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Objectives
Pathophysiology of ischemic stroke Imagistic aspects Etiology Clinical aspects Diagnosis Treatment
Cervical occlusion of ICA circulation can be compensated by ACoA or PoCoA. External carotid artery can be another source of supply, through ophtalmic artery or other anastomosis VA Occlusion compensatory flow can be provided by deep cervical arteries, , thyreocervical arteries or from the contralateral VA MCA/ACA occlusion (outside the circle of Willis) meningeal anastomosis In case of the occlusion of a big artery, the cerebral infarction can vary between 0 100% of the area vascularized by the occluded vessel
Neurovascular unit
lack of oxygen and glucose failure of energy production distruction of cell components, of membranes cell death
Depending on the duration of the vessel obstruction and on the level of the blood flow, theese changes can be permanent or reversible
In response to the increase of MTT the mechanisms of cerebral autoregulation determine the vasodilation of the vessels distally from the site of occlusion and the increase of oxygen extraction rate from the blood Vasodilation leads initially to an increase of CBF in order to maintain a constant level of blood flow supply despite the obstruction of the vessel When the capacity of vasodilation is exhausted, the MTT will continue to increase, the cerebral blood volume will decrease and finally the CBF will decrease upt to levels which are incompatible with survival
Hemodynamics
Normal CBF = 55 mL/100gr cerebral tissue /min CBF < 10-12ml/100gr/min leads to infarction irrespective of the duration of the occlusion
Critical hypoperfusion = 23-12 mL/ 100gr/ min neuronal function is abolished and the brain tissue is affected
EEG shows slow waves Below this level the EEG becomes flat (iso-electric)
MRI aspects
In the first hours, on T2 seq stroke is not visible, but it can be seen on DWI (red arrow)
Early signs
Noncontrast CT of the head is the first-line imaging modality for the assessment of strokes to differentiate ischemic from hemorrhagic strokes and to rule out other intracranial pathologies. It is very sensitive at detecting intracerebral and subarachnoid hemorrhages, as well as subdural hematomas. Hemorrhage appears as a readily identifiable hyperdense area within the brain.
The CT reveals early signs of a middle cerebral artery stroke, with loss of definition of the gyri and grey white boundary (arrow)
Early signs
In ischemic strokes, an early head CT may be grossly normal because edema and infarction have not yet developed adequately to be identified. However, other subtle findings may include: loss of the gray-white matter differentiation (red arrow) obscuration of the lentiform nucleus (white asterisk) sulcal asymmetry (yellow arrow) an insular ribbon sign Hyperdense MCA
This CT scan was taken 24 h after a stroke
M1 segment
Figure 4. A. Axial unenhanced CT image, obtained in a 73-year-old woman 21/2 hours after the onset of left hemiparesis, shows hypoattenuation and obscuration of the posterior part of the right lentiform nucleus (white arrow) and a loss of gray matterwhite matter . B. Normal aspect (I = insula, C= caudate nc, L= lentiform nc, IC = internal capsule), M1 M3 arterial territory of MCA
Hemorrhagic transformation
Presence of the blood (white arrow) in an area of brain ischemia, due to late recanalization of some of the occluded vessels and passage of the blood into the brain parenchima through the altered blood brain barrier
Old stroke
Old lesions are intensely hypodense, similar to CSF density (red arrows)
Modifiable
Arterial hypertension Hypercholesterolemia Diabetes Smoking Obesity Physical inactivity
Clinical aspects
Practically every neurological sign and symptom due to a dysfunction of the Central Nervous System can be caused by a transient or permanent occlusion of a vessel If the signs and symptoms are transient and the imagistic studies (MRI) do not show a lesion of the brain, we call this a transient ischemic attack (TIA) . The definition of the TIA admits a duration of the symptoms 24 h, but typical TIAs last 1 h. If the occlusion is permanent, a cerebral infarction will occur and we call this an ischemic stroke
The media campaign for increasing public awareness towards stroke included the most frequent signs of stroke, and stressed out the importance of acting fast, because time is brain Facial paresis, decrease in force of the arm or leg, dysarthria or aphasia are present in almost 2/3 of strokes Other signs, like cerebellar signs, hemianopia, brainstem signs can occur if the affected vessel is in the vertebro-basilar territory (see also the lecture about brain arteries for the clinical signs of different types of stroke)
Even if the patient is not hospitalized, he/she must be rapidly evaluated and treated
Stroke etiology
The Heart
Small vessels
Blood
Big vessels
The Heart
Left atrium
Thrombi due to atrial fibrillation Atrial mixoma
Endocarditis
Infectious Non- infectious
Marantic (para neoplastic) SLE (Liebman- Sachs)
The Heart
Ventricles
Myocardial infarction (hypokinesia, aneurysms and thrombi)
Paradoxical embolism
Persistent Foramen Ovale (PFO) Interatrial septal defect Interatrial septal aneurysm
Atrial fibrillation
The most common cause of cardioembolic stroke Any form of atrial fibrillation can cause a stroke (paroxysmal or permanent) AF is more frequent in men, but strokes due to AF are more frequent in women (reasons are not clear ) Prevalence of AF increases with age The majority of cases are nonvalvular AF, but AF can be associated with valvular disease (mitral stenosis) A person with AF and stroke must receive anticoagulant therapy (unless there are clear contraindications for long term oral anticoagulants)
PFO
In order to affirm a stroke due to paradoxal embolism:
Presence of PFO Right to left shunt Presence of deep vein thrombosis
Treatment :
Antiplatelet drugs/Anticoagulant drugs (not enough data) If under treatment, a recurrent stroke occurs we can consider PFO closure (Amplazer device is the most popular)
Epithelized device)
Preferential sites: low shear stress regions : ICA bulb, CCA bifurcation Do not forget the aortic crosa !!! (sometimes, even if the ICA is clean, we can identify ateromatous plaques with thrombosis on the aortic crosa by Trans Esophageal Ecocardiography)
There is endothelial dysfunction and the endothelium above the plaque is prone to rupture (exposes the lipid core, and causes thrombosis)
Thrombosis in situ, with complete acute occlusion of the vessel Arterial embolism : thrombus will be fragmented and will occlude smaller vessels
Atheromatous plaques
Doppler Ultrasound : extracranial (ECD) can visualize stenosis or occlusion (yellow arow)
Doppler ultrasound transcranial (TCD) Gives us information about the circle of Willis
Transtemporal approach; through a good window one can easily visualize MCA, ACA, PCA
Watershed infarction
II. Dissection
Young patients
Minor trauma Idiopatic Extension from aortic dissection (rare)
Clinical aspects :
Stroke or TIA Lateral cervical pain Claude Bernard Horner Syndrome Pulsatile Tinnitus headache Hypoglossus paralysis
Location : most frequent in the carotid channel (the bone channel through which the ICA enters into the skull) The mechanism : cleavage between intima and media; blood enters between intima and media, can cause stenosis or occlusion; about 30% of dissections recanalize
Small vessels
Small arteries : diameter between 100 400 mcrons Arterioles: Vessels with a diameter < 100 microns The strokes will have small dimensions and are called lacunar infarcts (yellow arrow); are situate in the subcortical white matter, basal ganglia, brainstem (especially pons) Main causes:
Arterial hypertension Diabetes mellitus Vasculitis
Inflammatory
Isolated CNS vasculitis Secondary (infectious, in cancer, toxic origin, autoimmune disorders)
Non- inflammatory
Susac syndrome Sneddon Syndrome Post-partum angiopathy
Fig. 2
Fig. 1 MRI aspect of CADASIL. Typical white matter lesions are seen as a hypersignal in FLAIR sequencewhite arrows Fig. 2 : evolutive pattern of CADASIL (it is not mandatory to have all the clinical manifestations but the majority of patients finally will be demented)
Blood
Red cells
Policytemia vera Sickle cells disease
White cells
Leukemias (acute or chronic) Lymphoma (there is a rare form of intravascular lymphoma)
Platelets
Thrombocytosis Thrombocytopenia (i.e in thrombotic thrombocytopenic purpura)
Plasma
Waldenstrm Macroglobulinema
Thrombophilias
Hyperhomocysteinemia Antiphospholipid antibodies
Clinical exam
From clinical point of vue, a sudden or a subacute onset can also be determined by:
Cerebral hemorrhage Subdural hematoma Necrosis or hemorrhage inside a brain tumor (primary tumor or a metastasis) Acute enkephalytis
In daily practice CT is usually enough for the diagnostic. If there is a problem of differential diagnostic, CT with contrast or an MRI will be neccesary
MCA
ACA
Small infarctions in the basal ganglia and cortex (blue arrows) and focal narrowings of the small vessels (yellow arrows) in a case of postpartum angiopathy
IV. Neurorehabilitation
Primary prevention
Treat the risk factors
Arterial hypertension (the best results seem to be with ACE inhibitors + indapamide) Diabetes mellitus: keep glycemia into normal ranges Dyslipidemia : use statins
Cholesterol dependent effects : they decrease LDL chol and triglycerides (use guidelines for the target level of LDL chol) Non- cholesterol dependent effects: statins improve endothelial dysfunction, stabilize the plaque, may determine the decrease of plaque dimensions)
Change lifestyle : less food, less alcohol, more sports, no smoking ! Use existing scores to calculate risk (i.e SCORE risk) Do not use routinely Aspirin for primary prevention of stroke. It was not proven to be efficient. Use Aspirin when the patient has a high risk of stroke, like high grade carotid stenosis Use anticoagulants if the patient has a proven source of cardiac emboli or if he/she has AF with a CHADS score 2
CHADS- vasc
Attention ! When a person already had a stroke we are speaking about secondary prevention !
Treat cerebral edema with Mannitol 20% 125 ml, iv perfusion, slow rhythm, maximum dose 6 perfusions/day Lower body temperature in case of fever *
* hypothermia (around 32 C can be an important method for neuronal protection, but it is not a routine for the moment
In the first 48 hours after stroke treat blood pressure only if it exceeds 220/120 mm Hg If the patient is a candidate for thrombolysis, the cut-off value is 185/110 mm Hg Stroke is a stressful condition for the patient and blood pressure increase is a compensatory reaction. Lowering blood pressure will aggravate the patients prognostic Do not lower fast the blood pressure Preferred drugs:
Thrombolysis
Check inclusion/exclusion criteria Cerebral CT scan Give 0.9 mg/kg body weight of rTpa (recombinant tromboplasminogen activated), but no more than 90 mg in one hour, with an initial bolus of 10% The patient is monitored in the next 24 hours, especially for blood pressure The sooner we give rTpa the greater are the chances to recanalize the vessel (Time is brain); always try to gain time ! Complications :
Bleeding (especially brain hemorrhage) Allergy to rTpa Re- thrombosis after an initial recanalization (we can not repeat thrombolysis)
Intravenous thrombolysis can be combined with intraarterial thrombolysis (bridging) In selected cases (especially in basilar occlusion) intrarterial thrombolysis (through catheterism) may be the irst choice
In a recent trial which compared thrombolysis/mechanical devices thrombolysis was proved to be more efficient
Secondary prevention
For all other strokes give antiplatelets
Clopidogrel 75 mg/day Aspirin + Extended release Dipiridamol (Agrenox) Aspirin 75 mg/day
If the patient is treated with Aspirin and has a recurrent stroke , Aspirin will be replaced by Clopidogrel The association of Clopidogrel + Aspirin increases the risk of hemorrhages and should be reserved to selected cases
Secondary prevention
Revascularization procedures If a stroke occurs in the distribution territory of the internal carotid artery and ICA has a stenosis of 70%, this stenosis is considered symptomatic. If no stroke occured and the discovery of the stenosis is incidental, the stenosis is considered asymptomatic Asymptomatic stenosis must not be re- vascularized routinely Symptomatic stenosis > 70% must be re-vascularized
The best results are obtained if the procedure is performed in the first 14 days after stroke
Revascularization
Endarterectomy
Proven efficacy in 2 large trials (NASCET, ECST) Possible complications:
Hypoglossus paresis Complications related to anesthesia Acute thrombosis after endarterectomy restenosis
Patients with endarterectomy should receive one antiplatelet drug, Clopidogrel or Aspirin
Carotid Stenting
ICA stenosis (white arrow), revascularization after introduction of the stent (red arrow), and the aspect of the stent inside the vessel (yellow arrow)
IV Neurorehabilitation
It is very important for the recovery of normal functions, for social and familial reinsertion of the patient Should be started very early, in the post acute period The neurorehabilitation team should include:
Neurologist, physiotherapist, logopedist, occupationl therapist, social worker
Every aspect should be assessed: motor function, spasticity, equilibrum, deglutition, speech, cognitive disorders Cognitive disorders are an important aspect in stroke patients. It is not correct to diagnose dementia immediatey after stroke, but the patients should be monitored and re- evaluated because incidence of dementia is 9 fold increased in the first year after stroke Depression also has an increased incidence and should be diagnosed and treated because if untreated it influences negatively the rehabilitation process