Nursing management of patient with chronic neurological problems

NURSING MANAGEMENT OF
PATIENT WITH CHRONIC
NEUROLOGICAL PROBLEMS
PARKINSON’S DISEASE
MYASTHENIA GRAVIS
GBS
MATHEW VARGHESE V
MSN(RAK),FHNP (CMC Vellore),CPEPC
Nursing officer
AIIMS Delhi
1
mathewvmaths@yahoo.co.in

PARKINSON’S DISEASE
 Parkinson's disease is a progressive nervous
system disorder that affects movement. Symptoms
start gradually, sometimes starting with a barely
noticeable tremor in just one hand. Tremors are
common, but the disorder also commonly causes
stiffness or slowing of movement.
 In the early stages of Parkinson's disease, your
face may show little or no expression. Your arms
may not swing when you walk. Your speech may
become soft or slurred. Parkinson's disease
symptoms worsen as your condition progresses
over time.
2

EPIDEMIOLOGY:
 Parkinson disease occurs worldwide and is present
in all races.
 Males are more affected than females.
 Prevention of Parkinson disease increase with
increasing age of 1% of person from age 60.
 It starts between 21 -40 years of age affecting 5 to
10% of Parkinson disease patients.
 China is the country world largest prevalence of
Parkinson disease.
 The incidence and prevalence of Parkinson disease
in India is lesser as compared to other country,
Rural population had a higher prevalence than
urban population 41:14.
3

DEFINITION
 Parkinson disease is characterized by tremor at
rest, rigidity and slowness or difficulty in
initiating and executing movement (Akinesis or
Bradykinesis). This combination of clinical
features is collectively known as Parkinsonism.
 Parkinsonism is a syndrome with numerous
causes of which Parkinson disease is the most
common.
4

CAUSES
 Genes. Researchers have identified specific
genetic mutations that can cause Parkinson's
disease. But these are uncommon except in rare
cases with many family members affected by
Parkinson's disease.
 However, certain gene variations appear to
increase the risk of Parkinson's disease but with a
relatively small risk of Parkinson's disease for each
of these genetic markers.
 Environmental triggers. Exposure to certain
toxins or environmental factors may increase the
risk of later Parkinson's disease, but the risk is
relatively small 5

RISK FACTORS
 Age. Young adults rarely experience Parkinson's
disease. It ordinarily begins in middle or late life, and the
risk increases with age. People usually develop the
disease around age 60 or older.
 Heredity. Having a close relative with Parkinson's
disease increases the chances that you'll develop the
disease. However, your risks are still small unless you
have many relatives in your family with Parkinson's
disease.
 Sex. Men are more likely to develop Parkinson's
disease than are women.
 Exposure to toxins. Ongoing exposure to herbicides
and pesticides may slightly increase your risk of
Parkinson's disease.
6

DIAGNOSIS
 No specific test exists to diagnose Parkinson's disease.
 Your doctor trained in nervous system conditions
(neurologist) will diagnose Parkinson's disease based
on your medical history, a review of your signs and
symptoms, and a neurological and physical
examination.
 Your doctor may suggest a specific single-photon
emission computerized tomography (SPECT) scan
called a dopamine transporter scan (DaTscan
 Your doctor may order lab tests, such as blood tests, to
rule out other conditions that may be causing your
symptoms.
10

DIAGNOSIS
 Imaging tests — such as an MRI, ultrasound of the
brain, and PET scans — also may be used to help
rule out other disorders..
 In addition to your examination, your doctor may
give you carbidopa-levodopa (Rytary, Sinemet,
others), a Parkinson's disease medication.
 Sometimes it takes time to diagnose Parkinson's
disease. Doctors may recommend regular follow-up
appointments with neurologists trained in
movement disorders to evaluate your condition and
symptoms over time and diagnose Parkinson's
disease. 11

COMPLICATIONS
 Parkinson's disease is often accompanied by these
additional problems, which may be treatable:
 Thinking difficulties. .
 Depression and emotional changes. ..
 Swallowing problems. .
 Chewing and eating problems. .
 Sleep problems and sleep disorders.
 Bladder problems. .
 Constipation. :
 Blood pressure changes.
 Smell dysfunction.
 Fatigue.
 Pain.
 Sexual dysfunction. 12

TREATMENT
MEDICATIONS
 Carbidopa-levodopa. Levodopa, the most effective
Parkinson's disease medication, is a natural chemical that
passes into your brain and is converted to dopamine.
 Levodopa is combined with carbidopa (Lodosyn), which
protects levodopa from early conversion to dopamine outside
your brain. This prevents or lessens side effects such as
nausea.
 Side effects may include nausea or lightheadedness
(orthostatic hypotension).
 After years, as your disease progresses, the benefit from
levodopa may become less stable, with a tendency to wax
and wane ("wearing off").
 Also, you may experience involuntary movements
(dyskinesia) after taking higher doses of levodopa. Your
doctor may lessen your dose or adjust the times of your doses
to control these effects.
13

MEDICATIONS
 Inhaled carbidopa-levodopa. Inbrija is a new brand-name
drug delivering carbidopa-levodopa in an inhaled form. It may
be helpful in managing symptoms that arise when oral
medications suddenly stop working during the day.
 Carbidopa-levodopa infusion. Duopa is a brand-name
medication made up of carbidopa and levodopa. However, it's
administered through a feeding tube that delivers the
medication in a gel form directly to the small intestine.
 Duopa is for patients with more-advanced Parkinson's who
still respond to carbidopa-levodopa, but who have a lot of
fluctuations in their response. Because Duopa is continually
infused, blood levels of the two drugs remain constant.
 Placement of the tube requires a small surgical procedure.
Risks associated with having the tube include the tube falling
out or infections at the infusion site.
14

MEDICATIONS
 Dopamine agonists. Unlike levodopa, dopamine agonists
don't change into dopamine. Instead, they mimic dopamine
effects in your brain.
 They aren't as effective as levodopa in treating your
symptoms. However, they last longer and may be used with
levodopa to smooth the sometimes off-and-on effect of
levodopa.
 Dopamine agonists include pramipexole (Mirapex), ropinirole
(Requip) and rotigotine (Neupro, given as a patch).
Apomorphine (Apokyn) is a short-acting injectable dopamine
agonist used for quick relief.
 Some of the side effects of dopamine agonists are similar to
the side effects of carbidopa-levodopa. But they can also
include hallucinations, sleepiness and compulsive behaviors
such as hypersexuality, gambling and eating. If you're taking
these medications and you behave in a way that's out of
character for you, talk to your doctor. 15

MEDICATIONS
 MAO B inhibitors. These medications include selegiline
(Zelapar), rasagiline (Azilect) and safinamide (Xadago).
They help prevent the breakdown of brain dopamine by
inhibiting the brain enzyme monoamine oxidase B (MAO
B). This enzyme metabolizes brain dopamine. Selegiline
given with levodopa may help prevent wearing-off.
 Side effects of MAO B inhibitors may include
headaches, nausea or insomnia. When added to
carbidopa-levodopa, these medications increase the risk
of hallucinations.
 These medications are not often used in combination
with most antidepressants or certain narcotics due to
potentially serious but rare reactions. Check with your
doctor before taking any additional medications with
an MAO B inhibitor.
16

MEDICATIONS
 Catechol O-methyltransferase (COMT)
inhibitors. Entacapone (Comtan) is the primary
medication from this class. This medication mildly
prolongs the effect of levodopa therapy by blocking
an enzyme that breaks down dopamine.
 Side effects, including an increased risk of
involuntary movements (dyskinesia), mainly result
from an enhanced levodopa effect. Other side
effects include diarrhea, nausea or vomiting.
 Tolcapone (Tasmar) is another COMT inhibitor that
is rarely prescribed due to a risk of serious liver
damage and liver failure. 17

MEDICATIONS
 Anticholinergics. These medications were used for many
years to help control the tremor associated with Parkinson's
disease. Several anticholinergic medications are available,
including benztropine (Cogentin) or trihexyphenidyl.
 However, their modest benefits are often offset by side effects
such as impaired memory, confusion, hallucinations,
constipation, dry mouth and impaired urination.
 Amantadine. Doctors may prescribe amantadine alone to
provide short-term relief of symptoms of mild, early-stage
Parkinson's disease. It may also be given with carbidopa-
levodopa therapy during the later stages of Parkinson's
disease to control involuntary movements (dyskinesia)
induced by carbidopa-levodopa.
 Side effects may include a purple mottling of the skin, ankle
swelling or hallucinations.
18

SURGERY
19

SURGERY
20

MYASTHENIA GRAVIS
23

MYASTHENIA GRAVIS
Myasthenia gravis is a chronic autoimmune neuromuscular
disease characterized by muscular weakness and fatigue that
worsens with exercise and improves with rest. The name
myasthenia gravis, which is Latin and Greek in origin, literally
means "grave muscle weakness."
24

EPIDEMIOLOGY
Prevalence 1-7 in
10,000 population
All age
groups
W:M--- 3:2
Women in 20-30’s
(young women)
Men in 40-60’s(old
male)
25

PATHOPHYSIOLOGY
↓No of
functional Ach
receptors
Complement
mediated damage
of the post synaptic
membrane
Functional blockage
of the Ach receptor
sites
Endocytosis &
degradation of Ach
receptors
26

FACTORS THAT WORSEN MYASTHENIC SYMPTOMS
 Emotional upset
 Exposure to bright sunlight
 Surgery
 Immunization
 Menstruation, Pregnancy
 Intercurrent illness-viral
infection
 Hypothyroidism or
hyperthyroidism
 Drugs
 Increased body temperature
27

MODIFIED OSSERMAN SCALE
1. Grade 1 - Ocular only
2. Grade 2 - Mild generalized symptoms sparing oropharyngial
muscles
3. Grade 3 - Moderate generalized weakness with mild to
moderate oropharyngeal symptoms
4. Grade 4 - Severe disability including oropharyngial and
respiratory muscles
5. Grade 5 - Myasthenic crisis
28

CLINICAL PRESENTATION
Muscles affected
 Ocular muscle
 Facial muscle
 Bulbar muscle
 Limb muscle
 Respiratory muscle
Characteristics of muscle weakness
 No muscle wasting
 No sensory loss
 No reflex changes
29

OCULAR MUSCLE WEAKNESS
Asymmetric
ptosis
Diplopia &
Nystagmus
Furrowing of
forehead
Raised
eyelids
30

FACIAL MUSCLE WEAKNESS
Expressionless
mask like face
Attempt to smile
causes snarl
31

BULBAR MUSCLE WEAKNESS
 Difficulty in chewing
 Dysphagia
 Nasal voice
 Nasal regurgitation
 Severe jaw weakness
- hang open jaw
Neck muscle weakness
 Risk for aspiration
32

LIMB MUSCLE WEAKNESS
 Upper extremity weakness is more common than lower extremity
weakness
 Weakness affects proximal muscles mainly and is often
asymmetric.
 Difficulty in raising the arms.
 Maintaining raised arms, as when shampooing the hair.
 Leg weakness can cause trouble climbing stairs, walking for
long distances, or getting up out of low chairs.
33

RESPIRATORY MUSCLE WEAKNESS
Neuromuscular emergency
 Intercostal muscle weakness
 Weakness of diaphragm
Difficulty in breathing
CO retention
 Pharyngeal muscle weakness
Collapse of upper airway
Respiratory failure
34

DIAGNOSIS
Bedside tests
 Looking upward for 30 seconds
 Looking at the feet while lying on the back for 60 seconds
 Keeping the arms stretched forward for 60 seconds
 Cogan lid twitch test
 Rapid eye blinking test
 Ice test
35

EDROPHONIUM TEST – (TENSILON CHALLENGE TEST)
• Edrophonium chloride-Ach Esterase inhibitor
BEFORE TEST
• A short acting drug that improves the muscle strength
• Initial dose -2 mg ,followed by 8 mg as IV
• Improvement very evident in ocular muscles
• Effect lasts for only 3-5 minutes
AFTER TEST
36

LAB TEST FOR ANTIBODIES
 Acetylcholine receptor antibodies
 Anti-MuSK antibody
( muscle specific receptor tyrosin kinase)
37

ELECTROMYELOGRAPHY
By repeatedly stimulating a muscle with electrical impulses,
the fatiguability of the muscle can be measured in graph
forms.
38

SINGLE FIBER ELECTROMYOGRAPHY (SFEMG)
 Most sensitive test which
shows increased jitter in
weak muscle.
 High jitter in facial
muscle predicts ocular
muscle weakness.
 Jitter in limb muscle
predicts generalized MG
39

CT SCAN
 To identify Thyoma
40

PULMONARY FUNCTION TEST
Incentive spirometry
41

MUSCLE BIOPSY
42

MEDICAL MANAGEMENT
The Therapeutic Approach
1) Drugs improving neuromuscular transmission- Cholinestrase
Inhibitors
2) Immunomodulating drugs interfering with autoantibody activity on
NMJ.
 Corticosteroids
 Immunosuppressants
 Plasmapheresis
 Intravenous immunoglobulins
3) Modification of the natural history of the disease, eg, thymectomy.
43

ACETYL CHOLINE ESTERASE INHIBITORS
 Pyridostigmine Bromide
 Neostigmine Bromide
 Ambenonium chloride
 Edrophonium chloride
44

CHOLINESTRASE INHIBITORS
Pyridostigmine bromide (Mestinon)
• 60 mg oral tablet
• Action starts in 15-30 mts, peaks in 2 hours,lasts for 3-4
hrs.
 A 120 mg sustained release tablet be used for night
symptoms
 Oral suspension of 12 mg/ml be used for those on NG
tube.
 Side effects
 Loose stools, nausea, vomiting, abdominal cramps
Blurred vision, constricted pupils, increased saliva,
sweating
45

CORTICOSTEROIDS
Prednisone
Dose
– Beginning15-25 mg/day
– Maximum 50 mg/day
– Maintained 3 months
– Gradually reduced to an alternate day regimen discontinued
 Side Effects
 peptic ulcer, hyperglycemia, fluid retention
46

IMMUNOSUPPRESSANT DRUGS
Mycophenolate mofetil 1-1.5mg BD
Azathioprine (Imuran) 50 mg OD
Cyclosporine 4-5 mg/ kg/day
Tacrolimus 0.1 mg/kg/day
Cyclophosphamide
47

WHAT IS NEW AMONG MEDICATIONS?
CK-2017357
Increases muscle strength, but not by affecting the patient’s
immune system
48

PLASMAPHERESIS
 Used to treat exacerbations
 A course of five exchanges (3–4 L
per exchange) is generally
administered over a 10- to 14-day
period.
 Improves the symptoms in 75%
 Benefits for 3-6 weeks
 Monitor for hypotension, electrolytes
& clotting factors
 Handle the catheter with utmost
care
 Obtain an order from physician to
hold medication before procedure.
49

INTRAVENOUS IMMUNOGLOBULIN (IVIG)
 A rapid improvement in difficult period of myasthenic
weakness or prior to surgery.The usual dose is 2 g/kg,
Administered over
5 days (400 mg/kg per day)
 The course of can be shortened to administer the entire dose
over a 3-day period. Patient may exhibit improvement in 2-4
days& may last for weeks/months
 Adverse reactions include headache, fluid overload, and rarely
aseptic meningitis or renal failure.
50

SURGICAL MANAGEMENT - THYMECTOMY
Indications :
 Refractory cases to medical management
• Thymoma
• The best responses
- In young people
- Early in the course of their disease
• The maximal favorable response - 2 to 5 years after
surgery
51

COMPLICATIONS
MYASTHENIC CRISIS CHOLINERGIC CRISIS
 By undermedication/sudden
withdrawal of medication
 May be precipitated by some
drugs, infection, surgery,high
temperature,pregnancy.
 Generalised weakness,
respiratory depression
 Tensilon test is positive
 Managed by increasing dosage
of cholinergic drugs
 By overmedication
 Symptoms aggravated by
tensilon administration
 Difficulty in speaking,
swallowing,breathing,increas
ed salivation
 Discontinuation of
medication is the main stay
of management
52

GBS
53

EPIDEMIOLOGY
55

REFERENCES-
 Medical surgical nursing – Joyce M Black, Jane
Hawks.
 Brunner and Suddarth’s textbook of Medical
Surgical Nursing.
 Harrison manual for internal medicine, 20 edition
89

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