CEREBRAL VASCULAR ACCIDENT Predisposing factors: 1. Advancing age 2. Gender (males) 3.Race (African Americans) 4.

Family history of stroke Precipitating factors: 1.Hypertension 2. Heart disease (atrial fibrillation) 3. Diabetes mellitus 4. Sleep apnea 5. Blood cholesterol levels 6. Smoking 7. Sickle cell disease 8. Substance abuse 9. Living in the stroke belt 10. Prior stroke, carotid stenosis, and a history of TIA 11.Heavy alcohol consumption 12. Obesity 13. Specific to women: oral contraceptive use, pregnancy, childbirth,menopause, migraine headaches with aura, autoimmune d/os (diabetes and lupus), clotting factor disorders

Atherosclerosis

Atherosclerotic plaques

LODGED Large blood vessel of the brain

Damage to the endothelial Lining of the vessel

STENOSIS

internal elastic lamina become thin and frayed CAUSING

platelets to adhere to the rough surface

RELEASE THE enzyme Adenosine Diphosphate

initiates the clotting sequence

THROMBUS FORMS

CAN DEVELOP ANYWHERE small, deep penetrating arteries( lenticulostriate arteries) from the middle cerebral artery LACUNAR STROKE OCCLUSION thrombus may remain in place and continue to enlarge

common site: internal carotid artery, vertebral arteries and the junction of the vertebral and basilar arteries

INFARCTION

cells DISTAL to the occlusion

cells CRITICALLY located

part of it may break off

completely occluding the lumen of the vessel

DIE

only minor deficits are seen since these areas are very small

more severe manifestations may develop including paralysis and sensory loss

EMBOLUS

disruption of the cerebral blood flow INITIATES

WITHIN FEW MONTHS OF THE INFARCTION

carried through the arterial system ISCHEMIC CASCADE Brain BEGINS WHEN

Necrotic brain cells are REABSORBED by macrophage activity

a very small cavity or lake is formed

lodged in a vessel too narrow to permit further movement (most common site: left middle cerebral artery)

cerebral blood flow falls to <25ml/100g/min

breaks up into smaller fragments

neurons can no longer maintain aerobic respiration Mitochondria switch Anaerobic respiration

absorbed by the body

not absorbed by the body large amounts of lactic acid manifestations will persist change in the pH level >drowsiness, stupor, coma RENDERS >contralateral hemiplegia of the arm and face neuron incapable of producing >contralateral sensory sufficient quantities of deficits of the arm and face adenosine triphosphate >global aphasia (if dominant (ATP) hemisphere is involved) >homonymous hemianopia NA- K pump fails

manifestations will disappear in a few hours to a few days

weakened vessel wall

INCREASING THE POTENTIAL HPN CEREBRAL HEMORRHA GE

OCCURS WHEN sudden onset of a severe headache

rupture of a cerebral aneursym BLOOD ENTRY INTO

Cerebral vessel ruptures SUDDEN ENTRY OF BLOOD

increase in intracellular calcium

release of glutamate

IF CONTINUED

SUBARACHNOID SPACE/ VENTRICLES

BRAIN TISSUE activate a number of damaging pathways RESULT

Irritates the meninges and brain tissue

brain tissue affected by pressure due to mass formation of blood clot

generation of free radicals, vasoconstriction, release of more calcium and glutamate, destruction of the cell membrane
MINI STROKE/ TRANSIENT ISCHEMIC If managed: tPA, ATTACK

displaces brain tissue Inflammatory reaction impairing absorption and circulation of CSF decreases cerebral blood flow

sudden onset and often disappears w/ minutes or hours

calcium channel blockers

Blood vessel spasm

edema ischemia and infarction

infarction

>contralateral numbness or weakness of the leg, hand, forearm and corner of the mouth( middle cerebral artery involvement) >aphasia (ischemia of the left hemisphere); >visual disturbances such as blurring (posterior cerebral artery involvement) IF NOT MANAGED

>weakness of one side (including the face, arm and leg) Putaminal & >slurred speech Internal >deviation of the capsule eyes

SEVERE HEMORRHAGE >hemiplegia >fixed and dilated pupils >abnormal body posturing >coma

IRREVERSIBLE CEREBRAL DAMAGE

Hemiplegia with more thalamus sensory than motor loss release of metalloprotease (zinc & calcium- dependent enzymes)

Problems w/ vision and eye movement subthalamus

breakdown of collagen, hyaluronic acid and other elements of connective tissue

severe headache, vomiting, loss of ability to walk, dysphagia, dysarthria, cerebellum eye movement disturbances

structural integrity loss of brain and tissue and blood vessels

>respiration affected >hemiplegia pons

breakdown of the protective blood brain barrier

>paralysis >coma >abnormal body posturing >fixed pupils >hyperthermia >DEATH

CEREBRAL EDEMA

VASCULAR CONGESTION

Compression of tissue

increase intracranial pressure

Impaired perfusion and function

Middle Cerebral Artery Lateral hemisphere, Frontal, parietal And temporal Lobes, basal ganglia

Anterior cerebral artery Frontal lobe

Posterior cerebral artery

Occipital lobe; Branches into opthalmic, Anterior & medial PCA, anterior Portion of temporal Choroidal,ACA, MCA lobe

Internal Carotid Artery

Vertebrobasilar System Cerebellum, brain stem

Anteroinferior cerebellar Cerebellum

Posteroinferior cerebellar Cerebellum

Contralateral hemiparesis or hemiplegia, unilateral Neglect, altered consciousness, homonymous anopsia, inability to turn eyes toward affected side, Vision changes, dyslexia, Dysgraphia, Aphasia, agnosia, Memory deficits, vomiting

Contralateral Alternating motor Hemiparesis, Weaknesses, Mild contralateral Foot and leg deficits Contralateral Ataxic gait, Hemiparesis, greater than the arm, Hemiparesis w/ dysmetria, Intention tremor, foot drop, Contralateral Facial asymmetry, Diffuse sensory gait disturbances, Hemisensory Contralateral Loss, Contralateral Impairments, Sensory Pupillary dysfunction, Hemisensory Double vision, Alterations, Loss of conjugate Alterations, Homonymous Homonymous Gaze, nystagmus, Deviation of Hemianopia, Hemianopsia, Loss of depth Eyes toward Nystagmus, Perception, Ipisilateral periods Conjugate gaze, Affected side, Cortical blindness, Expressive of blindness, Paralysis, Homonymous Aphasia, aphasia Dysarthria, Hemianopsia, Confusion, If dominant Memory loss, Perseveration, Amnesia, Hemisphere Disorientation, dyslexia, Flat affect, Tinnitus, is involved, Memory deficits, Apathy, shortened Hearing loss, Horner's Visual hallucinations Attention span, dysphagia, syndrome Incontinence, acuity vertigo,coma Carotid bruits Apraxia, acuity

Ipsilateral Ataxia, facial Paralysis, Ipsilateral loss of sensation in face, Sensation changes on Trunk and limbs, Nystagmus, Horner's syndrome, Tinnitus, hearing loss

Ataxia, paralysis Of the larynx And soft palate, Ipsilateral Loss of sensation In face, Contralateral on Body, Nystagmus, dysarthria, Horner's Syndrome, Hiccups And coughing, Vertigo, Nausea And vomting

If managed: Palliative care- monitoring v/s and neurovital signs, intubation, ICP monitoring, intubation, Mechnical ventilation, vasodilators, Osmotic, diuretics, ventriculostomy

If not managed

Continued insufficiency of Blood flow

Poor cerebral perfusion

Further compression Of tissues

coma Poor improvement Cerebral death

Loss of neural feedback mechanisms

Cessation of physiologic functions

Cardiovascula r system

Pulmonary system

GIT

GUT

Other systems

Loss of cardiac muscle function

Relaxation of venous valves

Failure of Accessory Muscles For breathing

Loss of lung movement

Relaxation of intestines and sphincters

Neurogenic bladder

Loss of sphincter control

Bradycardia

Hypotension Loss of bowel control

Restlessness, abnormal Thermoregulation, Mental Confusion, Increase Secretions, Decreased urinary output

Decreased Cardiac output apnea Cardiopulmonary arrest

Systemic failure

DEATH