1. PATHOLOGY OF STROKE dr. ISNANIAH, Sp. S
KILLER PRESENTATIONS Series “1001 Best Collections Power Template & Presentation Tools (2nd Edition)
© IDEASMAX - Presentation Services - – SMS Center : –
PATHOLOGY OF STROKE
dr. ISNANIAH, Sp. S

2. OVERVIEW Approximately 750,000 in USA annually
Third most common cause of death
#1 leading cause of disability
25% with initial stroke die within 1 year
50-75% will be functionally independent
25% will live with permanent disability
Physical, cognitive, emotional, & financial impact
A Guide to Understanding Stroke, Heart and Stroke Foundation of Canada, 1996

3. What is a Stroke
An interruption of the supply of blood and oxygen to an area of the brain.
This causes the brain cells in an area to die, and reduces the brain function in that area.
The area of the body controlled by the damaged area in unable to function properly.
There are two types of stroke.
Let’s start off with talking about what a stroke is. A stroke is an interruption in the supply of blood and oxygen to an area of the brain. When this happens the brain cells that rely on that blood and oxygen may die and the functions in the body that those brain cells were responsible for are not able to work. There are two types of strokes; an ischemic stroke and a hemohagic stroke.

4. What is a Stroke?
A stroke can happen when a blood clot blocks a blood vessel in the brain.
80% of strokes are this type.
This is an example of a stroke that results from a blood clot which has travelled to the brain and is now blocking one of the arteries “pipes” in the brain. This is called an ischemic stroke.
If you look at the picture you can see where the blood clot has lodged and is preventing the blood to continue to other parts of the brain. It is the region of brain cells behind the blood clot that is at risk of changing or dying. Depending on how quickly the blood and oxygen can be re-established will determine if there will be changes to those brain cells and the functioning that those brain cells are responsible for.
80% of stroke are this type.
A Guide to Understanding Stroke, Heart and Stroke Foundation of Canada, 1996

5. What is a Stroke?
A stroke can also happen when a blood vessel breaks and results in bleeding in the brain.
20% of strokes are this type.
This is a hemmorhagic stroke. This happens when one of the blood vessels in the brain bursts and bleeds into area around it.
20% of strokes are this type.
A Guide to Understanding Stroke, Heart and Stroke Foundation of Canada, 1996

6. RISK FACTORS Nonmodifiable:
Age – Occurrence doubles each decade >55 years
Gender – Equal for men & women; women die more frequently than men
Race – African Americans, Hispanics, Native Americans, Asian Americans -- higher incidence
Heredity – family history, prior transient ischemic attack, or prior stroke increases risk

7. Controllable Risks with Medical Treatment & Lifestyle Changes:
High blood pressure Diabetes Cigarette smoking TIA (Aspirin) High blood cholesterol Obesity Heart Disease Atrial fibrillation
Oral contraceptive use Physical inactivity
Sickle cell disease Asymptomatic carotid stenosis Hypercoagulability

8. Anatomy of Cerebral Circulation
Blood Supply
Anterior: Carotid Arteries – middle & anterior cerebral arteries
frontal, parietal, temporal lobes; basal ganglion; part of the diencephalon (thalamus & hypothalamus)
Posterior: Vertebral Arteries – basilar artery
Mid and lower temporary & occipital lobes, cerebellum, brainstem, & part of the diencephalon
Circle of Willis – connects the anterior & posterior cerebral circulation

16. Anatomy of Cerebral Circulation
Blood Supply
20% of cardiac output— ml/min
>30 second interruption– neurologic metabolism is altered; metabolism stops in 2 minutes; brain cell death < 5 mins.

17. Classification of Stroke
Two major categories:
Ischemic strokes, caused when a blood vessel supplying the brain is occluded by a clot. Responsible for 75% of all strokes.
Hemorrhagic strokes, caused when a cerebral artery ruptures.
Both forms are life threatening.
Classification of Stroke:
Strokes can be classified into two major categories:
Ischemic strokes - Occur because a blood vessel supplying the brain is occluded.
Hemorrhagic strokes - Occur because a cerebral artery ruptures.
Although both forms can be life threatening, ischemic stroke rarely leads to death within the first hour, whereas hemorrhagic stroke can be fatal at onset. Even among those who survive the first few hours after a stroke, brain injury progresses quickly and can lead to permanent disability. The classification of stroke as ischemic or hemorrhagic is important because management of the two differs markedly.

18. Causes Occlusion (50%) Atheromatous/thrombotic
1. Large vessel occlusion or stenosis (e.g. carotid artery)
2. Branch vessel occlusion or stenosis (e.g. MCA)
3. Perforating vessel occlusion (lacunar infarction)
Non-atheromatous diseases of the vessel wall
1. Collagen disease (e.g. systemic lupus erythematosis)
2. Vasculitis (e.g. polyarteritis nodosa)
3. Granulomatous vasculitis (e.g. Wegener’s granulomatosis)
4. Miscellaneous (e.g. syphilitic vasculitis, sarcoidosis, …)
Embolisation (25%) mostly from atheromatous
plaque in the intracranial or extracranial arteries or from the heart.
Haemorrhage (20%); parenchymal (15%), SAH (5%)

19. Pathophysiology Atherosclerosis: major cause of CVA
Thrombus formation & emboli development
Abnormal filtration of lipids in the intimal layer of the arterial wall
Plaque develops & locations of increased turbulence of blood - bifurcations
Increased turbulence of blood or a tortuous area
Calcified plaques rupture or fissure
Platelets & fibrin adhere to the plaque
Narrowing or blockage of an artery by thrombus or emboli
Cerebral Infarction: blocked artery with blood supply cut off beyond the blockage

20. Pathophysiology Ischemic Cascade Series of metabolic events
Inadequate ATP adenosine triphosphate production
Loss of ion homeostasis
Release of excitatory amino acids – glutamate
Free radical formation
Cell death
Border Zone: reversible area that surrounds the core ischemic area in which there is reduced blood flow but which can be restored (3 hours +/-)

21. Penumbra
Infarction

22. Infarction Cell Death Penumbra Ischemia 50 – 55 25 20 15 8
50 –
Edema Loss of Na/K+
electrical pump
↑lactate activity failure; ↓ ATP
Normal ml/100g/min
Cell Death

23. Ischemic Penumbra: Current Concept

24. Transient ischemic attacks (TIAs)
= episodes of focal neurological symptoms due to inadequate blood supply to the brain. Attacks are sudden in onset, resolve within 24 hours or less and have no residual deficit. These attacks are important as warning episodes or precursors of cerebral infarction.
The pathogenesis: A reduction of cerebral blood flow below ml/100 g/min produces neurological symptoms. The development of infarction is a consequence of the degree of reduced flow and the duration of such a reduction. If flow is restored within the critical period, ischemic symptoms will reverse.
Emboli are accepted as the cause of the majority of TIAs.

25. Occlusion of the internal carotid artery
The degree of deficit varies – it may be asymptomatic or a catastrophic infarction may result.
In the most extreme cases there may be: Unconsciousness, contralateral hemiplegia, contralateral hemisensory disturbance, homonymous hemianopia of the contralateral side and gaze palsy to the opposite side (eyes are deviated to the side of the lesion!). Occlusion of the dominant hemisphere side will result in a global aphasia.
Prodromal symptoms prior to occlusion may take the form of monocular blindness – AMAUROSIS FUGAX and transient hemisensory or hemimotor disturbance.

26. Occlusion of the anterior cerebral artery
Cortical branches supply the medial surface of the hemisphere: Orbital, frontal, and parietal ctx.
Deep branches pass to the anterior part of the internal capsule and basal nuclei.
Clinical features depend on the site of occlusion (especially in relation to the anterior communicating artery) and anatomical variation.
Occlusion proximal to the AComA is normally well tolerated because of the cross flow.
Distal occlusion results in weakness and cortical sensory loss in the contralateral lower limb with associated incontinence. Bilateral frontal lobe infarction may result in akinetic mutism or deterioration in conscious level.

27. Occlusion of the middle cerebral artery
MCA is the largest branch of the ICA. It gives off deep branches (perforating arteries) which supply the anterior limb of the internal capsule and part of the basal nuclei. It then passes out to the lateral surface of the hemisphere and here it gives off cortical branches temporal, frontal, and parietal.
Clinical features depend on the site of occlusion and whether dominant or non-dominant hemisphere is affected.
All cortical branches are involved – contralateral hemiplegia (leg relatively spared), contralateral hemianaesthesia and hemianopia, aphasia (dominant), neglect syndrome (non-dominant hemisphere).

28. Vertebral artery occlusion
The vertebral artery arises from the subclavian artery on each side. Underdevelopment of one vessel occurs in 10%. VA and its branches supply the medulla and the inferior surface of the cerebellum before forming the basilar artery.
Clinical features variable. When low in the neck, it is compensated by anastomotic channels. When one VA is hypoplastic, occlusion of the other is equivalent to basilar artery occlusion. Typical VA occlusion presents as a PICA syndrome: dysarthria, ipsilateral limb ataxia, vertigo and nystagmus, contralateral sensory loss (pain/temperature) of limbs and trunk, ipsilateral sensory loss (pain/temp.) of face, ipsilateral pharyngeal and laryngeal paralysis.

29. Basilar artery occlusion
The basilar artery supplies the brainstem from medulla upwards and divides eventually into posterior cerebral arteries which run forward to join the anterior circulation (circle of Willis).
Clinical features: Prodromal symptoms are common and may take the form of diplopia, visual field loss, intermitent memory disturbance and a whole constellation of other brainstem symptoms: vertigo, ataxia, paresis, paraesthesia.
The complete basilar syndrome following occlusion consists of: Coma, bilateral motor and sensory dysfunction, cerebellar signs and cranial nerve signs. Very serious condition!

30. Lacunar stroke
Occlusion of deep penetrating arteries produces subcortical arction characterised by preservation of cortical function – language, other cognitive and visual functions.
Clinical syndromes are distinctive and normally result from long-standing hypertension. In 80%, infarcts occur in periventricular white matter and basal ganglia, the rest in cerebellum and brainstem. Areas of infarction are cm in diameter and occluded vessels demonstrate lipohyalinosis, microaneurysms and microatheromatous changes.
Lacunar or subcortical infarction accounts for 17% of all thromboembolic strokes and knowledge of commoner syndromes is essential.

31. Lacunar stroke (cont’d)
Pure motor hemiplegia (lesion in posterior limb of internal capsule) – equal weakness of contralateral face, arm, end leg with dysarthria.
Pure sensory stroke (lesion in VPL nucleus of thalamus) – numbness and tingling of contralateral face and limbs. Sensory examination may be normal!
Dysarthria/clumsy hand (lesion in dorsal pons) – dysarthria due to weakness of ipsilateral face and tongue associated with clumsy but strong contralateral arm.
Ataxic hemiparesis (lesion in ventral pons) – mild hemiparesis with more marked ipsilateral limb ataxia
Severe dysarthria with facial weakness (lesion in anterior limb of internal capsule) – dysarthria, dysfagia and even mutism with mild facial and no limb weakness.
ventral posterolateral nucleus

32. Hemorrhagic Stroke
Hemorrhagic strokes account for 15% to 20% of cerebrovascular disorders and are primarily caused by intracranial or subarachnoid hemorrhage.

33. Hemorrhagic strokes are caused by bleeding into the brain tissue, the ventricles, or the subarachnoid space.
Primary intracerebral hemorrhage from a spontaneous rupture of small vessels accounts for approximately 80% of hemorrhagic strokes and is caused chiefly by uncontrolled hypertension.
Subarachnoid hemorrhage results from a ruptured intracranial aneurysm (a weakening in the arterial wall) in about half the cases

34. Another common cause of intracerebral hemorrhage in the elderly is cerebral amyloid angiopathy, which involves damage caused by the deposit of beta-amyloid protein in the small and medium-sized blood vessels of the brain.
Secondary intracerebral hemorrhage is associated with arteriovenous malformations (AVMs), intracranial aneurysms, intracranial neoplasms, or certain medications (eg, anticoagulants, amphetamines).

35. The mortality rate has been reported to be as high as 43% at 30 days after an intracranial hemorrhage . Patients who survive the acute phase of care usually have more severe deficits and a longer recovery time compared to those with ischemic stroke.

36. Pathophysiology
The pathophysiology of hemorrhagic stroke depends on the cause and type of cerebrovascular disorder. Symptoms are produced when a primary hemorrhage, aneurysm, or AVM presses on nearby cranial nerves or brain tissue or, more dramatically, when an aneurysm or AVM ruptures, causing subarachnoid hemorrhage (hemorrhage into the cranial subarachnoid space).

37. Normal brain metabolism is disrupted by the brain's being exposed to blood; by an increase in ICP resulting from the sudden entry of blood into the subarachnoid space, which compresses and injures brain tissue; or by secondary ischemia of the brain resulting from the reduced perfusion pressure and vasospasm that frequently accompany subarachnoid hemorrhage.

38. Intracerebral Hemorrhage
An intracerebral hemorrhage, or bleeding into the brain substance, is most common in patients with hypertension and cerebral atherosclerosis, because degenerative changes from these diseases cause rupture of the blood vessel. An intracerebral hemorrhage may also result from certain types of arterial pathology, brain tumors, and the use of medications (oral anticoagulants, amphetamines, and illicit drug use).
Bleeding occurs most commonly in the cerebral lobes, basal ganglia, thalamus, brain stem (mostly the pons), and cerebellum. Occasionally, the bleeding ruptures the wall of the lateral ventricle and causes intraventricular hemorrhage, which is frequently fatal.

39. Intracranial (Cerebral) Aneurysm
An intracranial (cerebral) aneurysm is a dilation of the walls of a cerebral artery that develops as a result of weakness in the arterial wall. The cause of aneurysms is unknown, although research is ongoing. An aneurysm may be due to atherosclerosis, which results in a defect in the vessel wall with subsequent weakness of the wall; a congenital defect of the vessel wall; hypertensive vascular disease; head trauma; or advancing age.
The cerebral arteries most commonly affected by an aneurysm are the internal carotid artery (ICA), anterior cerebral artery (ACA), anterior communicating artery (ACoA), posterior communicating artery (PCoA), posterior cerebral artery (PCA), and middle cerebral artery (MCA). Multiple cerebral aneurysms are not uncommon.

40. Arteriovenous Malformations
An AVM is caused by an abnormality in embryonal development that leads to a tangle of arteries and veins in the brain that lacks a capillary bed. The absence of a capillary bed leads to dilation of the arteries and veins and eventual rupture. AVM is a common cause of hemorrhagic stroke in young people

41. Subarachnoid Hemorrhage
A subarachnoid hemorrhage (hemorrhage into the subarachnoid space) may occur as a result of an AVM, intracranial aneurysm, trauma, or hypertension. The most common causes are a leaking aneurysm in the area of the circle of Willis and a congenital AVM of the brain.

42. Clinical Manifestations
The patient with a hemorrhagic stroke can present with a wide variety of neurologic deficits, similar to the patient with ischemic stroke.
The conscious patient most commonly reports a severe headache
Many of the same motor, sensory, cranial nerve, cognitive, and other functions that are disrupted after ischemic stroke are also altered after a hemorrhagic stroke. Other symptoms that may be observed more frequently in patients with acute intracerebral hemorrhage (compared with ischemic stroke) are vomiting, an early sudden change in level of consciousness, and possibly focal seizures due to frequent brain stem involvement .

43. Clinical Manifestations
Rupture of an aneurysm or AVM usually produces a sudden, unusually severe headache and often loss of consciousness for a variable period of time. There may be pain and rigidity of the back of the neck (nuchal rigidity) and spine due to meningeal irritation. Visual disturbances (visual loss, diplopia, ptosis) occur if the aneurysm is adjacent to the oculomotor nerve. Tinnitus, dizziness, and hemiparesis may also occur.
In other cases, severe bleeding occurs, resulting in cerebral damage, followed rapidly by coma and death.

44. Assessment and Diagnostic Findings
Any patient with suspected stroke should undergo a CT scan to determine the type of stroke, the size and location of the hematoma, and the presence or absence of ventricular blood and hydrocephalus.
CT scan and cerebral angiography confirm the diagnosis of an intracranial aneurysm or AVM. These tests show the location and size of the lesion and provide information about the affected arteries, veins, adjoining vessels, and vascular branches.
Lumbar puncture is performed if there is no evidence of increased ICP, the CT scan results are negative, and subarachnoid hemorrhage must be confirmed. Lumbar puncture in the presence of increased ICP could result in brain stem herniation or rebleeding.
When diagnosing a hemorrhagic stroke in a patient younger than 40 years of age, some clinicians obtain a toxicology screen for illicit drug use.

45. Prevention
Primary prevention of hemorrhagic stroke is the best approach and includes managing hypertension and ameliorating other significant risk factors.
Control of hypertension, especially in people older than 55 years of age, clearly reduces the risk for hemorrhagic stroke. Additional risk factors are increased age, male gender, and excessive alcohol intake).
A prevention effort unique to hemorrhagic stroke is to increase the public's awareness about the association between phenylpropanolamine (PPA, an ingredient found in appetite suppressants as well as cold and cough agents) and hemorrhagic stroke.

46. Complications
Potential complications of hemorrhagic stroke include rebleeding; cerebral vasospasm resulting in cerebral ischemia; acute hydrocephalus, which results when free blood obstructs the reabsorption of cerebrospinal fluid (CSF) by the arachnoid villi; and seizures.

47. Cerebral Hypoxia and Decreased Blood Flow
Immediate complications of a hemorrhagic stroke include cerebral hypoxia, decreased cerebral blood flow, and extension of the area of injury. Providing adequate oxygenation of blood to the brain minimizes cerebral hypoxia. Brain function depends on delivery of oxygen to the tissues.
Administering supplemental oxygen and maintaining the hemoglobin and hematocrit at acceptable levels will assist in maintaining tissue oxygenation.
Cerebral blood flow is dependent on the blood pressure, cardiac output, and integrity of cerebral blood vessels. Adequate hydration (IV fluids) must be ensured to reduce blood viscosity and improve cerebral blood flow. Extremes of hypertension or hypotension need to be avoided to prevent changes in cerebral blood flow and the potential for extending the area of injury.
A seizure can also compromise cerebral blood flow, resulting in further injury to the brain. Observing for seizure activity and initiating appropriate treatment are important components of care after a hemorrhagic stroke.

48. Vasospasm
The development of cerebral vasospasm (narrowing of the lumen of the involved cranial blood vessel. The mechanism responsible for the spasm is not clear, but vasospasm is associated with increasing amounts of blood in the subarachnoid cisterns and cerebral fissures, as visualized by CT scan. Monitoring for vasospasm may be performed through the use of bedside transcranial Doppler ultrasonography (TCD) or follow-up cerebral angiography).
Vasospasm leads to increased vascular resistance, which impedes cerebral blood flow and causes brain ischemia and infarction. The signs and symptoms reflect the areas of the brain involved. Vasospasm is often heralded by a worsening headache, a decrease in level of consciousness (confusion, lethargy, and disorientation), or a new focal neurologic deficit (aphasia, hemiparesis).

49. Increased ICP
An increase in ICP can occur after either an ischemic or a hemorrhagic stroke but almost always follows a subarachnoid hemorrhage, usually because of disturbed circulation of CSF caused by blood in the basal cisterns. If the patient shows evidence of deterioration from increased ICP (due to cerebral edema, herniation, hydrocephalus, or vasospasm).

50. Systemic Hypertension
Preventing sudden systemic hypertension is critical in the management of intracerebral hemorrhage. Although specific goals for blood pressure management are individualized for each patient, systolic blood pressure may be lowered to less than 150 mm Hg to prevent hematoma enlargement . If blood pressure is elevated, antihypertensive therapy .

51. THANK YOU