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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:

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clinical picture of tia
Clinical picture of TIA
  • Neurologic deficits are completelly and spontaneously reversiblein 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
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
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
diagnosis critical pathway
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
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 tests1
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 tests2
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
ischemic stroke management
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
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
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
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
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
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
criteria for iv thrombolysis other exclusion criteria
Criteria for IV Thrombolysis – other exclusion criteria
  • 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
anticoagulants
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
Drug Therapy in Ischemic Stroke
  • Majority of the patients are not thrombolysis candidates
    • secondary prevention
stroke 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 prevention1
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 stroke1
Drug Therapy in Ischemic Stroke
  • Cerebral vasodilators:
    • vincamine, vinpocetine, nicergoline, pentoxifylline
    • Ginkgo biloba
  • Cerebral trophic agents
    • Pyracetam, pramiracetam
    • Cerebrolysin, Actovegin
neuroprotective therapy
Neuroprotective therapy

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

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
stroke
Stroke

HaemorrhagicRupture of a vessel

Rupture producesinjury by distorting,compressing andtearing thesurrounding braintissue or byincreasingintracranialpressure

intracranial haemorrhage
Intracranial haemorrhage

Circle of Willis

Anteriorcerebral artery (ACA)

Middlecerebral artery (MCA)

Basilarartery

Blood in subarachnoid space

Vertebral arteries

Posterior cerebral artery

  • 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
cerebral hemorrhage etiology
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
slide28

Microaneurysms

in penetrating

arteries

cerebral hemorrhage etiology1
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
Topographical forms
  • Basal ganglia
  • Lobes
    • localized – “intrecerebral hematoma”
topographical forms1
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
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
causes of sah
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
subarrachnoid hemorrhage1
Subarrachnoid hemorrhage
  • Bleed into the subarachnoid space in the brain.
subarrachnoid hemorrhage2
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 hemorrhage
subarrachnoid hemorrhage3
Initial 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

Subarrachnoid hemorrhage
vasospasm
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
cerebral 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
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 trombosys1
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 trombosys2
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 trombosys3
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 trombosys4
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