Degenerative

Disorders of Central
Nervous System
Muhammad Ali. Diagnosed with Parkinson's in 1984,
due to the head trauma he endured while boxing
Famous actor, Michael j. Fox diagnosed with
parkinson’s in 1991
PARKINSON’S DISEASE
 Learning Objectives:

1. Define Parkinson’s disease

2. State the risk factors of Parkinson's disease
3. Describe the pathophysiology of Parkinson's disease
4. State the clinical manifestations of patient with
parkinson’s disease
5. State the stages of Parkinson's disease based on clinical
manifestations
6. Explain your nursing management or interventions for
patient with Parkinson's disease
 Parkinson’s disease

A slowly progressive neurologic disease that is

characterized by a fixed inexpressive face, tremor
at rest, slowing of voluntary movements, gait with
short accelerating steps, peculiar posture and
muscle weakness .
 Parkinson’s disease

Parkinson's disease is a progressive

neurodegenerative disorder that is common, age-
related and chronic.

It is caused by loss or degeneration of dopaminergic

neurons in the substantia nigra of the midbrain.
 Parkinson’s disease

 Onset of symptoms and progression of the disease is

gradual.Motor signs and symptoms include resting
tremor, rigidity, bradykinesia (slow movement) and
postural instability.

 In Parkinson's disease dementia indicates loss of

intellectual functions including memory, significant
deterioration in the ability to carry out day-to-day
activities and changes in social behavior.
 Risk factors (believe to be)

1. Advancing age (60 years above, more men than

women) – reason unclear

2. Environmental factors: rural living, exposure to well

water, agricultural pesticides and herbicides or
carbon monoxide exposure (toxin induced)

3.Genetic (family history of PD)-genetic mutations

4.Others e.g. Head trauma, encephalitis, drugs

(
 Pathophysiology of Parkinson’s disease

Destruction of dopaminergic neuronal cells in the substantia

nigra in the basal ganglia

Depletion of dopamine stores

Degeneration of the dopaminergic nigrostriatal pathway

Imbalance of acetylcholine(excitory nuerotransmitter) and

dopamine(Inhibitory ) in the corpus striatum

Impairment of extra pyramidal tracts controlling complex body

movements
Tremors Rigidity Bradykinesia Postural
changes

( Slow movement)
Dopamine pathway

Basal
ganglia
EXTRAPYRAMIDAL TRACT
Parkinson’s Disease
Clinical features

1. Tremor - more prominent at rest

(initial sign of parkinson’s disease)

2. Bradykinesia -slowness in initiating movement

3. Muscle rigidity - stiffness when the arm, leg, or

neck is moved back and forth.

4. Postural instability

5. Shuffling gait
Clinical features

.
6 Akinesia- absence, loss, or impairment of the

power of voluntary movement.

7. Slowed speech (hypophonia) & Dysarthria(

difficulty speaking )less facial expression.

8. Trunk tilted forward

Clinical features
 Clinical features

9. Decrease arm swing when walking

10. Difficulty rising from chair
11. Micrographia (small, cramped
handwriting)
12. Decrease eye movement
13. Slowed activities in daily living (e.g.
eating, dressing, bathing etc.)
14. Difficulty turning in bed
 Clinical features

15. Remaining in certain position for a

long period of time
16. Skin problem: Seborrhoea
17. Excessive sweating in face in neck
18. Absence sweating on arms and
extremities
19. constipation
 Clinical features

20. Postural hypotension

21. Diminished sense of smell
22. drooping, drooling
23. Painful foot cramps
24. Urinary frequency/urgency
25. male, erectile dysfunction

Cognitive and psychological sign and symptom:

26. Dementia( decrease in the ability to think and
remember)
27. Depression
28. Anxiety
29. Sleep disturbance
 Clinical features

Patient with parkinson’s may develop

(complication):
• Falls, fracture
• Skin breakdown
• Dizziness
• Social isolation (low self esteem)
 Stages of Parkinson’s based on
clinical manifestations
stage Clinical features

Stage 1: Unilateral movement, minimal or no functional

impairment
Stage 2: Bilateral/midline involvement without impairment
of balance
Stage 3: Impaired reflexes e.g. unsteadiness by Romberg
test
Stage 4: Fully develop, severely disabling disease. Unable
to walk without assistance

Stage 5: On bed/wheel chair unless aided

 Investigations

1. No specific investigations
2. EEG – Slow pattern and disorganize
3. FBC – Hb low due to anemic
4. Upper GI X-ray – colon distention due to
constipation
5. PET scan
 Treatments

Anticholinergic Artane (trihexypinedyl) – 1mg 1st day, Block the excitatory

2mg 2nd day, and increase to 2mg action on
daily neurotransmitter
ii. Cogentine (benztropine) – 1mg acetylcholine
daily •Used during the early
iii. Aameton (bipenden) stage of the disease
•Reduced tremor,
rigidity, drooling
➢Side effects: dry
mouth, constipation,
blurred vision,
tachycardia, urinary
retention
 Treatments

Dopaminergics Levodopa (levadopa) 100mg 1 tab Increase mobility,

TID reduce muscle rigidity
and tremor
Sinemet (carbidopa) 25mg 1 tab TID,
1oomg/25mg (100mg levadopa, Use to stimulate
25mg carbidopa) dopamine receptor to
balance the dopamine

Side effects: nausea,

vomiting (common),
dark urine, sweating,
 Treatments
Dopamine i. Bromocriptine (pariodel) 1.25mg ➢ Act directly to
agonist daily for 1ST week activate dopamine
ii. Puanipexole (mirapex) receptor in the
brain
➢ Combination with
levadopa
COMT (Catechol-O- methyltransferase) Responsible for
inhibitors i. Tolcapone (Tasmar) metabolizing dopamine
ii. Entacapone (comtass)
iii. Given with Levodopa
 Other
treatment

Activa TM Tremor control

therapy

• Similar with pacemaker,

patient will control the
device as required
• Deliver mild electrical
stimulation to block the
impulse that causes tremor
 Activa TM Tremor control therapy

Brain Implant for Parkinson’s

 Pacemaker-like pulse generator

that is implanted in the chest

and attached to wire leads that

connect to electrodes placed

in thalamus to block nerve

pathway associated with PD .

Portable brain Stimulator
 Other treatment

b. Stereotaxic thalamotomy
Insertion of needle into the specific
area under x-ray guidance
Destroy small amount of tissue in the
thalamus
 Rehabilitation

1. Consult occupational therapy (OT)

 To adapt to change: abilities to work, self care and
recreational
 Concentrate upper extremities activity
 Skill related to cooking, grooming

2. Physical or physiotherapist (PT)

 Improve coordination, balance, gait, posture and
preventing contractures
 Improve muscle tone, strength
 Improve lower extremities
 Rehabilitation

Adjust pants, clothes – button to zip

Elastic shoe lace that can tied permanently
Clip ties which slip under the collar

3. Speech therapist
Evaluate speech ability and potential benefits
of assistive devices e.g. voice synthesizer
To improve speech and swallowing, gag reflex
 Rehabilitation

It is important for the nurse to assess the patient’s

ability to perform activities of daily living before
any nursing care plans.

Goal of nursing care is to maintain optimal body

function
 Health Education or Teaching

Maintaining a safe environment :

1. Advice patient or patient’s family to remove all
loose or scatter rugs – risk for fall
2. Remove all objects (put aside furniture) that
will block patient’s way
3. Remove any sharp objects that may hurt or
injure the patient
 Rehabilitation

Maintaining a safe environment

4. Avoid flight of stairs
5. Install metal or wooden handles on the wall
adjacent to door knobs and rail
6. Modify bed or chair for easy movement and
support
7. Use support to brush teeth, walking
 Rehabilitation

 Exercise
1. Advise walking outdoor with guidance
2. Provide exercise apparatus to maintain
tone and strength of the muscle
3. Driving out of busy area might be safe
and develop confidence to
independence
 Diet

1. Intake at least 8 meals a day

2. Weigh patient daily
3. Use spoon when eating
4. Soft and blended diet
5. Consult physician if weight loss remains
 Diet

Medication and follow up

1. Don’t stop medication without consulting the
Doctor
2. Always come to the hospital for routine liver
function test – to rule out the side effects of
medications
3. Come for follow as scheduled to monitor the
effectiveness of the medication
 Nursing Care Plan

1. Impaired physical mobility related to rigidity and

weakness of the muscle
2. Self care deficit related to tremor
3. Impaired verbal communication related to loss of
muscular control and diminished vocal amplitude
4. Impaired sleeping pattern due to rigidity and
weakness of muscle tone
5. nutritional status less than body requirement
related to impaired chewing and swallowing
 ..\..\..\..\..\What is Parkinsons disease.mp4
ALZEIMERS DISEASE
(AD)
 Learning Objectives:

At the end of the topic the learners will be able to:

1. Define Alzheimer’s disease

2. State the etiology of Alzheimer’s disease

3. State the Clinical Manifestations of Alzheimer’s disease

4. Describe the Patho-physiology of Alzheimer’s disease

5. Explain your Nursing Management of a patient suffering

from Alzheimer’s disease
 Alzheimer’s disease
Definition

 Also Senile dementia .

 Alzheimer’s type is a chronic, progressive and

degenerative brain disorder that is accompanied by
profound effects on memory, Cognition and ability for self
care.

 Alzheimer’s disease is a brain disease that slowly destroys

memory and thinking skills and, eventually, the ability to
carry out the simplest tasks. It begins slowly and gets worse
over time. Currently, it has no cure.
 Etiology/Risk factors
A combination of various risk factors of AD

1. Idiopathic.

2. Increasing age (age 65 and above – due to

degeneration of neurons which causes tangles and
plaques.)- but AD is not a normal part of aging.

3. Genetic or family history of AD (account for 10%) of AD

cases.

4. Presence of seizure disorder at risk for AD – reason

unclear.

5. Obesity may contribute.

 Patho-physiology of Alzheimer’s
disease

Idiopathic or other risk factors e.g. increasing age

Structural AND Biochemical and changes in the

brain (Brain degeneration)

Formation of neurofibrillary tangles and beta

amyloid plaques deposit in the brain
 Pathophysiology of Alzheimer’s
disease Contd……

Death of neuron (Neural damage) and brain atrophy

Loss of acetylcholine and other neurotransmitters

+
Disruption of nerve impulse transmission

Dementia –memory loss, personality changes, difficulty

to carry out activities of daily living (ADL )
Histo-pathological changes in AD
Amyloidal plaques in AD
 Clinical manifestations

Stage 1 (2-4 years)

1. Usually noticed by family members

2. short term memory loss

3. > Forget any object and location. Long term memory

is unaffected

4. Decrease attention span

5. Denial, irritability, restless and depression

 Clinical manifestations

Stage 1 (2-4 years)

6. Apathetic( feeling of no interest)

7. Loss of spontaneity and initiative

8. Neglect of personal hygiene and appearance

9. Suspicious of other’s motives w/ a tendency to blame

them for one’s incapacity

10.Loss of spatial orientation (e.g: place, reading)

11.Motor aphasia- cannot recall words she wishes to say.

 Clinical manifestations
Stage 2 (2- 12 years)

Changes in the 1st stage intensify

1. Personality changes

2. Easy agitated and irritability may have hallucination and

delusion

3. Sleep disturbance :Restlessness at night – causes insomnia

4. Memory loss becomes severe – cannot recognized close

friends and relatives , cannot recognize himself in the mirror.
 Clinical manifestations

Stage 2 (2- 12 years)

5. Changes in the 1st stage intensify

6. Confused

7. Reading, mathematical skills deteriorate

8. Loses weight –poor nutrition and shows no interest in

meals
 Clinical manifestations
Stage 2 (2- 12 years)
8. Unable to tell time (time disorientation) and
calculation

9. Sun downing – characteristic of increase

agitation, time disorientation, wandering
behavior afternoon and evening

10.Impaired judgment

11.> inability to make decision, inability to drive a

car
Unable to recognize self in
the mirror
 Clinical manifestations

Stage 3 (approximately 2 – 14 years or longer) the final stage

1. cognitive abilities decrease or absent; disorientated to time,

place and person

2. Communication skill is absent (inability to use language) – mute

3. Motor skill impaired or absent – limb rigidity, posture and flexion

of the lower extremities

4. Bowel and bladder incontinence

 Clinical manifestations

Stage 3 (approximately 2 – 14 years or longer) the final stage

5. Weight loss

6. Becomes bedridden and totally helpless

7. Tendency to grasp objects and put them in the

mouth

8. Seizure

9. Skin infection
 Investigations

1. EEG

2. Complete medical history

3. CT Brain scan/MRI – Shrinkage of the hippocampus

4. Psychometric evaluation – assess the motor and cognitive skills

5. PET Scan – to visualize the activity and interaction of functions.(The

hippocampus is the part of the brain that is involved in memory
forming, organizing, and storing.
 Diagnosis

6. Mini Mental Status Examination

Orientation to time What is the date month ,year?

Registration 3 words and repeat up 5 times.
House, car and lake
Naming What is this?...e.g. pencil/pen

Reading Read and apply: ‘CLOSE YOUR EYES’

 Treatment

Cholinesterase inhibitor – to improve memory in mild to moderate AD

dementia
1. Taurine hydrochloride (Cognex)
2. Donepezil hydrochloride (Aricept) 5mg TDS –
3. Rivastigmine tartace (Exelon) 1.5mg BD, increase to 3mg BD
 Improve in carrying out ADL
 Reduce Agitation and delusion

Alternative treatment:
i. Herbs (Gingko Biloba) – believe to be improving cognitive abilit
ii. Coenzyme (Q10) – Antioxidant that naturally occurs in the body
30mg daily
 Nursing Responsibilities

Health Education:
Activity
1. Assist in ADL
2. Label -medication box –using calendar
3. Always be with the patient and communicate as they
will assist patient to memorized.
4. Communicate in the low voice and speak in calm.
5. Identify any risk of injury or fall to patient e.g. staircase,
slick floor, lighting and matches.
 Nursing Responsibilities

6. Orientate to the environment, person and time

every time conversation with the patient begins
especially in the morning.Simple conversation:
close ended – ‘yes’ or ‘no’ answer
7. Provide safe environment e.g. adjust water heater
to safe temperature
8. Provide sufficient light on dark area
9. Provide fence to avoid wandering
10. Develop emergency call bell system, emphasize
the importance of safe improvement
 Nursing Responsibilities

➢ Exercise
1. Render therapeutic touch and gentle hand
massage
2. Meditation – encourage relaxation
3. Play patient’s favorite music (soft melody)
4. Involve patient in simple activity like
gardening but with guidance

➢ Diet
1. Encourage high fluid and fiber diet
2. Provide well balance diet
 Nursing Responsibilities
Medication and follow up

1. Follow instruction of medication intake and provide

information about the side effect of the medication

2. Give tranquilizer to reduce agitation and hallucination as

ordered by the Doctor

3. Come for follow up as scheduled and involve patient in

specific association to develop self confidence and
continuous improvement for patient and family

4. Provide latest information regarding care of patient with

Alzheimer’s disease
 Reference
 Hinkle, J. L. (2014). Brunner & Suddarth's textbook of medical-surgical
nursing (Edition 13.). Philadelphia: Wolters Kluwer Health/Lippincott
Williams & Wilkins.
New Evidence Shows that Depression May
Be a Risk Factor for Dementia

‘University of Massachusetts medical school’

(researchers).
 Learning Objectives

1. Define Multiple Sclerosis

3. State the etiology of Multiple Sclerosis
2. Describe the pathophysiology of Multiple Sclerosis
3. State the clinical manifestation of Multiple Sclerosis
4.Describe the diagnostic investigation for Multiple
Sclerosis.
5.Explain the treatment for Multiple Sclerosis.
5. Formulate the nursing care plan for a patient
suffering from Multiple Sclerosis
 Multiple sclerosis
• Is an autoimmune , inflammatory , progressive
demyelinating disease (destruction of axonal
myelin ) in the brain and spinal cord. The disease
is chronic, degenerative disease.

• The immune system attacks the protective sheath

(myelin) that covers the nerves and causes
demyelization throughout the brain and spinal
cord.
 Multiple sclerosis

• Myelin damage disrupts communication between

your brain and the rest of the body.
DEMYELINATION
 Multiple Sclerosis (MS)

Etiology:
1. Autoimmune
2. Age 20-40 years women
3. Pathogen mediated –previous h/o viral infection
with insult to nervous system.
4. Genetically susceptible individuals
 Pathophysiology

Autoimmune response (T cells B cells; cytokines production)

Inflammation - destroys the myelin and dendrocytes

Axon dysfunction (spinal cord, optic nerve and brain stem)

Demyelination interrupts the flow of nerve impulses

Multiple Sclerosis – Variety of manifestations appear

depending on the nerves affected
 Classification
1. Relapsing – Remitting( the return of an illness after a period of
improvement)
Common in MS, characterized by exacerbation (acute attack) with
partial or full recovery.

2. Progressive
Begin with relapsing-remitting and becomes worse

3.Primary progressive
Steady/slow worsening of the disease from onset -minor recovery

4. Progressive Relapsing
 Rare from continuous to progress from the onset but has
exacerbation
 Clinical Manifestations
1. General fatigue
2. Involvement of the optic nerve:
 Blurr vision
 Diplopia
 Impaired color perception
 Altered papillary reaction to light
3. Brain stem (CN III & XII)
Nystagmus (uncontrolled repetitive movement of eyes)
 Clinical Manifestations
3. Dysarrthythmia
4. Deafness
5. Reduce concentration
6. Depression
7. Weakness numbness both extremities
8. Bladder dysfunction (urgency, hesitancy and
incontinence)
9. Constipation
10. Night blindness
 Investigations

Lumbar Puncture - •High lymphocyte with reactive antigen that

CSF indicate presence of autoimmune response
•High IgG in the CSF

MRI •Multifocal lesions in the white matter of the

brain
•Optic/spinal lesion

CT Scan Atrophy with white matter

 Treatment
Immunomodulato  To prolong onset of Inteferon Beta 1a (IM
rs disability. Avonex) 30mcg weekly
ii. Inteferon Beta 1b (S/C
 Side effect: confusion, Betaferon) 0.25mg OD
depression, with suicidal
tendencies

adenocorticothropine Prednisolone 200mg daily

Adenocorticos Hormone (ACTH). followed by 80mg OD
teroid as ordered
 Largely replaced by Iii. Methylprednisolone
synthetic corticosteroids 1gm/day as ordered
– depends on patient
condition
 Treatment

Muscle relaxant Combination of i.Baclofen (Lioresal)

muscle relaxant 30mg TDS
and minor Ii. Diazepam (Valium) 5-
tranquilizer 10mg daily – minor
manage to tranquilizer
suppress CNS •To relieve muscle spasm
reflexes that can
regulate muscle
activity and reduce
the anxiety
Immunosuppressant cytotoxic drugs – i.Azathiopine (Imuran)
suppress the pending on patient progress
autoimmune component not more than 3mg/kg/day
Ii. Cyclophosphamide 50-
200mg/kg/day –
 Nursing care

1. Impaired physical mobility related to

muscle weakness
2. Fatigue related to disease process
3. Disturbed sensory perception related to
disease process.
4.Impired urinary elimination related to
disease process.
 Impaired physical mobility related to muscle
weakness
1. Determine current activity level and physical condition. Assess
degree of functional impairment using 0–4 scale.
2. Provides information to develop plan of care for rehabilitation.
Note: Motor symptoms are less likely to improve than sensory ones.
3. Encourage patient to perform self-care to the maximum of ability as
defined by patient. Do not rush patient.
4. Promotes independence and sense of control; may decrease feelings
of helplessness.
5. Encourage scheduling activities early in the day or during the time
when energy level is best.
6. Patients with MS expend a great deal of energy to complete ADLs,
increasing the risk of fatigue, which often progresses through the day
 Impaired physical mobility related to muscle
weakness
7. Allot sufficient time to perform tasks, and display patience when
movements are slow.
8. Decreased motor skills and spasticity may interfere with ability to
manage even simple activities.
9. Anticipate hygienic needs and calmly assist as necessary with care
of nails, skin, and hair; mouth care;
10. Provide assistive devices and aids as indicated: shower chair,
elevated toilet seat with arm supports.
11. Reduces fatigue, enhancing participation in self-care.
 Impaired physical mobility related to muscle
weakness

7. Reposition frequently when patient is immobile (bed or chair bound).

8. Provide skin care to pressure points, such as sacrum, ankles, and
elbows.
9. Position properly and encourage to sleep prone as tolerated.
10. Reduces pressure on susceptible areas, prevents skin breakdown.
 Impaired physical mobility related to muscle
weakness
17. active or passive ROM exercises on a regular schedule. Encourage
use of splints or footboards as indicated.
18. Prevents problems associated with muscle dysfunction and disuse.
19. use of medications, cold packs, and splints and maintenance of
proper body alignment, when indicated.
20. Helps decrease spasticity and its effects.
 Fatigue related to disease process

1. Accept when patient is unable to do.

2. Nonjudgmental acceptance of patient’s evaluation of
capabilities promote independence.
3. Determine need for walking aids. Provide braces, walkers, or
wheelchairs.
4. Review safety considerations.
5. Mobility aids can decrease fatigue, enhancing independence
and comfort, as well as safety.
 Fatigue related to disease process

1. Schedule ADLs in the morning if appropriate.

2. Plan care consistent rest periods between activities. Encourage
afternoon nap.
3. Reduces fatigue, aggravation of muscle weakness.
4. Assist with physical therapy. Stress need for stopping exercise or
activity just short of fatigue.
5. Pushing self beyond individual physical limits can result in
excessive or prolonged fatigue and discouragement. In time,
patient can become very adept at knowing limitations.
 Disturbed sensory perception related to disease
process
1. Catheterize as indicated.
2. May be necessary as a treatment and for evaluation if patient is
unable to empty bladder or retains urine.
3. Teach self-catheterization and instruct in use and care of indwelling
catheter.Helps patient maintain autonomy and encourages self-care.
4. Obtain periodic urinalysis and urine culture and sensitivity as
indicated.Monitors renal status. Colony count over 100,000 indicates
presence of infection requiring treatment.

Administer anti-infective agents as necessary: Nitrofurantoin; co-

trimoxazole (Bactrim); ciprofloxacin (Cipro)
Bacteriostatic agents that inhibit bacterial growth and destroy
susceptible bacteria.
 Disturbed sensory perception related to disease
process
▪ Encourage adequate fluid intake, avoiding caffeine and use of
aspartame, and limiting intake during late evening and at bedtime.
Recommend use of cranberry juice/ vitamin C.
▪ Sufficient hydration promotes urinary output and aids in preventing
infection.
▪ Encourage patient to observe for sediments or blood in urine, foul
odor, fever, or unexplained increase in MS symptoms.

▪ Indicative of infection requiring further evaluation or treatment.

▪ Refer to urinary continence specialist as indicated.Helpful for
developing individual plan of care.
 TEACHING

▪ Review disease process, treatment and prognosis

▪ Discuss importance of daily routine of rest, exercise, activity, and

eating, focusing on current capabilities. Instruct in use of appropriate
devices to assist with ADLs, e.g., eating utensils, walking aids.

▪ Helps patient maintain current level of physical independence and

may limit fatigue.

 TEACHING

▪ Stress necessity of weight control.

▪ Excess weight can interfere with balance and motor abilities and
make care more difficult.
▪ Problems that may arise-UTI
▪ Injury prevention
▪ Medication
▪ Vocational rehab