c Tests(Neuro)

7/28/2019 c Tests(Neuro)

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Care of Clients withNeurologic Deficit

By: Elmer G. Organia, RN


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Organization of the Nervous System


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Gray and White Matter in the Brain


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Gray Matter and White Matter in the SpinalCord


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Gray and White Matter in the PNS


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The Cerebral Hemispheres


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Longitudinal Fissure


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Cerebral Lobes


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Figure 13.15


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Diencephalon

Figure 13.16a


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Midbrain, Pons, MedullaOblongata, Cerebellum


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Pons, Medulla Oblongata


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Cerebellum


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Cerebrospinal Fluid (CSF)


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Cerebrospinal Fluid (CSF)


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Cerebrospinal Fluid


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CSF


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CSF


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Blood Brain Barrier

S i l C d


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Spinal Cord


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Spinal Cord


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Anatomy of Spinal Cord


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S i l C d


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Spinal Cord


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Anatomy of the Spinal Cord


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M i


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Meninges


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The Meninges


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Patellar Reflex

rgan za on o e ervous


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rgan za on o e ervousSystem


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Th 12 P i f C i l


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The 12 Pairs of CranialNerves

12 Pairs of Cranial Nerves


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12 Pairs of Cranial Nerves

CN I (Olf N )


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CN I (Olfactory Nerves )

CN II (Optic Nerve)


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CN II (Optic Nerve)

CN III (Oculomotor Nerve)


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CN III (Oculomotor Nerve)

CN IV (T hl N )


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CN IV (Trochlear Nerve)

CN V (T ig i l N )


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CN V (Trigeminal Nerve)

CN VI (Abd N )


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CN VI (Abducens Nerve)


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CN VIII

(Vestibulocochlear Nerve)


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CN IX (Glossopharyngeal Nerve)

CN X (Vagus Nerve)


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CN X (Vagus Nerve)

CN XI (Accessory Nerve)


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CN XI (Accessory Nerve)

CN XII (Hypoglossal Nerve)


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CN XII (Hypoglossal Nerve)

CN DYSFUNCTION INTERVENTIONS


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I Decreased sense of smell Is often accompanied by impaired taste and weightloss

II Decreased visual acuity and

visual fields

Frequent reorientation to environment. Position

objects around client in deference to visualimpairment

IIIIV,VI

Double vision (diplopia) Intermittent eye patchingLubricate eyes to protect against corneal abrasions

V Decreased facial sensationInability to chewDecreased corneal reflexes

Caution in shaving and mouth care. Choose easy tochew foods with high caloric content. Protectcorneas from abrasion by using lubricant

VII Facial weakness and

decreased taste(ant. tongue)

Oral hygiene. Account for decreased food intake.

Cosmetic approach to hiding facial weakness.VIII Hearing loss, imbalance,

vertigo, tinnitusSAFETY! Move slowly to prevent nausea andemesis. Assist ambulation

IXX

Dysarthria, Dysphagia,cardiac and respiratoryinstability

Maintain airway. Prevent aspiration. Swallowtherapy


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Structure of Spinal Nerves


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Spinal Nerve

Spinal Nerves Dorsal Root and


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Spinal Nerves-Dorsal Root andVentral Root


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S h i N S


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Sympathetic Nervous System


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Autonomic Reflexes

Control of Autonomic Functions by


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yHigher Brain Centers


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Key Concepts Oxygen Supply - 20% of Oxygen in

the body.

Glucose Supply 65 75% of glucosein the body. Blood Supply 1/3 of Cardiac Output


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Acid Base Balance

Acidosis cerebral vasodilation-increase ICP- CNS depressant-COMA.

Alkalosis Vasoconstriction IncreaseICP CNS stimulant - SEIZURE


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Impairment of short term memory Blood supply lessens Alteration of sleep-wake ratio


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Diagnostic Tests

N i i T t


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Non-invasive Test

1.) SKULL &SPINAL X-RAY

b l


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Nsg Responsibilities:

PREPROCEDURE

1.)Explain the procedure

2.)Provide support for the confused, combative and ventilated dependent

3.)Maintain immobilization of neck if spinal fracture is suspected

4.)Fasting is not required

5.)Remove metal items from body parts.

6.)If the client has thick and heavy hair, this should be documented.

2 ) COMPUTED TOMOGRAPHY SCAN


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2.) COMPUTED TOMOGRAPHY SCAN

HemorrhageTumors

Abscess

EmboliCV disorders

Fractures

Degenerative disorders

b l


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Nsg Responsibilities:Preprocedure:

1. Explain the procedure2. Obtain consent if dye is to be used3. Assess for allergies to the dye4. Instruct the patient the need to lie flat and still during the test5. Remove objects from the head6. Assess for claustrophobia7. Inform the patient about the possible mechanical noise8. Inform about the possible effect of the dye as injected.9. Sedate as ordered


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Post procedure:

1.Provide fluid replacement2.Monitor for allergic reaction3.Assess dye injection site

3 ) Magnetic Resonance Imaging


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3.) Magnetic Resonance Imaging

Identifies types of braintissues

Tumors Vascular abnormalities Abnormal degenerative

disorders Ischemic areas Edema Demyelinization

Oops! Neurons break


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Oops! Neuron s break

1.) Give one contraindication for MRIand the rationale!

4 )P i E i i T h


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4.)Positron Emission Tomography Used to measure cerebral b

flow Cerebral glucose metabolis Oxygen extraction Epilepsy Tumor

ELECTOENCEPHALOGRAM


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( EEG)

Is an amplified recording ofthe electrical activity of the brain.

Used to dx: Epilepsy Cerebral damage (coma,

drug overdose, retardation,organic brain syndrome)

Cerebral death

N ibili i


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Nsg responsibilities:

1. Explain the purpose of the test2. Wash the clients hair 3. Inform that electrodes are attached to the head4. Withhold stimulants, antidepressants, tranquilizers,

anticonvulsants5. Breakfast is allowed6. Wash the clients hair

7. The test will take 45-2 hours.

Pre-procedure


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Invasive Diagnostic Test

LUMBAR PUNCTURE


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LUMBAR PUNCTURE

Introducing a hollow needle intoSAS between L4& L5, is used to:

Measure CSF pressure Collect CSF for lab exam

Inject contrast medium Reduce ICP Introduce anesthetics

Reference Abnormal


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ReferenceValue:

AbnormalFindings

1.) Color Crystal, clear,colorless Cloudy

bloody

2.) Pressure 60-180mmH2O increased

decreased

3.) Protein 15-45 mg/dl increased

4.) Glucose 50-75mg/dl increaseddecreased

5.) IgG 1-4 mg/dl increased

N g ibiliti


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Nsg responsibilities: Pre-procedure:1. Explain the

procedure2. Obtain consent3. Have patient

empty the bladder.


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Queckenstedts test


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Queckenstedts test

To test for subarachnoid obstruction. Compression of jugular vein noting

pressure of spinal fluid.

MYELOGRAM


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MYELOGRAM

Is a radiograph of the spinalcanal after injection ofcontrast media into the SASthru LP.

Used to detect: Herniated intravertebral

disk Spinal cord tumor spondylosis


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CEREBRAL ANGIOGRAM


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CEREBRAL ANGIOGRAM

Is an invasive method ofvisualizing the intracranial andextra-cranial blood vessels by

using an intra-arterial injection ofradiopaque contrast medium

Used to detect:


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Used to detect: Structural abnormalities of BV Malformations

Aneurysms

Thrombi

Occlusions

Arterio-venous malformation

Nsg Responsibilities:


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Nsg Responsibilities:PRE-PROCEDURE:

1. Explain the procedure2. Obtain consent3. Assess for allergies4. NPO 4-6 hours prior to the test5. Obtain baseline neurological status6. Mark peripheral pulses7. Remove metal items

8. Administer pre-medications.

POST-PROCEDURE:


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POST-PROCEDURE:

1. Monitor Vs and Neurological Status2. Monitor fro swelling in the neck and dysphagia3. Bed rest for 12 hours

4. Elevate head of the bed 15-30 degrees5. Keep the bed flat if the femoral artery is used6. Assess peripheral pulses7. Immobilize the puncture site for 12 hours8. Apply pressure dressing to the injection site9. Apply ice to the punctured site10.Force fluids

Electromyography


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Electromyography Is used to measure anddocument electrical

currents produced byskeletal muscles.

Small needle electrodes areinserted into the muscles

Used to detectneuromuscular disorder


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Neurological Assessment

I Consciousness & Mental State


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I. Consciousness & Mental State

Cognitivefunctions

Emotions

Personality &psychological

status

Physiologicchanges

COGNITIVE FUNCTIONS


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COGNITIVE FUNCTIONS

Attention SpanOrientationMemory & Concentration

IntellectFlow of SpeechPerception

CalculationsJudgment & Insight

II VITAL SIGNS


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II.VITAL SIGNS

Temperature

Pulses in all ext

Respiratory rate &Pattern

Blood pressure

III LEVEL OF CONSCIOUSNESS


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III. LEVEL OF CONSCIOUSNESS

1.) FULL CONSCIOUSNESS Alert, oriented, comprehends spoken &written words.

2.) CONFUSEDUnable to think rapidly & clearlyPoor Memory & Short attention span.

3.) DISORIENTED

Not aware or not oriented to time, place or person.

CONT


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CONT.

4.) OBTUNDEDLethargic, somnolent; responsive to verbalor tactile stimuli but quickly drifts back tosleep.

5.) STUPORGenerally unresponsive; maybe brieflyaroused by vigorous, repeated, or painful

stimuli; may shrink away from or grab @ thesource of stimuli.


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Glasgow Coma Scale

Eye Opening


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Eye Opening4 - Spontaneous3 On Request2 To painful stimuli1 No eye opening

Verbal Response


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Verbal Response5 Oriented to time , place and person.4 Engages in conversation, confused in

content

3 Words spoken but conversation notsustained.2 Groans on evoked pain1 No response even evoked with pain.

Motor Response


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Motor Response6 Obeys command5 Localizes painful stimuli4 - Flexion Withdrawal3 Decortication2- Decerebration

1 No response


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A score of 15 indicates client is awake and

oriented.A score of 7 to 4 is considered coma.The lowest score is 3,client is considered in deepcoma.

Assessment of Pupils


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Size: 1.5-2mm (2-3mm)Equality: isocuricReaction to light

Unusual Eye movement

p

Assessment of Motor Function


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1.) Muscle Strength

Interpretation:

5/5: Normal Full Strength

4/5: Muscle is able to move actively through thefull ROM against effect of gravity with

weakness to applied resistance

3/5: Muscle is able to move actively against theeffect of gravity alone


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2/5: Muscle is able to move across asurface but cannot overcomegravity

1/5: Muscle contraction is palpable &visible; trace or flicker movt occurs

0/5: Muscle contraction or movt isundetectable


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Apraxia - inability to perform finemotor activities.

Agraphia inability to write

2. Motor Function


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General Appearance uncoordinated movements andasymmetry of face.

Muscle Power Weakness ( paresis )

Paralesis (plegia )

CRANIAL SURGERY


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CraniectomyExcision of the cranial bone without replacingit.

Burr hole- A small hole 12 mm less, used for decompression, evacuation of clot, draining,abscess, insertion of ICP monitor.

Craniotomy An opening to the craniumDrilling 3-six holes and then cutting.

Approaches of Surgery


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Supratentorial- above the double foldsof dura, provide access to the frontal,temporal, parietal, and occipital lobes.

Head of the bed elevated . gravity will cause displacement of

remaining tissue into empty space. Headelevation approximates normal ICP.


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INCREASED INTRACRANIAL PRESSURE


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an intracranial hypertension associated with altered states of consciousness

Normal ICP: 5-15 mmHg/10-20mmHg

The brain requires 60-150 mmHg of


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Cerebral perfusion pressure for

adequate function .


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Autoregulation: the manner in which

the brain protects itself frominadequate blood flow. If the ICP willincrease the MAP will increaselikewise to increase CP. This action iscalled CUSHING REFLEX.


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Monroe Kelly Hypothesis states thatbecause of the limited space forexpansion within the skull, anincrease in any of the components

causes a change in the volume of others.


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Head injuryIntracranial Bleeding

HydrocephalusEdema from surgery


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Compensatory Mechanism


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1.) Displacement

2.) Reduction of blood volume


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Deterioration of LOC: due to reduced


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Deterioration of LOC: due to reducedoxygen supply to the brain.

Unisocuric: due to varying pressureupon CN III.

Vomiting: occurring from pressure in thebrainstem

Seizure

Cushings triad


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Increased SBP: results from ischemia of the vasomotor center , which thenreleases a general sympathetic

discharge.

Bradycardia: because heart is trying to


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to pump blood into cerebral vessel with

extreme high resistance.

Hyperthermia: results from hypothalamicdysfunction but may be due to infection.

C shings lcer


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Cushings ulcer

- result from hypothalamic stimulationfro ICP with resulting vagal activation.The ulcers results from increasedserum gastrin levels, which stimulateshypersecretion of HLC acid.

Management


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1. Surgery: removal of the cause, or decompression.2. Fluid restriction: kept slightlydehydrated to reduce ICP, 800 ml/dayonly.3. Positioning: Head elevation- toassist on venous return fromintracranial circulation and preventfurther congestion.


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4: Meds:MannitolCortecosteroids( dexamethasone)- iseffective in reducing vasogenicedema

AntacidStool softener( docusate sodium:colace)- to prevent straining

Acetaminophen: reduce temperature


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Acetaminophen: reduce temperatureof the client.

Chlorpromazine-if hypothermia is

needed to prevent shivering.

No antihypertensive if the cause is

cushings response to IICP.

Nursing Mgt:


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Goal: To

decrease ICP

VS & NVS monitoringElevate head of bed 30-40

Avoid Trendelenburg positionPrevent flexion of the knee & hipsMonitor respiratory statusMaintain body temp

Avoid shiveringDecrease environmental stimuli

Avoid valsalva maneuver


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Etiology


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ETIOLOGY:Pathologically acquired epilepsy-cerebral birth injuries, CNS infections,high fever, trauma, tumors.Idiopathic


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Biochemical epilepsy: alcohol ingestion,drug overdose, metabolic disorders,electrolyte imbalances.

Posttraumatic : results from cerebraltrauma.

Clinical Findings: TYPES OFSEIZURE


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S U

I. PARTIAL SEIZURE1.) SIMPLE-PARTIAL

Originate in the motor cortex of the frontallobe.

2. ) COMPLEX-PARTIAL Originate in the temporal lobe and limbic

system

II. Generalized Seizure


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1.) GRANDMAL SEIZUREBegins with an Aura 2 phases:

TONIC- muscular rigidity/

extension of extremitiesCLONIC- muscular jerking.

Post-ictal sleep

It would last for 2 minutes


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It would last for 2 minutes

The patient is is generally in deepsleep, confused and lethargic.


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3.) MYOCLONICInvolve a sudden uncontrollable jerkingmovements of either a single musclegroup.

4.) ATONIC Associated with total loss of muscletone. Will cause the person to dropsuddenly to the floor.

TREATMENT


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Medications:Phenytoin- the drug of choicePhenobarbitalCarbamazepine- when seizure is notcontrolled by phenytoin.Ethosuximide( Zarontin)- drug of choicefor Absence seizure

Valproic acid (Depakene)Diazepam


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Provide oxygen


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patient may become hypoxic

turn to side when possible this positions allow secretions to drain

Remove pillow and top sheets

elevation of head in the pillow may blockthe airway.Do not restraint

resistance against strong muscle

contraction may cause injury.Reorient the client.


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Complication:STATUS EPILEPTICUS- continuous

seizure lasting for more than 30minutes without full recovery inbetween.

TRIGEMINAL NEURALGIA


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IdiopathicCN 5 disorder characterized by pain alongone or more branches of the CN 5.

( Maxilary, ophthalmic, mandibular)Classic Finding: intense, lightning-like painin paroxysms about hundred times daily.Trigger zone; cold breeze, talking or chewing.

CN V (Trigeminal Nerve)


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Treatment:C b i ( l) li f f


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Carbamazepine(tegretol)- relief from

paroxysm of pain:Nerve block for 8-16 monthsPercutaneous radiofrequency rhizotomy-heat controlled electrocoagulation of thepain fibers without compromising touchsensation and motor control.


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Avoid food and beverages of extremetemperatureChew on unaffected side

Oral care

BRAIN ATTACKS (STROKE)


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Is a syndrome of a group of suddenfocal neurological deficit resultingfrom interruption

Major Predisposing factors
http://www.ucalgary.ca/UofC/Others/CAN/frames.html


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Atherosclerosis- thickens the intimallayer of arteries over a period of 20-30 years.

- Cerebral vessel have a thinner intima with less elasticity thanextracranial vessel and are severely

affected by atherosclerotic changes.

Emboli- Aggregate of platelets at an


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Emboli Aggregate of platelets at an

atheromatous site such as carotidartery.

Arrhytmias

Hypertension


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Intracranial hemorrhageDM

Polycythemia- causes increased


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y yblood viscosity.

Classification of Brain Attacks:


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Classification of Brain Attacks:

Ischemic (emboli, Thrombus)Hemorrhagic

Pathophysiology


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An abrupt interruption of circulationfro 4-8 minutes will producepermanent brain damage, because

neurons are unable to regenerate.

When circulation to an area isimpaired gradually collateral


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impaired gradually, collateral

circulation is often able to developand maintain an adequate supply of blood to that area of the brain.

Once infarction occurs, the damage is


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girreversible. Cellular death occur within 5 minutes. Symptoms such asLOC occurs when oxygen isinterrupted fro 10 seconds butirreversible when circulation isreestablished.

TIME COURSE CLASSIFICATION

1 TRANSIENT ISCHEMIC


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1. TRANSIENT ISCHEMIC

ATTACK

2. REVERSIBLE ISCHEMIC

NEUROLOGIC DEFICIT

3. STROKE IN EVOLUTION

4. COMPLETED STROKE

A.) TRANSIENT ISCHEMIC ATTACK


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Are sudden, brief,episode of neurologicdysfunction caused

by temporary, focalcerebral ischemia


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Usually last for 5-30 minutes andoccasionally up to 24 hours but never longer.

B.) REVERSIBLE ISCHEMIC NEUROLOGIC

DEFICIT (RIND)


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Signs andsymptoms areconsistent with butmore pronounced

than TIAs

Also c lled s sm ll stroke s me s


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Also called as small stroke, same asTIA but the signs persist for longer than 24 hours.

c.) STROKE IN EVOLUTION


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Worsening of neurologic signsand symptomsover several

minutes or hours.This is aprogressing stroke.


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Generally, large artery disease exists.

4.) COMPLETED STROKE


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Stabilization of theneurologic sign andsymptoms

Thrombotic stroke occurs during sleep


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Thrombotic stroke occurs during sleep.

Embolic stroke occurs suddenly during

waking activities.

Left Hemisphere Right Hemisphere

Aphasia Spatial percept al deficits


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Aphasia

Agraphia (loss of ability towrite) Alexia (Loss of ability toread, word blindness) Acalculia Dysarthria Hemiplegia Homonymous hemianopsia Short-term memory Depression frustration

Spatial-perceptual deficits

Lack of inhibitions Inappropriate social

behavior Short attention span Poor judgment Hemiplegia Hemiparesis Anosognosia (Denial of

affected Side) Apraxia (Inability to use

objects or words)

Medical Management


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Prevention of strokePrevention of recurrenceImmediate brain resuscitation

Stabilization and Rehabilitation

Medications


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Antihypertensive- used to graduallyreducing the hypertension so thatcerebral infarction does not occur

from inadequate CP because of decreasing Bp rapidly.The immediate elevation of BP after infarct is a compensatory mechanismand is not treated.

Platelet Aggregant


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Aspirin

AnticoagulantHeparinWarfarin

Thrombolyticsurokinase- convert plasminogen to


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urokinase convert plasminogen to

plasmin, which lysis fibrin and releasesfibrin degeneration which inhibits clotformation.

Calcium channel blockers-due tocell death secondary to ischemiarelated to calcium influx.MannitolDexamethasone

Nursing Care


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Positioning;MHBRPatent airway-to prevent hypoxiaOxygen Admin

Suctioning

Guillain-Barr syndrome


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Is an autoimmune neuromuscular disorder in which there is chronic,progressive decreased amplitude of

the nerve impulse at the myoneural junction.

an autoimmune disorder affecting the


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an autoimmune disorder affecting theperipheral nervous system, usuallytriggered by an acute infectious process.


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Signs and Symptoms


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Bilateral weakness or tingling in thelegs.Loss of reflexes

ParalysisMuscle weakness on both sides of the body in the legs, arms, and face.

Difficulty speaking, chewing, andswallowing.


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Inability to move the eyes.Back pain.Horners syndrome - ipsilateral ptosis

due to sympathetic damage

Diagnosis


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CSF ANALYSIS As opposed to infectious causes, thisis an elevated protein level (100 -1000 mg/dL).PA

Nerve conduction velocity (NCV) test


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Nerve conduction velocity (NCV) test can figure out how well nerves are sendingsignals down to the arms and legs.

Treatment


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Supportive careEarly intubationhigh-dose intravenous

immunoglobulin (IVIg)GlucocorticoidsPlasmapheresis


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Analgesics AntibioticsChest physiotherapy

Suctioning

Prognosis


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80% of patients have a completerecovery within a few months to ayear

20 50 years


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20-50 years Female>male Impaired transmission of nerveimpulse to muscle cells

possibly because of acetylcholinedeficiency

Pathophysiology


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Normally: Acetylcholine attach to receptor

sites.

Contraction

Myasthenia Gravis:


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Impaired transmission of impulses.

Decrease receptor for stimulation

Muscle weakness


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Signs and symptomsMuscle weakness


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FatiguePtosisSnarl smileMass like faceDroolingRespiratory difficulty

Thymus gland enlargement (antibodyproduction).

MedicationsNeostigmine Pyridostigmine


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Neostigmine , PyridostigminePrednisoneThymectomy
http://en.wikipedia.org/wiki/File:Myasthenia.jpg


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http://en.wikipedia.org/wiki/File:Myasthenia.jpg


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DiagnosisEdrophonium chloride


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(Tensilon Test).

(+) increase muscle strength.

It is important that pt does not know themeds.Administer 2mg IV one at a time = 10 mg

Ptosis and facial weakness must be solvedin 5 min.

Myasthenic Crisis Cholinergic CrisisCaused by under medication.

Caused byovermedication. Extreme


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Extreme weakness.Relieved by Tensilon Test.Managed by cholinergics

weakness.Worsens by Tensilon Test.Managed byanticholinergics (atropine)

Stop the medication


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Steroids (dec. antibody production)


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Thymectomy Assess gag/swallowing reflex Administer meds on time. (resp. arrest).

Protect from falls. Adequate ventilation.

Avoid Drugs

Muscle Relaxant


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Muscle RelaxantBarbiturates

Morphine

Tranquilizer Neomycin

Increases weakness

Survival Guide

Secure handicapped sticker


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Secure handicapped sticker.Frequent restTake meds on time (alarm clock)

BELLS PALSY


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Is a sudden loss of motor control onone side of the face.Causing flaccid paralysis of facial

muscles, loss of taste.

Occurs in 20-60 years old


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Inflammation, capillary damage, andischemia develops and nerve

degeneration may result


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Due to GBS, viral infection, genetics,s/sx: pain behind the ear 1-2 daysprior to paralysis, unable to smile,

frown, close eyelids, puff out cheeks,close the lips.

TX: Steroids for 7 days Analgesics


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gWarm or moist applicationElectrical nerve stimulation to preventfacial sagging and stimulate muscle

tone.

Chew on unaffected side


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Oral care Artificial tear

Soft diet


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Myasthenia Gravis

HEADACHE


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Classification & Etiology:

1.) TENSION HEADACHE

results from muscle contraction

describe as a tight band-like discomfort that isunrelenting; with few h/a free intervals

d/t fatigue/stress

2.) CLUSTER HEADACHE have cyclical pattern of 1-3 short-

lived attacks of periorbital pain


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lived attacks of periorbital pain

occurs more often in men

triggered by ROH consumption

pain described as deep, boring,intense pain of such severity that

the client has difficulty remainingstill

3.) MIGRAINE HEADACHE

considered as vascular h/a vasospasm


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-considered as vascular h/a , vasospasm& ischemia of intracranial vessel being thecause of pain

h/a is most often unilateral, but pain mayoccur on alternate sides with differentattack

Etiology: IdiopathicPATHOPHYSIOLOGY:


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Menstrual Cycle Stress Depression Sleep Deprivation Fatigue Overuse of Meds Tyramine-rich foods

Dysfunction of brainstem pathway

Abnormal metabolism of serotonin

Increase plasma serotonin level

Dilates cerebral blood vessel

4 Phases of Migraine:


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Prodrome

Aura

Headache phase

Recovery Phase

4.) Lumbar Puncture H/Aloss of CSF volume with LP


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decreases the brain supportivecushion

5.)Post Concussion H/Aafter seemingly trivial head injuries &particularly after rear-end motor

Vehicle collisions

NURSING MANAGEMENT


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M -I -

G -

R -

A -

I -

N -

E -

Seizure Disorder


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is a sudden, abnormal electrical discharge from the brain that results in changes in sensation,behavior, movts, perception or consciousness

Epilepsy Greek word. epilepsia seizure

- is a chronic disorder of recurrent

seizure.

Status Epilepticus


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involves rapid succession of epileptic spasm without intervalof consciousness

Etiology: Idiopathic


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Severe penetrating trauma Tumor Infection

Circulatory & metabolic disorders Toxicity Brain surgery Hypoglycemia

STROKE


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TIME COURSE CLASSIFICATION

1. TRANSIENT ISCHEMIC


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ATTACK

2. REVERSIBLE ISCHEMICNEUROLOGIC DEFICIT

3. STROKE IN EVOLUTION

4. COMPLETED STROKE

A.) TRANSIENT ISCHEMIC ATTACK

Are sudden, brief,


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, ,episode of neurologicdysfunction causedby temporary, focal

cerebral ischemia

B.) REVERSIBLE ISCHEMICNEUROLOGIC DEFICIT

Signs and symptoms
http://www.ucalgary.ca/UofC/Others/CAN/frames.html


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g y pare consistent withbut more pronouncedthan TIAs

c.) STROKE IN EVOLUTION

Worsening of


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gneurologic signs andsymptoms over several minutes or

hours. This is aprogressing stroke.

4.) COMPLETED STROKE

Stabilization of the


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neurologic sign andsymptoms

Date post:	03-Apr-2018
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c Tests(Neuro)

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