Response to Altered Perception:

Neurologic Disturbances
 Multiple Sclerosis
 Parkinson’s Disease
 Myasthenia Gravis
 Amyotrophic Lateral Sclerosis

Multiple Sclerosis

1. Review of Anatomy and Physiology (AnaPhy)

Affected Part: Central Nervous System (Brain, Spinal Cord, Optic

Nerves)
Function:

 Brain: Coordinates sensory input, motor function,

cognition, and autonomic control
 Spinal Cord: Transmits nerve signals from brain to body
 Optic Nerves: Carry visual information from eyes to the
brain

In MS: Myelin sheath (protective layer around nerves) is damaged,

leading to impaired nerve transmission.

2. Overview

Incidence :

 Affects approximately 400,000 people in the United States

 Peak age of onset: 20 to 50 years old
 Occurs three times more often in women than in men
 More common in northern temperate regions like Europe, New Zealand, southern Australia, the
northern U.S., and southern Canada
 Less prevalent in Asians
 Geographic and environmental factors influence risk

Definition :

Multiple Sclerosis is an immune-mediated, progressive demyelinating disease of the central nervous

system (CNS).

 Demyelination involves destruction of myelin, a protective layer around nerve fibers, resulting in
impaired transmission of nerve impulses.
Etiology:

 Exact cause is unknown, but autoimmune

activity plays a major role

 The specific antigen that triggers the immune response remains unidentified

 Possible contributing factors:

 Genetic predisposition (not directly inherited but over 200 gene variations are linked)
 Environmental factors:
o Obesity
o Low vitamin D exposure
o High salt intake during adolescence
 Viral theory: Certain viruses may mimic myelin proteins, triggering a cross-reactive immune
response in genetically susceptible individuals

Types:

A. Early Forms:

 Radiologically Isolated Syndrome (RIS):

o MRI shows MS-like lesions with no clinical symptoms
o About 1/3 progress to MS within 5 years
 Clinically Isolated Syndrome (CIS):
o First clinical episode of neurologic symptoms lasting at least 24 hours
o May or may not progress to MS

B. Main Clinical Forms:

1. Relapsing-Remitting MS (RRMS):
o Most common type
 o Periods of new or worsening symptoms followed by remission
2. Secondary Progressive MS (SPMS):
o Initially RRMS, followed by gradual worsening without recovery periods
3. Primary Progressive MS (PPMS):
o Steady worsening from the start without early relapses or remissions
4. Progressive-Relapsing MS (PRMS):
o Rare form
o Progressive decline with occasional relapses

3. Assessment

Clinical Manifestations

MS presents with a wide range of symptoms depending on the location and extent of demyelination. The
disease follows varied courses, with some patients experiencing mild symptoms (benign MS) and others
facing progressive disability.

1. Disease Progression & Forms

 Benign MS & Radiologically Isolated Syndrome (RIS): No or minimal symptoms.

 Clinically Isolated Syndrome (CIS): Unilateral optic neuritis, focal symptoms, or partial
myelopathy.
 Relapsing-Remitting MS (RRMS) – 85% of cases: Periods of symptom exacerbation and
remission. Residual deficits may accumulate over time.
 Secondary Progressive MS (SPMS): Progressive worsening with or without relapses.
 Primary Progressive MS (PPMS) – 15% of cases: Steady functional decline with few or no
remissions. May lead to quadriparesis, cognitive dysfunction, and visual loss.
 Progressive-Relapsing MS (PRMS) – 5% of cases: Continuous worsening with acute relapses.

2. Common Symptoms

 Fatigue: Most disabling symptom, worsened by heat, depression, anemia, and medications.
 Pain: Due to lesions on sensory pathways, may require analgesics, anticonvulsants, or
antidepressants.
 Weakness, Numbness, & Spasticity: Affects lower extremities in 90% of cases, leading to muscle
stiffness and increased reflexes.
 Visual Disturbances: Blurred vision, double vision (diplopia), blind spots (scotoma), or total
blindness.
 Cognitive Impairment: Memory loss, difficulty concentrating, emotional instability, and rare
cases of dementia.
 Ataxia & Tremors: Due to cerebellar and basal ganglia involvement, affecting coordination.
 Bladder, Bowel, & Sexual Dysfunction: Leads to urinary tract infections (UTIs), constipation, and
incontinence.
 Complications: Pressure injuries, pneumonia, osteoporosis, contractures, and pedal edema due
to immobility.

3. Exacerbations & Remissions

 Exacerbations (relapses) involve worsening symptoms and may be triggered by emotional or

physical stress.
  Remissions bring partial or complete symptom relief, though some deficits may persist.

 Objective:

 Method: Neurologic examination, MRI, lumbar puncture

 Findings: Muscle weakness, spasticity, intention tremor, nystagmus
 Justification: Reflects demyelination and disrupted nerve conduction

 Subjective:

 History: Onset of symptoms often episodic

 Verbal Complaints: Fatigue, visual disturbances, numbness, tingling, difficulty walking, memory
loss

4-Pathophysiology

Sensitized T & B cells enter CNS

➡️
T cells stay and activate immune response
➡️
Inflammation damages myelin & oligodendrocytes
➡️
Demyelination of nerve fibers
➡️
Interrupted nerve impulse transmission
➡️
Formation of plaques in CNS
➡️
Axonal damage & degeneration
➡️
Permanent, irreversible nerve damage
➡️
Neurologic symptoms vary by affected area

5. Nursing Diagnosis

 Impaired physical mobility related to neuromuscular impairment

 Self-care deficit related to fatigue and muscle weakness
 Disturbed visual perception related to optic nerve involvement
 Risk for injury related to sensory and motor deficits

6.Planning

 The patient will perform range-of-motion exercises twice daily and ambulate 10 meters with
assistance within 7 days to promote mobility.
  The patient will identify three energy-conservation techniques and implement rest periods within
3 days to manage fatigue.

 The patient will maintain intact skin with no signs of pressure injury throughout the hospital stay
by repositioning every 2 hours.

 The patient will verbalize feelings and demonstrate one coping strategy during daily interactions
within 5 days to improve emotional adjustment.

7. Health Promotion

1. Vaccination and Infection Control: Prevent triggers for exacerbations

2. Stress Management: Reduce frequency of flare-ups

8. Health Restoration

1. Rehabilitation Programs: Physical and occupational therapy for mobility and ADLs
2. Bladder and Bowel Training: Prevent complications and improve quality of life

9. Independent Nursing Care

Physiologic Care

 Promote mobility through ROM exercises – prevents contractures and maintains function
 Monitor fatigue levels – pacing activity prevents overexertion

Psychosocial Care

 Provide emotional support – helps cope with chronic nature of illness

 Facilitate support groups – reduces isolation

Spiritual Care

 Offer chaplain services – fosters hope and peace

 Respect beliefs and rituals – holistic care

Client Education

 Educate on symptom management – empowers self-care

 Teach medication adherence – reduces relapses and slows progression

10. Dependent Care

Medical Management

 Corticosteroids (e.g., methylprednisolone) – reduce inflammation during relapse

 Immunomodulators (e.g., interferon-beta) – decrease frequency of relapses

Diagnostic Tests

 MRI: Detects brain and spinal plaques

 Lumbar puncture: Detects oligoclonal bands (indicative of MS)

Pharmacologic Care

 Baclofen or tizanidine: Muscle spasticity

 Amantadine: Fatigue
 Gabapentin: Neuropathic pain

Therapeutic Care

 Physical Therapy: Improves muscle tone and balance

 Speech Therapy: For dysphagia or dysarthria

Complementary and Alternative Therapy

 Yoga and meditation: Improve flexibility and reduce stress

 Acupuncture: May help with pain management

Nutritional and Diet Therapy

 High-fiber diet: Prevent constipation

 Adequate fluid intake: Avoid urinary infections

📚 Reference: Brunner & Suddarth’s, 15th ed., p. 2079-2082

11. Surgical Intervention

 Rare in MS; considered for severe spasticity (e.g., tendon release surgery) or neurostimulator
implantation

12. Evaluation: Expected Outcome of Care

 Improved mobility and self-care

 Reduced severity/frequency of relapses
 Patient demonstrates understanding of disease and care regimen
 Maintains optimal function in ADLs
13. Reporting and Documentation of Care

 Document neuro assessments and changes in mobility or sensation

 Record response to medications and therapies
 Note education provided and patient understanding
 Monitor for adverse effects and complications

14. Evidence-Based Practice of Care

 Early use of disease-modifying therapies (DMTs) significantly reduces relapse rates and delays disability
progression
📌 Source: Rae-Grant A. et al. (2018). Practice guideline recommendations summary: Disease-modifying
therapies for adults with multiple sclerosis. Neurology, 90(17), 777–788.
 Exercise and fatigue management interventions improve quality of life and functionality
📌 Source: Latimer-Cheung, A. E., et al. (2013). Effects of exercise training on fitness, mobility, fatigue, and
health-related quality of life in multiple sclerosis: a systematic review to inform guideline development.
Archives of Physical Medicine and Rehabilitation, 94(9), 1800-1828.

15. Relevant Legal, Moral, and Ethical Standards of Care

 Informed Consent: Ensure the patient is aware of treatment options and risks
 Confidentiality: Respect patient privacy in documentation and discussions
 Autonomy: Support the patient’s right to make decisions
 Beneficence & Non-maleficence: Aim for beneficial interventions while avoiding harm
 ADA Compliance: Ensure accessibility and accommodation for disabled patients

Parkinson’s Disease

1. Review of Anatomy & Physiology (Affected Parts & Function)

Parkinson’s Disease (PD) primarily affects the basal ganglia, especially the substantia nigra, a structure responsible
for producing dopamine, a neurotransmitter crucial for regulating voluntary movement. As dopamine decreases,
there is an imbalance with acetylcholine, causing the motor symptoms of PD such as tremors, rigidity, and
bradykinesia. The nigrostriatal pathway, which links the substantia nigra to the striatum, is significantly affected.
2. Overview of Disease

 Incidence:
Parkinson’s Disease affects approximately 1 million people in the U.S., with 60,000 new cases annually. It
usually manifests after the age of 50, with men slightly more affected than women (Brunner & Suddarth,
15th ed.).
 Definition:
Parkinson’s Disease is a chronic, progressive, neurodegenerative disorder characterized by depletion of
dopamine in the central nervous system, particularly within the basal ganglia, leading to motor and non-
motor symptoms.
 Etiology:
The exact cause remains unknown, but contributing factors include genetic mutations (e.g., SNCA,
LRRK2), oxidative stress, environmental toxins (e.g., pesticides), and aging. Secondary parkinsonism may
result from medications, encephalitis, or brain injuries.
 Types:
o Primary/Idiopathic Parkinson’s Disease (most common)
o Secondary Parkinsonism (due to medications or other diseases)
o Parkinson-plus Syndromes (e.g., multiple system atrophy, progressive supranuclear palsy)

3. Assessment (with Rationale)

 Clinical Manifestations:
o Motor symptoms: Resting tremor ("pill-rolling"), bradykinesia, rigidity, postural instability
o Non-motor symptoms: Depression, cognitive decline, sleep disturbances, constipation
 Objective:
o Method: Neurologic examination using criteria like UK Parkinson’s Disease Society Brain Bank
Diagnostic Criteria
o Findings: Bradykinesia plus either tremor or rigidity; shuffling gait, masked facies, stooped
posture
o Justification: Objective signs confirm dopamine loss and basal ganglia dysfunction.
 Subjective:
o History: Gradual onset of tremors, stiffness, and slowing of movement
o Verbal Complaints: “I feel stiff,” “I have trouble writing,” or “I freeze when I try to walk.”
4. Pathophysiology (Simplified Arrow Form)

Neuronal degeneration in substantia nigra → ↓ dopamine production → imbalance between dopamine and
acetylcholine → impaired motor control in basal ganglia → motor symptoms (tremors, rigidity, bradykinesia) →
progressive disability

5. Nursing Diagnosis (Examples)

 Impaired physical mobility related to neuromuscular impairment

 Risk for aspiration related to impaired swallowing reflex
 Disturbed sleep pattern related to altered neurotransmitter levels

6. Planning (SMART, One-Sentence Goals)

 The patient will ambulate 20 feet with minimal assistance within 3 days to promote mobility.
 The patient will maintain a safe swallowing technique during all meals within 48 hours to prevent
aspiration.

7. Health Promotion

 Encourage regular physical activity to preserve mobility and reduce stiffness

 Promote early screening and neurologic evaluation in patients over 50 with motor symptoms

8. Health Restoration

 Implement physical and occupational therapy to restore motor function

 Promote medication adherence to restore dopaminergic balance and control symptoms

9. Independent Nursing Care (with Rationales)

Physiologic Care

 Assist with ambulation and transfers → Prevent falls due to postural instability
 Provide soft, easy-to-chew meals → Accommodate dysphagia and reduce aspiration risk

Psychosocial Care

 Encourage expression of feelings → Helps cope with depression and anxiety

 Include family in care discussions → Enhances support and treatment adherence

Spiritual Care

 Provide spiritual resources or chaplain visit → Supports emotional and existential needs
  Create a quiet, private space for reflection → Reduces stress and supports holistic well-being

Client Education

 Teach medication schedules and side effects → Ensures proper use and recognition of adverse effects
 Instruct on home safety modifications → Prevents injuries from falls or motor complications

10. Dependent Care (with Brief Rationales)

 Medical Management: Neurologist evaluates disease progression and adjusts treatment plan
 Diagnostic Tests: MRI to rule out other neurologic conditions; DaTscan to assess dopamine levels
 Pharmacologic Care:
o Levodopa-Carbidopa (mainstay for dopamine replacement)
o MAO-B inhibitors (e.g., selegiline) to prolong dopamine action
 Therapeutic Care: Physical therapy to improve gait and flexibility
 Complementary Therapy: Tai chi or yoga to improve balance and reduce fall risk
 Nutritional and Diet Therapy: High-fiber diet to manage constipation; small, frequent meals to reduce
fatigue and tremors

11. Surgical Intervention

 Deep Brain Stimulation (DBS): Electrodes implanted in basal ganglia to modulate abnormal impulses—
used in advanced PD unresponsive to medication (Brunner & Suddarth, 15th ed.)

12. Evaluation: Expected Outcome of Care

 The patient demonstrates improved mobility and balance, adheres to the medication regimen, maintains
nutritional intake, and experiences fewer falls or complications.

13. Reporting and Documentation of Care

 Document motor symptom changes, medication responses, patient teaching, fall incidents, and
communication with family and healthcare providers.

14. Evidence-Based Practice of Care

 Exercise interventions (aerobic training, resistance training) significantly improve gait, balance, and quality
of life (Tomlinson et al., Cochrane Database, 2013).
 DBS shows long-term improvement in motor symptoms and reduces medication dosage (Weaver et al.,
NEJM, 2009).
 Music therapy improves motor function and emotional well-being (Pacchetti et al., Neurological Sciences,
2010).
15. Relevant Legal, Moral, and Ethical Standards of Care

 Informed consent before initiating DBS or pharmacologic trials

 Right to autonomy and decision-making in advanced-stage planning
 Moral obligation to advocate for palliative care and dignity in late stages

Myasthenia Gravis

Myasthenia Gravis: Comprehensive Nursing Overview

1. Review of AnaPhy (Affected Parts and Function)

 Affected Part: Neuromuscular junction, specifically the acetylcholine (ACh) receptors

on the motor end plate of skeletal muscles.
 Function: ACh receptors are essential for the transmission of nerve impulses to initiate
voluntary muscle contraction. In Myasthenia Gravis (MG), autoantibodies block or
destroy these receptors, impairing communication between nerves and muscles.

2. Overview of Disease

 Incidence: MG is a rare disorder, with an estimated prevalence of 14 to 20 per 100,000

population. It affects women more frequently under age 40 and men over age 60
(Brunner & Suddarth, 15th ed.).
 Definition: MG is a chronic autoimmune disorder characterized by weakness and rapid
fatigue of voluntary muscles due to impaired transmission of nerve impulses at the
neuromuscular junction.
 Etiology: Caused by autoantibodies against ACh receptors, often associated with thymic
abnormalities such as hyperplasia or thymoma.
 Types:
o Ocular MG: Affects only eye muscles.
 o Generalized MG: Affects multiple muscle groups including facial, limb, and
respiratory muscles.

3. Assessment

 Clinical Manifestations:
o Ptosis, diplopia, muscle weakness, dysphagia, dysarthria, fatigue that worsens
with activity, and respiratory difficulty in severe cases.
 Objective:
o Method: Neurological assessment, Tensilon test.
o Findings: Improved muscle strength after administration of edrophonium.
o Justification: Confirms impaired neuromuscular transmission typical in MG.
 Subjective:
o History: Fatigue, muscle weakness, difficulty in chewing, swallowing, and
breathing.
o Verbal Complaints: "My eyelids droop by the end of the day," "I feel weak after
walking."

4. Pathophysiology – Simple Arrow Genetic/immune trigger → Autoantibody production →

Destruction/blockade of ACh receptors → Decreased neuromuscular transmission → Muscle
weakness and fatigue

5. Nursing Diagnosis

 Ineffective airway clearance related to respiratory muscle weakness.

 Fatigue related to impaired neuromuscular transmission.
 Impaired verbal communication related to muscle weakness.

6. Planning (SMART Goal) The patient will demonstrate improved muscle strength by
performing ADLs independently within 1 week of nursing interventions.

7. Health Promotion

 Educate patient on energy conservation techniques.

 Encourage regular follow-up and medication adherence.

8. Health Restoration

 Initiate respiratory muscle training and incentive spirometry.

 Collaborate with PT for muscle strengthening exercises.

9. Independent Nursing Care

 Physiologic Care:
o Elevate head of bed to prevent aspiration (rationale: reduces risk of choking due
to dysphagia).
 o Monitor respiratory effort and pulse oximetry (rationale: detect early signs of
respiratory compromise).
 Psychosocial Care:
o Provide emotional support during flare-ups (rationale: reduces stress which can
exacerbate symptoms).
o Encourage social interaction (rationale: combats isolation from chronic illness).
 Spiritual Care:
o Offer chaplain referral if requested (rationale: addresses spiritual needs).
o Encourage participation in spiritual practices (rationale: enhances coping).
 Client Education:
o Instruct on medication timing and side effects (rationale: prevents overdose or
crisis).
o Teach signs of myasthenic and cholinergic crisis (rationale: enables early
intervention).

10. Dependent Care

 Medical Management: Immunosuppressants, corticosteroids to reduce immune activity.

 Diagnostic Test: Antibody titers (AChR, MuSK), EMG, CT/MRI for thymoma.
 Pharmacologic Care: Anticholinesterase drugs (e.g., pyridostigmine) to enhance
neuromuscular transmission.
 Therapeutic Care: Plasmapheresis, IVIG during crisis.
 Complementary Therapy: Relaxation therapy to manage stress.
 Nutritional Therapy: Soft diet, small frequent meals to manage dysphagia.

11. Surgical Intervention

 Thymectomy is indicated in patients with thymoma or generalized MG to reduce

symptoms or induce remission.

12. Evaluation

 Patient maintains adequate respiratory function, performs ADLs with minimal fatigue,
and reports understanding of disease management.

13. Reporting and Documentation of Care

 Document respiratory rate, muscle strength, fatigue level, medication adherence, and
education provided.

14. Evidence-Based Practice of Care

 IVIG and plasmapheresis are proven effective in myasthenic crisis (Sanders et al., 2016,
Neurology).
 Early thymectomy improves outcomes in non-thymomatous MG (Wolfe et al., 2016,
NEJM).
15. Relevant Legal, Moral, and Ethical Standards of Care

 Respect for patient autonomy in treatment decisions.

 Informed consent for procedures like thymectomy or plasmapheresis.
 Confidentiality in patient records and ethical allocation of ICU resources during crises.

Amyotrophic Lateral Sclerosis

1. Review of AnaPhy
Affected parts: Motor neurons in the brain, brainstem, and spinal cord. These neurons control voluntary muscle
activity including speaking, walking, breathing, and swallowing. In ALS, these neurons degenerate and die, leading
to muscle weakness and atrophy. (Brunner & Suddarth, 15th ed.)

2. Overview of Disease

 Incidence: ALS affects approximately 2 per 100,000 people annually worldwide, with onset typically
between ages 40–70.
 Definition: ALS is a progressive neurodegenerative disorder characterized by the degeneration of upper
and lower motor neurons, leading to muscle weakness and eventually paralysis.
 Etiology: The cause is largely unknown; however, genetic mutations (e.g., SOD1 gene) and environmental
factors are implicated.
 Types:

Sporadic ALS: This is the most common form of ALS, accounting for about 90–95% of cases. It occurs
randomly with no known family history or genetic link. The exact cause remains unknown, but
environmental and lifestyle factors may contribute.

Familial ALS (FALS): This type is inherited and accounts for about 5–10% of cases. It results from
genetic mutations passed down through families, most commonly involving mutations in the SOD1,
C9orf72, or other ALS-associated genes.

3. Assessment

 Clinical Manifestations: Progressive muscle weakness, fasciculations, dysarthria, dysphagia, respiratory

dysfunction, and eventual paralysis.
 Objective:
o Method: Neurological exams, electromyography (EMG).
o Findings: Muscle atrophy, decreased reflexes, abnormal EMG patterns.
o Justification: Confirms involvement of both upper and lower motor neurons.
 Subjective:
o History: Gradual onset of muscle weakness, difficulty speaking or swallowing.
o Verbal Complaints: “I feel weaker every day,” “I have trouble breathing at night.”

4. Pathophysiology (Simple Arrow)

Genetic/environmental factors → Motor neuron degeneration → Loss of communication to muscles → Muscle
atrophy and weakness → Progressive paralysis → Respiratory failure

5. Nursing Diagnosis

 Ineffective breathing pattern related to progressive respiratory muscle weakness.

  Impaired physical mobility related to motor neuron degeneration.
 Imbalanced nutrition: less than body requirements related to dysphagia.

6. Planning

 Assist patient in maintaining oxygen saturation > 92% through pulmonary support within 7 days.
 Promote safe ambulation with assistive device at least once per shift within 5 days.
 Ensure patient consumes 75% of meals with modified consistency within 3 days.

7. Health Promotion

 Encourage smoking cessation to reduce respiratory complications.

 Promote routine neurologic evaluations for early detection and management.

8. Health Restoration

 Provide respiratory therapy (e.g., BiPAP) to support breathing.

 Initiate physical and occupational therapy to preserve mobility.

9. Independent Nursing Care

 Physiologic Care:
o Position patient to facilitate breathing (semi-Fowler's); prevents aspiration.
o Provide suctioning and oral care; reduces risk of pneumonia.
 Psychosocial Care:
o Encourage verbalization of fears; provides emotional support.
o Involve patient in care planning; promotes autonomy and dignity.
 Spiritual Care:
o Facilitate chaplain visits; provides spiritual comfort.
o Offer quiet moments for reflection or prayer.
 Client Education:
o Teach signs of respiratory distress; enables early intervention.
o Educate on use of assistive devices and home safety.

10. Dependent Care

 Medical Management: Monitor for signs of respiratory compromise; consult neurologist regularly.
 Diagnostic Test: EMG, MRI, pulmonary function tests; confirm diagnosis and monitor progression.
 Pharmacologic Care: Riluzole (delays disease progression); Edaravone (may slow functional decline).
 Therapeutic Care: Physical therapy to maintain joint function and muscle strength.
 Complementary and Alternative Therapy: Massage therapy for muscle relaxation; mindfulness for
anxiety.
 Nutritional and Diet Therapy: Soft or pureed diet, high-calorie supplements to maintain weight.

11. Surgical Intervention

 Tracheostomy may be considered for long-term ventilatory support in advanced stages.

12. Evaluation: Expected Outcome of Care

 Patient maintains adequate oxygenation and nutrition.

 Patient communicates effectively using assistive devices.
  Patient expresses feelings and participates in decision-making.

13. Reporting and Documentation of Care

 Document respiratory status, nutritional intake, motor function changes, and psychosocial needs each shift.

14. Evidence-Based Practice of Care

 Use of non-invasive ventilation like BiPAP improves quality of life and survival (Radunovic et al.,
Cochrane Review, 2017).
 Multidisciplinary ALS care teams improve functional outcomes (Ng et al., JAMA Neurology, 2015).

15. Relevant Legal, Moral, and Ethical Standards of Care

 Ensure informed consent and advanced directives are discussed.

 Respect for patient autonomy in end-of-life decisions.
 Maintain confidentiality and dignity in care (ANA Code of Ethics).