure > 130 mm Hg Lowering BP too much reduces perfusion to

penumbra converting reversible injury to infarction Use easily titratable Rx (labetalol or enalaprilat) SL Ca-channel blockers should be avoided

Ischaemic stroke treatment – other management issues Surgical:

– Decompression (in selected cases)– Removal of clot, stenting, I.V.

administration of thrombolitycs Brain edema prevention /treatment –

mannitol, loop diuretics (Furosemidum)

Ischaemic stroke - treatment Ethiologic

– Trombolysis rTPA – tissue plasminogen activator 3 hours from the start of stroke I.V., generally or directly in the obstructed artery

– Heparin – prevents extension of clot/ formation of new clots

Thrombolysis Background

NIH/NINDS study– 624 patients, trial with I.V. tPA vs placebo

Treatment w/in 3 hrs of onset– At 3 months, patients treated with tPA were at least

30% more likely to have minimal/no disability; absolute favorable outcome in 11-13 percent

– 6.4% of patients treated with tPA developed symptomatic ICH compared with 0.6% in placebo group

– Mortality rate at 3 months not significantly different– tPA group had significantly less disability– FDA approved in 1996

tPA Dose and Complications

IV tPA –Total dose 0.9 mg/kg, max. 90mg– 10% as bolus, remaining infusion over 60

min.– Blood pressure and Neurological checks

every 15 min for 2 hours initially Treatment must begin within 4,5

hours of symptoms and meet inclusion and exclusion criteria

No ASA or heparin given x 24 hours after thrombolysis

Thrombolysis Criteria in Ischemic Stroke Inclusion criteria

– Age 18 years or older– Time since onset well established to be < 3 hrs– Clinical diagnosis of ischemic stroke

Exclusion criteria– Minor/rapidly improving neurologic signs– Evidence of intracranial hemorrhage on

pretreatment noncontrast head CT– History of intracranial hemorrhage– High suspicion of SAH despite normal CT– GI or GU bleeding within last 21 days

Exclusion criteria– Known bleeding diathesis

Platelet count < 100,000 /mm3 Heparin within 48 hours and has an elevated PTT Current use of anticoagulation or PT > 15 seconds or INR > 1.7

– Intracranial surgery, serious head trauma or previous stroke within 3 months

– Major surgery within 14 days– Recent arterial puncture at non compressible site– Lumbar puncture within 7 days– Seizure at onset of stroke– History of ICH, AVM or aneurysm– Recent MI– Sustained pretreatment systolic pressure > 185 mmHg or

diastolic pressure > 110 mmHg despite aggressive treatment to reduce BP to within these limits

– Blood glucose < 50 or > 400 mg/dL

Criteria for IV Thrombolysis – other exclusion criteria

Anticoagulants

Heparin: unproven– Patients may expect fewer strokes but

benefit is offset by increased ICH– Similar results with low molecular weight

heparin– Use of heparins or heparinoids for a

specific stroke subtype or TIA cannot be recommended based on available evidence.

– Prevention of decubitus complications

Drug Therapy in Ischemic Stroke

Majority of the patients are not thrombolysis candidates– secondary prevention

Stroke secondary prevention Prevention of risk factors – correct

treatment of diabetes, arterial hypertension, dyslipidemia, giving up smoking

Antiplatelet agents– ASA: ↓ risk 20-25% vs placebo

50-300 mg dose and will not interfere with tPA therapy– Dipyridamole: alone (200mg BID) ↓ risk 15%

Dipyridamole + ASA (Assasantin, Aggrenox)– Clopidogrel: (75 mg qd) 0.5% absolute annual risk

reduction when compared to ASA– Triflusalum (Aflen)

Good for pts who cannot tolerate or fail ASA

Stroke secondary prevention Anticoagulation - vitamin K

antagonists– warfarine, Acenocumarol – first line in secondary prevention in

patients with atrial fibrilation or other cardiac emboligene conditions

– < 75 years – embolic risk – atrial fibrillation

– >75 years (individual evaluation of risk/benefit)

– INR 2.5 (2 –3) lifelong or whole duration of AF (Vidal, Martindale)

Drug Therapy in Ischemic Stroke Cerebral vasodilators:

– vincamine, vinpocetine, nicergoline, pentoxifylline

– Ginkgo biloba Cerebral trophic agents

– Pyracetam, pramiracetam– Cerebrolysin, Actovegin

Neuroprotective therapy

Neuroprotection targets· Growth factors· Calcium channels· Glutamate receptors· Free radicals· Nitric oxide· Proteases· Cell membrane components· Apoptotic pathway molecules

(e.g. Bcl-2 promoters)

· Neuroprotective drugs: Cerebrolysin, calcium blockers

Neuroprotective therapy is designed to save the penumbra, or the area surrounding the core of the primary ischaemia, from the damage caused by reduced blood flow to this region

Hemorrhagic stroke

Stroke

Rupture producesinjury by distorting,compressing andtearing thesurrounding braintissue or byincreasingintracranialpressure

HaemorrhagicRupture of a vessel

Intracranial haemorrhage

· Intraparenchymal haemorrhage may be relatively benign· Bleeding into the region of previous infarction causes no additional functional loss· At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed

tissue, and blood or its breakdown products in the parenchyma damages brain tissues

Anteriorcerebral artery (ACA)

Middlecerebral artery (MCA)

Basilarartery

Vertebral arteries Posterior cerebral artery

Circle of Willis

Blood in subarachnoid space

Cerebral hemorrhage - etiology

Arterial hypertension– Segmentar arteriolosclerosys: fibrinoid

necrosis, hyalinosys, sclerosis of the media: lipohyalinosys

Small diameter arteries (0,08-0,3 mm)– Microaneurisms – arteries with 0,3-1 mm

diameter Damages the intraparenchimal arteries

– Penetrating arteries, near their origin in large arterial trunks

(MCA, basilary trunk, superior cerebellar artery, anteroinferior cerebellar artery)

More frequent location of hemorrhageae within the basal ganglia, internal capsula, thalamus, pons, cerebellum

Microaneurysmsin penetratingarteries

Cerebral hemorrhage - etiology Vascular malformations

– Arterial aneurysms– Arteriovenous malformations– Other small blood vessel malformations (cavernoma,

telangiectasia)– Micotic aneurysms

Amyloid angiopathy– Amyloid deposits in the arterial walls– All types of intracranial bleeding– Tendency to recidivate

Coagulation abnormalities– Genetic, leucemy– Anticoagulant treatment– Drug/alcohol abuse, tumors, systemic diseases,

pregnancy, cerebral venous obstruction

Topographical forms Basal ganglia Lobes

– localized – “intrecerebral hematoma”

Topographical forms

Brainstem: – Primary: pontine– Secondary:

mesencephalon, in rapid rising of the intracranial pressure in tumors, hemorrhage above the tentorium

Cerebellar– May lead to severe

respiratory problems, coma, decerebration

– Decompression may be urgently needed

Brain hemorrhage - treatment

Prevention:– Correct treatment of arterial hypertension, – vessel malformations’ surgical treatment, – correct monitoring of anticoagulant treatment

Non surgical:– General measures of support– Treatment of seizures, other complications– Treatment of brain edema – loop diuretics, manitol

Surgical:– Bleeding control– Removal of hematoma– In lobe hemorrhages, cerebellar hematoma

Rehabilitation

Subarrachnoid hemorrhage

Causes of SAH

Rupture of an existing aneurysm– 85% anteriorly– Especially the anterior communicating

artery– Aneurysmal size often >7mm and <10mm

Rupture of an AV malformation Trauma Tumour

Distribution of congenital cerebral aneurysms

Arterial aneurysms

Vascular malformations

Subarrachnoid hemorrhage

• Bleed into the subarachnoid space in the brain.

Subarrachnoid hemorrhage

Clinical picture– Sudden onset– Intense headache– Vomiting– Meningeal syndrome

– but no fever– Consciousness

alterations– Usually no other focal

signs

Diagnosis– History– Non-contrast CT– May need LP

If CT is negative or equivocal

If CT unavailable

Subarrachnoid hemorrhageInitial Management ABC Bed rest SBP < 160 mm Hg

– Treat any pain/anxiety– Hydralazine/SNiP/

Others– May also increase risk

of infarction Prevention of seizure

– Load with phenytoin Monitor closely for signs

of raised ICP– Intubated (if not

already)– Hyperventilated– Mannitol

Surgery (clips/coils/drains)

Complications: Early:

– Rebleeding– Arterial spasm– Acute hydrocephalus

Late:– Recurrence– Psychiatric sequelae– Chronical

hydrocephalus

Vasospasm

Occurs 3-30 days after the initial bleeding Peaks at 4-12 days (worst time for surgery!) Associated with increased mortality in the

first 2 weeks post bleed. Occurs in 70% of patients presenting with

SAH Diagnosis

– Angiogram or MRA– Doppler (increased velocity of blood)

Prevention:– Hypervolaemic Hypertensive Haemodilution– Nimodipine

Vasospasm

Venous system

Cerebral venous system

Superficial system:– Drains into the venous

synuses Central system

– Drain in a large, short venous trunk – the great vein of Galien

Basal system – Drains the blood into

the basilar vein and then to the great vein of Galien

Jugular veins

Cerebral venous trombosys

Causes: Infectious – significantly decreased since

antibiotics– Local– General

Non infectious– Local: trauma, surgical interventions, tumors,

arterialtrombosys, malformations– General: surgicale, pregnancy, post partum/post

abortum, drugs, dehydration, advanced liver or kidney disease

Idiopatic

Cerebral venous trombosys

Venous synus thrombosis:– Increased pressure in the preceding veins

(depending on the anastomosys system)– increased intracranial pressre

Superior longitudinal synus: role in resorbtion of the CSF

Cerebral veins thrombosys– Secondary hemorrhage is more frequent– Cerebral edema, venous infarcts– Seizures

Cerebral venous trombosys

Clinical picture:– Increased intracranian pressure

(headache, nausea, papillary edema, consciousness abnormalities)

– Focal or generalized seizures– Meningean syndrome– Focal signs

– Septic CVT: fever, other signs of severe infection

Cerebral venous trombosys

Cavernous synus thrombosys– Staphilococcus infections of the face, orbitary,

synuses, teeth other ENT infections– Trauma– Usually the clinical picture is marked by the septic

syndrome– Venous stasis:

Palpebral edema, chemosis, exoftalmia VI-th and then IIIrd, IV-th, and ophtalmic ramus of the

Vth nerves palsies– Often clinical signs are bilateral – the 2 synuses are

conected

Cerebral venous trombosys

Investigations – CT, MRI

Thrombus image Empty vessel (CT with contrast substance) Infarctus or hemorrhages images

– Arteriography– CSF analysis – differential diagnosys of an infection– EEG, funduscopy

Treatment: Etyologic treatment Antithrombotic treatment (anticoagulants) Treatment of cerebral edema, raised intracranian

pressure, seizures