NEURO 2009

THE CONCEPT OF PERCEPTION

AND COORDINATION (NEUROLOGIC NURSING)

Perception- is defined as the perception and awareness of sensory stimuli.

- it is a mental act involving memory and the intellectual interpretation of new sensory data in terms of previously encountered information.

Coordination- maybe defined as “the working together of

muscles to produce movement or of systems to accomplish a given process.

- it implies perception of the movement or reaction that is necessary and the subsequent completion of that action via the appropriate bodily activity.

Management of coordination and perception within the

human body is controlled by the Central Nervous System, the Peripheral, the Autonomic Nervous System and the Neuro-endocrine System.

ANATOMY AND

PHYSIOLOGY

DIVISION

BASIC STRUCTURES

NEURONS

NEUROGLIA

NEUROTRANSMITTERS

NERVE

NEURON Cell body - contains

nucleus and cytoplasm where metabolic activity takes place. Collection clusters of nerve cells bodies are called ganglia or nuclei. Ganglia with same functions are called centers.

Axons- generate and conduct impulses away from the cell body and release a neurotransmitter

Dendrites- carry electrical current towards the cell body

NEURONS

Types:

Based on Function (direction of impulse transmission

1. Sensory neurons (afferent)

2. Motor neurons (efferent)

Based on Structure

1. Unipolar: most sensory neurons

2. Bipolar: sensory neurons- ear and eye

3. Multipolar: motor and association neurons

Classification

1. Based on Function (direction of impulse transmission A. Sensory neurons

(afferent) B. Motor neurons

(efferent) 2. Based on Structure

A. Unipolar: most sensory neurons

B. Bipolar: sensory neurons- ear and eye

C. Multipolar: motor and association neurons

NEUROGLIA

– makes up about 85 % of the CNS cells. They provide, nourishment, support and protection to the neurons

Types:

1. Astrocytes – star-shaped supportive cells

2. Oligodendrocytes

3. Microglia

4. Ependymal cells

NEUROTRANSMITTERS – chemicals that carry messages between different nerve

cells or between nerve cells and muscles. Released by an axon across the synaptic cleft to bind to specific receptors in the postsynaptic bulbs of another neuron or cell.

- It acts to potentiate, terminate or modulate a specific action.

Types:

1. Excitatory – acetylcholine (PNS), Norepinephrine (SNS), Gamma-aminobutyric acid, enkephalins or endorphins

2. Inhibitory – acetylcholine (Heart via vagal nerve), Dopamine, Serotonin

Concentration:

1. PSNS – acetylcholine

2. SNS – norepinephrine

NERVES- bundles of neurons processes wrapped in connective tissue

coverings found outside the CNS.

MAJOR PARTS

CNS

1. Brain

2. Spinal Cord

PNS

1. Cranial Nerves

2. Spinal Nerves

ANS

1. Parasympathetic

2. Sympathetic

CNS:BRAIN

PARTS OF BRAIN

CEREBRUM

CEREBELLUM

DIENCEPHALON

BRAIN STEM

PROTECTION OF BRAINSKULL

MENINGES

CSF

BLOOD BRAIN BARRIER

BLOOD-BRAIN BARRIER

CNS is inaccessible to many substances that circulate in the blood plasma (dye, meds).

Barrier is formed by the endothelial cells of brain capillaries, which form continuous tight junctions, creating a barrier to macromolecules and many compounds.

Has an implication in the tx and selection of meds for CNS disorders as well as serving a protective function.

CEREBRAL CIRCULATION

Receives 15% of cardiac output or 750ml/min.

Brain does not store nutrients and has high metabolic demands that require high blood flow.

Blood flow is against gravity as arteries fill in below and veins drain from above.

Can’t tolerate decreased blood flow for it will result to irreversible tissue damage when blood flow is occluded even for a short period of time.

CIRCLE OF WILLIS

Located at the base of the brain surrounding the pituitary gland.

It is a formed ring of arteries between vertebral and internal carotid artery chains (internal carotid, anterior and middle cerebral artery, anterior and posterior communicating artery)

The most frequent site of aneurysm – weakening or bulge in the arterial wall.

CNS: SPINAL CORD

Spinal cord - reflex center and conduction pathway

-located within the vertebral canal

-extends from the foramen magnum to L1 to L2

-has central area of gray mater surrounded by columns of white mater, which carry motor and sensory tracts from the brain.

- Serves as a connection bet. brain and the periphery.

- About 45cm (18in) long and about the thickness of a finger.

- Surrounded by meninges, dura, arachnoid and pia layers.

SPINAL CORD PROTECTION

MENINGES VERTEBRAL COLUMN- The bones of the vertebral column surround

and protect the spinal cord.- It consists of 7 cervical, 12 thoracic, 5 lumbar,

1 sacrum, and 1 coccyx.- They are all separated by disks except for the

1st (atlas) and the 2nd (axis), sacral and coccygeal.

PNS: CRANIAL NERVES

CRANIAL NERVES (12)

- 3 Sensory (1, 2 and 8)

- 5 motor (3, 4, 6, 11 and 12)

- 4 mixed (5, 7, 9 and 10)

I. Olfactory sensory smell

II. Optic sensory visual acuity

III. Oculomotor motor muscle that move the eye &

lid pupillary constriction.

IV. Trochlear motor muscle that move the eye

V. Trigeminal mixed facial sensation,

mastication, corneal reflex

VI. Abducens motor muscle that move the eye

VII. Facial motor facial expression and movement, salvation and tearing, ear sensation

VIII. Acoustic sensory hearing and equilibrium

IX. Glossopharyngealmixed taste, sensation in

pharynx and tongue, pharyngeal muscles

X. Vagus mixed muscles of pharynx and larynx, soft palate, external ear sense, pharynx,

larynx, thoracic,

abdominal viscera, parasympathetic innervation of thoracic and abdominal organs.

XI. Spinal accessory

motor sternocleidomastoid and trapezius muscle

XII. Hypoglossal

motor tongue movement

PNS:SPINAL NERVES

SPINAL NERVES

-thirty one (31) pairs of nerves formed by the union of the dorsal and ventral roots of the spinal cord on each side-splits into:

a. dorsal rami – serve the posterior body trunk

b. ventral rami – serve the limbs through the plexuses (cervical, brachial , lumbar, sacral)

AUTONOMIC NERVOUS SYSTEM

ANS - regulates the activity of smooth muscles, cardiac muscles and glands

2 divisions:

1. Sympathetic ”fight or flight” response; prepares the body to cope with stress

e.g. increased heart rate, blood pressure pre ganglionic neurons are in the sympathetic chains or in

collateral ganglia post ganglionic axons secrete norepinephrine

2. Parasympathetic ”house keeping” system; in control most of the time maintains homeostasis first motor neurons are in the brain or the sacral region of the

cord second motor neurons are in the terminal ganglia close

to the organ served post ganglionic axons secrete acetylcholine

EFFECTS OF ANS

PNS SNSPupil of eye constricted dilatedHR decreased increasedHeart vessels constricted dilated Vessels in:Skeletal mus. No effect dilatedAbd’l viscera/skin No effect constrictedBP decreased increasedBronchioles constricted dilated Breathing decreased increasedDigestive peristalsis increased decreasedd. Tube sphincter relaxed constricted

Secretion of glands thin, watery saliva thick, viscid saliva

Digestive secretion increased no effectGlycogen-glucogenConversion of liver no effect increasedUrinary bladder wall contracted relaxedUrinary sphincter relaxed contractedUterine mus. Relaxed; variable contracted;

varies in mens& pregnancy

Ext. genitalia mus. Dilated no effectSecretion of sweat no effect increasedPilomotor mus. no effect contracted

(goose flesh)Adrenal medullae no effect secretion of

epinephrine and norepinephrine

ASSESSMENT: NEUROLOGICASSESSMENT

I. NURSING HEALTH HISTORY

history of present illness (COLD SPA) review of medical history system by system evaluation

***are important and critical in order to come up with to an accurate diagnosis.

II. CLINICAL MANIFESTATIONS1. Pain - a multidimensional unpleasant experience which may

occur from neurologic disorders like: Acute - Spinal disk disease, Trigeminal neuralgia, Painful

neuropathies Chronic - Cerebral palsy

2. Seizures - results from abnormal paroxysmal discharges or neuronal firing in the cerebral cortex, which then manifest as an alteration in consciousness, sensation, behavior, movement or perception. It may also be a sing of brain lesion.

3. Dizziness and Vertigo Dizziness - abnormal sensation of balance or movement, fairly

common in elderly and most common complaint encountered by health professionals, can be caused by virus, hot weather, roller coaster ride, middle ear infection, etc.

Vertigo – specific form of dizziness, usually a manifestation of vestibular dysfunction, can be severe as to result in spatial disorientation, loss of equilibrium, and nausea and vomiting.

II. CLINICAL MANIFESTATIONS4. Visual disturbances - visual effects that cause people to seek

health care, can range from decreased visual acuity associated with aging to sudden blindness caused by glaucoma, normal vision depends upon functioning visual pathways through the retina and optic chiasm and the radiations into the visual cortex in the occipital lobe, lesions of the eye itself (cataract), lesion along the pathway (tumor), lesion in the visual cortex (from stroke) interfere with normal visual acuity, abnormality of eye movement (nystagmus associated with multiple sclerosis) can compromise vision by causing diplopia or double vision.

5. Weakness - especially muscle weakness is a common manifestation of neurologic disorder. Frequently coexists with other symptoms of disease and can affect variety of muscles causing a wide range of disability. It can be sudden or permanent as in stroke, or progressive as in amyotrophic lateral sclerosis.

II. CLINICAL MANIFESTATIONS6. Abnormal Sensation - numbness, abnormal or loss

of sensation is a neurologic manifestation of both central & peripheral nervous system disease. It can significantly affect balance and coordination.

7. Impact on lifestyle - limitations imposed to the patient by any deficit & the patient’s role in society including family & community roles. Plan of care that the nurse develops to address & support adaptation to the neurologic deficit & continued function to the extent possible within patient’s support system.

III. CEREBRAL FUNCTIONS1. Mental status – Assess patient’s appearance, behavior,

dressing, grooming, personal hygiene, posture, gesture, movements, facial expressions and motor activity. Assess orientation to time, place and person.

2. Intellectual Function – Assess IQ, serial 7 test (100 minus 7), capacity to interpret well – known proverbs, ability to recognize similarities and make judgments. Check also for the memory (remote and recent).

3. Thought content – Assess if thought are spontaneous, natural, clear, relevant and coherent. Assess for presence of fixed ideas, illusions, hallucinations, preoccupations with morbid and paranoid ideation.

4. Emotional status – Assess the affect or the external manifestation of mood: natural and even, irritable or angry, anxious, apathetic, flat, euphoric, jumping of ideas, and consistency between verbal and non verbal cues.

III. CEREBRAL FUNCTIONS5. Perception – having an insight into the patient’s cortical ability Agnosia – inability to interpret or recognize objects seen through the

special senses.Types of agnosia Affected cortical area

Visual (show pencil) occipital lobe Auditory temporal (lateral/superior) Tactile (hold coin) parietal Body parts/relationship parietal (postero-inferior)

6. Motor Ability - asking the patient to perform a skilled act (throw a ball, move a chair), failure means cerebral dysfunction

7. Language Ability- person with normal neurologic function can understand and communicate in written & spoken language.

Aphasia – a deficiency in language functionTypes of aphasia Brain area involvedAuditory-receptive temporal lobeVisual-receptive parietal-occipital lobeExpressive speaking inferior posterior frontal areasExpressive writing posterior frontal areas

IV. CRANIAL NERVE FUNCTION

Cranial Nerve Clinical ExamI. Olfactory - with eyes closed, the pt. identifies

familiar odor (coffee, tobacco). Each nostril is tested separately

II. Optic - Snellen eye chart; visual fields, opthalmoscopic exam

III. Oculomotor - for CNs 3, 4 & 6; tests for ocularIV. Trochlear rotations, conjugate mov’ts.,VI. Abducens nystagmus. Test for pupillary

reflexes & inspect eyelids for ptosisV. Trigeminal - have pt. close the eyes. Touch a

wisp of cotton to forehead, cheeks& jaw. Sensitivity to superficial pain is tested the sharp & dull ends ofa broken tongue blade.

V. Trigeminal - alternate bet. the sharp & dull end - patient reports dull & sharp with

each mov’t. If reports are incorrect, test for temp sensation.

- while the patient looks up, lightly touch a wisp of cotton against the

temporal surface of each cornea. A blink and tearing are normal

responses.- have the patient clench & move

the jaw from side to side. Palpate the masseter & temporal muscles, noting strength & equality.

VII. Facial - observe symmetry while patient performs facial mov’t.;

smiles, whistles, elevates eyebrows, frowns, tightly closes eyes (examiner opens them); flaccidity

VIII. Acoustic - whisper or watch-tick technique; test for lateralization (weber); test for air & bone conduction (Rinne)

IX. Glossopharyngeal- assess patient’s ability to

discriminate bet. Sugar & salt on posterior 3rd of the tongue

X. Vagus - depress a tongue blade on posterior tongue or stimulate posterior pharynx to elicit gag reflex note any harshness in voice. Have pt. say “ah”, observe for symmetric rise of uvula & soft palate.

XI. Spinal Accessory- palpate & note strength of trapezius muscle on shrugging & sternocleidomastoid muscle as pt. turns head against pressure

XII. Hypoglossal - while pt. protrudes tongue, any deviation or tremors are

noted. Strength of the tongue is tested by having the protruded tongue move from side to side against a tongue depressor.

V. REFLEXES Involuntary contractions of muscle in response to abrupt

stretching or striking with a reflex or percussion hammer near the site of muscle insertion. Valid findings depend on proper use of reflex hammer, proper positioning of extremities & a relax patient.

2 TYPES: Superficial, Deep Tendon Reflexes

1. Superficial or Cutaneous Reflexes - graded as (+) or (-) Corneal reflex – cotton wisp is touched to outer sclera of each

eye. Normal response is a blink. Gag reflex – tongue depressor is touched to uvula. Normal

response is gag. Cremasteric reflex – inner thigh of male client is stroked. Normal

response is penile erection. Plantar or Babinski reflex – lateral sole is stroked with tongue

blade, normal response is toe flexion or negative babinski.

V. REFLEXES

2 TYPES: Superficial, Deep Tendon Reflexes

2. Deep tendon reflex – graded as:+4 -hyperactive+3 -more brisk than avg. maybe normal or indicative of a dse.+2 -average or normal response+1 -hypoactive or diminished 0 -No response

Biceps reflex (C5C6) -Arm is slightly flexed at the elbow with the palm down. The examiners thumb is placed on the biceps tendon and a blow is stuck over the thumb. The biceps muscles should contact and flexion of the forearm at the elbow should occur.

Brachioradialis reflex (C5C6) - The forearm should rest in the person’s lap. The hand is supported in a semi prone position and the tendon over the radius is struck about 1 to 2 inches above the wrist. The result should be flexion and supination of the forearm.

V. REFLEXES

Triceps reflex (C7C8) - The client’s arm is flexed at the elbow with forearm held across the abdomen. The hand of that arm is supported with the palm toward the body and a blow is struck over the triceps tendon. The triceps muscle should extend at the elbow.

Patellar reflex (L2L3L4)

Ankle reflex (S1S2) - With the person’s leg somewhat flexed at the knees and the foot supported with the examiner’s hand the Achilles tendon is struck above the heel. Normal response is plantar flexion.

Clonus – very hyperactive reflexes which may indicate CNS disease abd require further evaluation

VI. MOTOR FUNCTIONS1. Muscle Strength

2. Balance and coordination

1. Muscle Strength- Patient is asked to walk across the room while examiner observes for posture & gait. Muscles are palpated for size & symmetry. Any evidence of atrophy or involuntary mov’t. (tremors, tic), muscle tone (tension present in a muscle at rest) is evaluated by palpating various muscle groups @ rest & during passive mov’t. Abnormalities include spasticity (inc. Muscle tone), rigidity (resistance to passive stretch) & flaccidity. Strength is assessed to know the ability to flex or extend against resistance. Graded as:

0- no contractility 1- some contractility but no joint motion 2- complete ROM without gravity 3- complete ROM with gravity 4- complete ROM with some resistance 5- normal function against full resistance

VI. MOTOR FUNCTIONS2. Balance & Coordination - Cerebellar influence on the motor system

is reflected in balance, control & coordination. Hand & extremity coordination is tested by having the pt. perform alternating mov’ts & point to point testing (thigh patting with alternate hands, pronate & supinate, thumb with each fingers). Speed, symmetry & degree of difficulty are noted. Patient’s finger then examiner’s finger touching)

Check for Ataxia - incoordination of voluntary muscle action, particularly of muscle group used in activity (rhythmic, involuntary mov’ts)

Check for maintenance of standing position: (Romberg’s test)- screening test for balance.

Patient stands with feet together with arms @ the side, with eyes open first then both eyes closed for 20-30 seconds. Loss of balance means (+) Romberg test.

Ask the person to stand erect with both heels together and both eyes open. Note any swaying or loss of balance.

Ask the person to maintain that position but to close both eyes. Note any abnormal swaying or tendency to fall.

VII. SENSORY FUNCTIONS

GENERAL TYPES OF SENSATION:

1. Superficial - concerned with touch, pain, temperature

2. Deep sensation - concerned with muscle and joint sense

3. Combined – superficial and deep sensory mechanism combined in steriognosis (recognition and naming of familiar objects placed on hand) and in the ability to localize cutaneous stimuli


1. Tactile Sensation – lightly touch a cotton wisp to a body part. Compare proximal to distal sensation.

2. Vibration Sensation - Ask the client to close both eyes. Vibrate a tuning fork by knocking it against the palm of the hand. Apply the tuning fork to the bony prominences to ensure that the person is responding to vibration and not sound both eats should be blocked from receiving sound. Ask the client to report the feeling of a “buzz” and to say when the “buzz” stop

3. Pain and Temperature Sensation

3. Position Sensation or Proprioception – moves toes up, down, side to side


5. Integration of Sensation Two point discrimination - Ask the client to close both eyes. Hold

one pin in each hand and apply them so that the fingers of the examiner slide down the pin. Simultaneously apply the two pins to the same body part. Ask the person to report when one or two pins is/are felt

Test for stereognosis – the ability to recognize an object of touch

Test for extinction phenomenon - Ask the client to close both eyes and to report where he or she is touched. The answer should not just state “on the side” but should state which side it is.

VIII. BOWEL FUNCTIONS

IX. BLADDER FUNCTIONS

ASSESSMENT: KEY SYMPTOMS OF NEUROLOGIC

DISORDERS

1. Altered Level of Consciousness

2. Altered memory, orientation, concentration

3. Speech difficulties

4. Altered movement and coordination (weakness, paralysis)

5. Pain

6. Seizures

7. Dizziness (Vertigo)

8. Visual disturbances

9. Taste & Smell alterations

10. Abnormal Sensation (numbness, paresthesia)

11. Altered temp regulation

12. Altered pain perception

13. Altered bowel and bladder elimination

DIAGNOSIS:DIAGNOSTIC

TESTS

I. GLASGOW COMA SCALE

1. Verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

None 1

2. Eye opening

Spontaneous 4

To voice 3

To pain 2

None 1

3. Best motor response

Obeys command 6

Localizes pain 5

Withdraws from pain 4

Abnormal flexion (decorticate) 3

Abnormal extension 2

None 1

Levels of consciousness

Deep coma 3 - 5

Coma 6 - 8

Lethargic 9 - 11

Stuporous 12 -14

Normal 15

Coma – a clinical state of unconsciousness in which the patient is unaware of self or the environment for prolonged periods (days to months or even years)

Persistent vegetative state – condition in which the patient is described as wakeful but devoid of conscious content, without cognitive or affective mental function

Brain Death – irreversible loss of all functions of the entire brain, including the brain stem

II. LUMBAR PUNCTURE AND CSF ANALYSIS

Carried out by inserting a needle into the lumbar SA space to withdraw CSF.

Done to obtain CSF for examination, measure & reduce CSF pressure, determine the presence or absence, detect spinal SAB & administer medications intrathecally.

Needle is inserted into the SA space between 3rd & 4th or 4th & 5th lumbar vertebrae.

Specimens are obtained for cell count, culture & glucose & protein testing.

Specimen should be sent to lab immediately because changes will take place & alter result if allowed to stand.

Other form include Queckenstedt’s test.


RESULT:

a. 70-200mmH20- normal CSF pressure with the pt in lateral recumbent

b. Should be clear & colorless

c. Pink, blood-tinged or grossly bloody CSF may indicate a cerebral contusion, laceration or SA hemorrhage

COMPLICATIONS:

a. Herniation of intracranial contents

b. Spinal epidural abscess/hematoma

c. Meningitis

d. Temporary voiding problems

e. Slight increase of temperature

f. Backache or spasms

g. Stiffness of neck

h. Post lumbar puncture headache


POST LUMBAR PUNCTURE HEADACHE :

Caused by CSF leakage @ the puncture site. The fluid continues to escape into the tissues by way of the needle track, from the spinal canal. It is then absorbed promptly by the lymphatics.

As a result, the supply of CSF in the cranium is depleted @ point @ which it is insufficient to maintain proper mechanical stabilization of the brain.

This leakage of CSF allows settling of the brain when the patient assumes an upright position, producing tension & stretching the venous sinuses & pain-sensitive structures.

Both traction & pain are lessened & the leakage is reduced when the pt lies down.


NURSING INTERVENTIONS:

1. Signed consent and void before the procedure. Use small gauged needles

2. Instruct to relax to avoid traumatic or bloody tap, fetal position. A local anesthetic will be used.

3. Patient remains on prone position 2 – 3 hours post procedure

4. Headache is managed by rest, analgesics & hydration

5. Assist with EPIDURAL BLOOD PATCH – blood is withdrawn from antecubital area & injected into the epidural space, usually @ the site of previous spinal puncture

*** Blood acts as gelatinous plug to seal the hole in the dura, preventing further loss of CSF

III. CT SCAN

- a non-invasive & painless procedure & has a high degree of sensitivity for detecting lesions.

- makes use of a narrow x-ray beam to scan the head in successive layers. The images provide cross sectional views of the brain or other organs.

- performed first without contrast then with IV contrast enhancement.

- patient lies in adjustable table with the head in fixed position while the scan system rotates around the head & produces cross-sectional images. The patient must stay still because motion will distort the image

III. CT SCAN


1. teaching the pt about the need to lie quietly & still throughout the procedure

2. sedation can be used if agitation, restlessness or confusion will interfere with a successful study

3. instruct pt to be on NPO for at least 4 hours

4. monitoring pt for allergic reaction of contrast agent & other side effects

5. increase hydration to flush out contrast

IV. POSITRON EMISSION TOMOGRAPHY

Computerized nuclear imaging technique that produces images of actual organ functioning.

Patient either inhales radioactive gas or injected, that emits positively charged particles.

It is useful in showing metabolic changes in the brain (Alzheimer’s dse), locating lesion (tumor, epileptogenic lesion), identifying blood flow & O2 metabolism in pts with strokes, evaluating new therapies for brain tumors & revealing biochemical abnormalities associated with mental illness.


1. Patient preparation; explanation of the test & teaching patient of inhalation techniques & sensation (dizziness, lightheadedness, headache)

V. ELECTROENCEPHALOGRAPHY Represents a record of the electrical activity generated in the brain.

Obtained through electrodes applied in the scalp or through electrodes applied within the brain tissue.

Provides a physiologic assessment of cerebral activity. Useful test for diagnosing & evaluating seizure disorders, coma, or

organic brain syndromes. Tumors brain abscesses, blood clots, & infection may cause abnormal patterns in electrical activity


1. Patient is deprived of sleep

2. Anti-seizures, tranquilizers, stimulants, depressants are withheld 24-48 hours (can alter/mask abnormal wave patterns of seizure disorders.

3. No coffee, tea, chocolate & cola (all stimulants)

4. Meal should NOT be omitted - altered blood glucose change brain wave

5. Patient is informed that it would take 45-60 minutes for awake & 12 hours for sleep EEG.

VI. MYELOGRAPHY

An x-ray of the spinal subarachnoid space taken after the injection of contrast agent into the spinal subarachnoid space through a lumbar puncture.

Shows any distortion of the spinal cord or spinal dural sac caused by tumors, cysts, herniated vertebral disks or other lesions


1. Information of the procedure; meal prior to procedure is omitted; sedative may be given

2. After procedure, pt may lie in bed with HOB @ 30-45 degrees for 3 hours

VII. ELECTROMYELOGRAPHY

Obtained by introducing needle electrodes into the skeletal muscles to measure changes in the electrical potential of the muscle & the nerves leading to them.

Useful in determining the presence of neuromuscular disorders & myopathies and help distinguish weakness due to neuropathy from weakness due to other causes


1. Explanation of the procedure & patient is warned to expect a sensation similar to that of an IM injection as the needle is inserted into the muscle

2. Inform that muscles examined may ache for a short of time after the procedure

VIII. MAGNETIC RESONANCE IMAGING

Helps identify cerebral abnormality more early and clearly than other test by using a highly magnetic field.

The test may be done with or without a contrast. The magnet causes hydrogen ions in the body (protons) to align

like small magnets and emit signals which are converted into images.

NURSING REPONSIBILITIES:

1. Remove all metal objects from the patient and inside the examination room.

2. Instruct patient that it is painless but he may hear loud thumping

3. Inform that he or she may communicate to the staff via a microphone inside the scanner.

4. For claustrophobic patients, sedation may be used.

IX. CEREBRAL ANGIOGRAPHY

X- ray study of cerebral circulation after injection of a dye to a selected artery (usually femoral artery) under local anesthesia and heparinized saline.

Valuable for detection of aneurysm, AV malformations and other vascular diseases.

NURSING RESPONSIBILITIES:

1. Ensure well hydration and clear liquids before the test

2. Instruct to void before the test

3. Location of peripheral pulses are marked with a felt – tip pen

4. Shave the are (groin)

5. Instruct to remain immobile during the test, brief feeling of warmth behind the eyes, face, jaw, teeth, tongue and lips and a metallic taste after dye injection.

6. After the test, monitor VS, affected extremity for s/s of occlusion, apply cold compress to relive hematoma.

X. NON – INVASIVE CAROTID FLOW STUDIES & TRANSCRANIAL DOPPLER

Uses UTZ imagery and Doppler measurements of arterial blood flow to assess carotid and deep orbital circulation and presence of Stenosis or obstruction.

Transcranial Doppler assesses flow velocities in deep cranial arteries and helpful in detection of vasospasm.

NURSING RESPONSIBILITIES:

1. Inform that it is non – invasive, hand held transducer is placed over the neck and orbits of the eyes with water soluble jelly.

2. It is done at bedside.

XI. CHEST X - RAY Makes images of the heart, lungs, airway, blood vessels and

the bones of the spine and chest. An x-ray (radiograph) is a painless medical test that helps

physicians diagnose and treat medical conditions. Radiography involves exposing a part of the body to a small

dose of ionizing radiation to produce pictures of the inside of the body.

X-rays are the oldest and most frequently used form of medical imaging.

NURSING RESPONSIBILITIES:1. Check the doctor’s order.

2. Inform the patient about the procedure.

3. Provide privacy.

4. Instruct the patient to remove clothing’s and jewelries.

5. Instruct the patient to take full inspiration during the procedure.

DIAGNOSIS: NURSING

DIAGNOSES

1. Altered Cerebral Tissue Perfusion2. Impaired Physical Mobility3. Ineffective Breathing Pattern4. Ineffective Airway Clearance5. Impaired Gas Exchange6. Pain7. Self – Care Deficit8. Activity Intolerance9. Impaired Urinary / Bowel Elimination, Incontinence, Retention10. Altered Nutrition Less than Body Requirement11. Impaired / Risk for Impaired Skin Integrity12. Risk for Injury13. Impaired Verbal Communication14. Disturbed Sensory Perception15. Altered Thought Process16. Confusion: Acute / Chronic17. Anxiety18. Low Self Esteem19. Ineffective Individual Coping20. Risk for Ineffective Family coping21. Sexual Dysfunction

MANAGEMENT OF

NEUROLOGIC DISORDERS

INTRACRANIAL SURGERIES LAYERS OF SCALP & MENINGES: (SCALP – SKULL - DAP)

1. Skin

2. Connective tissue

3. Aponeurosis

4. Loose Connective Tissue (vascular layers)

5. Pericranium (skull)

6. Dura, Arachnoid, Pia matter

TYPES OF SURGERIES:

1. Supratentorial

2. Infratentorial

3. Transphenoidal

4. Burr Holes

I. UNCONSCIOUSNESS & COMA TERMS:

1. Altered LOC – disorientation, difficulty in following commands and needs persistent stimuli to achieve a state of alertness.

2. Coma – state of unarousable unconsciousness wherein purposeful response to external and internal stimuli are absent except for involuntary responses to painful stimuli and brain stem reflexes.

3. Akinetic mutism – unresponsiveness to the environment in which the patient makes no voluntary movements.

4. Persistent vegetative state - condition in which the unresponsive patient is described as wakeful or resumes sleep – wake cycles after coma but is devoid of conscious content, without cognitive or affective mental function.

5. Locked-in syndrome - inability to speak, tetraplegia but with intact vertical eye movements and eyelid elevation . Results from lesions in Pons.

I. UNCONSCIOUSNESS & COMA S/S:1. Glasgow coma scale result below 152. Presence of multiple pathophysiologic phenomenon3. Comatose w/ localized abnormal pupillary & motor response –

neurologic problem4. Comatose but w/ pupillary light reflexes – toxic or metabolic

disorder COMPLICATIONS:1. Respiratory failure2. Pneumonia3. Pressure ulcers4. Venous stasis5. Musculoskeletal deterioration6. Disturbed GI Functions7. Aspiration

I. UNCONSCIOUSNESS & COMA MEDICAL/SURGICAL/NURSING MGT:1. Maintain patent airway Semi – Fowler’s position, lateral or semi-prone position, suction

secretions with hyper-oxygenation, monitor breath sounds, prepare intubation set.

2. Protect the client Side rails: 2 @ day, 3 @ night, privacy during nursing activities3. Maintain fluid balance and proper nutrition IV (slow), NGT, gastrostomy4. Mouth care Cleanse, rinse, remove secretions, apply thin petrolatum on lips,

move ET tube to side regularly5. Maintain skin and joint integrity Regular turning, proper moving in bed, passive ROM, assistive

devices, proper positioning, fluidized or low – air loss bed

I. UNCONSCIOUSNESS & COMA MEDICAL/SURGICAL/NURSING MGT:6. Preserve corneal integrity Cleanse with cotton moistened w/ NSS, artificial tears every 2

hours, cold compress for periorbital edema, proper eye patching7. Maintain Body temperature Proper ventilation, clothes, TSB, IV hydration, antipyretics,

monitor temperature8. Prevent urinary retention Regular palpation of bladder, IFC, bladder training9. Promote bowel function Monitor bowel sounds and movements, rectal exam, fecal

collection bags, stool softeners; glycerin suppositories, enema.10. Provide sensory stimulation Orientation, patience 11. Meet family’s needs12. Monitor and manage complications

II. INCREASED ICP PREDISPOSING FACTORS:

1. Cerebral edema

2. Head injury

3. Hydrocephalus

4. Inflammatory conditions

5. Tumor

SITUATION: Imbalance among the 3 major determinants of ICP.

ICP exceeds 20 mmHg (normal is 10 – 20 mmHg ,measured at the lateral ventricles)

II. INCREASED ICP3 major determinants of ICP:1. Brain tissue – 1,400 grams (increased by space

occupying lesions/tumor, abscess, edema)

2. Blood supply – 75 ml (affected by thrombosis, embolism, aneurysm, AV malformation)

3. CSF – 75 ml (increased by obstruction to flow or overproduction d/t a tumor in choroid plexuses)

**** CSF and Blood supply undergo constant minor changes due to increase in the intra-thoracic pressure when the person sneezes, coughs, strains; posture, BP, systemic oxygen and CO2 levels.

II. INCREASED ICP CEREBRAL RESPONSE TO INCREASED ICP:

1. Monro – Kellie Hypothesis

2. Autoregulation

3. Cushing’s Reflex

EFFECTS:

1. Ischemia – cell death

2. Cerebral edema

3. Fatal complication - Herniation of brain tissue (brain stem)

4. Secondary complications – SIADH, Diabetes insipidus (> 250ml urine/hour in 2 consecutive hours)

II. INCREASED ICP Early Signs:1. Change in LOC – earliest sign, restlessness to confusion2. Slowing of speech – delayed response to verbal suggestions 3. Pupillary changes – anisocuria 4. Constant Headache

Late Signs:1. Change in VS – Cushing’s triad plus hyperthermia2. Deterioration of LOC - disorientation to lethargy, stupor to coma3. Cheyne-stokes breathing4. Ataxic breathing – irregular with random sequence of deep and

shallow respiration5. Projectile vomiting6. Decorticate and Decebrate posture, flaccidity, hemiplegia7. Loss of brainstem reflexes – pupillary (fixed, dilated pupils),

corneal reflex, gag, swallowing reflex

II. INCREASED ICPMedical Nursing

1. Monitoring ICP and Cerebral Oxygenation

a. Ventriculostomyb. Subarachnoid screw or bolt

ICP c. Epidural monitord. Fiberoptic monitore. Jugular Venous Bulb (SjvO2)f. LICOX - measures O2 and

a. Evaluate ICP as orderedb. Perform regular neurologic

checkc. Prompt referral of

significant abnormal findings


2. Decreasing cerebral edema

a. Osmotic diuretics – mannitolb. Loop diuretics – furosemidec. Potassium sparing diuretics –

spironolactoned. For Hypokalemia – KCLe. For Hyperklaemia – Insulin,

kayexalate, Na CHO3, Calcium Gluconate

f. Corticosteroidsg. Negative fluid balance - Fluid

restrictionsh. Ventriculostomyi. IFC

a. Administer meds ad orderedb. Monitor for electrolyte

imbalance with use of diuretics especially Potassium

c. Record I and Od. Emphasize fluid restriction

to patient and SOe. Position properly to facilitate

drainage – HOPB elevated by 30 degrees

f. Regulate IVF properlyg. Oral care during fluid

restrictions


3. Maintaining Cerebral Perfusion and oxygenation

a. Inotropic agents - Dobutamine HCL (dobutrex) and Norepi. bitartrate (Levophed)

b. Oxygenation administration mechanical ventilation

c. CPP monitoringd. ABG, Hgb, Pulse oximetry

a. Administer meds as ordered

b. Proper positioning, use of cervical collar

c. Maintain oxygen as ordered


4. Reducing CSF and Intracranial Blood Volume

a. CSF drainageb. Promoting mild cerebral

vasoconstriction – PaCO2 at 30 – 35 mmHg

a. Proper positioningb. Maintain integrity of

intraventricular catheter for CSF drainage


5. Preventing further increase in ICP

a. Cough suppressants (dextrometorphan)

b. Antivomiting (plasil)c. Stool softeners (dulcolax)d. Surgery – burr hole

a. Proper positioning, use of cervical collar, preventing hip flexion

b. Instruct to conscious client to avoid valsalva maneuver, bending, stooping, lifting heavy objects

c. Prevent vomiting and coughing


6. Controlling Fever and reducing metabolic demands

a. Antipyreticsb. Hypothermic blanketc. High doses of barbiturates –

Pentobarbital (nembutal), Thiopental (pentothal)

d. Paralyzing agents – propofol (Diprivan) with analgesia and sedation

e. Induced hypothermia

a. Monitor VS esp. Temperature – use rectal or tympanic thermometer

b. Provide adequate ventilationc. Administer meds as orderedd. Monitor for adverse effects of

paralyzing agents and barbiturates

e. Assist in induction of hypothermia


7. Maintaining a patent airway

a. Intubation a. Suction secretions as needed –

with oxygenationb. Monitor breath sounds

8. Preventing Infection

a. Prophylactic antibiotics especially if with intraventricular catheter

a. Maintain aseptic technique when caring for tubes and intraventricular catheter

b. Monitor for signs and symptoms of meningitis and other infections

II. INCREASED ICP

Medical Nursing

9. Monitoring and managing complications

a. Diabetes Insipidus – electrolyte replacement, vasopressin

b. SIADH – fluid restriction, monitoring F & E status

a. Perform frequent and regular neurologic assessments

b. Monitor urine and record outputc. Proper use of monitoring devicesd. Educate family regarding

monitoring technology/equipment and their purposes.

III. HEADACHE/CEPHALGIA DEFINITION:

A symptom rather than a disease which may indicate organic disease, stress response, vasodilatation, skeletal muscle tension, or combination of factors.

TYPES:1. PRIMARY HEADACHE – no organic cause is identified.

Includes: Migraine Tension – type headache Cluster headaches Cranial arteritis Other primary headaches

2. SECONDARY HEADACHE - associated with organic cause such as brain tumor or aneurysm.

III. HEADACHE/CEPHALGIA ASSESSMENT:

1. Migraine

a. Prodrome

b. Aura Phase

c. Headache Phase

d. Recovery and Postdrome

2. Other headache types

a. Tension headache

b. Cluster headaches

c. Cranial arteritis

III. HEADACHE/CEPHALGIAMedical Nursing

1. Prevention

Migraine: 1. Beta blockers – propanolol,

metoprolol2. Calcium channel blockers for clients

with asthma, DM, bradycardia – verapamil

3. Amitriptyline HCL (elavil)

4. Divalproex (valproate)5. Flunarizine 6. Serotonin antagonist (pizotyline)

Others:a. Ergotamine tartrateb. Lithium naproxen (naprosyn) c. Methysergide (sansert)

a. Educate patients regarding causes and predisposing factors and the need to avoid them.

b. Teach relaxation techniques

c. Administer meds as ordered

III. HEADACHE/CEPHALGIAMedical Nursing

2. Relieve Pain

a. 100 % oxygen via face mask for 15 minutes

b. Ergotamine tartratec. Corticosteroidsd. Other analgesics

a. Provide comfort measures, quiet, dark environment

b. Assist with comfortable positioning – usually HOB elevated by 30 degrees

c. Apply warm compress and massage to area with muscle tension

d. Administer meds as ordered

IV. SEIZURE DISORDERConvulsion Seizure Epilepsy

- can be best described as a sudden, excessive, disorderly discharge of neurons in either a structurally normal or diseases cortex which arises from an instability of the neuronal membrane caused by an excess of excitation or a deficiency of normal inhibitory mechanism.

-refers only to those violent, involuntary muscular contraction of voluntary muscle.

- includes clinical manifestation such as disturbances in sensation, alteration in perception and or coordination, LOC, convulsive movements or a combination of any or all of the aforementioned.

- when seizures become recurrent or chronic in nature

- a paroxysmal disturbance in consciousness with autonomic, sensory and /or motor dysfunction

- a manifestation of excessive neurological discharge in the brain.

IV. SEIZURE DISORDERConvulsion Seizure Epilepsy

- can be best described as a sudden, excessive, disorderly discharge of neurons in either a structurally normal or diseases cortex which arises from an instability of the neuronal membrane caused by an excess of excitation or a deficiency of normal inhibitory mechanism.

-refers only to those violent, involuntary muscular contraction of voluntary muscle.

- includes clinical manifestation such as disturbances in sensation, alteration in perception and or coordination, LOC, convulsive movements or a combination of any or all of the aforementioned.

- when seizures become recurrent or chronic in nature

- a paroxysmal disturbance in consciousness with autonomic, sensory and /or motor dysfunction

- a manifestation of excessive neurological discharge in the brain.

IV. SEIZURE DISORDER CAUSES:

1. Idiopathic

2. Acquireda. Cerebrovascular disease

b. Hypoxemia of any cause

c. Fever (childhood)

d. Head injury

e. Hypertension

f. CNs infections

g. Brain tumor

h. Drug and alcohol withdrawal

i. Agents - (INH) isoniazid

j. Allergies

k. Metabolic and toxic conditions – hypoglycaemia, hypocalcemia, hyponatremia, renal failure, pesticides

IV. SEIZURE DISORDER PATHOPHYSIOLOGY:

1. Depletion of K+ and a gain of Na+ in the neuronal cell produce seizure2. Alteration in the blood brain barrier system can precipitate a shift in K+

concentration lowering the convulsive threshold3. An altered O2 and glucose concentration – produce rapid marked potassium loss

and a sodium accumulation within the cells depolarizing the membrane and producing those paroxysmal discharges.

4. Infectious process – as a result of cell destruction, fever, inflammation and possible bacterial toxicity.

5. Vitamin B6 deficiency whether dietary or drug antagonized. Since Vit B6 is involved in the metabolism of GABA, a shift of the normal excitatory inhibitory balance occur with excitation prevailing and a results to seizure.

6. The duration of a seizure varies greatly. It may last a few seconds or persists for several minutes. Although investigators do not know why seizure stops at a given time. It is thought to be related to exhaustion of the neurons involved and to certain unknown factor which inhibits further electrochemical transmission. Some individuals may experience them once or twice a year, while others may have 2 or 3 episodes in a single day. It is unpredictable which is especially frightening to the individual.

IV. SEIZURE DISORDER CLASSIFICATION:1. Generalized seizure Grand mal or major motor Petit mal Myoclonic seizure Infantile spasms Atoning seizure Tonic seizure Febrile seizures Status epilepticus

2. Partial seizure Localized motor seizures or Jacksonian seizure Psychomotor (complex partial seizure) Partial seizure with secondary generalization

3. Unilateral

4. Unclassified epileptic seizures

IV. SEIZURE DISORDER MEDICAL MANAGEMENT:1. Prevention – removal of precipitating factors2. Anticonvulsant Therapy Phenytoin (Dilantin) – DOC Phenobarbital (Luminal) Mephobarbital (Mebaral) Primidone (Mysoline) Succinamides Ethosiximide (Zarontin) Methsuximide (Celontin) Others Diazepam (Valium) Clonazepam (Clonopin) Valproic Acid (Depakene) Acetazolamide (Diamox) Carbamazepine (Tegretol) 3. Surgery

IV. SEIZURE DISORDER NURSING MANAGEMENT:

1. General – C-A-E-S-A-R

2. During the Seizure

3. After the Seizure

V. CEREBROVASCULAR ACCIDENT V. CEREBROVASCULAR ACCIDENT (STROKE)(STROKE)

SITUATION: Sudden loss of brain function resulting from a

disruption of blood supply to part of the brain causing temporary or permanent dysfunction.

May be caused by thrombosis, embolism, hemorrhage.

Also known as Ischemic stroke and brain attack

MAJOR CAUSES:

1. Ischemic

2. Hemorrhagic

V. CVA/STROKE RISK FACTORS:1. HPN2. DM3. MI4. Aortic valve disease5. CHF6. Arterio/Atherosclerosis

TYPES ACCORDING TO TIME:1. Transient Ischemic Attack (TIA)2. Reversible ischemic Neurologic deficit3. Stroke in Evolution4. Completed Stroke

TYPES ACCORDING TO CAUSE:1. Ischemic2. Hemorrhagic

STROKE CLASSIFICATION STROKE CLASSIFICATION ACCORDING TO TIMEACCORDING TO TIME

1. Transient Ischemic Attack (TIA)- temporary episode of neurologic dysfunction (loss of motor, sensory & visual dysfunction)Management: Anticoagulant therapy heparin, coumadin, aspirin

2. Reversible ischemic Neurologic deficit- signs & symptoms are consistent with but more pronounced than TIA. S/Sx resolve in days without neurologic deficit

3. Stroke in Evolution- worsening of neurologic S/Sx over several minutes or hours. Also called Progressing stroke

4. Completed Stroke- stabilization of neurologic S/Sx. No further progression of hypoxic insult to the brain.

TYPES ACCORDING TO CAUSE (ISCHEMIC):TYPES ACCORDING TO CAUSE (ISCHEMIC):1.1. Large artery thrombosis Large artery thrombosis

– – due to atherosclerotic plaques in the large blood vessels of due to atherosclerotic plaques in the large blood vessels of the brain. Thrombus formation & occlusion @ the site of the brain. Thrombus formation & occlusion @ the site of atherosclerosis result in ischemia & infarction.atherosclerosis result in ischemia & infarction.

2. Small penetrating artery thrombosis- affect one or more vessels & are the most common type of ischemic stroke.- also called lacunar stroke.

3. Cardiogenic Embolic stroke - associated with cardiac dysrhytmias, usually atrial fibrillation.

Emboli originate from the heart & circulate to the cerebral vasculature, most commonly the left middle cerebral artery, resulting in a stroke. Embolic strokes may be prevented with use of anticoagulants.

4. Cryptogenic- no known cause

5. Others- cocaine use, coagulopathies, migraine & spontaneous dissection of the carotid or vertebral arteries.

Pathophysiology:Obstruction of blood vessels

(of different causes)

↓↓

IschemiaIschemia

↓↓

Energy failureEnergy failure

AcidosisAcidosis ↓↓ Ion imbalanceIon imbalance

↓ ↓ inc. glutamateinc. glutamate depolarizationdepolarization

Intracellular calcium increaseIntracellular calcium increase

↓ ↓Cell membranes & protein breakdownCell membranes & protein breakdown

Formation of free radicals;Formation of free radicals;

Decrease protein productionDecrease protein production

↓ ↓Cell injury & deathCell injury & death

Ischemic cascade begins when cerebral blood flow falls to less than 25 ml/100g/min. at this point, neurons can no longer maintain aerobe respiration.

Mitochondria switches to anaerobic respiration which generates large amounts of lactic acid, causing change in Ph, also renders the neuron incapable of producing large quantities of ATP to fuel depolarization process. Membranes pump that maintain electrolyte balance begin to fail & cells cease to function.

An area of low cerebral blood flow (penumbra region) exists around the area of infarction. It is ischemic brain tissue that can be salvaged with timely intervention.

TYPES ACCORDING TO CAUSE:TYPES ACCORDING TO CAUSE:

(HEMORRHAGIC STROKE)(HEMORRHAGIC STROKE)

1. Intracerebral Hemorrhage

2. Intracranial/Cerebral Aneurysm

3. Subarachnoid Hemorrhage

4. Arterio-Venous Malformation

V. CVA/STROKERISK FACTORSRISK FACTORS

1. HPN – BP vasoconstriction pressure in blood vessels rupture of vessels thrombus in the blood vessel of brain blood supply to the brain

2. DM - blood sugar levels viscosity of blood perfusion of blood stasis of blood flow thrombus formation blood supply to the brain

3. MI – decrease O2 to myocardium decreased cardiac output decreased perfusion stasis thrombus decreased blood supply to brain

4. Aortic valve dse - decreased cardiac output decreased perfusion stasis thrombus decreased blood supply to brain

5. CHF – inability of heart to pump sufficient amount of blood back to heart decreased cardiac output decreased perfusion stasis thrombus decreased blood supply to brain

6. Arterio/Atherosclerosis – narrowing of blood vessels decreased cardiac output decreased perfusion stasis thrombus decreased blood supply to brain

V. CVA/STROKECLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

Stroke can cause a wide variety of neurologic deficits, depending on the location of lesion, size of area of inadequate perfusion & the amount of collateral blood flow.

1. Ischemic

2. Hemorrhagic

3. Motor disturbances

4. Communication problems

5. Perceptual/ Sensory disturbance lesion; numbness & tingling of extremities.

6. Cognitive deficit

7. Emotional deficits


Ischemic: Numbness or weakness of face, arm or leg especially on one side of the body

Hemorrhagic: “Exploding headache”, decreased LOC, focal seizures, nuchal rigidity


MOTOR hemiplegia – most common motor dysfunction, due

to lesion of the opposite side of the brain (paralysis of one side of the body)

hemiparesis – weakness of one side of the body. Ataxia – staggering, unsteady gait; unable to keep feet together, needs a broad base to stand

Dysphagia – swallowing difficulty. apraxia – inability to perform a previously learned

action (picks up a fork but attempts to comb hair)


COMMUNICATIONCOMMUNICATION dysarthria – difficulty in speaking, caused by

paralysis of muscles responsible for producing speech

dysphasia/aphasia – defective or loss of speech. Could either be expressive, receptive or mixed/global


PERCEPTUAL DISTURBANCEPERCEPTUAL DISTURBANCE- Perception is the ability to interpret sensation. Disturbances are due to disturbances of primary sensory pathways between the eye & cerebral cortex.

Homonymous hemianopsia – loss of half of the visual field. It corresponds to the paralyzed side of the body.

Loss of peripheral vision – difficulty seeing @ night.

Diplopia – double vision, unaware of objects or borders of objects.

Paresthesia – occurs on side opposite to lesion; numbness & tingling of extremities.

PERCEPTUAL DISTURBANCEPERCEPTUAL DISTURBANCE

PERCEPTUAL DISTURBANCEPERCEPTUAL DISTURBANCE


COGNITIVE DEFICITCOGNITIVE DEFICIT Short & long term memory loss Decreased attention span Impaired ability to concentrate Poor abstract reasoning Altered abstract reasoning

EMOTIONAL DEFICITSEMOTIONAL DEFICITS Loss of self control Emotional lability Decreased tolerance to stressful situations Depression Withdrawal Fear, hostility & anger Feelings of isolation


USUAL SIGNS & SYMPTOMSUSUAL SIGNS & SYMPTOMS1. Headache

2. Vomiting

3. Seizures

4. Confusion

5. Decreased LOC

6. Nuchal rigidity

7. Fever

8. Hypertension

9. Slow bounding pulse

10. Cheyne-stokes respirations

V. CVA/STROKEDIAGNOSTIC TESTS

1. CT scan show lesion – to determine if the event is ischemic or hemorrhagic; to determine treatment

2. 12 lead ECG3. Carotid Ultrasound4. Cerebral arteriography shows occlusion or

malformation of vessels5. Transcranial Doppler6. Transthoracic or transesophageal echocardiogram7. MRI of brain8. Single photon emission CT

V. CVA/STROKEMEDICAL MANAGEMENTMEDICAL MANAGEMENT

Ischemic Stroke1. Thrombolytic therapy – Recombinant t-PA

2. Anticoagulants – heparin – Coumadin (after 24 hours)

3. Antiplatelets - Aspirin

4. Statins - simvastatin

5. AntiHPN – ACE Inhibitors

6. Thiazide Diuretics

7. Intubation

8. Surgery: Carotid Endarterectomy – removal of an atherosclerotic plaque or thrombus from carotid artery to prevent stroke in patients with occlusive diseases of the extracranial cerebral arteries.

9. Manage complication – pulmonary care, maintenance of patent airway, & administration of supplemental oxygen


Hemorrhagic Stroke1. Analgesics – codeine, acetaminophen

2. Sequential compression devices – prevent DVT

3. Surgery: endovascular treatment, aneurysm coiling, removal of aneurysm


COMMUNICATION:Aphasia right hemiplegicsReceptive – inability to decode spoken word (WERNICKE”S area affectation) give one command at a time, simple instructions, non verbal communicationExpressive – inability to speak (BROCA’S area affected) encourage attempts at speech – anticipate needs, allow to verbalize, no matter how long it takes, do not finish sentences for him

HOMONYMOUS HEMIANOPSIA AND LOSS OF HALF OF EACH VISUAL FIELD

- approach patient on unaffected side place belongings on unaffected side teach scanning technique (turn head to sides)


MANAGING COMPLICATIONS:- pulmonary care, maintenance of patent airway, & administration of supplemental oxygen

ENDARTERECTOMY – removal of an atherosclerotic plaque or thrombus from carotid artery to prevent stroke in patients with occlusive diseases of the extracranial cerebral arteries.

NURSING MANAGEMENT POST OP 1. Close cardiac monitoring2. Maintenance of adequate BP

V. CVA/STROKENURSING MANAGEMENTNURSING MANAGEMENT

1. Maintain Patent airway

2. Monitor VS , neurological checks

3. Promote Bed rest

4. Perform GI decompression (NGT)as ordered

5. Maintain Fluid electrolyte balance

6. Reposition q2h

7. Promote Skin integrity

8. Improve mobility

9. Support Elimination – offer bed pan every 2 hours – catheterize if necessary – stool softeners and suppositories

10. Ensure safety

11. Facilitate Communication

12. Administer drugs as ordered

VI. NEUROLOGIC TRAUMA

CLASSIFICATION:

1. Brain Trauma Primary trauma –is the direct result of some force applied to the

skull resulting in a fracture, hemorrhage, contusion, or concussion. Secondary trauma - is one in which some other medical condition

causes a person to fall or otherwise to sustain a blow to the head. These conditions include diabetic, cardiac, epileptic or hysterical problems and situations following drug and/or alcohol ingestion in which the person falls, strikes the head and loses consciousness.

a. Fractureb. Hemorrhagec. Contussiond. Concussion

2. Spinal Cord Injury

BRAIN TRAUMA: FRACTURES

BRAIN TRAUMA: FRACTURES

1. Linear fracture- are those in which there is a simple break in the continuity of the bone/skull

2. Comminuted fracture- are fragmented interruptions of the skull from multiple linear fractures

3. Depressed fracture - comminuted bone fragments penetrate the brain tissue

4. Compound fracture- any of the preceding which also has an opening through the sinuses, eardrums or scalp.

BRAIN TRAUMA: HEMORRHAGE

1. Linear fracture- are those in which there is a simple break in the continuity of the bone/skull

2. Comminuted fracture- are fragmented interruptions of the skull from multiple linear fractures

3. Depressed fracture - comminuted bone fragments penetrate the brain tissue

4. Compound fracture- any of the preceding which also has an opening through the sinuses, eardrums or scalp.

BRAIN TRAUMA: HEMORRHAGE

1. Epidural Hematoma

2. Subdural Hematoma

3. Intra-cerebral Hematoma

BRAIN TRAUMA: CONCUSSION

Concussion - It is essentially a disruption of normal activity among some of

the synapses of the neurons. It is a temporary disarrangement of normal neurons activity. Muscular activity and mental clarity usually return within a few minutes after trauma, although there may be residual amnesia for the event.

BRAIN TRAUMA: CONTUSION

Contusions - Resemble bruises. There is only slight injury to small vessels

with a small amount of bleeding into the surrounding tissues. The resulting effects of increased ICP are dependent upon the amount of contused brain tissue.

SPINAL CORD INJURY

Primary Injury - results from initial insult or trauma and produces permanent damage

Secondary Injury – results from contusion or tear injury in which nerve fibers begin to swell and disintegrate. Damage is reversible up to 4 – 6 hours after the injury.

Effects:1. Central Cord Syndrome

2. Anterior Cord Syndrome

3. Brown Sequard Syndrome

SPINAL CORD INJURY

COMPLICATIONS:

1. Spinal and Neurogenic shock “areflexia”

2. Autonomic Dysreflexia “hyperreflexia”

3. Tetraplegia and Paraplegia

4. Deep Vein Thrombosis and Thrombophlebitis

5. Orthostatic Hypotension

SPINAL CORD INJURY

MANAGEMENT:

1. Cord Damage – immobilize

2. Respiration – stabilize, intubation

3. Urinary and bowel function – training, IFC, enema, suppositories, don’t allow bladder to distend

4. Thrombosis – anticoagulants, elastic compression stockings

5. Cardiovascular stability

6. Help assess meurologic status

7. Encourage adequate fluid, nutrition

8. Support skin to prevent breakdown, watch out for Shock

VII. HYDROCEPHALUS DEFINITION:

A.k.a. water on the brain

Can be caused by impaired CSF flow and re-absorption, or excessive CSF production.

Flow obstruction, hindering free passage of CSF through the Ventricular System & SA space (e.g. stenosis of cerebral aqueduct or obstruction of Foramen of Monro) due to tumors hemorrhages, infection or congenital malformations.

Overproduction of CSF (e.g. papilloma of choroid plexus)

VII. HYDROCEPHALUS

TYPES:

1. Congenital

2. Acquired

3. Communicating or Non – obstructive

4. Non – communicating or Obstructive

VII. HYDROCEPHALUS

MEDICAL MANAGEMENT:1. Drugs

2. Surgical removal of obstruction

3. Surgical placement of shunting devices

a. VP shunt

b. VA shunt

c. EVD

MEDICAL MANAGEMENT:1. Prevent Increase ICP

2. Prevent Infection

3. Promote proper nutrition

4. Educate SO

5. Post – op care

VIII. NEURAL TUBE DEFECTS DEFINITION:

Failure of neural tube to close or fully develop at 3 – 5 weeks of gestation.

CAUSE:

Genetics, heredity, drugs, radiation, chemicals or toxins, maternal malnutrition, maternal use of antiepileptic drugs, infectious diseases and FOLIC ACID DEFICIENCY (normal intake 0.4 - 4 mg/day).

CLASSIFICATION:1. Anencephaly - cerebrum2. Encephalocele – cerebrum, meninges, glial cells3. Spina Bifida – spinal cord, meninges, usually L5 and S1 regiona. Spina Bifida occultab. Spina Bifida cystic Meningocele Myelomeningocele

VIII. NEURAL TUBE DEFECTS GENERAL MANAGEMENT FOR NTD:

1. All – protect from LATEX allergy, NO to balloons, vinyl gloves2. Anencephaly – no cure, support parents3. Encephalocele – protect from infection, support perio-peratively,

and educate parents about possible intellectual impairment.4. Spina bifida occulta - facilitate work ups, referral to surgery,

monitor for development of s/s.5. Meningocele – protect sac from rupture, drying or infection, place

in prone position, facilitate early sac excision (24 – 48 hours of life), complete closure of spinal column, monitor for development of complications.

6. Myelomeningocele – cover sac with non-adhesive, sterile, moist saline gauze, place infant in prone position, facilitate surgery (repair and shunt placement), emphasize to parents that surgery has its risks (lower extremities paralysis), monitor for development of complications like increase ICP and HYDROCEPHALUS.

IX. MULTIPLE SCLEROSIS DEFINITION:

Immune-mediated progressive demyelination or destruction of myelin sheath that surrounds certain nerve fibers in brain and spinal cords resulting to impaired transmission of nerve impulses. Affects the CNS. May be Relapsing-remitting, Primary progressive, Secondary progressive, Progressive-relapsing.

CAUSE: Possibly Human Leukocyte Antigen in cell wall, presence of sensitized T – Cells that remain within the CNS.

DX: MRI, Electophoresis of CSF (several bands of IG G)

MAIN S/S: FATIGUE, CHARCOAT’S TRIAD

MGT: Analgesics, immunosuppressive agents and steroids, GABA agonist, Benzodiazepines (valium), Symmetrel, Cylert, Prozac, Inderal, Vitamin C, antibiotics.

NSG. CARE: AVOID FATIGUE, AVOID PREGNANCY during remission

MULTIPLE SCLEROSIS

A degenerative disease characterized by demyelination of nerve fibers within the spinal cord and brain. Destruction of an area of a myelin sheath occurs, followed by a proliferation of neuroglial cells, scar formation and damage to the nerve fiber with ensuing loss of transmission of impulses.

Etiology and incidence:

The cause is unknown. At present theories undergoing investigation are concerned with auto immune mechanisms and viral infections as possible etiologic factors. It most prevalent in colder climates. It has a slightly higher incidence in females between 20 to 40 years of age.

Course and manifestations:Characterized by remissions and relapses, and the course is extremely variable and unpredictable.

Early symptoms:Transient tingling sensations, numbness and muscular weakness in one or both arms and legs and visual disturbances (nystagmus, diplopia or blurring of vision); emotional lability, evidenced bv alternating periods of euphoria, depression, irritability.

Late symptoms:With relapses and increasing damage, the patient may develop paralysis, impaired speech, dysphagia, increasing loss of sensation, bladder and bowel incontinence, increasing visual difficulties, personality changes, and intellectual impairment. Weakness of the respiratory muscles and cough reflex may also be present, predisposing him to pulmonary complication.

Diagnostic test:At present there are no specific diagnostic tests. The CSF shows an elevated gamma globulin and a positive colloidal gold precipitation test (Lange colloidal gold curve)

Treatment and Nursing Care:During remissions – the patient is encouraged to resume his usual pattern of life modifying it as necessary to avoid fatigue, emotional stress and infection. Well balanced diet adequate rest and learning to accept what cannot be readily change are stressed. Avoid pregnancy.

During relapses – confine to bed for a period of 2 to 3 weeks or until symptoms begin to disappear. Warm baths, massage, pleasant quiet surroundings, encouraging reading and listening to radio, chat. The limbs are passively moved through the full range of motion twice daily.

Steroid therapy:Dexamethasone (Decadron), Adrenocorticotropin (ACTH) or Prednisone

X. MYASTHENIA GRAVIS DEFINITION:

Immune-mediated varying degrees of voluntary muscle weakness. Affects the MYONEURAL JUNCTION.

CAUSE: Presence of ANTIBODIES directed towards Ach receptors.

DX: Achetylcholinesterase inhibitor test: TENSILON TEST, Presence of Ach receptor antibodies in serum, Successive nerve stimulation, Evaluation of Thymus gland.

S/S: Ptosis, descending paralysis, muscle weakness in late afternoon, risk for respiratory failure.

COMPLICATIONS: Respiratory Failure and Crisis: Myasthenic crisis Cholinergic crisis Brittle Crisis – extreme under meds

Etiology: Predisposing factor:Etiology: Predisposing factor: - autoimmune - auto immune disease - autoimmune - auto immune disease

- viral infection, Thymoma, rheumatoid arthritis, - viral infection, Thymoma, rheumatoid arthritis, - systemic lupus erythematous- systemic lupus erythematous

│ │--------------------------------------------------------------------------------------│--------------------------------------------------------------------------------------│ ↓ ↓ auto antibodiesauto antibodies ↓ ↓ blocking the binding of acetylcholineblocking the binding of acetylcholine ↓ ↓ destruction of ACH receptordestruction of ACH receptor ↓ ↓ impaired transmission of impulses across the myoneural junctionimpaired transmission of impulses across the myoneural junction

---------------------------------------------------------------------------------------------------------------------- ---------------------------------------------------------------------------------------------------------------------- ↓ ↓ ↓ ↓ ↓ ↓ ↓ ↓ ↓ ↓ ↓ ↓

facial expression limb movements laryngeal chewing & eye & eyelid facial expression limb movements laryngeal chewing & eye & eyelid involvement swallowing movementsinvolvement swallowing movements

-myasthenic smile - unstable - dysphonia - dysphagia - diplopia-myasthenic smile - unstable - dysphonia - dysphagia - diplopia - waddling gait - dysarthria - choking - ptosis- waddling gait - dysarthria - choking - ptosis

- weak arms, - slurred speech - aspiration- weak arms, - slurred speech - aspiration legs, handslegs, hands & fingers& fingers

DiaphragmDiaphragm - Shortness of breath- Shortness of breath

Complications:Complications: - Myasthenia crisis or Brittle Crisis- Myasthenia crisis or Brittle Crisis - Cholinergic crisis- Cholinergic crisis

PTOSIS

CRISIS: acute episodes to severe muscular weakness in which respiratory insufficiency and the inability to swallow are manifested.

Categories:Myasthenic type – is attributed to a temporary resistance to or inadequate dosage of the cholinergic preparation being administered. Manifested by extreme weakenss. Tensilon relieves symptoms

Cholinergic crisis – is caused by excess of anticholinesterase medication. Patient becomes pale and manifests diarrhea, nausea, vomiting, diaphoresis, increased salivation and bronchial secretions, abdominal cramps and blurred vision. Symptoms worsen in Tensilon. Atropine as antidote.

X. MYASTHENIA GRAVIS MGT: 1. Drugs – ANTICHOLINESTERASE/pyridostigmine bromide

(Mestinon) and Neostigmine (Prostigmin), immunosuppressive agents (Prednisone), cytotoxic agents NO TO MORPHINE, CURARE, QUININE, NEOMYCIN, STREPTOMYCIN

2. IVIG, Plasmapheresis, Thymectomy, Intubation, Mechanical Ventilation

NSG. CARE:1. Avoid overfatigue.2. Support nutrition. 3. Administer meds at precise time. 20 – 30 minutes before meals. 4. Protect patient from fall.5. Aspiration precaution. 6. Monitor respiratory status and provide adequate ventilation. 7. Avoid exposure to infection.8. Provide eye care. “Crutches” to eyelids, patch one eye and give

artificial tears.

XI. GUILLAIN BARRE SYNDROME DEFINITION:

An acute inflammatory demyelinating disease of the peripheral nervous system.

CAUSE: Unclear. It is believed to be associated with an viral infections 1-4 weeks before.

DX: Spinal Tap - High Protein levels in CSF, EMG – slow conduction of impulses to muscles

S/S:

1. Initial phase - Bilateral muscle weakness in the lower extremities, with an ascending pattern. Can result in potential life-threatening respiratory compromise.

2. Plateau phase - May last days to weeks. It is an interim period in which no changes occur.

3. Recovery phase - Synonymous with re myelination and axonal regeneration. Paralysis resolves gradually in a descending symmetrical pattern following a proximal to distal pattern.

Pathophysiology:

Schwann cells, which cover the nerve axons, form the myelin sheath.Degeneration of these cells occurs, causing a flaccid paralysis, which is usually in an ascending pattern. It is primarily the motor neurons affected. Sensory involvement is limited and is usually confined to the hands and feet in what is termed the glove and stocking pattern. Spontaneous regeneration of the myelin sheath occurs with complete recovery within 6 months to 1 year. Management is aimed at supporting body functions and preventing complications associated with paralysis until recovery occurs.

GB Planning and Intervention:

1. Assess for respiratory compromises - evaluate ABGs and pulse oximetry

2. Be prepared to provide respiratory support – mech. vent and later on, intubation

3. Perform pulmonary toilet to prevent pneumonia, suction as necessary, hyperoxygenate/hyperventilate

4. Monitor Vital signs, ECG5. Assess for urinary retention6. Maintain optimal positioning

a. Elevate head of bed as tolerated to promote lung expansion and decrease risk for aspiration

b. Turn and reposition every 2 hoursc. Assist with active and passive ROM

7. Prevent DVT & pulmonary embolism – Anti-embolic stockings, sequential compression boots, anticoagulants

8. Administer medications as indicated and ordered, including:

1. IVIG – therapy of choice, followed by plasmapheresis

2. Analgesics

3. Anti-anxiety agents

4. Corticosteroids

5. Antibiotics for prophylaxis

6. Antacids to control gastric irritation

7. H2 blockers to reduce gastric acid secretion and prevent ulcer

8. Anticoagulants

9. A short – acting alpha adrenergic blockers for HPN in autonomic dysfunction

XII. PARKINSON’S DISEASE DEFINITION:

A progressive degenerative neurologic disorder affecting the brain centers that are responsible for control and regulation of movement (extrapyramidal) caused by deficiency of dopamine. Occurs in the elderly.

CAUSE: Dopamine deficiency

DX: EEG, CT Scan, SPECT (PET)

S/S: 1. Resting tremors2. Rigidity3. Bradykinesia4. Postural instability

Manifestations:1. Tremors of the upper limbs; “Pill rolling”

2. Rigidity; “cogwheel rigidity”

3. Bradykinesia (moves slowly)to hypokinesia (diminished movements)

4. Stooped posture, loss of postural reflexes

5. “Shuffling, propulsive gait/ festinating” gait

6. Monotone speech; “microphonia, dysphonia”

7. Mask like facial expression

8. Increased salivation, drooling, dysphagia

9. Excessive sweating, seborrhea

10. Lacrimation, constipation

11. Decreased sexual capacity

12. Alteration in handwriting; “micrographia”

13. Dementia, depression, sleep disturbances and hallucinations

XII. PARKINSON’S DISEASE MGT: Drugs, Surgery

1. Antiparkinsonians2. Anticholinergics3. Antihistamines4. Dopamine agonist5. Antidepressants6. MAO Inhibitors 7. Antiviral8. Stereotactic Procedures - Thalamotomy and Pallidotomy 9. Neural Tranplantation10. Deep Brain Stimulation

NSG. CARE:1. Aspiration precaution2. Educate on drug therapy3. Physical therapy and gait training4. Diet5. Safety6. Emotional support7. Promote independence8. Skin care

Drug Function Generic Name (Trade Name)

Levodopa Enhances conversion of levodopa to dopamine in the brain.

Levodopa (Laradopa); levodopa/carbidopa (Sinemet, Sinemet CR,Atamet); levodopa/benserazide (Madopar)

Dopamine agonist Mimics the action of dopamine by activating nerve cells in the brain.

Bromocriptine (Ergoset, Parlodel); pergolide (Permax); pramipexole (Mirapex); ropinirole (Requip)

Anticholinergic Blocks action of acetylcholine, a brain chemical that becomes overactive when dopamine levels drop.

Trihexiphenidyl (Artane, Trihexy); biperidine (Akineton); benztropine (Congentin)

MAO-B inhibitor Blocks action of an enzyme that breaks down dopamine in the brain.

Selegiline (Eldepryl, Movergan)

COMT inhibitor Blocks action of an enzyme that breaks down levodopa in the body, permitting more levodopa to reach the brain.

Tolcapone (Tasmar); entacapone (Comtan)

Amantadine Stimulates release of dopamine from nerve cells in the brain and may block acetylcholine action.

Amantadine (Symadine, Symmetrel)

BELL’S PALSYIt is a lower motor neuron lesion of the 7 th cranial nerve, resulting in paralysis of one side of the face. It is usually self-limiting to a few weeks.

Manifestations:

Facial paralysis involving the eyeTearing of eyePainful sensations in the faceSagging of one side of mouth; drooling

Management:

Steroids and analgesicsProtect involved eyeActive facial exercises

CEREBRAL PALSYCEREBRAL PALSY- Is an umbrella term encompassing a group of non-progressive, non-contagious neurological disorders that cause physical disability in human development, specifically movement & posture.

- Neurological disability or difficulty controlling voluntary muscles (caused by damage to some portion of the brain, with associated sensory, intellectual, emotional or convulsive disorders.

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NEURO 2009