MODULE G SECTION 1 Nervous System

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Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

MODULE G

SECTION 1

Nervous System

NUR 202

Instructor: Dr. Dowanda D. Pullom, RN

OBJECTIVES

• The student will:

�Understand the anatomy & physiology of the nervous system.

�Compare and contrast the etiology, clinical manifestations, collaborative care, and nursing management of tension-type, migraine, and cluster headaches.

�Differentiate the etiology, clinical manifestations, diagnostic studies, collaborative care, and nursing management of multiple sclerosis, Parkinson’s disease, and myasthenia gravis. 2

TOPICS

• ANATOMY & PHYSIOLOGY REVIEW

• Central nervous system

• Peripheral nervous system

• Neuron

• Neuroglia

• Neurotransmitter

• Myelin

• Autonomic nervous system

• HEADACHES

• MAJOR CHRONIC DISEASES

• Multiple sclerosis

• Parkinson’s disease

• Myasthenia gravis

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COMPONENTS OF THE

NERVOUS SYSTEM

Central Nervous

System includes

both Spinal and

Cranial Nerves

4

CELLS OF THE

NERVOUS SYSTEM: NEURON

5

1. Excitability

2. Conductivity

3. Influence

CELLS OF THE NERVOUS SYSTEM:

GLIAL (NEUROGLIA)

Provide to Neurons

• Support

• Nourishment

• Protection

6

What is the function of the Glial

Cells?

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NEUROTRANSMITTERS

7

8

Circle of Willis

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CRANIAL NERVES

10

CRANIAL NERVES

On Olfactory

Old Optic

Olympus Oculomotor

Towering Trochlear

Tops Trigeminal

A Abducens

French Facial

And Auditory

Vestibulocochlear

German Glossopharyngeal

Viewed Vagus

Some Spinal Accessory

Hops Hypoglossal

11

EFFECTS OF AGING

• Fall Risks

• Nutritional Risks

• Risk for Temperature,

BP Problems

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Assessment of Nervous System

• Past Health History

• Medications

• Surgery or other treatment

• Functional health Patterns

� Substance abuse, smoking, nutrition, blood pressure control

� Participation in recreational activities

• Seat belts, and Helmets

• Elimination

• Sleep/Rest Pattern

• Physical exam Findings

� Mental Status

� Cranial Nerve Assessment

Table 56-6 Normal physical assessment or nervous system p. 1349 13

Diagnostic Studies of Nervous

System

• Lumbar Puncture

• Computed Tomography

• Magnetic Resonance Imaging

• Cerebral Angiography

• Electroencephalography

• Electromyography and Nerve Conduction Studies

P. 1351 Table 56-8 1352-1353

Please read purpose of the tests and the nursing responsibilities

related to the test.14

LUMBAR PUNCTURE **

15

Tube # 1 Chemistries – GLUCOSE

Tube # 2 Bacteria

Tube # 3 or 4 Blood (WBC and RBC)

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Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Chapter 57 Acute

Intracranial Problems

COMA

INCREASED INTRACRANIAL PRESSURE

(IICP)

NORMAL INTRACRANIAL PRESSURE

17

� DEFINED

� 3 components

� Normal limit

ICP Normal 5-

15%

Compliance :

Is the expandability of the brain

• Monro-Kelly doctrine

18

NORMAL INTRACRANIAL PRESSURE cont…

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• DEFINITION: The amount of blood in milliliters passing through

100grams of brain tissue in 1 minute.

• NORMAL RANGE: Approx. 50mL/min per 100g of brain tissue.

• AUTOREGULATION: Automatic adjustments in the diameter of the

cerebral blood vessels in order to maintain a constant blood flow

during changes in systemic BP.

CEREBRAL BLOOD FLOW

19

20

**CBF and ICP are NOT the same thing. Increased ICP causes decreased

CBF.

• The pressure needed to ensure blood flow to the brain.

• CPP = MAP − ICP

• Normal CPP 60 to 100

• CPP of less than 50 is associated with ischemia and neuronal

death

21

CPP (Cerebral Perfusion Pressure)

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Intracranial Pressure (ICP)

22Table 57-1. Calculation of Cerebral Perfusion Pressure

22

Increased Intracranial Pressure (ICP)

23

Fig. 57-2. Intracranial pressure-volume curve. (See text for descriptions of 1, 2, 3, and 4.)

Compliance :

Is the expandability of the brain

With HIGH compliance

the brain’s

autoregulation is intact

and accommodating

changes in volume

With LOW compliance

the brain’s

compensation

mechanisms start to

fail.

Compliance

23

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Increased Intracranial Pressure (ICP)

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INCREASED

INTRACRANIAL PRESSURE:

25

Fig. 57-3. Progression of increased intracranial pressure (ICP).

25

• DEFINITION:

• LOC- A range of signs/symptoms from headache coma.

• Coma- a state of extreme unresponsiveness, in which an individual

exhibits no voluntary movement or behavior.

� SIGNIFICANCE:

� Level of consciousness is the most sensitive and reliable indicator of

the patient’s neurologic status.

� RAS (Reticular Activating System)

located in brain stem.

Damage to RAS can cause coma

ALTERED LEVEL OF CONSCIOUSNESS

(LOC) COMA

26

Personality and Behavioral Signs of

Increasing ICP

• Irritability, restlessness

• Drowsiness, indifference, decrease in physical

activity and motor skills

• Diminished physical activity

• Inability to follow commands, memory loss

• Lethargy and drowsiness

• YAWNING

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Late Signs of Increasing ICP• Decreased LOC

• Decreased motor response to command

• Decreased sensory response to painful stimuli

• Alterations in pupil size and reactivity

• Papilledema

• Decerebrate or decorticate posturing

• Cheyne-Stokes respirations

https://www.youtube.com/watch?v=DH2GElqrK8o

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COMPLICATIONS OF ICP

• In adequate cerebral perfusion

• Cerebral Herniation

29

• Rise in systolic BP

• Widening Pulse Pressure

• PP= SP - DS

• Bradycardia with a full bounding

pulse and altered respirations.

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*CUSHING’S TRIAD*

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LOCs

(in Descending Order)

↓Full consciousness

↓ Confusion: impaired decision

making

↓ Disorientation: to time and place

↓ Lethargy: sluggish speech

32

LOCs

(in Descending Order)—cont’d

↓ Obtundation: arouses with stimulation

↓ Stupor: responds only to vigorous and repeated

stimulation

↓ Coma: no motor or verbal response to noxious stimuli

↓ Persistent vegetative state: permanently lost function of

cerebral cortex

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� Assessment:

� Vigilant and frequent neuro-assessment is

mandatory.

� Change in affect, orientation, attention

� EEG: electroencephalogram

� Vital Signs

� Labs: CBC, CMP, PT-INR, PTT, Ammonia, Drug

Screen

� CSF for WBC, culture, protein and glucose

34

Diagnostics in Altered LOC

Neurologic Examination

• Vital signs

• Skin

• Eyes

• Motor function

• Posturing

• Reflexes

35

Coma Assessment• Glasgow Coma Scale

• Three-part assessment

• Eyes

• Verbal response

• Motor response

• Score of 15: unaltered LOC

• Score of 3: extremely decreased LOC (worst possible

score on the scale)

• LESS THAN 8 LESS THAN 8 LESS THAN 8 LESS THAN 8 –––– ComaComaComaComa----INTUBATEINTUBATEINTUBATEINTUBATE

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Fig. 51-1. Pediatric coma scale. 37

PE

DIA

TR

IC

Nursing Management: Increased Intracranial

Pressure (ICP)

38

Fig. 57-11. Pupillary check for size and response.

38

Fig. 51-2. Variations in pupil size with altered states of consciousness. A, Ipsilateral pupillary constriction with slight ptosis. B, Bilateral small pupils. C, Midposition, light fixed to all stimuli. D,Bilateral dilated and fixed pupils. E, Dilated pupils, left eye abducted with ptosis. F, Pinpoint pupils.

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Fig. 51-3. A, Flexion posturing. B, Extension posturing. 40

�ABC

� INJURY

�SKIN

�MUSCULOSKELETAL

�NUTRITIONAL

COMA CARE: PRIORITIES

41

ICP Monitoring

• Indications for ICP monitoring

• Glasgow Coma Scale of 8

• Glasgow Coma Scale <8 with

respiratory assistance

• Deteriorating neurologic condition

• Subjective judgment regarding clinical

appearance and response

42

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Methods of Measuring ICP

• Ventriculostomy

• Subarachnoid bolt (Richmond

screw)

• Fiberoptic Catheter

43

Increased Intracranial Pressure

(ICP)

44

44

Collaborative Therapy

�Elevation of head of bed to 30 degrees with head in a neutral

position

�Intubation and mechanical ventilation

�ICP monitoring

�Cerebral oxygenation monitoring (PbtO2, SjvO2)

�Maintenance of PaO2 ≥100 mm Hg

�Maintenance of fluid balance and assessment of osmolality

�Maintenance of systolic arterial pressure between 100 and

160 mm Hg

�Maintenance of CPP >60 mm Hg

�Reduction of cerebral metabolism (e.g., high-dose

barbiturates)45

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Collaborative Therapy

Drug therapy�Osmotic diuretic (mannitol)

�Hypertonic saline

�Antiseizure drugs (e.g., phenytoin [Dilantin])

�Corticosteroids (dexamethasone [Decadron]) for brain tumors,

bacterial meningitis

�Histamine (H2)-receptor antagonist (e.g., cimetidine

[Tagamet]) or proton pump inhibitor (e.g., pantoprazole

[Protonix]) to prevent GI ulcers and bleeding

46

MANNITOL

47

Oliguria, edema, ICP-Indications

Stops reabsorption of water

Mannitol

Output of urine, electrolytes-monitor

Tissue dehydration-UE

Increased urination

Circulatory overload - UE

HYPERTONIC SOLUTION

• D5NSS (5% Dextrose in normal saline solution)

•

D5 in 0.45% NaCl ( 5% Dextrose in half strength normal saline)

•D5LR (5% Dextrose in Lactated Ringer's Solution)

•

D10W ( 10% Dextrose in water)

•

D50W50 (50% Dextrose in 50 ml of water)

• 3% Saline

48

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CORTICOSTEROIDS

Side Effects:

�Cushing like syndrome (moon face, wasting of arms and legs, buffalo hump resulting from excess fat deposits.

�Weight gain

�Changes in Labs - Some People Get Cold (SPGC)

Sodium

Potassium

Glucose

Calcium

Education:

• Administer with food or milk

• Withdraw medicine slowly

• Avoid infections and large crowds

• Don’t take ASPIRIN without consulting physician first 49

BARBITURATES

• Pentobarbital {Nembutal}

• Thiopental { Pentothall}

50

Nursing Care of the Client with

Increased ICP

• Patient positioning

• Avoid activities that may increase ICP

• Eliminate or minimize environmental noise

• Suctioning issues

• Strict aseptic technique during dressing changes or sampling

of CSF is imperative to prevent infection With the ventricular

catheter in place

51

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Increased Intracranial Pressure

(ICP)

52

Fig. 57-9. A, Leveling a ventriculostomy. B, CSF is drained into a drainage system.52

• OXYGENATION

• FLUIDS

• METABOLIC DEMANDS

• OTHER INTERVENTIONS

Safety Alert

• Be alert to altered breathing patterns.

• Snoring sounds indicate obstruction and require immediate intervention.

IICP: INTERVENTIONS

53

Chapter 59 Chronic

Neurological Problems

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TYPES OF HEADACHES

• TENSION

• CLUSTER

• MIGRAINE

• LP/ POSTCONCUSSION

55

Headache

• Probably the most common type of pain

experienced by humans

• Majority of people have functional headaches

• Migraine or tension-type headaches

56

Pain Location for Common Headache

Syndromes

57Fig. 59-1. Location of pain for common headache syndromes.

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Tension-Type Headache

• Most common type

• Bilateral, band-like feeling of pressure around the head

• Constant, squeezing tightness

• Not aggravated by physical activity

Etiology and Pathophysiology

• Mechanism in all patients with tension-type headaches has neurovascular factors similar to those involved in migraine headaches.

58


Clinical Manifestations

• May involve sensitivity to light and sound

• May occur intermittently

• Can have combination of migraine and tension-

type headaches

59


Diagnostic Studies

• Careful history taking

• Electromyography (EMG) may be performed.

• May reveal sustained contraction of neck,

scalp, or facial muscles

• May not show increased tension even when test

is done during headache

60

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Gender Differences

MEN

• Cluster headaches are

more common than in

women (6:1).

• Exercise-induced

headaches are more

common than in women.

WOMEN

• Migraine headaches are

more common than in

men (3:1).

• Tension headaches are

more common than in

men.

61

Migraine Headache

• Recurring

• Characterized by unilateral or bilateral throbbing

pain

• Strong family history

• More common in females than males

• In United States, prevalence highest in those of

lower socioeconomic status

62

Migraine Headache


• Evidence suggests vascular, muscular, and

biochemical factors are involved.

• Exact cause is unknown.

• Can be preceded by an aura and prodrome

• May precede by days or hours

63

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Migraine Headache


• May be precipitated or triggered by

• Food

• Hormonal fluctuations (Post Partum)

• Head trauma

• Physical exertion

• Fatigue

• Stress

• Pharmacologic agents

64

Migraine Headache


• Subdivided into categories. Two most important are:

• Migraine with aura

• Migraine without aura

Signs/Symptoms

• Generalized edema

• Irritability

• Pallor

• Nausea, vomiting

• Sweating 65

Migraine Headache


• During headache, some patients “hibernate.”

• Seek shelter from noise, light, odors, people,

and problems

• Headache is described as steady, throbbing pain

that matches the pulse.

• Pain is usually unilateral but may switch to other

side in another episode.

66

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Migraine Headache

Diagnostic Studies

• No specific laboratory or radiologic tests

• Diagnosis is usually made from history.

• Neurologic and diagnostic examinations are

normal.

67

Cluster Headache

• Rare form of headache

• Characterized by repeated headaches that occur

for weeks or months at a time, followed by

periods of remission

• One of the most severe forms of head pain

68

68

Cluster Headache


• Neither cause nor pathophysiologic mechanism is

known.

• Extracranial vasodilation

occurs in affected part of face.

• Trigeminal nerve is

implicated.

69

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Cluster Headache


• Sharp stabbing

• Intense pain typically lasting from a few

minutes to 3 hours

• Pain is usually located around the eye,

radiating to the temple, forehead, cheek, nose,

or gums.

• Swelling around the eye, Constriction of the

pupil

• Facial flushing or pallor70

70

Cluster Headache


• During the headache, patient is often agitated and

restless.

• Headaches occur with regularity.

• Usually occur at same time of day

• Typically last daily for 2 weeks to 3 months, then

into remission for months or years

� Apply 6-8 liters O2 as a first priority.

71

71

Cluster Headache

Diagnostic Studies

• Diagnosis may be based primarily on

history.

• Headache diaries are helpful.

• CT scan, MRI, or MRA may be performed

to rule out aneurysm, tumor, or infection.

72

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Headache

Other Types

• Can be first symptom of a more serious illness

• Can accompany subarachnoid hemorrhage; brain

tumors; other intracranial masses; arteritis;

vascular abnormalities; trigeminal neuralgia;

diseases of the eyes, nose, and teeth; and

systemic illness

73

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As we consider drugs for headache, keep three basic principles

in mind:

• First, anti-headache drugs may be used in two ways…to abort an

attack or to prevent an attack.

• Second, not all patients with a particular type of headache

respond to the same drugs and therefore treatment must be

individualized.

• Third, several of the drugs employed to treat severe headaches

can cause physical dependence

The objective of abortive therapy is to eliminate

headache pain and suppress nausea and vomiting.

�Treatment should begin at the earliest sign of attack.

�Route: rectally, injection, inhalation.

�Drug selection depends on intensity of attack.

�Use of abortive meds should be limited to 1-2 days

per week.

Abortive Therapy

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Tension Headache

DRUG THERAPY• Aspirin

• Acetaminophen

• Nonsteroidal anti-inflammatory drugs (NSAIDS)

• Sedative

• Muscle relaxant

• Tranquilizer

Decrease Reoccurrence

�Tricyclic antidepressant (elavil, nortriptyline)

�Topiramate (topamax)

�Divalproex (depakote)

�Mirtazapine (Remeron) 76

• Used with severe migraine that has not responded to first-line

medications.

• Examples: Meperidine (Demerol),and Butorphanol (Stadol)

nasal spray.

• Disadvantages of Demerol versus Stadol:

• Adverse effects of Demerol are the 6 D’s

� Depressed respirations

� dizzy

� Drowsy

� Drug dependence

� Decreased blood pressure

� Decreased GI peristalsis & urine output

Opioid Analgesics

• Mechanism of action providing relief: unknown.

• Possible mechanism of action: act as serotonin agonists,

resulting in a vasoconstriction effect = decrease blood

flow to area and decreases painful pulsations. Also

possibly blocks inflammation.

• Therapeutic uses: drug of choice to stop an ongoing

migraine. Also used to treat cluster headaches that are

characterized by tearing, rhinnorhea, sharp on sided pain

from neck to temporal area.

• Risk of dependency…should not be taken on a daily basis

for a long time.

Ergot Alkaloids

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• Drug therapy to prevent migraines.

• Goal of therapy: to reduce the frequency and intensity

of migraine attacks.

• Indicated for patients who have not responded

adequately to abortive therapy and for patients whose

attacks are frequent or especially severe.

• Examples: beta blockers (Inderal used most often),

antiepileptic drugs (Depakote, Topramax), Tricyclic

(amitriptyline), Calcium Channel blocker (verapamil,

Calan), and estrogens (for menstrual migraines).

Preventive Therapy

Migraine Headache

Drug Therapy• NSAIDs

• Aspirin

• Caffeine-containing combination analgesics

� triptans have become the first line of therapy

� sumatriptan (Imitrex) affect selected serotonin receptors

Drug Alert

Sumatriptan (Imitrex)

• Should not be given to patients with the following:

•History or manifestations of ischemic cardiac, cerebrovascular, or peripheral vascular problems

•Uncontrolled hypertension, since it may increase blood pressure

• Excess dosage may produce tremor and decrease respirations. 80

�Therapeutic uses:

• To abort ongoing migraine attacks.

• Relieves pain, nausea, photophobia, phonophobia.

• Effects begin in 15 minutes after SC or IN, and 30-60 minutes

after PO

• 40% of patients have return of HA within 24 hours.

�Adverse effects:

• Generally well tolerated. Coronary vasospasm biggest concern.

• Sumatriptan should be avoided during pregnancy.

• Others include dizziness, malaise, vertigo, tingling, warm/hot

sensation, chest symptoms including heaviness, pressure,

tightness, angina, and injection site reaction.

Sumatriptan

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• Drug interactions:

• Do not give with any other drug causing vasoconstriction unless

discontinued for 24 hours.

• MAOI’s cause decreased metabolism of Imitrex, Zomig, and Maxalt.

Preparations:

prefilled SQ syringes

stat-dose pen

Oral/PO

Nasal spray

Sumatriptan

SUMATRIPTAN (IMITREX)

I schemic heart disease

Maoi’s may lead to MAOI toxicity

Iintial dose evaluate B/P 1 hr before and after administration

Teach to use adequate contraception during therapy

Remind to allow 1 hr between doses; no > than 2 doses in 24hrs

Evaluate EKG for changes if angina occurs

X outa migraine headache-not just to prevent headaches83

• Drug therapy to prevent migraines.

• Goal of therapy: to reduce the frequency and intensity

of migraine attacks.

• Indicated for patients who have not responded

adequately to abortive therapy and for patients whose

attacks are frequent or especially severe.

• Examples: beta blockers (Inderal used most often),

antiepileptic drugs (Depakote, Topramax), Tricyclic

(amitriptyline), Calcium Channel blocker (verapamil,

Calan), and estrogens (for menstrual migraines).

Preventive Therapy

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Beta Blocker Propranolol

BLOCKER – 5 B’s

BRADYCARDIA

BLOOD PRESSURE – TOO LOW

BRONCHIAL CONSTRICTION

BLOOD SUGAR – MASK LOW

BLOCKS (HEART) > 1ST DEGREE

85

Headache

Nursing Management

• Nursing assessment

• Health history

• Seizures, cancer, stroke, trauma, asthma or allergies, mental illness, stress, menstruation, exercise, food, bright lights, noxious stimuli

• Medications

• Surgery and other treatments

• Specific details about the headache

• Objective data

• Anxiety or apprehension

• Diaphoresis, pallor, unilateral flushing with cheek edema, conjunctivitis

86

86

Headache

Nursing Management

• Nursing diagnoses

• Acute pain

• Anxiety

• Hopelessness

87

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Headache

Nursing Management

• Planning

• Have decreased or no pain

• Experience increased comfort and reduced anxiety

• Demonstrate understanding of triggering events and treatment strategies

• Use positive coping strategies to deal with chronic pain.

• Experience ↑ quality of life88

88

Headache

Nursing Management

• Nursing implementation

• Daily exercise, relaxation, and socializing help

reduce recurrence.

• Suggest alternative pain management such as

relaxation, meditation, yoga, and self-hypnosis.

• Massage and heat packs.

• *Oxygen therapy for cluster headaches

89

89

Headache

Nursing Management

• Nursing implementation (cont’d)

• Patient should make a written note of

medications to prevent accidental overdose.

• Teach patient about prophylactic treatment.

• Dietary counseling for food triggers

• Avoid smoking and smoke exposure and other

environmental triggers.

90

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SEIZURES AND

SEIZURE DISORDER (EPILEPSY)

�DEFINITION : �Seizure: Paroxysmal, uncontrolled

electrical discharge of neurons in the brain, interrupting normal function.

�Epilepsy or seizure disorder : Is the condition in which a person has reoccurring seizures due to an underlying, chronic condition.

�PATHOLOGY : Causes can be intracranial,

extracranial, metabolic, and genetic.

RISK FACTORS

• Decreasing in children and increasing in

the elderly.

• Males are more likely to develop disorder

than females.

• Persons with traumatic brain injury and

stroke are at high risk.

Algorithm

Classification of Seizures

Fig. 59-2. Algorithm for classification of seizures.

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Seizures Phases

�Prodromal phase

�Aural phase

� Ictal phase

�Postictal phase

Absence Seizures• Formerly called petit mal or lapses

• Brief loss of consciousness

• Minimal or no change in muscle tone

**Almost always appear in childhood

(4 to 12 years old)

PARTIAL SEIZURE

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TONIC/CLONIC PHASES

Febrile Seizures

• Transient disorder of childhood

• Affect approximately 3% to 8% of children

• Usually occur between ages 6 months and

3 years

• Rare after age 5

• Twice as frequent in males

98

Complications � Status epilepticus is state of constant seizure or

condition when seizures recur in rapid

succession without return to consciousness

between seizures.

� Neurologic emergency

� Can involve any type of seizure

� Neurons become exhausted and cease to

function.

� Permanent brain damage can result.

�Other complications.

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Diagnostic Studies

� Table 59-7 Page 1422 Collaborative Care

� Accurate, comprehensive description of seizures

with patient’s health history

� EEG

� Labs

� Radiology

� MANAGEMENT

� Goals

� Principles of drug therapy

� Care during/after seizure

� Review Care Plans

Nursing AssessmentAssessment

1.Seizure history

2.Type of seizure

3.Occurrences before, during, and after the seizure

4.Prodromal signs, such as mood changes, irritability, and

insomnia

5.Aura: Sensation that warns the client of the impending

seizure

6.Loss of motor activity or bowel and bladder function or loss

of consciousness during the seizure

7.Occurrences during the postictal state, such as headache,

loss of consciousness, sleepiness, and impaired speech or

thinking

102

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Nursing Interventions1. Note the time and duration of the seizure.

2. Assess behavior at the onset of the seizure: If the client has experienced an aura, if a change in facial expression occurred, or if a sound or cry occurred from the client

3. If the client is standing or sitting, place the client on the floor and protect the head and body.

4. Support the ABCs—airway, breathing, and circulation.

5. Administer oxygen.

6. Prepare to suction secretions.

7. Turn the client to the side to allow secretions to drain while maintaining the airway.

8. Prevent injury during the seizure.

9. Remain with the client.

10. Do not restrain the client.

103

Nursing Interventions Cont’11. Loosen restrictive clothing.

12. Note the type, character, and progression of the movements during the seizure.

13. Monitor for incontinence.

14. Administer intravenous medications as prescribed to stop the seizure.

15. Document the characteristics of the seizure.

16. Provide privacy, if possible.

17. Monitor behavior following the seizure, such as the state of consciousness, motor ability, and speech ability.

18. Instruct the client about the importance of lifelong medication and the need for follow-up determination of medication blood levels.

19. Instruct the client to avoid alcohol, excessive stress, fatigue, and strobe lights.

20. Encourage the client to contact available community resources, such as the Epilepsy Foundation of America.

21. Encourage the client to wear a Medic-Alert bracelet.

104

If the client is having a seizure,

maintain a patent airway. Do

not force the jaws open or place

anything in the client’s mouth. 105

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Antiepileptic Drugs

107

108

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Therapeutic Goal: to reduce seizures to an extent that

allows the patient to live a normal/near normal life.

�Drugs can benefit 60-70% of patients.

�Noncompliance is a nursing problem because

treatment is continuous and not curative.

�Monitoring plasma drug levels

�Withdrawing antiepileptic drugs

Antiepileptic

Antiepileptic Drugs

Classifications:

• Traditional AED’s (such as Tegretol, Dilantin)

• Newer AED’s (such as Neurontin, Lyrica, Topamax)

KEY: Neither group is superior to the other, so drugs

from both groups must be considered when selecting

appropriate pharmacological therapy.

110

Phenytoin (Dilantin): Tonic-Clonic Seizures

• Most widely used AED. Used PO and IV.

• Suppresses seizures without depressing the entire CNS.

• Absorption varies greatly among patients…dosage must be highly individualized.

• Small changes in dosage can cause disproportionately large changes in serum drug levels, thus producing toxicity.

• Half-life varies in relation to dosage (lower dose has shorter half-life of 8 hours where a higher dose can have a half-life of up to 60 hours).

• Therapeutic uses: epilepsy, digoxin induced dysrhythmias.

Traditional Antiepileptic Drugs

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• At therapeutic levels (10-20), sedation and other CNS

symptoms are mild.

• At levels above 20, toxicity can occur with nystagmus,

sedation, ataxia, diplopia, and cognitive impairment.

• Others: gingival hyperplasia, skin rash, hypotension,

dysrhythmias, gastric upset.

• Must gradually withdraw drug.

Phenytoin (Cont.)

• Regular and meticulous mouth care.

• Narrow therapeutic index.

• IV administration: give slowly, do not add to an

existing IV solution, and flush before and after with NS.

• Recommended administration: 50 mg over 1 minute

or so. Giving faster may cause cardiovascular collapse

Phenytoin (Cont.)

NURSING Interventions�Tube feedings may interfere with the absorption of the enteral

form of phenytoin and diminish the effectiveness of the medication; therefore, feedings should be scheduled as far as possible away from the time of phenytoin administration.

�Monitor therapeutic serum levels to assess for toxicity.

�Monitor for signs of toxicity.

�When administering phenytoin intravenously, dilute in normal saline because dextrose causes the medication to precipitate.

�When administering phenytoin intravenously, infuse with an inline filter and no faster than 25 to 50 mg/minute; otherwise, a decrease in blood pressure and cardiac dysrhythmias could occur.

�Assess for ataxia (staggering gait).

�Instruct the client to consult with the HCP before taking other medications to ensure compatibility with anticonvulsants.

114

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DILANTIN

Gingival hyperplasia

Use alternate birth control

Mouth care-preventative dental

Soft toothbrush, don’t stop abruptly

115

Adverse effects of PHENYTOINP Plasma level monitoring needed because of its zero order

kinetics

H Hypertrophy of gums, can be minimized by good oral hygiene

E Enzyme induction so interacts with many drugs including other antiepileptics

N Neutropenia and other hypersensitivity reactions

Y Young girls beware! Causes hirsutism, coarsening of facial features and acne

T Teratogenic, married girls beware! Causes Fetal HydantoinSyndrome

O Osteomalacia due to interference with calcium absorption

I Interference with folate absorption leads to megaloblastic anemia

N Neurological manifestations at higher doses: Ataxia, vertigo, headache and nystagmus

116

117

Phenytoin must be given slowly to

prevent hypotension and cardiac

dysrhythmias. Also, it may decrease the

effectiveness of some birth control pills

and may cause teratogenic effects, if

taken during pregnancy.

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• Used to treat tonic-clonic, and partial but not absence. Also can be used in treatment of bipolar disease and neuralgias.

• Therapeutic levels: 5-12

• Adverse effects:

• Bone marrow suppression (rare) such as aplastic anemia, leukopenia, anemia, thrombocytopenia, agranulocytosis.

• Birth defects (cleft palate, growth retardation).

• Hypo-osmolarity

• Photosensitivity, rash, SJS

Carbamazepine (Tegretol)

Stevens–Johnson Syndrome

119

Adverse effects (Cont.)

• Minimal effect of cognitive ability

• Others: visual disturbances, ataxia, vertigo, unsteadiness, HA especially in the first weeks of treatment with tolerance developing with continued use.

• Grapefruit juice can increase the peak and trough levels by 40%!

Carbamazepine (Tegretol)

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TEGRETOL

Trigeminial neuralgia, tonic clonic seizures

Evaluate for anorexia, nausea, dizziness sedation, HA, sore throat

Give with food, milk to GI distress

Review levels, maintain 4-12mcg/ml

Evaluate for anorexia-indicate toxic level

Tablet-chewable, do not swallow whole

Open & mix with food (extended capsule)

Look for other drug interactions 121

122

• Used to treat all major seizure types.

• Widely used.


• GI upset is common (transient N/V) so take with food or use enteric coated formulation.

• Severe adverse effects are limited to rare cases of severe hepatotoxicity (usually first few months of therapy and in children less than 2 years old)and pancreatitis (soon after starting or years later).

Valproic Acid (Depakote,

Depakene)

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• Valproic acid is highly teratogenic.

• Hyperammonemia (if combined with Topamax).

• Will also potentiate levels of Dilantin and phenobarbital.

• Others: (not common) rash, weight gain, hair loss,

tremor, blood dyscrasias)

• Also used to treat bipolar disorder and prevention of

migraine.

Valproic Acid (Depakote,

Depakene) (Cont.)

125

Adverse effects of VALPROICV Vomiting, Nausea

A Alopecia

L Liver toxicity (Hepatoxicity)

P Pancreatitis

R Rashes & thrombocytopenia are rare

hypersensitivity reactions

O Oedema

I Ingestion

C Cell count will decrease, platelet & wbc =

Blood Dyscrasias

• One of our oldest drugs used for epilepsy.


• Unfortunately, can cause significant lethargy, depression,

learning impairment.

• Largely replaced by newer drugs.

Phenobarbital (Luminal)

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Adverse effects: drowsiness (tolerance will develop),

depression, confusion and agitation in the elderly, physical

dependence.

• When phenobarbital is withdrawn, dosage should be

reduced gradually.

• If administering IV, give slowly. If done too fast, excessive

CNS depression may result.

• Monitor BP during IV infusion.

Phenobarbital (Luminal)

(Cont.)

Antiseizure Medications

128

• Better tolerated.

• Smaller risk to developing fetus.

• Examples: Trileptal, Topamax, Keppra, Lamictal,

Neurontin, Lyrica.

• Most recommended for adjunctive therapy versus

monotherapy (Trileptal/monotherapy).

Newer Antiepileptic Drugs

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• Lyrica also widely used for neuropathic pain and

fibromyalgia.

• Unlike most other anti-seizure agents, Lyrica is regulated

under the Controlled Substance Act (schedule V).

Newer Antiepileptic Drugs (Cont.)

Benzodiazepines

Benzodiazepines are used to treat absence seizures.

�Clonazepam (Klonopin)

�Clorazepate (Tranxene)

�Diazepam (Valium)

�Lorazepam (Ativan)

Side/adverse effects

a. Sedation, drowsiness, dizziness, blurred vision

b. For intravenous injection, administer slowly to prevent bradycardia.

c. Medication tolerance and drug dependency

d. Blood dyscrasias: Decreased platelet count and decreased white blood cell count

e. Hepatotoxicity

131

132

Flumazenil (Romazicon) reverses

the effects of benzodiazepines. It

should not be administered to

clients with increased intracranial

pressure or status epilepticus who

were treated with benzodiazepines

because these problems may recur

with reversal.

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DEGENERATIVE DISEASES

• CHARACTERISTICS

�MS

�Parkinson’s

�Myasthenia Gravis

133

MULTIPLE SCLEROSIS

• ETIOLOGY/PATHOPHYSIOLOGY

134

MS: MYELIN LOSS

135

� Initially, the myelin sheaths of the neurons in the brain

and spinal cord are attacked, but the nerve fiber is not

affected.

� Patient may complain of noticeable impairment of

function.

� Myelin can be replaced by glial scar tissue.

� Nerve impulses slow down without myelin.

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Risk Factors for Multiple

Sclerosis�Infection

�Smoking

�Physical injury

�Emotional stress

�Excessive fatigue

�Pregnancy

�Poor state of health

�Pathogenic agents(controversial)

136

137

Early Multiple Sclerosis

Diagnosis

138

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MRI of the Brain/MS Plaque

139

MRI of the Brain Scan

140

Chronic Multiple Sclerosis

141

141

Fig. 59-4. Chronic multiple sclerosis. Demyelination plaque (P) at gray-white junction and

adjacent partially remyelinated shadow plaque (V).

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142

Multiple Sclerosis

143

144

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• Common signs and symptoms include

�Motor problems

• Weakness or paralysis of limbs, trunk, and head

• Diplopia

• Scanning speech

• Spasticity of muscles

�Sensory problems

• Numbness and tingling

• Blurred vision

• Vertigo and tinnitus

• ↓ hearing

• Chronic neuropathic pain 145

Clinical Manifestations�Cerebellar problems

• Nystagmus

• Ataxia

• Dysarthria

• Dysphagia

�Cognitive problems

• Short-term memory attention

• Information processing

• Visual perception

• Word finding

�Emotional problems

• Anger

• Depression

• Euphoria

� Other Physical

�Spastic bladder, retention or flaccid bladder may occur

Diagnostic Testing

• Based primarily on history, clinical

manifestations, and presence of multiple lesions

over time measured by MRI

• Cerebral spinal fluid (CSF) analysis

• ↑ in oligoclonal immunoglobulin G

• Contains higher numbers of lymphocytes and

monocytes

147

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DRUG THERAPYThe initial treatment of MS is the use of immunomodulator drugs to modify the disease progression and prevent relapses.

β-Interferon

�Avonex*

�Betaseron*

�Rebif*

�Copaxone

�Aubagio

** Drug Alert

• Rotate injection sites with each dose.

• Assess for depression, suicidal ideation.

• Wear sunscreen and protective clothing while exposed to sun.

• Know that flu-like symptoms are common after initiation of therapy.

148

Drug Therapy for Active and

Aggressive forms of MS

�Tysabri (Natalizumab)

�Novantrone (Mitoxantrone)

149

150

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Drugs for Symptom

ManagementCholinergics� bethanechol (Urecholine)

� neostigmine (Prostigmin)

Anticholinergics� propantheline (Pro-Banthine)

� oxybutynin (Ditropan)

Muscle Relaxants� diazepam (Valium)

� baclofen (Lioresal)

� dantrolene (Dantrium)

� tizanidine (Zanaflex)

151

Anticholinergic Medications

152

Cholinergic Overdose

This is an example of a mnemonic that is commonly used in the

real world to diagnose cholinergic overdose

Diarrhoea

Urination

Miosis/muscle weakness

Bronchorrhea

Bradycardia

Emesis

Lacrimation

Salivation/sweating 153

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Nursing Assessment

Subjective data

�Health history

�Viral infections or vaccinations

�Residence in cold or temperate climates

�Physical and emotional stress

�Medications

�Elimination problems

�Weight loss, dysphagia

�Anger, depression, euphoria, isolation

�Presence of frequent UTI or incontinence154

154

Nursing Assessment

Objective Data:

�Apathy, inattentiveness

�Pressure ulcers

�Scanning speech

�Tremor

�Nystagmus

�Ataxia

�Spasticity

155

155

Nursing Assessment

Objective Data (con’t):

�Hyperreflexia

�↓ hearing

�Muscular

�Weakness

�Paresis

�Paralysis

�Foot dragging

�Dysarthria 156

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Managing Relapse of MS

The most common treatment regimen is:

� a three-to-five-day course of high-dose

�intravenous corticosteroids to reduce inflammation and end

the relapse more quickly (Solu-Medrol)

�followed with a slow taper of oral prednisone (Deltasone)

�H.P. Acthar Gel

• Given to PATIENTS who are unable to cope with the side effects of

high-dose corticosteroids,

• have been treated unsuccessfully with corticosteroids

• do not have access to intravenous therapy

• have trouble receiving medication intravenously because of

difficulty accessing the veins.157

Nursing Diagnosis, Planning and

Implementation

�Impaired physical mobility

�Impaired urinary elimination

�Interrupted family processes

�Ineffective self-health management

158

PARKINSON’S DISEASE

159

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• Diagnosis increases with age, with peak onset in the seventh decade.

• More common in men, ratio of 3:2

• Other causes of parkinsonism

• Encephalitis lethargica (type A encephalitis) has been associated with onset.

• Incidence has dwindled since 1920s.

• Symptoms have occurred after intoxication with a variety of chemicals.

160

Parkinson’s Disease (PD)

• Disease of basal ganglia

characterized by

• Slowing down in the initiation and execution

of movement

• ↑ muscle tone

• Tremor at rest

• Gait disturbance

161

162

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• Onset is gradual and insidious.

• Classic triad of PD

• Tremor

• Rigidity

• Bradykinesia

• Beginning stages may involve only mild tremor, slight limp, or ↓ arm swing.

• Later stages may have shuffling, propulsive gait with arms flexed, and loss of postural reflexes.

163


�Tremor

�So minimal initially that only the patient may

notice it

�More prominent at rest and is aggravated by

emotional stress or ↑ concentration

�Described as pill rolling because thumb and

forefinger appear to move in rotary fashion

�Benign essential tremor, which occurs during

voluntary movement, has been misdiagnosed as

Parkinson’s disease (PD). 164


• Rigidity

• Increased resistance to passive motion.

• Typified by a jerky quality when the joint

is moved.

Caused by sustained muscle contraction and consequently

elicits the following:

• Complaint of soreness

• Feeling tired and achy

• Pain in the head, upper body, spine, or legs

• Inhibits the alternating contraction and relaxation in

opposite muscle groups.165

165

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PARKINSON’S: HANDWRITING

CHANGES NOTED:

Cramped

Shaky, especially with upward strokes

166


• Bradykinesia

• Slowing down in initiation and execution of

movement

• Evident in loss of autonomic movements

• Blinking

• Swinging of arms while

walking

• Swallowing of saliva

• Self-expression with facial movements

167

167

Appearance of Patient With PD

168

168

Fig. 59-9. Characteristic appearance of a patient with Parkinson’s disease.

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Complications

• Non-motor symptoms

• Depression

• Anxiety

• Impotence

• Short-term memory

impairment

• Sleep disorders are common and potentially

severe.

• Effective management of sleep disturbances can

greatly improve quality of life. 169

169

• Apathy

• Fatigue

• Pain

• Constipation

Complications

• As disease progresses, complications increase

�Motor symptoms

�Weakness

�Akinesia

�Neurologic problems

�Neuropsychiatric problems

• Dementia occurs in 40% of patients.

170

Complications

• Dysphagia may result in malnutrition and

aspiration.

• General debilitation may lead to

pneumonia, UTIs, and skin breakdown.

• Orthostatic hypotension may occur.

• Could result in falls and injuries171

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NOW…

• A CLIENT IS

DIAGNOSED WITH

PARKINSON’S

DISEASE. WHAT

PROBLEMS DO

YOU ANTICIPATE?

172

Diagnostic Tests

• No specific tests

• Diagnosis based solely on history and

clinical features

• Firm diagnosis can be made when at least

two of three characteristics of the classic

triad (tremor, rigidity, and bradykinesia)

are present.

173

173

174

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59

Collaborative Care

Drug Therapy

• Aimed at correcting imbalances of

neurotransmitters within the CNS

• Antiparkinsonian drugs either

�Enhance or release supply of DA

�Antagonize or block the effects of overactive

cholinergic neurons in the striatum

• Levodopa with carbidopa (Sinemet) is often the

first drug used.

175

175

Collaborative Care

Drug Therapy

• Anticholinergics are also used in management.

�↓ activity of acetylcholine

• Antihistamines with anticholinergic or β-adrenergic blockers are used to manage tremors.

• Antiviral agent amantadine is effective, although exact mechanism is unknown.

• MAO-B inhibitors, selegiline, and rasagiline (Azilect) may be combined with Sinemet.

• Entacapone and tolcapone block the enzyme that breaks down levodopa in the peripheral circulation.�Prolong the effects of Sinemet 17

6

176

Collaborative Care

Drug Therapy

• Within 3 to 5 years of treatment, patients experience episodes of hypomobility.

• Treated with apomorphine (Apokyn)

�MUST NOT BE taken with an antiemetic drug

• Aricept is used to treat Parkinson’s dementia.

• Elavil may be used to treat depression. 177

177

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Nursing Interventions

1. Assess neurological status.

2. Assess ability to swallow and chew.

3. Provide high-calorie, high-protein, high-fiber soft diet with

small, frequent feedings.

4. Increase fluid intake to 2000 mL/day.

5. Monitor for constipation.

6. Promote independence along with safety measures.

7. Avoid rushing the client with activities.

8. Assist with ambulation and provide assistive devices.

9. Instruct the client to rock back and forth to initiate

movement. 178

Nursing Interventions Cont’d10. Instruct the client to wear low-heeled shoes.

11. Encourage the client to lift feet when walking and to avoid prolonged sitting.

12. Provide a firm mattress and position the client prone, without a pillow, to facilitate proper posture.

13. Instruct in proper posture by teaching the client to hold the hands behind the back to keep the spine and neck erect.

14. Promote physical therapy and rehabilitation.

15. Administer antiparkinsonian medications to increase the level of dopamine in the CNS.

16. Instruct the client to avoid foods high in vitamin B6 because they block the effects of antiparkinsonian medications.

17. Instruct the client to avoid monoamine oxidase inhibitors because they will precipitate hypertensive crisis.

179

Parkinson’s Disease• Goal of treatment: to improve the patients

ability to carry out activities of daily living.

• Drugs do not cure, but will treat symptoms

of the disorder.

• Two types of agents used for this:

• Dopaminergic agents (drugs that either

directly or indirectly activate dopamine

receptors).

• Anticholinergic Agents (drugs that block

receptors for acetylcholine).

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Levodopa• Introduced in 1960’s

• Stimulates dopamine production or increases sensitivity of dopamine receptors.

• A “prodrug”: no effect orally until it is converted to dopamine once in the body. This process is facilitated by an enzyme decarboxylase and enhanced by pyridoxine (vitamin B6).

• Very effective (if drug not effective, diagnosis of Parkinson's disease should be questioned).

• Beneficial effects diminish over time.

• Most troubling side effect: dyskinesias.

• Full therapeutic effects may take several weeks or months (6) to develop. Patients should be informed that beneficial effects are likely to increase steadily over the first few months.

• Symptoms usually well controlled for 2 years; at end of 5 years, back to pretreatment level (one reason it is reserved for patient’s that have been treated with other agents in the initial stages of Parkinson’s).

Levodopa continues…Acute loss of effect:

• Occurs in 2 patterns:

• 1. Gradual loss – “wearing off”

developing near the end of the dosing

interval when drug levels have declined

to a sub therapeutic level. May be

minimized by shortening the dosing

interval, and giving a drug that prolongs

levodopa’s half-life (Comtan), and giving a

direct-acting dopamine agonists

(Mirapex, Requip, Parlodel).

Levodopa….2. Abrupt loss of effect

• Often referred to as the “on-off” phenomenon.

• Can occur at any time during the dosing interval.

• “Off” times may last from minutes to hours and are

likely to increase in both intensity and frequency as

treatment continues.

• The patient has and abrupt loss of effect.

• Avoiding high-protein meals may help (amino acids

compete with levodopa for intestinal absorption)

(page 185).

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Levodopa…

Drug holiday:

• Defined as a brief (i.e.10 day) interruption

of treatment.

• When holiday is successful, beneficial

effects are achieved with lower doses, and

therefore the incidence of dyskinesias and

psychosis is lowered as well.

• Drug holidays do not eliminate “off” times.

• These holidays are dangerous and must

take place in a hospital.

Levodopa….Adverse effects:

• Nausea and vomiting: common. May be helped if administered with food

(watch protein).

• Dyskinesias: in 80% of patients..Ironic. Develop just before or soon after

optimal levodopa dosage has been achieved. May be head bobbing, tics,

grimacing, or ballismus (uncoordinated swinging of the limbs and jerky

movements), choreoathetosis (irregular involuntary movements giving the

appearance of restlessness).

• CV effects: postural hypotension (especially early in treatment. May be

helped by increasing intake of salt and water, or by an alpha-adrenergic

agonists).

• Psychosis (manifested initially by hallucinations): in 20% of patients. May

be reduced by lowering dosages, but this will also decrease beneficial

effects too. Clozaril and Seroquel used to treat symptoms. Why wouldn’t

traditional antipsychotics be used???

• Others: dark sweat and urine (harmless but patients need to be told),

activation of malignant melanoma and therefore should be avoided in

patients with undiagnoses skin lesions.

Levodopa/Carbidopa

• Brand names: Sinemet and Paracopa .

• Combination of levodopa and carbidopa.

• The addition of carbidopa results in the most effective

therapy for PD..much more effective than levodopa

alone.

• Carbidopa enhances the effects of Levodopa by

increasing the amounts of dopamine available in the

brain. How?? By inhibiting peripheral conversion of

dopamine in the periphery, more levodopa will be

converted to dopamine in the brain.

• Carbidopa has no effect on its own.

• Vitamin B6 not a problem.

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Levodopa/Carbidopa

Advantages:

• Because carbidopa increases levels of dopamine in

the brain, dosages of levodopa can be reduced by

about 75%.

• Cardiovascular responses to levodopa are reduced

as well as nausea and vomiting.

• By causing direct inhibition of decarboxylase,

carbidopa eliminates concern about decreasing the

effects of levodopa by taking vitamin preparations

that contain vitamin B6.

Dopamine Agonists• Act to directly activate dopamine receptors in the brain.

• For patients with mild or moderate symptoms, these are drugs

of first choice.

• Advantages: not dependent on conversion by enzymes to be

active, don’t compete with dietary proteins, lower incidence

of response failures, and are less likely to cause disabling

dyskinesias.

• Disadvantage: cause more serious SE’s, like hallucinations,

day-time sleepiness, and postural hypotension.

• Usually reserved for younger patients, who tolerate their side

effects better than do the elderly.

• Examples: Mirapex, Requip, Permax, Parlodel.

Dopamine Agonist

Renal impairment

Extrapyramidal symptoms

Seeing things (hallucinations)

Thirsty (dry mouth)

Lethargy

Express concern of falling asleep during activity

Sickness (nausea)

Stuck up (constipation) 189

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Other agents used to treat Parkinson’s

Disease• Anticholinergic agents: Cogentin, Artane (how would these

work and what would be their side effects????). Used for

younger patients with mild symptoms. Usually avoided in the

elderly because of CNS side effects (sedation, confusion,

hallucinations).

• Antiviral agent: Symmetrel (not considered a first-line drug

because responses begin to diminish within 3-6 months).

• MAO-B inhibitor: Eldepryl (MOA remember inactivates

catecholamine's in the brain, such as dopamine).

Collaborative Care

• Surgical therapy

• Procedures aimed at relieving symptoms

• Used in patients who are usually unresponsive to drug therapy or have developed severe motor complications

• Ablation surgery

• Has been used to treat PD for over 50 years

• But has been recently replaced by deep brain stimulation (DBS) 19

1

191

Collaborative Care

• Deep brain stimulation

�Involves placing an electrode in the thalamus,

globus pallidus, or subthalamic nucleus

�Connected to a generator placed in the upper chest

�Device is programmed to a to deliver specific

current to targeted brain

location.

192

192

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Collaborative Care

• Transplantation of fetal neural tissue into the basal

ganglia provides DA-producing cells in the brains

of patients.

�Still in experimental stages

193

193

Collaborative Care

• Nutritional therapy

�Malnutrition and constipation can be serious

consequences.

�Patients with dysphagia and Bradykinesia need

food that is easily chewed and swallowed.

�Adequate roughage

194

194

NURSING CARE OF THE CLIENT

WITH PD: MOBILITY

• PROMOTE EXERCISE

• MAINTAIN SAFETY

• USE ADAPTIVE DEVICES

195

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NURSING CARE OF THE CLIENT

WITH PD: NUTRITION

• AID SWALLOWING

• OFFER APPROPRIATE FOODS

• USE ADAPTIVE DEVICES

196

197

MYASTHENIA GRAVIS

• DEFINITION

• INCIDENCE

• PATHOLOGY

• MANIFESTATIONS

198

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MG: BLOCKED RECEPTORS

199

Myasthenia Gravis

200

200

Fig. 59-9. “Peek” sign in myasthenia gravis. During sustained forced eyelid closure he is unable

to bury his eyelashes (left) and, after 30 seconds, he is unable to keep the lids fully closed (right).


• Weakness and fatigue

• Difficulty chewing and swallowing

• Dysphagia

• Ptosis

• Diplopia

• Weak, hoarse voice

• Difficulty breathing

• Diminished breath sounds

• Respiratory paralysis and failure201

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HORNER’S SYNDROME

• Unilateral:

• Ptosis

• Tearing

• Rhinitis

• Pupillary constriction202

MYASTHENIA GRAVIS

• DIAGNOSIS

• H & P

• Sustained force test

• Labs

• EMG

203

Tensilon (edrophonium chloride) Test

• The Tensilon test is an injection.

• Tensilon blocks the action of acetylcholinesterase.

• To stimulate a muscle, a nerve cell (neuron) releases

acetylcholine.

• To prevent prolonged muscle response to a single nerve signal,

acetylcholine is broken down by acetylcholinesterase after the

muscle is stimulated.

• The Tensilon test involves the IV injection of a small amount

of Tensilon.

• The needle is left in place. If no adverse reaction is observed

within 30 seconds, an additional volume is injected.

• Results are apparent within one minute.204

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205

Anticholinesterase drugs

Prostigmin

Mestinon

Mytelase

Corticosteroids

206

MYASTHENIA GRAVIS:

FOCUS ON TEACHING

• MEDICATION

• SAFETY

• LIFESTYLE ADJUSTMENTS

• CRISIS MANAGEMENT

207

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MYASTHENIA GRAVIS:

CRISIS MANAGEMENT

• MYASTHENIC CRISIS

• An acute ↑ in requirement for anticholinesterase therapy

• Symptoms

• Response

• CHOLINERGIC CRISIS

• An acute ↓ in the need for anticholinesterase medication

• Symptoms

• Response 208

Assessment of MG Crisis

�Increased pulse, respirations, and blood

pressure

�Dyspnea, anoxia, and cyanosis

�Bowel and bladder incontinence

�Decreased urine output

�Absent cough and swallow reflex

209

Cholinergic Crisis

a. Abdominal cramps

b. Nausea, vomiting, and diarrhea

c. Blurred vision

d. Pallor

e. Facial muscle twitching

f. Hypotension

g. Pupillary miosis210

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Cholinergic Overdose

This is an example of a mnemonic that is commonly used in the

real world to diagnose cholinergic overdose

Diarrhoea

Urination

Miosis/muscle weakness

Bronchorrhea

Bradycardia

Emesis

Lacrimation

Salivation/sweating211

Edrophonium test

Have atropine sulfate available

when performing the Tensilon test.

212

Nursing Interventions

1. Monitor respiratory status and ability to cough

and deep-breathe adequately.

2. Monitor for respiratory failure.

3. Maintain suctioning and emergency equipment

at the bedside.

4. Monitor vital signs.

5. Monitor speech and swallowing abilities to

prevent aspiration.

6. Encourage the client to sit up when eating.

7. Assess muscle status.

213

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Nursing Interventions8. Instruct the client to conserve strength.

9. Plan short activities that coincide with times of

maximal muscle strength.

10. Monitor for myasthenic and cholinergic crises.

11. Administer anticholinesterase medications as

prescribed.

12. Instruct the client to avoid stress, infection,

fatigue, and over-the-counter medications.

13. Instruct the client to wear a Medic-Alert

bracelet.

14. Inform the client about services from the

Myasthenia Gravis Foundation.

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THE DIEASES MS, PD, AND MG ALL

INVOLVE MOVEMENT PROBLEMS

215

� MS: Demyelination of nerve fibers of

the brain and spinal cord

� PD: Degeneration of dopamine

producing neurons in the substantia

nigra

� MG: Reduction in the number of these

receptor sites for acetylcholine

Myasthenia Gravis• Cholinestrerase: Reversible cholinesterase inhibitors are

the mainstay of therapy.

• Prevent ACh inactivation, anticholinesterase agents can

intensify the effects of ACh released from motor

neurons, and can thereby increase muscle strength.

• Cholinesterase inhibitors do not cure MG. Rather, they

only produce symptomatic relief, and hence patients

usually need therapy lifelong.

11/7/2016

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Myasthenia Gravis (Cont.)Most commonly used:

� Ambenonium

� Neostigmine

� Pyridostigmine

• Route: PO, IM, SQ, IV & Topical

• Side Effects:

� Causes ACh to accumulate at muscarinic junctions

�If muscarinic responses are excessive, atropine may be

given to suppress them.

�Atropine should not be employed routinely.

�Atropine can mask the early signs (eg, excessive

salivation) of overdose with anticholinesterase agents.

QUESTIONS

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MODULE G SECTION 1 Nervous System

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