Stroke

1. Stroke

2. Stroke • Second important cause of death • Physical and pshychosocial handicap • Lesions of brain parenchima due to pathology of cerebral circulatory system that leads to hemorrhageae or ichemic lesions

3. Cerebral Anatomy • Vascular circulation: Anterior and Posterior • Anterior circulation • Origin: carotid system • supplies 80% brain- optic nerve, retina, frontoparietal and anterotemporal lobes of brain • Posterior circulation: • supplies 20% of brain • Derived from vertebral arteries • Supplies brainstem, cerebellum, thalamus, auditory centers and visual cortex

4. Important arteries of the brain

5. Blood supply of the brain

6. Anastomosys of main arterial systems • Circle of Willis • 2 anterior cerebral arteries • Anterior communicating artery • Postrior communicating arteries • Posterior cerebral arteries

7. Compensation via 1. Aortic arch 2. Subclavian – vertebral aa 3. Internal – external carotis communications 4, 5 Willis polygone 6. Cortical and meningean anastomosys Extracranial Intracranial Anatomosys

8. Cerebral perfusion • Blood flow: 50-55 ml/100g/min (20% of the heart output) • Values above 20 ml/100g/minno consequences • Values below 12 ml/100g/min cell death • Flow regulation • Mechanisms are active at an average BP under 60 mmHg, or above 160 mmHg • Quick acting

9. Stroke • Sudden onset (seconds- minutes, rarely 1-2 days) of a focal neurological deficit • Evolution towards stabilization or remission • Risk factors for vascular disease: arterial hyoertension, embolic conditions, etc

10. Stroke Types • 80% ischemic • Thrombosis • Embolism • Hypoperfusion • 20% hemorrhagic • Intracerebral • Subarachnoid

11. Ischemic Strokes • Thrombosis-most common cause • Etiology • Atherosclerotic disease-most common • Vasculitis • Dissection • Polycythemia • Hypercoagulable states • Infectious Diseases-HIV, TB, syphilis • Evolution of mural thrombi: • Lysis – fragmentation (eventally emboli formation) or resorbtion • Fibrous evolution • Extension

12. Ischemic stroke – other type of vascular obstruction • Inflamatory angeitis – Takayasu disease, Horton temporal arteritis, Lupus erithematosus, granulomatous angeitis) • Infectious angeitis (lues, tuberculosys, AIDS) • Arterial dissection • Radiotherapy associated stenosys

13. Ischemic Strokes • 1/5th due to Embolism • Etiology • Cardiac • More often in the carotidian system • Valvular Vegetations • Mural thrombi- caused by A-fib, MI, or dysrhythmias • Paradoxical emboli – from ASD, VSD • Cardiac tumors-myxoma • Arterial emboli (trombi, atheroma plaque fragments) • Fat emboli • Particulate emboli – IV drug injections • Septic Emboli • Spontaneous lysis and clinical remission may happen, depending of the nature of the embolus • Usually multiple ischemic lesions of different ages • More often secondary hemorrhageae

14. Hemorrhageae in the infarctus area

15. Ischemic Strokes • Hypoperfusion- less common mechanism • Typically caused by cardiac failure • More diffuse injury pattern vs thrombosis or embolism • Usually occur in watershed regions of brain • Focal hypoperfusion – arterial stenosis; collateral circulation may compensate • Global hypoperfusion – consequences depend on the dynamics of the flow reduction (duration, intensity) • Systolic AT <7 mmHg • Watershed infarct

16. Flow decrease  increase of oxygen extraction Celular death  dramatic decrease of oxygen extraction,vasoplegia (due to acidosys, release of other substances)  increase of flow Penumbra: Critical flow, enough for some of the processes required for cell survival Not enough for cell function Recovery if blood flow increases Cerebral infarctus

17. Atherosclerosis • Arteries with a diameter above 1 mm • Potentiated and caused by the risk factors • Main cause of ischemic stroke • Is thought to start around the age of 40

18. General Comments • Arteriosclerosis • Thickening and loss of elasticity of arterial walls • Hardening of the arteries • Greatest morbidity and mortality of all human diseases • Two major processes in plaque formation: • Intimal thickening • Lipid accumulation

19. Non-Modifiable Risk Factors • Age • A dominant influence • Atherosclerosis begins in the young, but does not precipitate organ injury until later in life • Gender • Men more prone than women, but by age 60-70 about equal frequency • Family History • Familial cluster of risk factors • Genetic differences

20. Modifiable Risk Factors(potentially controllable) • Hyperlipidemia • Hypertension • Cigarette smoking • Diabetes Mellitus • Elevated Homocysteine • Factors that affect hemostasis and thrombosis • Infections: Herpes virus; Chlamydia pneumoniae • Obesity, sedentary lifestyle, stress

21. Normal Artery

24. Summary of Atherosclerotic Process • Multifactorial process (risk factors) • Initiated by endothelial dysfunction • Up regulation of endothelial and leukocyte adhesion molecules • Macrophage diapedesis • LDL transcytosis • LDL oxidation • Foam cells • Recruitment and proliferation of smooth muscle cells (synthesis of connective tissue proteins) • Formation and organization of arterial thrombi

25. Complicated Lesions Fibrous Plaques

26. Complicated Lesions

27. Types of stroke • Transitory ischemic attacs • Neurologic deficits are completelly and spontaneously reversible in less than 24 hours • Stroke “in evolution” • Defficit aggravates during hours, but lasts more than 24 h • Pathologic process continues: tromobsys/bleeding; • Cerebral oedema may lead to dangerous intracranian hypertension • Stroke

29. 1 2 3 5 4 5 Cerebral Arteries Areas 1. anterior cerebral 2. Middle cerebral 3. Penetrating branches of middle cerebral 4. anterior choroidal 5. Posterior cerebral

30. Anterior cerebral artery syndrome

31. Anatomy • Initial part – before the anterior communicating artery • Anterior communicating A – near the genu of the corpus calosum • Curved portion (anterior convexity) over the corpus calosum • Pericalosal artery (deep in the interhemisferic fissure)

32. Surface branches supply cortex and white matter of : inferior frontal lobe medial surface of the frontal and parietal lobes (and a narrow territory of the lateral surface along the margin) anterior 4/5 of the corpus callosum Penetrating branches supply: deeper cerebrum limbic structures head of caudate inferior part of the anterior limb of internal capsule anterior part of the lenticulate nucleus anterior hypothalamus Anterior Cerebral Artery

33. Anterior Cerebral Artery Infarction • Clinical picture: • Contralateral weakness/numbness greater in leg than arm • Dyspraxia (apraxia of left arm (sympathetic apraxia) if anterior corpus callosum is affected) • Speech perseveration • Slow responses • In 10% of cases stroke is bilateral due to common origin of both ACA • Akinetic muteness (apathy, inertia, suppresion of verbal, emotional and gestual expression) • Forced prehension reflex bilaterally • Paraparesis/paraplegia • Urinary incontinence

34. Middle cerebral artery syndrome

35. Middle Cerebral Arteries • Surface branches supply • Most of the cortex & white matter of hemispheric convexity • (all four lobes and insula). • Penetrating branches • deep white matter (including the upper part of anterior and posterior limbs of the internal capsule, external capsula) • some diencephalic structures • Basal ganglia – putamen, caudate, external pallidus)

36. Middle cerebral artery occlusion • contralateral motor and sensory deficits in the face and arm > leg, and aphasia in the dominant (left) hemisphere. (Netter, Part II, p. 58)

37. Middle cerebral artery occlusion • Most common stroke syndrome. • Dominant Hemisphere (usually the left) • Contralateral weakness/numbness in arm and face greater than leg • Contralateral hemianopia • Gaze preference toward side of infarct • Aphasia (Wernicke’s -receptive, Broca’s –expressive, or complete) • Dysarthria • Nondominant hemisphere • Contralateral weakness/numbness in arm and face greater than in the leg • Constructional Apraxia • Dysarthria • Inattention, neglect, or extinction

38. Middle cerebal artery stroke • Stroke in the surface branches’ territory • Hemiplegia (facio-brachial) • Hemihipestesia (sometimes limited to astereognosia); • Homonime lateral hemianopia (temporal radiations); also (space agnosia in nondominant hemisphere involvement) • Impaired spatial perception, spatial neglect, anosognosiaor hemiasomatognosia(nondominant hemisphere) • aphasia • dressing apraxia, constructional apraxia(dominant hemisphere) • Stroke in the deep branches’ territory • Severe complete hemiplegia (destruction of the internal capsula) • Hemianopia, sensory damage, speech problems

39. Middle cerebal artery stroke • Complete MCA obstruction • Frequent • Controlateral: hemiplegia; sensory loss; hemianopia; • anosognosia/global aphasia • Eyes and head deviated towards the lesion • Early counsciousness problems • Massive oedema -> herniation risk –> death

41. Posterior communicating artery • Joins the MCA with the PCA • Branches for the hypothalamus, thalamus, posterior limb of the IC, Luys body • Long, small diameter • Goes backward around the cerebral peduncles, following the optic bandelete until the geniculate body • Supplies for the anterior hippocampus, posterior limb of the internal capsule • Stroke in the territory of the anterior choroidian artery: • Massive controlateral hemiplegia, hemianopia (optic hemianopsie homonimă laterală (bandeleta optică sau fibrele geniculo-calcarine) Anterior Choroidal Arteries

42. Posterior cerebral artery syndrome

43. Vertebral Arteries • Rise from subclavian artery • Branches • anterior spinal arteries & • posterior inferior cerebellar arteries. • 2 vertebral arteries join at the junction of the pons and medulla • form basilar artery • basilar divides into 2 posterior cerebral arteries

44. Posterior Cerebral Artery • Is born from the basilary artery  around the cerebral peduncles  inferior face of hemispheres (occipital lobe)  calcarine fissure • Surface branches supply • cortex and white matter of medial occipital lobes • inferior temporal lobes • posterior corpus callosum • Penetrating branches supply: • parts of the thalamus, hypothalamus, geniculate bodies • parts of the midbrain

45. Posterior cerebral artery (PCA) supplies: midbrain diencephalon temporal and occipital lobes (Netter, Part II, p. 65)

46. Posterior Cerebral Artery • Complete proximal occlusion • contralateral hemisensory loss, and hemiplegia • spontaneous pain and dysesthesia if thalamus affected (thalamic pain syndrome) • contralateral severe proximal chorea (hemiballism) (red nucleus) • Hemianopia • Cerrebelar disturbances • Sensory aphasia (dominant hemisphere) • Vertical gaze palsy, nerve III palsy

47. Posterior Cerebral Artery • Visual disturbances • Contralateral homonymous hemianopsia (central vision is often spared) • May be associated to visual agnosia, alexia • Bilateral lesions: cortical blindness • patients unaware they cannot see • Possible sparing of central vision; light pupilary reflexes are maintained • Usually associated with halucinations, agnosia, colour blindness, other psychic disorders • Memory impairment if temporal lobe is affected

48. Posterior Cerebral Artery stroke

49. Basilar artery • Arises from the jcn of paired vertebral arteries • Supplies: occipital lobe, medial temporal lobe, medial thalamus, posterior limb of internal capsule, entire brainstem and cerebellum • Clinical Presentation: • Often results in death; bilateral neurological signs • Occlusion involving the dorsal/tegmentum portion of the pons • Uni or bilateral CN VI palsy, vertical nystagmus, pupils constricted but are reactive to light,h emi or quadroplegia • Coma - common • Occlusion involving the ventral portion of the pons: remains conscious, but quadriplegic; locked-In Syndrome

50. Clinical picture of TIA • TIA is usually characterized by focal neurological symptoms. The last usually dominate over general brain symptoms. Thus TIA is regional DCBCD. They are usually acute and develop suddenly. 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