STROKE -Contains the cerebrospinal fluid.

-Leading cause of disability in adults AVM

-AKA “Brain attack”
-Blood Clot Blocks an artery or a blood vessel or breaks -Is the abnormal tangle of blood vessels that connects the artery and the vein.
-Interrupts blood flow to an area of the brain —> cells begin to die and brain damage occurs -A tangle can disrupt the normal blood flow which increases the risk of having subarachnoid hemorrhage
-Affects a part of the brain which the affected part cannot receive oxygen rich blood which can lead to the death of the
brain cells. Intracerebral hemorrhage
-It can happen to anyone, but it can be prevented and treated if quickly diagnosed
-Abrupt onset-focal neurologic deficit that lasts at least 24 hours and is of presumed vascular origin.
-Speech, vision, hearing problems, Weakness in the left arm, Plegia, Paresis -When bleeding occurs in the brain parenchyma itself, with the formation of a hematoma within the brain.
-Has an uncontrolled HTN, Anti-thrombotic therapy, Cerebral amyloid angiopathy, and can lead to drug abuse.
ISCHEMIC STROKE -Occurs when blood vessel within the brain ruptures causing bleeding within the brain tissue, or cerebrum.
-Elevated HTN—>Can weaken blood vessels which cause rupture thus leading to bleeding
-87%
- Most common type of stroke
-Caused by clot that blocks the brain which caused decrease supply of oxygen rich blood the brain leading to ischemia
- symptoms: Headache

Cerebral amyloid angiopathy

-Buildup of amyloid proteins on the artery walls of the brain.

Subdural hematomas
HEMORRHAGIC STROKE
-Collection of blood below the dura.
-13% -Trauma
-Occurs when an artery in the brain ruptures which prevents the blood flow into the brain the cause bleeding inside, or
around the brain making hemorrhagic stroke more little than ischemic stroke.
- Symptoms: Very severe pain and headache
- is more painful compared to ischemic
stroke.
-due to aneurysm with high incidence of delayed cerebral ischemia in 2 weeks after bleeding.

Dura

-Thick outermost membrane the surrounds the brain.

Non-modifiable Risk Factors

-Age, Gender, Race, FH of stroke, low birth weight.

Modifiable Risk Factors

THROMBOTIC STROKE
-HTN, Atrial fibrillation, other cardiac disease, DM, Dyslipidemia, cigarette smoking, alcohol, sickle cell disease, asymptomatic carotid
-When damaged cerebral arteries become blocked by the formation of a blood clot within the brain -What do you call the stenosis, postmenopausal hormone therapy, lifestyle factors
blood clot -It can be modified through lifestyle modifications and management of diseases that can increased the risk of stroke

THROMBUS HTN

-A clot attached to the artery wall. -single most important risk factor for ischemic stroke.
-Usually seen in older people that has a high level of cholesterol which can make them at risk of atherosclerosis

EMBOLIC STROKE Dyslipidemia

-Caused by a blood clot that develops elsewhere in the body and then travels to one of the blood vessels in the brain – complications f stroke.
through the bloodstream -increase the risk of stroke for 2 to 4 times.
-Usually forms in the heart, Larger arteries of the upper chest, or necks
-When a part of the clot breaks away and travel into the bloodstream until it flows into the brain and blocks an artery Sickle cell disease

– inherited red blood cell disorder in which the red blood cells contains hemoglobin S.
ATRIAL FIBRILLATION
Hemoglobin S
-HR is 100-175bpm -can distort red blood cells into crescent shape or moon shape, sickle shape.
-Rapid or irregular HR which happens if the upper chamber of the heart(atria) does not function or beat well
-Can lead to blood clot formation in the heart which increased risk of embolic stroke Stenosis
-the most important cardiac cause of stroke that is treatable. -narrowing of the carotid artery. Carotid artery is the blood vessel that carry blood from the heart to the brain. Stenosis is caused by plaque
formation.
EMBOLUS
Lifestyle factors
-A part of the blood clot that breaks away and travels into the blood streams is called? -Obesity, Sedentary lifestyle, diet can contribute to stroke.

SUBARACHNOID HEMORRHAGE Paresis

-When blood enters the subarachnoid space - mild paralysis; weakened muscle movement.
-Causes trauma, rupture of intracerebral aneurysm, and rupture of arteriovenous malformation (AVM)
-Occurs when an artery on the surface of the brain rupture causing bleeding in the subarachnoid space Plegia
-Can cause permanent brain damage
- no muscle movement at all; can affect one or more muscles

Neurologic deficit

-impairment of the nerve, spinal cord, or brain function that can affect the specific region of the body.

Transient Ischemic Attack

-“Mini stroke”
-Lasts <24 ours and usually less than 30 minutes.
-Without evidence of infraction.
-Occurs when the flow of blood in the part pf the brain is temporarily blocked by a clot.
-Presents the same symptoms with stroke but it does not last long.
- can be a warning sign of a future stroke; it requires urgent assessment and intervention to reduce the risk of stroke
- symptoms: Weakness on the side on the body, Inability to speak, Loss of Vision, Vertigo, Trouble walking
-signs: Hemiparesis or Monoparesis
SUBARACHOID SPACE
Hemisensory deficit
-Space between the arachnoid membrane, and the brain tissue. -Patients with vertigo and double vision are likely to have posterior circulation involvement.
 - Determine whether the patient has a high degree of stenosis in the carotid arteries supplying blood to the brain.
Aphasia -Imaging test but uses an ultrasound to examine the carotid arteries in the neck; and can help determine whether the patient has a high
-is seen commonly in patients with anterior circulation strokes. degree of stenosis in the carotid arteries due to atherosclerosis.

Dysarthria
-Altered levels of consciousness

Infarction
– “Necrosis”; tissue death cause by prolonged lack of oxygen.

MUST KNOW!
If the left part of the brain is affected, that could affect the right part of the body. (e.g. Left part of the brain is affected, it
can cause numbness to the right part of the body).

Hemiparesis
– weakness on one entire side of the body. Electrocardiogram (ECG)
– Determine whether the patient has atrial fibrillation.
Monopoiesis
– weakness of one limb. TREATMENTS

Hemisensory deficit Desired Outcomes

– a feeling of altered sensation on one side of the body (Usually involves the face, arms, and legs)
-Reduce the ongoing neurologic injury and decrease mortality and long-term disability.
Posterior circulation -Prevent complications secondary to immobility and neurologic dysfunction
– brainstem, cerebellum, occipital lobe is affected. -Prevent stroke recurrence

Brainstem and Cerebellum General Approach

-is involved in regulating balance and coordination; if these parts are affected the patient may experience vertigo.
-Respiratory and cardiac support
Occipital lobe -Determine quickly whether the lesion is ischemic or hemorrhagic by CT scan.
-involve in vision, the patient may experience double vision if this area is affected. -Ischemic stroke patients presenting within hours of symptom onset should be evaluated for reperfusion therapy.
-Patients with BP should remain untreated unless: (Increase risk of cerebral blood flow if not followed) BP > 220/120 mm Hg and Evidence of
Aphasia aortic dissection, acute myocardial infraction (AMI), pulmonary edema, or hypertensive encephalopathy.
-communication disorder, that makes the patient unable to speak and understand words. The part affected are the areas -If BP is treated in the acute phase, short-acting parenteral agents (e.g. Labetalol, nicardipine, nitroprusside) are preferred.
responsible for language.
Reperfusion Therapy
Dysarthria – therapy for restoring blood flow which included the use of fibrinolytic agents or by surgery, stenting, grafting.
-difficulty in speaking; but it is caused by a problem in the control of the muscles used in speaking
Permissive Hypertension.
Laboratory Tests for Acute Strokes:
- Common for ischemic patients.
-Blood glucose test, Platelet count, Coagulation test -It should remain untreated for the first 7 days after the ischemic stroke.
-The purpose of the BGT, PC, CoagT. are used in order to determine the treatment eligibility of the patient, and to select the
appropriate treatment for the patient. Aortic dissection
-the inner walls of the aorta separate.
Acute stroke
- 1st 24-hour period of a stroke event. Hypertensive encephalopathy
– elevated BP and there are neurologic disfunction.
Test for hypercoagulable states

-Done only when the cause of the stroke cannot be determined based on the presence of well-known risk factors for stroke.
- This test is reserved for patient who are young (<50 years old) and had multiple venous/ arterial thrombotic events.
- If the cause of the stroke if not determined these tests are done.

Protein C deficiency
-Vit. K dependent protein that regulates coagulation; it also helps maintain the permeability of the blood vessel wall. If it’s
deficient the patient will be at risk of Thrombosis (blood clotting).

Protein S deficiency
-co-factor that helps protein C in preventing the blood from clotting too much. If protein S is deficient, it will also increase
the risk of Thrombosis, as well as for deep vein thrombosis (DVT) which is the formation of clot in the deep areas of the
body (e.g. in the legs)

Antiphospholipid antibody
-Group of antibodies that the body mistakenly produces and these antibodies attacks phospholipids, and if these antibodies
are formed it increases the risk of excessive bleeding because they considered phospholipids as foreign substances.
Hypercoagulable states
– tendency for the blood to clot easily; the blood tends to clot too much.

CT Scan

- Reveal an area of hypersensitivity (white) in hemorrhage and will be normal or hypointense (dark) in the area of infection.
- “Computer Tomography Scan”
- White area reveals hemorrhage; dark area reveals infarction.
-For general image.

Ischemic Stroke w/ Alteplase:

-You should not administer alteplase if the blood pressure of the patient is not maintained into an SBP of <185 and DBP of <110

Non-pharmacologic Therapy

Surgical Decompression
-Cases of significant swelling associated with cerebral infraction.
-Craniectomy

Craniectomy
- Removal of part of the skull to relieve pressure on the brain.

MRI
REHABILITATION
- Very effective in reducing long-term disability
–Reveal areas of ischemia with higher resolution.
- Early stroke rehabilitation involves exercise, cognitive activities etc. which can help the patient relearn the skills that they have loss.
Additional Notes:
- “Magnetic Resonance Imaging”
CAROTID ENDARTERECTOMY
-Effective in reducing stroke incidence and recurrence.
MUST KNOW!!
- Surgical removal of plaque in the carotid artery in the neck that is to restore normal blood flow and to prevent stroke.
-Both CT Scan and MRI can help view the internal structures of the body and show the stroke information.
For more detailed image.
CAROTID STENTING
-Effective in reducing recurrent stroke risk in patients at high risk of complications with endarterectomy
Diffusion Weighted Imaging (DWI)
- Surgical procedure that involves inserting a long- narrow mesh tube (Stent) into the narrow carotid artery in order to improve the blood
flow, and to prevent the artery from narrowing again.
- Reveal an evolving infarct within minutes on stroke onset.
-For detecting early stage diagnosis.

Carotid Doppler (CD)

subarachnoid hemorrhage
- due to ruptured intracranial aneurysm or arteriovenous malformation .
-Surgical intervention to clip or ablate the vascular abnormality substantially reduces mortality from bleeding.
Life threatening Secondary Prevention of Stroke

Surgical clipping
- ANTIPLATELET
-involves placing a tiny metal clip on the neck of the aneurysm to stop the blood flow.
- Extended-release Dypiridamole + Aspirin
- Dual antiplatelet Therapy
Endovascular coiling
-ANTICOAGULANT
-involves inserting a soft flexible wire by a catheter into the aneurysm and then the wire coil inside the aneurysm which
seals it off.
ANTIPLATELET

- Used in Non-cardioembolic strokes

-Long-term antithrombotic therapy to patients who have had acute ischemic stroke TIA.
-1st line antiplatelet agents: ● Aspirin (50-325 mg daily) ● Clopidogrel (75 mg daily) ● Extended-release Dipyridamole + Aspirin (ERDP-ASA)
(200/50 mg BID)

Pharmacologic Therapy

Acute Treatment of Ischemic Stroke

-Intravenous t-PA (Alteplase)
-ASPIRIN

Intravenous t-PA (Alteplase)

- Initiated within 4.5 hours of stroke onset.

-It is more effected if initiated within 4.5 hours. Clopidogrel (Plavix)
-ADR: High risk for bleeding, ICH
Inclusion Criteria: -75 mg daily
▪ Age ≥ 18 years old -Adenosine Diphosphate (ADP) inhibitor
▪ Clinical diagnosis of ischemic stroke with neurologic deficit -Clopidogrel is a prodrug
▪ Time of symptom onset well established to be <4.5 hours from treatment initiation.
-It is metabolized by CYP450 enzymes in the liver into its active metabolite which inhibits the binding of ADP to the P2Y12 receptor. The
Protocol:
binding activates the glycoprotein GP2B3A which bind to fibrinogen causing platelet aggregation.
▪ Alteplase 0.9mg/kg IV (maximum 90mg), 10% bolus over 1 min. The remainder given over 1 hour in
selected patients
Drug Interactions:
▪ Identify if the patient has a history of ICH, head trauma, previous stroke within 3 months = not required
for Alteplase therapy. ▪ CYP4502C19
▪ CT scan to rule out hemorrhage ▪ Omeprazole
▪ Avoidance of antithrombotic therapy (anticoagulant or antiplatelet) for 24 hours after alteplase. ▪ Esomeprazole
▪ SBP >185, DBP >110mm Hg Adverse Effects:
▪ Diarrhea
▪ Rash
Alteplase

– acts by activating plasminogen into plasmin

-exhibits significant fibrin specificity and affinity, however it increases the risk of bleeding and intracranial hemorrhage.
Plasmin
-active enzyme for responsible for the degradation of clot, or the dissolution of fibrin.

ASPIRIN
Extended-release Dypiridamole + Aspirin
-168-325 mg daily started within 24-48 hours of stroke onset. -Phosphodiesterase (PDE) inhibitor
-Onset of effect <60 mins. - Not used alone
-Patients receiving alteplase, are generally held for 24 hours after alteplase administration to reduce risk of hemorrhage.
- Duration of effect of Aspirin last for 7-10 days that is based on the lifespan of platelets. PDE inhibitor
-Ensure that the patient is not allergic to Aspirin.
-Aspirin acts by irreversibly inhibiting the enzyme COX- 1 (enzyme involve in the synthesis of prostaglandins which prevents
- is responsible for the degradation of CAMP into Adenosine Monophosphate which increases the concentration of CAMP thus potentiate
the formation of thromboxane A2 that is involve in platelet aggregation)
PGI2 (inhibitor of platelet aggregation).
-It should be taken with food. -It should be combined with Aspirin and others because if given alone it can cause headache.
-– can also be used for the management of acute coronary syndrome, and other coronary artery disease are treated with -Dose: 200mg/50 mg (High dose of Dypiridamole)
aspirin for the rest of their lives. Adverse Effects:

Adverse Effects: ▪ May worsen angina, dizziness, headache, syncope, GI disturbances, rash
▪ GI distress
▪ GI bleeding
Drug Interaction:
▪ NSAIDS – Administer ASA 2 hours before NSAID or 4 hours after NSAID
Dual antiplatelet Therapy
-Aspirin + Clopidogrel

Aspirin + Clopidogrel

-Ultra-low dose of Aspirin

-Patients with ischemic stroke, history of MI, and coronary stent placement
-Short term only (3 months)

ANTICOAGULANT
-Cardioembolic strokes
- Treatment of choice in patients with Atrial fibrillation, history of recent stroke or TIA.
- acts by delaying the clotting of blood.
-Also known as “blood thinners”

STROKE RISK QUIZ

Warfarin
-Antithrombotic agent of 1st choice for secondary prevention in patients with atrial fibrillation and a presumed cardiac -Developed by the AHA and ASA.
source of embolism. -can help identify if the individual has a high risk or low risk for stroke
- INR: 2.5

MOA:

▪ Inhibits Vit K. epoxide reductase (responsible for activating Vit. K) →

▪ decrease Factor X, IX, VII, II (1972)
▪ First 2 days (Procoagulant): Warfarin + Heparin
▪ Effect is seen after 5 days.

Contraindicated

▪ Pregnant (it can cause the placenta) → Hemorrhagic fetal disorder

INR (International Normalize Ratio)

- determines how long it takes for a blood to clot and monitoring patient who are in the anticoagulant therapy.
-High INR = Risk of bleeding
-Low INR = blood clot is fast occurring
-High INR but no symptoms of bleeding = Lower the dose of the warfarin, stop the Tx, or restart the TX at a low dose.
-High INR with Symptoms = Tx should be stopped.

Direct Oral Coagulant

-Dabigatran (150 mg BID)

-Apixaban (5 mg BID)
-Rivaroxaban (20 mg OD)
-Edoxaban (60 mg OD)

Edoxaban (60 mg OD)

-Less food and drug interactions

-Evaluated patient’s renal function prior to drug therapy (reduces the risk for kidney damage)
-7 days in order to decrease the cerebra blood flow.

Blood Pressure Management (According to JNC7 and ACC, ASA)

-Recommended anti-hypertensive agent for patients with stroke and TIA:

ACE Inhibitors
Diuretics
ARBs – for patients unable to tolerate ACE inhibitor
Additional Notes:

Statin Therapy

-For all ischemic stroke patients

-Reduce the risk of stroke by approximately 30% in patients with coronary artery disease and elevated plasma lipids.
-Ischemic stroke and TIA = Coronary risk equivalent (National Cholesterol Education Program (NCEP))
-LDL goal = <100 mg/dL
-Age ≤ 75 years old →High-intensity statin (Atorvastatin and Rosuvastatin)
Age > 75 years old → Moderate or high-intensity statin
-If the patient is on maximally tolerated statin therapy, but still has an LDL cholesterol ≥ 70 mg/dL (1.81 mmol/L) +
→Ezetimibe

Heparin

-Low-molecular weight heparins or low-dose subcutaneous unfractionated heparin (5,000 units TID)
-Recommended for the prevention of DVT in hospitalized patients with decreased mobility

Nimodipine

-Reommended deficits to reduce incidence and severity of neurologic deficits from delayed ischemia.
-60 mg every 4 hours continue for 21 days.
- If hypotension occurs 30 mg every 2 hours.