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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