PATHO Alterations in Neurologic Function

Reticular Activating System (RAS) Picture

Ability to respond to stimuli = intact RAS Different levels of being in a coma, cant arouse them

Data Processing Deficits Aphasia and Acute confusional states

Aphasia -The loss of the comprehension or production of language Acute confusional states - Result from cerebral dysfunction secondary to drug intoxication or nervous system disease May begin either suddenly or gradually depending on the amount of toxin exposure Inability to concentrate on incoming sensory information or on any particular mental or motor task

Antibrain Antibodies

Autoimmune etiology Once plaques form, it is possible that complement proteins attach to the plaques and attract microglia-type of glial cell brain- resonates microphages of the brain or anti-inflammatory cells, which release toxins in an attempt to destroy the plaques - the assault is endless Aging and injury decrease oxygen and glucose transport, impair the blood-brain barrier, and cause mitochondrial defects that alter cell metabolism and processing of amyloid proteins

AD: An Issue of Brain Tissue

Brain tissue of AD patient's has three distinguishing features: Neurofibrillary tangles formed out of proteins in the neurons Beta amyloid plaques Granulovascular degeneration of neurons Disease causes degeneration of neutrophils (dense complexes of interwoven cytoplasmic processes of nerve cells & neuroglial cells), especially in the frontal, parietal, and occipital lobes Causes enlargement of the ventricles Early cerebral changes include formation of microscopic plaques, consisting of a core surrounded by fibrous tissue Later- atrophy of cerebral cortex

Traumatic Brain Injuries Blunt and Open

Broadly categorized into: Blunt (closed) trauma -Head strikes a hard surface or a rapidly moving object strikes the head -Dura remains intact and brain tissues are not exposed to the environment -May result in both focal brain injuries and diffuse axonal injuries Open (penetrating) trauma -A break in the dura exposes the cranial contents to the environment -Results in focal brain injuries

TIA= Transient Ischemic Attack

Caused by thrombotic particles causing an intermittent blockage of circulation or spasm Affects 50,000 people / yr Neurologic deficits must be completely clear within 24 hours, leaving no residual dysfunction Recurrence of symptoms in 30% at 3 months, 60% at 6 months and 80% at 1 year without definitive treatment

Ups and Downs of MS

Characterized by exacerbations and remissions MS is a major cause of chronic disability between ages 18 and 40 Incidence is highest in: Women Northern urban areas Higher socioeconomic groups Family history

Treating MS-Medication

Corticotropin, prednisone, or dexamethasone is used to reduce edema of the myelin sheath during exacerbations - relieving symptoms and hastening remissions Do not prevent future exacerbations Acute attack - short course of methylprednisolone, with or without a short prednisone taper Interferon beta-1a or interferon beta-1 b To decrease relapses (not clearly understood) Chlordiazepoxide (Librium) - mitigate mood swings Baclofen or dantrolene - relieve spasticity Bethanechol - relieve urine retention and minimize urinary frequency and urgency

Data Processing Deficits Dementias

Dementias Characterized by the loss of more than one cognitive or intellectual function May be decrease in orientation, general knowledge & information, vigilance, recent memory, remote memory, concept formation, abstraction, reasoning, or language Causes include degeneration, CVA, compression, toxins, metabolic disorders, biochemical imbalances, demyelinization, and infections Not be used simultaneously with Alzheimer's Dementias is the umbrella, Alzheimer's is a part of it

Stage I AD

Duration of Disease: 1 to 3 years Memory -New learning defective, impaired declarative memory Visuospatial Skills -Topographic disorientation, poor construction Language -Poor word list generation Personality -Apathy, irritability, depression Motor System -normal EEG -normal CT -Normal

Stage II AD

Duration of Disease: 2 to 10 years Memory -More severely impaired declarative memory Visuospatial Skills -Poor construction, spatial disorientation Language -Fluent aphasia Personality -Indifference and apathy EEG -Slowing CT -Normal or ventricular dilation and sulcal enlargement

MS symptoms include 2

Emotional lability (white matter-frontal lobe) Dysphagia Poorly articulated speech (cerebellar involvement) Muscle weakness & spasticity (lesions in corticospinal tracts) involuntary movements Hyperreflexia Urinary problems Intention tremor - one area not in both hands for example Gait ataxia

Epilepsy

Epilepsy is a term that is applied to conditions in which no correctable cause for seizure is found, seizure activity recurs without treatment Generalized seizures-(30%), bilateral neurons involved. Consciousness always lost or impaired Partial-focal (60%). Simple: maintain consciousness, Complex: consciousness impaired & person unable to respond normally to stimuli Tonic seizure- losing 60% of oxygen in brain- people become disabled because losing brain cells and CNS

Types of Strokes Hemorrhagic

Hemorrhagic -Most common causes are HTN, ruptured aneurysms, AVM, bleeding disorders or anticoagulation, head trauma, and illicit drug use -Hemorrhages are described as massive, small, slit, or petechial Lacunar Stroke -Are microinfarcts smaller than 1 cm in diameter and involve the small perforating arteries -Cause motor and sensory deficits

Pupillary changes

Hypothermia-may cause fixed pupils Hypoxia & severe ischemia cause large (5 mm) and fixed pupils - eyes where is the oxygen looking for it -Occasionally pupils remain small even if severe hypoxia

Prognosis for Emergence from a Coma

In traumatic coma: 95% death rate if pupillary reflexes or reflective eye movements are not present 6 hours after onset coma & 91 % if not present 24 hrs after Absence of eye opening & muscle tone for 24 hours predicts death or severe disability Recovery of consciousness within 2 weeks is associated with good outcome. Recovery of consciousness after 6 months is associated with severe disability

Seizure Activity

Maintenance of seizure activity demands increased ATP and increased cerebral oxygen consumption As available serum glucose is depleted, lactate accumulates in the brain and produces acidosis leading to cerebral injury and destruction ATP cannot be reproduced as fast as neurons firing Acidosis - respiratory arrest

CNS and Control of Voluntary Muscle Movement

Motor output to skeletal muscles travels down the spinal cord in two types of descending tracts Cerebral cortex plays major role in controlling precise, voluntary muscular movements Pyramidal tracts Extrapyramidal tracts

Signs and Symptoms Infarction

Sudden numbness, tingling or weakness of the face, arm or leg - especially if unilateral Sudden confusion, trouble speaking or understanding Sudden trouble seeing in one or both eyes Sudden trouble walking, dizziness, loss of balance or coordination Sudden, severe HA with no known cause

Absence of Acetylcholine

Suggested that problems with neurotransmitters and the enzymes associated with their metabolism may play a role in the disease The severity of dementia is directly related to reduction of the amount of the neurotransmitter acetylcholine On autopsy, the brains of Alzheimer's patients may contain as little as 10% of the normal amount

The Part Plaques Play

The more beta-amyloid plaques present, the more severe the dementia The amyloid in the plaques are hypothesized to exert neurotoxic effects Evidence suggest that plaques play an important part in bringing about cell death

Prognosis of MS

Varies May progress rapidly, causing death in a few months or disability by early adulthood About 70% of patients lead active, productive lives with prolonged remissions

Seizure Defined

"A sudden, explosive, chaotic discharge of cerebral neurons that is characterized by a sudden, transient alteration in brain function that usually -------------involves motor, sensory, autonomic, or psychic clinical manifestations and an alteration in the level of arousal." Alteration in level of arousal is temporary Chaos in the brain within the nerves Portion of brain become overly excited-hyper activated, nerves fire in an abnormal fashion

Hemorrhagic Infarction

"red strokes" Bleeding occurs into the infarcted area as a result of restoration of blood flow Most hemorrhagic infarcts are located in the cerebral cortex Produces ischemia and subsequent vasogenic edema Increased ICP results Ruptured and seepage into the ventricular system often occurs

Ischemic Infarction

"white strokes" Pale infarcts- stopping blood, cytotoxic ischemic events & interaction between blood elements & blood vessels combine to produce brain injury Affected area becomes slightly discolored & softens about 6-12 hours after occlusion Necrosis, swelling appears by 48-72 hours after infarct Cellular events occur such as failure of energy production, cytotoxic edema, and fall in extra & intracellular pH

Confirmation of emergence from a coma:

1. Ability to respond yes/no questions about self or environment 2. Ability to discriminate among objects in environment Can you squeeze my hand

CVA Statistics

500,00 persons / yr Third leading cause of death in the U.S. -150,000 deaths / yr 5% - 14% of survivors have a second stroke within 1 year of their first stroke By 5 years, 24% of females & 42% of males have a second stroke Incidence higher in African-American (Black) than white AA/Black suffer greater physical impairments and are 2 times as likely to die from their stroke Intracranial atherosclerosis more common in AA/Black & Asian Americans Extracranial more common in White population Can reoccur because of hypertension Some paralyzed survivors

Risk Factors CVA

65 years or older Male Family member-CVA Arterial HTN Systolic & diastolic Smoking > risk 50% Diabetes Insulin resistance

Seizure- Pathophysiology

A group of neurons that has a depolarization shift Plasma membranes of these cells appear to be more permeable-flexable able to be moved, making them more easily activated by hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation, and certain sleep phases Neurons are hypersensitive and remain in a chronic, partially depolarized state The firing of neurons spread to subcortical thalamic & brain stem areas (tonic phase) causing increased muscle tone & loss of consciousness Phase of alternating contraction & relaxation of muscles (clonic phase). Inhibitory neurons interrupt the seizure discharge causing the contraction & relaxation pattern

Testing for Alzheimers

AD cannot be confirmed until death, when an autopsy is performed Test to rule out other disorders PET scan: measures the metabolic activity of the cerebral cortex; confirm an early diagnosis CT scan shows more brain atrophy than occurs with normal aging MRI evaluates the condition of the brain & rules out intracranial lesions as the source of dementia EEG evaluates the brain's electrical activity & may show brain wave slowing late in the disease; also identifies tumors, abscesses, & other intracranial lesions that might cause symptoms CSF-cebral fluid analysis r/o infection Cerebral blood flow studies

CVA: CEREBRAL VASCULAR ACCIDENT/ Acute Stroke

According to the American Stroke Association A cerebrovascular accident (CVA) occurs when a blood vessel bringing oxygen to the brain gets blocked (ischemic) or ruptures (hemorrhagic) so brains cells do not get the flow of blood (oxygen & nutrients) that they need "brain attack"

Data Processing Deficits Agnosia

Agnosia - loses ability to sense things Deficit of recognition of the form and nature of objects Involves the loss of recognition through one sense, although the object or person by still be recognized by other senses Can be tactile, visual, or auditory Produced by dysfunction in the primary sensory area or in the interpretive areas of the cerebral cortex.

Extradural Hematomas Signs and Symptoms

Also called epidural hematomas Most often have arteries as source of bleeding May result in herniation through the foramen magnum Classic signs & Symptoms LOC at time of injury - some lucid periods follow As mass accumulates -h/a of increasing severity ▪ confusion -Vomiting ▪ seizure -Drowsiness -Hemiparesis

Cerebral Hemorrhage

As blood accumulates and volume increases, adjacent brain tissue is displaced and compressed

What to Look for AD 2

As the disease progresses, signs & symptoms indicate a degenerative disorder of the frontal lobe, such as: Difficulty with abstract thinking & activities that require judgment Progressive difficulty in communicating Severe deterioration of memory, language, & motor function progressing to coordination loss & an inability to speak or write Repetitive actions - disorientation Restlessness- nocturnal awakenings Irritability, depression, mood swings, paranoia, hostility & combativeness

Seizure-Phases

Aura- a partial seizure that immediately precedes the onset of a generalized tonic-clonic seizure- like a warning Prodroma- an early manifestation occurring hours to days before a seizure- headache, sense of depression Tonic Phase- muscle contraction with excessive muscle tone Clonic Phase- alternating contraction and relaxation of muscles Postictal Phase- the time period immediately following the cessation of seizure activity Depolarization- sudden change in the cell, dramatic electrical change. Most cells have negative charge inside. Rapid shift from negative to positive TIME SEIZURES- very important

Coma

Bilateral hemisphere damage or suppression by medications, hypoglycemia - low sugar want more sugar instead of less, toxins OR Brain stem lesion(tumor) that suppresses reticular activating system Coma-no verbal response to environment or stimuli/nonpurposeful movement on stimulation Light coma-purposeful movement on stimulation Deep coma-no response to any stimulation Suppressing the RAS system 80-120 normal blood sugar, 50-60 systematic for hyperglycemia 600-800 sometimes not in a coma

Pathological Mechanism Cerebral Infarction

Brain looses blood supply because of vascular occlusion Can be global or focal process with a central zone of cell loss surrounded by a zone of injured cells (penumbra) Can be ischemic or hemorrhagic

Brain Stem Areas

Brain stem areas that control arousal are next to areas that control pupils, so changes in pupillary size can give information about level of brain stem dysfunction Changes in pupil size can give info on brain steam function Serves as message system between the brain

Effects of Injury on Myelin

Can be injured by -Hypoxia -Toxic chemical -Vascular insufficiency -Autoimmune response Sheath becomes inflamed & the membrane layers break down into smaller components These components become well-circumscribed plaques filled with microglial elements, macroglia, and lymphocytes Damaged myelin sheath impairs normal conduction

Genes and Alzheimer's Disease FAMILIAL AD

Cases are rare; identified in relatively same number of families; many people in multiple generations are affected The affected person has inherited an abnormal mutation in one of three genes -PS1, PS2, or APP An individual who carries one of the mutated genes has a 50% chance of passing the gene onto his children Those who inherit the mutated gene will most likely develop the disease Not totally understood how these mutations cause the disease - they all influence beta-amyloid production

Acute Subdural Hematoma

Classically begins with -Headache -Drowsiness -Restlessness or agitation -Slowed cognition and confusion Symptoms worsen over time and progress -Loss of consciousness -Respiratory pattern changes -Pupillary dilation

Extradural Hematomas Clincial Manifestations

Clinical manifestations of temporal lobe herniation begins Ipsilateral pupillary dilation Contralateral hemiparesis - if have right side will have left side SURGICAL THERAPY EVACUATES THE HEMATOMA THROUGH BURR HOLES FOLLOWED BY LIGATION OF THE BLEEDING VESSEL(S) Worst than acute Gravity brings blood down

Neurological Exam

Confirms many of the problems revealed during the history In addition reveals: -Impaired sense of smell (early symptom) -Inability to recognize & understand the form and nature of objects by touching them, gait disorders, and tremors Positive snout reflex; in response to a tap or stroke of the lips or the area under the nose, the patient grimaces or puckers his/her lips Final stages -Urinary or fecal incontinence -Twitching -Seizures

Levels of Acute Coma

Confusion-can't think rapidly or clearly, impaired judgment Disorientation-beginning LOC, disorientation to time, then to place & poor memory, followed by loss of ability to recognize self Lethargy - deep sleep, but arousal to speaking. When opening eyes very flat and tired Obtundation-mild to mod decrease in awakness, limited response to environment - have to yell in the year Stupor-deep sleep or unresponsive Coma-no verbal response to environment or stimuli -Light coma-purposeful movement on stimulation -Coma-nonpurposeful movement on stimulation -Deep coma-no response to any stimulation

Stage III AD

Duration of Disease: 8 to 12 years Intellectual Functions -Severely deteriorated Motor -Limb rigidity and flexion posture Sphincter Control -Urinary and fecal incontinence EEG -Diffusely slow CT -Ventricular dilation and sulcal enlargement

Supportive Measures For MS

During acute exacerbations Bedrest Massage Prevention of fatigue and pressure ulcers Bowel and bladder training - catheter Treatment of bladder infections with antibiotics Physical therapy Counseling

Data Processing Deficits Dysphasia

Dysphasia - can not understand what they say, speech impairment The impairment of comprehension or production of language (semantic processing) Comprehension or use of symbols, in either written or verbal language is disturbed or lost Usually associated with CVA that involve the middle cerebral artery or one of its many branches Results from dysfunction in left cerebral hemisphere & usually involves the frontal temporal region May be non-fluent or fluent -Non-fluent- cannot find words & difficulty in writing -Fluent- verbal language is produced, but is meaningless; inappropriate words

AD: It's in the Genes

Early-onset of familial AD Includes gene defects on chromosomes: -21 -14 -1 Late-onset of familial AD Linked to a defect on chromosome: -19

AD STATS

Estimated 5.5 million Americans have Alzheimer's disease Number has more than doubled since 1980 One in 10 individuals older than age 65 and nearly one-half of those older than 85 are affected A primary progressive dementia with a poor prognosis Most patients die 2 - 20 years after onset of symptoms The average duration of the illness before death is 8 years

How Does MS Happen?

Exact cause is unknown May be caused by a slow-acting viral infection, an autoimmune response of the nervous system, or and allergic response Other possible causes include trauma, anoxia, toxins, nutritional deficiencies, vascular lesions and anorexia nervosa, all of which may help destroy axons and the myelin sheath In Addition, emotional stress, overwork, fatigue, pregnancy, or an acute respiratory tract infection may precede the onset Genetic factors may also play a part

AD: How It Happens

Exact cause is unknown, but four factors are thought to contribute: Neurochemical factors- deficiencies in acetylcholine, somatostatin, substance P, and norepinephrine Antibrain antibodies - don't know why Viral factors such as slow-growing CNS viruses Trauma Genetic factors Pain not associated with AD

ACRONYM DETECTION OF STROKE- FAST

FAST is an acronym used as a mnemonic to help detect and enhance responsiveness to stroke victim needs. The acronym stands for: Facial drooping, - ask to smile Arm weakness, Speech difficulties - repeat sentences Time. TPA- drug plasminogen activator- huge blood clot busters- can cause hemorrhage Has extreme side effects - need to witness stroke Hemorrhage- need to drain the blood

Clinical Manifestations- Meningitis

Fever, chills Tachycardia Throbbing headache Photophobia Nuchal rigidity Decrease in consciousness Seizures Diagnosis- physical exam, CSF cultures (spinal tap) Treatment- bacterial and fungal meningitis are treated with the appropriate antibiotics

Clinical Manifestations of Contusion

Immediate loss of consciousness Loss of reflexes Transient cessation of respiration Brief period of bradycardia and drop in BP Vital signs may stabilize in a few seconds Reflexes return next Regain of consciousness Return to full alertness takes variable periods of time (minutes to days)

What to Look For AD

Insidious onset, barely perceptible at first Patient history is almost always obtained from a family member or caregiver Early changes include: -Forgetfulness -Subtle memory loss without loss of social skills or behavior patterns -Difficulty learning & retaining new information -Inability to concentrate -Deterioration in personal hygiene & appearance

Intracerebral Hematomas

Intraparenchymal hemorrhages Small blood vessels are traumatized by shearing forces Intracerebral hematoma expands, increases intracranial pressure, and compresses brain tissues As ICP rises, clinical manifestations of temporal lobe herniation may appear

Alzheimer's Disease (AD)

Is a progressive degenerative disorder of the cerebral cortex Accounts for more than one-half of all cases of dementia Cortical degeneration is most marked in the frontal lobes, but atrophy occurs in all areas of the cortex Once you have the disease- try to manage and stop plaque formation. NOT going away Can get hostile and aggressive

Seizure Activity Causes

Lack of sleep Stress Excess water ingestion Constipation - cant correlate with symptoms Stimulant drugs Depressant drug withdrawal Environmental Stimuli Blinking lights, loud noises, certain odors Hypoglycemia Hypothermia

Extrapyramidal tracts

Lower motor neurons, arise from the cortex and project to the cerebellum & basal ganglia before they descend to innervate the motor neurons; they do not cross to the opposite side Convey nerve impulses that program automatic movements, help coordinate body movements with visual stimuli, maintain skeletal muscle tone & posture, and play a major role in equilibrium

Myelin Breakdown

MS affects the white matter of the brain & spinal cord by causing scattered demyelinated lesions that prevent normal neurologic conduction After myelin is destroyed, neuroglial tissue in the white matter of the CNS proliferates, forming hard yellow plaques of scar tissue called gliosis

MS Symptoms Include

May be unpredictable and difficult to describe May be transient or may last for hours or weeks Patient reveals two initial symptoms -Vision problems (optic neuritis) -Blurred vision or diplopia Sensory impairment 50% have weakness, numbness in one or more limbs (Spinal type MS). Can have bowel or bladder problems. Symmetric cerebellar problems with ataxia and nystagmus Can get hostile Start looking at you and crying

Infections in the brain Meningitis

Meningitis Pathophysiology- CNS entry is through the choroid plexus or areas of altered blood brain barrier. The bacteria or their toxins function as irritants and induce an inflammatory reaction by the meninges, the CSF, and the ventricles The blood cells migrate into the subarachnoid space, producing an exudate that thickens the CSF and interferes with normal CSF flow around the brain and spinal cord. Meningeal cells become edematous, and the combined exudate increase intracranial pressure Eitiology Bacteria, virus, fungi, parasites, toxins Test spinal tap and cerebral spinal fluid - clear like water

What Does Myelin Do?

Myelin plays a key role in speeding electrical impulses to the brain for interpretation The myelin sheath is a lipoprotein complex formed of glial cells - protects the neuron's long nerve fiber (axon) much like the insulation on a electrical wire Because of its high electrical resistance and weak ability to store an electrical charge, the myelin sheath permits conduction of nerve impulses from one node of Ranvier to the next

Pyramidal tracts

Originate in the motor cortex & terminate in the brainstem Cross to the opposite side at the medulla-spinal cord junction Also known as upper motor neurons, consists of lateral cortiocospinal, anterior cortiocospinal, and corticobulbar tracts that convey impulses - let the brain know that impulse is coming in

Risk Factors CVA 2

Polycythemia and thrombocythemia Presence of elevated lipoprotein-a Impaired cardiac function Hyperhomocysteinemia - lack of viatmin b12 and folic acid Non-rheumatic Afib - clots Chlamydia pneumoniae (infects & injures endothelium)

Multiple Sclerosis

Results from progressive demyelination of the white matter of the brain and spinal cord Leads to widespread neurologic dysfunction Structures usually involved are the optic and oculomotor nerves and the spinal nerve tracts Does not affect the PNS Cause may be viral insult to nervous system in a susceptible person that then has an autoimmune response. T cells become autoreactive to one myelin protein

Structural Modulators of Consciousness

Reticular activating system (RAS) affects many CNS activities including sleep and wakefulness; arousal and awareness Ascends from the lower brainstem through the midbrain and thalamus and projects throughout the cerebral cortex Following prolonged wakefulness, the neurons in the RAS gradually fatigue & become less excitable - when occurs, neuronal mechanisms revert to lower-level functioning and sleep The ability to respond to stimuli or arousal depends on an intact RAS in the brainstem and the ability to respond to the environment Cognition relies on an intact cerebral cortex - needs to get stimuli - ability to respond to stimuli(shaking and pinching) or arousal depends on intact and active RAS system and the ability to respond to you RAS - huge communicating system where we think, deep into cortical part of brain IT IS CONCIOUNESS, different levels, AROUSAL

Focal Brain Injuries

Specific, grossly observable brain lesions that are seen in cortical contusions, epidural hemorrhage, subdural hematoma, intracerebral hematoma and open-head trauma Force of impact typically produces contusions (bruises) on the brain Contusion in turn, causes tears in blood vessels May be coup (direct impact area) or contrecoup (area that lies opposite of the line of force) Coup - initial injury Contrecoup- hurt anywhere else because of initial blow

Status Epilepticus

Status epilepticus-30 min or longer seizure duration, or subsequent seizures one right after another. Emergency due to cerebral hypoxia putting at risk for aspiration, mental retardation, brain damage Occurrence of a second, third, or multiple seizures before the person has fully regained consciousness from the preceding seizure Most frequently results from abrupt discontinuation of anti-seizure medications or in untreated or inadequately treated persons- compliance- people not taking medications need to maintain blood level Serious or potentially fatal - development of cerebral hypoxia Seizure activity demands a 250% increase in ATP & cerebral oxygen consumption increases by 60% All medication cause depression- suppresses the brain, serotonin levels

Dementia Symptoms and Types

Symptoms of dementia are grouped according to type of memory deficit Amnestic dementia- loss of recent memory Cognitive dementia- loss of remote memory Intentional dementia- loss of vigilance & executive function- want to do something but cant, impulses are slow Altered behavior- agitation

Subdural Hematoma

Tearing of the bridging veins is the major cause of rapidly developing and subacutely developing subdurals Other sources include: torn cortical veins or venous sinuses and contused tissue Subdural space gradually fills with blood and herniation can result

M/S Depend on Four Factors

The extent of myelin destruction The site of myelin destruction The extent of remyelination The adequacy of subsequent restored synaptic transmission

AD- Sporadic AD/ and APOE

The most researched gene in sporadic AD APOE is responsible for the production of a protein that transports cholesterol & other fats throughout the body Protein that also may involved in the structure & function of the outer wall of a brain cell APOE has 3 common forms: -APOE-epsilon 2 -APOE-epsilon 3 -APOE-epsilon 4 (sporadic)- younger People who carry at least one of this type of gene are at higher risk for developing AD 35-50% of people with AD have at least one copy of this form of gene - people with 2 have even higher risk - when develop disease, show symptoms younger

Types of Stoke Ischemic

Thrombotic: occlusion caused by thrombi formed in arteries supplying the brain or in the intracranial vessels Embolic: fragments that break from a thrombus formed outside the brain or the heart-usually involves small vessels & obstructs at a bifurcation or other point of narrowing Fat emboli: fracture of long bones; post-op