Neurological Disorders

Comprehensive Nursing Care & Clinical Management

Adult Health II - Exam 3

6 Major Disorders Covered

Ch 64-65 Brunner & Suddarth's

CNS/PNS System Involvement

Understanding Neurological Disorders

OVERVIEW

Neurological disorders encompass a wide range of conditions affecting the central nervous system (CNS) and peripheral nervous system (PNS). These disorders can significantly impact motor function, sensory perception, cognition, and overall quality of life. Understanding the pathophysiology, clinical manifestations, and nursing management of these conditions is essential for providing comprehensive patient care.

This guide covers six major neurological disorders that you must understand for comprehensive patient care:

Multiple Sclerosis (MS)

Immune-mediated demyelinating disease of the CNS affecting young adults.

Myasthenia Gravis (MG)

Motor disorder affecting the myoneural junction with muscle weakness.

Guillain-Barré Syndrome (GBS)

Acute inflammatory demyelinating polyneuropathy with ascending weakness.

Trigeminal Neuralgia

Chronic pain condition affecting cranial nerve V with severe facial pain.

Bell's Palsy

Unilateral facial paralysis affecting cranial nerve VII.

Amyotrophic Lateral Sclerosis (ALS)

Progressive motor neuron disease with no sensory impairment.

LEARNING OBJECTIVES

Describe the pathophysiology, clinical manifestations, diagnostic evaluation, and management of major neurological disorders
Use the nursing process as a framework for care of patients with neurological disorders
Identify critical complications and implement appropriate nursing interventions
Educate patients and families about disease management and long-term care

Multiple Sclerosis (MS)

PATHOPHYSIOLOGY

Multiple Sclerosis is an immune-mediated, progressive demyelinating disease of the central nervous system (CNS). The immune system mistakenly attacks the myelin sheath that protects nerve fibers, causing inflammation and eventual damage to the myelin and underlying nerve fibers. This results in disrupted nerve impulse transmission and progressive neurological dysfunction.

The disease is characterized by lesions (plaques) scattered throughout the white matter of the CNS, particularly in the optic nerves, brainstem, spinal cord, and periventricular areas.

Risk Factors & Epidemiology

Age

Typically onset between 20-50 years, with peak incidence in the third and fourth decades of life.

Gender

Women are affected 2-3 times more frequently than men.

Genetics

Family history increases risk. Certain genetic markers (HLA-DR2) are associated with increased susceptibility.

Environmental Factors

Lack of Vitamin D, obesity, high salt diet during teenage years, and geographic location (higher incidence away from equator).

Clinical Presentation

Initial Presentation (CIS - Clinically Isolated Syndrome)

Unilateral optic neuritis: Vision loss, eye pain with movement, altered color perception
Focal symptoms: Weakness, numbness, or tingling in limbs
Partial myelopathy: Incomplete spinal cord dysfunction

Common Clinical Manifestations

Fatigue

Overwhelming tiredness, often worse in heat. Most common and disabling symptom.

Motor Symptoms

Weakness, difficulty with coordination and balance, spasticity affecting mobility.

Sensory Changes

Numbness, tingling, burning sensations, loss of proprioception.

Visual Disturbances

Diplopia (double vision), scotoma (blind spots), nystagmus, blurred vision.

Pain

Neuropathic pain, Lhermitte's sign (electric shock sensation with neck flexion).

Cognitive Changes

Memory problems, difficulty with attention, executive function deficits.

Emotional Changes

Depression, mood swings, pseudobulbar affect (inappropriate laughing/crying).

Speech/Swallowing

Dysarthria (slurred speech), dysphagia (difficulty swallowing).

Complications

Immediate Complications

Bladder, bowel, and sexual dysfunction
Urinary tract infections (UTIs)
Constipation
Pressure injuries
Pneumonia (aspiration risk)

Long-term Complications

Total blindness
Dementia or severe cognitive impairment
Contracture deformities
Dependent pedal edema
Osteoporosis (from immobility)

MS symptoms often worsen with heat exposure (Uhthoff's phenomenon). Patients should avoid hot baths, excessive exercise in heat, and febrile illnesses. Cooling strategies can temporarily improve symptoms.

Diagnostic Studies

DIAGNOSTIC PROCEDURES

MRI (Magnetic Resonance Imaging): Shows demyelinating lesions in the CNS; gadolinium enhancement indicates active inflammation
Lumbar Puncture/CSF Analysis: Electrophoresis reveals oligoclonal bands and elevated IgG index
Evoked Potential Studies: Detect slowed nerve conduction (visual, brainstem auditory, somatosensory)
Urodynamic Studies: Assess bladder dysfunction
Neuropsychological Testing: Evaluate cognitive function
Bone Mineral Density Testing: Screen for osteoporosis risk

Disease Classifications:

RIS (Radiologically Isolated Syndrome): MRI findings without clinical symptoms
CIS (Clinically Isolated Syndrome): First neurological episode; may or may not progress to MS
Relapsing-Remitting MS (RRMS): Distinct relapses followed by complete or partial recovery (85% of cases initially)
Secondary Progressive MS (SPMS): Gradual worsening after initial RRMS phase
Primary Progressive MS (PPMS): Steady decline from onset without distinct relapses (10-15% of cases)

Medical Management

TREATMENT GOALS

Delay the progression of the disease
Manage chronic symptoms and improve quality of life
Treat acute exacerbations
Prevent and manage complications

Disease-Modifying Therapies (DMTs)

Medication Class	Examples	Mechanism/Notes
Interferons	Interferon beta-1a, Interferon beta-1b	Modulate immune response; reduce relapse rate
Glatiramer Acetate	Copaxone	Synthetic protein that may block myelin-damaging cells
Oral DMTs	Teriflunomide, Fingolimod, Dimethyl fumarate	Various mechanisms; convenient oral administration
Monoclonal Antibodies	Ocrelizumab, Natalizumab	Target specific immune cells; highly effective
Chemotherapy Agents	Mitoxantrone	Reserved for aggressive MS; significant side effects

Acute Exacerbation Management

RELAPSE TREATMENT

Methylprednisolone: High-dose IV corticosteroids (1g daily for 3-5 days) to reduce inflammation
Plasma Exchange (Plasmapheresis): For severe relapses not responding to steroids
Rest and supportive care

Symptom Management Medications

Spasticity

Baclofen: First-line; GABA agonist
Diazepam: Benzodiazepine
Tizanidine: Alpha-2 agonist
Dantrolene: Acts on muscle directly

Fatigue

Amantadine: First-line treatment
Modafinil: Wakefulness-promoting agent
Dalfampridine: Improves walking speed

Ataxia/Tremor

Propranolol: Beta-blocker
Gabapentin: Anticonvulsant
Clonazepam: Benzodiazepine

Bladder/Bowel

Anticholinergics: For overactive bladder
Alpha-adrenergic blockers: For urinary retention
Antispasmodics: For bladder spasms
Stool softeners/laxatives: For constipation

Nursing Management

PRIORITY NURSING INTERVENTIONS

Assessment

Conduct comprehensive neurological assessment including motor strength, sensation, coordination, and cranial nerve function
Monitor for signs of exacerbation: new symptoms or worsening of existing symptoms
Assess mobility, fall risk, and need for assistive devices
Evaluate bladder and bowel function
Screen for depression, anxiety, and cognitive changes

Safety Measures

Implement fall prevention strategies (non-slip footwear, clear pathways, assistive devices)
Ensure adequate lighting and remove environmental hazards
Teach energy conservation techniques and pacing activities
Monitor skin integrity and implement pressure injury prevention

Symptom Management

Develop bowel and bladder retraining programs
Implement scheduled voiding and intermittent catheterization if needed
Provide cooling measures to manage heat sensitivity
Assist with ADLs while promoting independence

Patient & Family Education

Medication Management

Proper administration techniques for injectable DMTs, importance of adherence, recognizing and reporting side effects.

Energy Conservation

Prioritize activities, plan rest periods, use assistive devices, modify work/home environment.

Environmental Modifications

Adapt home for safety and accessibility, install grab bars, use mobility aids, optimize temperature control.

Complication Prevention

Recognize signs of UTI, maintain skin integrity, prevent pneumonia through deep breathing exercises.

MS is highly variable and unpredictable. Each patient's experience is unique. Focus on individualized care plans that address specific symptoms and functional limitations. Encourage patients to maintain hope while being realistic about disease progression.

Myasthenia Gravis (MG)

PATHOPHYSIOLOGY

Myasthenia Gravis is an autoimmune neuromuscular disorder affecting the myoneural junction. Antibodies attack and destroy acetylcholine receptors at the neuromuscular junction, preventing normal muscle contraction. This results in progressive muscle weakness that characteristically worsens with activity and improves with rest.

MG is a motor disorder with no effect on sensation or coordination. The hallmark feature is fatigable weakness - muscles become progressively weaker with repeated use and recover strength after rest.

Epidemiology & Risk Factors

Bimodal age distribution:
- Women: Typically affects those in their 2nd and 3rd decades of life (20-40 years)
- Men: More common after age 50, with peak incidence in 60s-70s
Thymus abnormalities: 75% have thymic hyperplasia; 10-15% have thymoma
Association with other autoimmune diseases: Thyroid disorders, rheumatoid arthritis, lupus

Clinical Manifestations

Ocular Symptoms (Often First to Appear)

OCULAR MYASTHENIA

Ptosis: Drooping of one or both eyelids, worsens as day progresses
Diplopia: Double vision due to weak extraocular muscles
Symptoms worsen with sustained upward gaze
May remain isolated to eyes (15-20% of cases) or progress to generalized MG

Generalized (Bulbar) Symptoms

Facial Weakness

Expressionless face, difficulty closing eyes completely, weak smile ("snarl").

Dysphonia

Voice impairment; voice becomes weaker, hoarse, or nasal with prolonged speaking.

Dysphagia

Difficulty swallowing; risk of aspiration, choking, nasal regurgitation.

Limb Weakness

Proximal muscle weakness affects shoulders, hips. Difficulty rising from chair, climbing stairs, lifting arms.

Respiratory Weakness

Weakness of diaphragm and intercostal muscles; can lead to respiratory failure.

Chewing Difficulty

Jaw becomes progressively weaker during meals; may be unable to finish eating.

MG symptoms characteristically fluctuate during the day, typically worsening in the evening and improving after rest. This fatigability pattern is a key diagnostic feature.

Diagnostic Studies

DIAGNOSTIC TESTS

Acetylcholinesterase Inhibitor Test (Tensilon Test)

IV administration of edrophonium (Tensilon) or neostigmine
Rapid, temporary improvement in muscle strength confirms diagnosis
CRITICAL: Have atropine at bedside to counteract potential cholinergic side effects (bradycardia, bronchospasm)
Monitor cardiac rhythm during test

Ice Test

Alternative for patients with cardiac conditions or asthma (safer than Tensilon test)
Apply ice pack to affected eye for 2 minutes
Improvement in ptosis suggests MG

Additional Diagnostics

Single Fiber Electromyography (EMG): Most sensitive test; shows abnormal neuromuscular transmission
Serum Acetylcholine Receptor Antibodies: Present in 80-90% of generalized MG
MRI of chest: Detect thymoma or thymic hyperplasia
Pulmonary function tests: Assess respiratory muscle strength

Medical Management

TREATMENT GOALS

Improve neuromuscular transmission and muscle function
Reduce or remove circulating antibodies
Prevent myasthenic and cholinergic crises
Maintain respiratory function

Pharmacotherapy

FIRST-LINE THERAPY

Pyridostigmine Bromide (Mestinon) - Anticholinesterase Inhibitor

Mechanism: Prevents breakdown of acetylcholine at neuromuscular junction, prolonging its action
Dosing: Typically 60-120 mg every 3-4 hours; timing is crucial
Onset: 30-60 minutes; peak effect at 2 hours
Common side effects: Diarrhea, abdominal cramps, excessive salivation, nausea
Nursing consideration: Administer with food or milk to minimize GI upset; time doses to optimize function during important activities

Second-Line Immunomodulators

Medication	Action	Key Nursing Considerations
Corticosteroids (Prednisone)	Suppress immune response; reduce antibody production	Monitor for infection, hyperglycemia, bone loss. May cause temporary worsening initially. Taper slowly.
Azathioprine (Imuran)	Immunosuppressant; steroid-sparing agent	Monitor CBC for bone marrow suppression. Takes 6-12 months for full effect.
Mycophenolate (CellCept)	Inhibits lymphocyte proliferation	Monitor for GI effects, infection risk. Check CBC regularly.
Cyclosporine	T-cell suppression	Monitor kidney function, blood pressure. Numerous drug interactions.

Third-Line Therapies

Rituximab: Monoclonal antibody targeting B cells; used for refractory cases
Eculizumab: Complement inhibitor for refractory generalized MG
IV Immunoglobulin (IVIG): For acute exacerbations; provides temporary improvement

Therapeutic Plasma Exchange (Plasmapheresis)

PLASMAPHERESIS

Removes circulating antibodies from blood
Indications: Myasthenic crisis, pre-operative preparation, acute exacerbations
Effects temporary (weeks to months); typically 5-7 treatments over 10-14 days
Nursing considerations: Monitor vital signs, assess vascular access site, watch for hypotension and bleeding

Surgical Management: Thymectomy

Indications: Thymoma present (absolute indication), generalized MG in patients age 10-65
Benefits: 50-60% achieve remission or significant improvement; may take months to years for full benefit
Timing: Best results when performed early in disease course

Myasthenic Crisis vs. Cholinergic Crisis

Both crises are life-threatening emergencies requiring immediate intervention! The key difference lies in the cause and treatment approach.

Myasthenic Crisis

Cause: Undermedication or disease exacerbation

Triggers:

Respiratory infection
Medication changes or missed doses
Pregnancy, surgery, stress
Medications that worsen MG (aminoglycosides, beta-blockers, quinolones)

Manifestations:

Severe generalized weakness
Respiratory failure
Dysphagia
Minimal secretions

Treatment:

Increase anticholinesterase medication
Plasmapheresis or IVIG
Mechanical ventilation

Cholinergic Crisis

Cause: Overmedication with anticholinesterase drugs

Trigger:

Excessive doses of pyridostigmine
Medication accumulation

Manifestations:

Muscle weakness
Respiratory failure
PLUS cholinergic symptoms:
Excessive salivation, lacrimation
Diarrhea, abdominal cramps
Miosis (constricted pupils)
Bradycardia
Fasciculations

Treatment:

STOP anticholinesterase medication
Atropine to counteract cholinergic effects
Mechanical ventilation

CRISIS MANAGEMENT

Immediate Interventions for Both Crises:

Airway protection is priority! Assess respiratory status continuously
Provide non-invasive ventilation or mechanical ventilation as needed
Monitor vital signs, ABGs, oxygen saturation continuously
Maintain NPO status initially; risk of aspiration
Monitor fluid and electrolyte balance
Suction secretions as needed
Provide emotional support to patient and family

Nursing Management

PRIORITY NURSING CARE

Assessment

Monitor respiratory status: rate, depth, oxygen saturation, ability to cough effectively
Assess muscle strength regularly using standardized scale
Evaluate swallowing ability before meals; watch for signs of aspiration
Document medication effectiveness and timing of symptom relief
Monitor for signs of crisis (increasing weakness, respiratory distress)

Medication Management

Administer anticholinesterase medications precisely on schedule; timing affects function
Give medications 30-45 minutes before meals to optimize swallowing strength
Monitor for medication side effects (GI upset, excessive secretions)
Teach patients to recognize signs of under- and over-medication

Nutrition Support

Recommend soft foods that are easier to chew and swallow
Encourage eating larger meals in the morning when strength is better
Provide smaller, more frequent meals in the afternoon/evening
Position patient upright during and after meals
Allow adequate time for meals without rushing

Patient & Family Education

Self-Care

Energy conservation, activity pacing, recognizing symptoms of worsening disease, when to seek help.

Medication Management

Strict adherence to schedule, not skipping doses, recognizing side effects, keeping medication diary.

Ocular Management

Tape eyelids closed during sleep if needed, use artificial tears, wear eyeglasses with prism lenses for diplopia, alternate eye patching.

Safety at Home

Keep suction equipment available, wear medical alert identification, avoid triggers, maintain emergency plan.

Patients with MG should avoid medications that can exacerbate symptoms: aminoglycoside antibiotics, fluoroquinolones, macrolides, beta-blockers, calcium channel blockers, magnesium, muscle relaxants, and some anesthetics. Always check drug compatibility!

Guillain-Barré Syndrome (GBS)

PATHOPHYSIOLOGY

Guillain-Barré Syndrome (also known as acute idiopathic polyneuritis) is an acute, immune-mediated disorder of the peripheral nervous system. It involves a cell-mediated and humoral immune attack on peripheral nerve myelin proteins, causing inflammatory demyelination.

The immune attack typically targets ganglioside GM1b, leading to progressive muscle weakness that characteristically begins in the lower extremities and ascends upward. GBS is purely motor with no altered sensation, though patients may experience paresthesias. Importantly, cognition and level of consciousness remain intact throughout the illness.

Etiology & Triggers

GBS typically occurs 1-3 weeks after a triggering event, most commonly:

Campylobacter jejuni

Most common bacterial trigger (30-40% of cases). Associated with diarrheal illness.

Viral Infections

Cytomegalovirus (CMV), Epstein-Barr virus (EBV), influenza, Zika virus.

Respiratory Infections

Mycoplasma pneumoniae, Haemophilus influenzae.

Other Triggers

Recent surgery, vaccinations (rare), immunizations, lymphoma.

Clinical Manifestations

Classic Presentation

HALLMARK FEATURES

Ascending weakness: Begins in lower extremities and progresses upward symmetrically
Areflexia: Loss of deep tendon reflexes (early and consistent finding)
Motor involvement only: No sensory loss (though paresthesias common)
Cranial nerve involvement: Facial weakness (50%), dysphagia, ophthalmoplegia
Respiratory failure: Can occur in 20-30% of cases due to diaphragm/intercostal muscle weakness
Intact cognition and LOC: Patient remains fully alert and aware

Progression Timeline

Acute phase (progression): Symptoms worsen over 2-4 weeks
Plateau phase: Symptoms stabilize; lasts days to weeks
Recovery phase: Gradual improvement over months to years
Note: If progression continues beyond 4 weeks, consider diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP)

Respiratory failure can occur rapidly in GBS! Continuous monitoring of respiratory function is essential. Watch for declining vital capacity, weak cough, difficulty managing secretions, shortness of breath, and use of accessory muscles.

Autonomic Dysfunction

Occurs in 65% of patients and can be life-threatening:

Cardiac: Tachycardia, bradycardia, arrhythmias, blood pressure fluctuations
Gastrointestinal: Ileus, constipation, diarrhea
Genitourinary: Urinary retention, incontinence
Temperature regulation: Hyperthermia, hypothermia, excessive sweating

Diagnostic Studies

DIAGNOSTIC FINDINGS

Lumbar Puncture/CSF Analysis

Elevated protein (>45 mg/dL), often markedly elevated (100-1000 mg/dL)
Normal white blood cell count (albuminocytologic dissociation - classic finding)
Protein elevation peaks at 4-6 weeks

Electrophysiologic Studies

Nerve conduction studies: Show progressive loss of nerve conduction velocity
Prolonged distal latencies, conduction blocks
Findings may be normal early in disease

Pulmonary Function Tests

Monitor forced vital capacity (FVC) and negative inspiratory force (NIF)
Declining values indicate need for respiratory support

Medical Management

TREATMENT GOALS

Provide supportive care and prevent complications during acute phase
Reduce severity and duration of symptoms through immunotherapy
Maintain respiratory and cardiovascular function
Prevent complications of immobility
Support recovery and rehabilitation

Immunotherapy

Therapeutic Plasma Exchange (TPE/Plasmapheresis)

Removes circulating antibodies and inflammatory mediators
Most effective when started within 2 weeks of symptom onset
Typically 5 exchanges over 8-10 days
Reduces time on ventilator and shortens recovery

IV Immunoglobulin (IVIG)

Modulates immune response
Dose: 0.4 g/kg/day for 5 days (total 2 g/kg)
Equally effective as plasmapheresis
Easier to administer; fewer side effects
Preferred in patients with cardiovascular instability

Note: Corticosteroids are NOT effective in GBS and are not recommended.

Respiratory Support

RESPIRATORY MANAGEMENT

Non-invasive ventilation (NIV): BiPAP for early respiratory muscle weakness
Mechanical ventilation: Required in 20-30% of patients
- Indications: FVC <20 mL/kg, NIF <-30 cm H2O, PaO2 <70 mmHg
- Average duration: 2-4 weeks
Tracheostomy: Consider if prolonged ventilation (>2 weeks) expected

DVT Prophylaxis

Pharmacologic: Low molecular weight heparin or unfractionated heparin
Mechanical: Sequential compression devices, early mobilization when safe
GBS patients at high risk due to immobility and autonomic dysfunction

Additional Supportive Care

Pain management: Gabapentin, carbamazepine for neuropathic pain
Alpha-adrenergic blockers: For urinary retention
Cardiac monitoring: Continuous for autonomic dysfunction
Nutrition support: Enteral feeding if dysphagia present

Complications

Acute Complications

Respiratory failure
Pulmonary embolism
Autonomic dysfunction
Cardiac arrhythmias
Aspiration pneumonia
Sepsis

Long-term Complications

Persistent weakness (10-20%)
Fatigue
Neuropathic pain
Depression/anxiety
Recurrence (3-5%)

Nursing Management

PRIORITY NURSING INTERVENTIONS

Respiratory Monitoring (HIGHEST PRIORITY)

Assess respiratory rate, depth, pattern continuously
Monitor oxygen saturation, ABGs
Measure vital capacity and NIF regularly (every 2-4 hours initially)
Assess ability to cough and handle secretions
Suction as needed; position for optimal lung expansion
Watch for signs of respiratory distress: dyspnea, tachypnea, use of accessory muscles, anxiety

Cardiovascular Monitoring

Continuous cardiac monitoring for arrhythmias
Monitor blood pressure frequently (autonomic instability)
Assess for orthostatic hypotension before position changes
Avoid sudden position changes

Enhancing Physical Mobility

Perform passive range of motion exercises to prevent contractures
Reposition every 2 hours to prevent pressure injuries
Use pressure-relieving devices (specialty mattress, heel protectors)
Begin physical therapy as soon as patient stabilizes
Progress from passive to active exercises as strength improves

Additional Nursing Care

Nutrition

Assess swallowing ability before oral intake. Provide enteral nutrition if dysphagia present. Monitor for aspiration.

Communication

Provide alternative communication methods if facial weakness or intubation. Be patient; allow time for responses.

Anxiety Reduction

Explain all procedures. Reassure about cognition remaining intact. Provide emotional support. Remember: patient is AWARE but unable to move.

Fatigue Management

Balance rest with activity. Prioritize essential activities. Plan rest periods. Gradually increase activity as tolerated.

The psychological impact of GBS is profound. Patients remain fully conscious and aware while experiencing progressive paralysis and potential ventilator dependence. Provide frequent reassurance that recovery is expected. Many patients experience anxiety, depression, and PTSD. Psychological support is essential.

Patient & Family Education

Disease course: Explain three phases - worsening, plateau, recovery
Recovery expectations: Most patients recover fully, but it takes time (months to years)
Rehabilitation: Physical and occupational therapy crucial for optimal recovery
Recurrence: Rare (3-5%) but possible; report new symptoms immediately
Support resources: GBS/CIDP Foundation International for education and support

Prognosis

Full recovery: 70-80% of patients recover completely or near-completely within 6-12 months
Mortality: 3-5% despite treatment (usually from complications)
Persistent deficits: 10-20% have long-term weakness or fatigue
Poor prognostic factors: Older age, rapid progression, need for mechanical ventilation, axonal variant

Trigeminal Neuralgia

PATHOPHYSIOLOGY

Trigeminal Neuralgia (also known as "Tic Douloureux") is a chronic pain condition affecting the trigeminal nerve (Cranial Nerve V). The disorder is caused by demyelination of axons in the trigeminal ganglion, root, and nerve, typically from compression by blood vessels (most commonly the superior cerebellar artery) or, less frequently, by a demyelinating disease like multiple sclerosis.

The trigeminal nerve has three major branches: ophthalmic (V1), maxillary (V2), and mandibular (V3). The maxillary and mandibular branches are most commonly affected.

Epidemiology & Risk Factors

Age: Typically affects individuals 50-60 years old
Gender: Slightly more common in women
Multiple sclerosis: 2-4% of MS patients develop trigeminal neuralgia; consider MS in younger patients with bilateral symptoms
Vascular compression: Most common cause in older adults

Clinical Manifestations

CLASSIC PAIN PRESENTATION

Character of Pain:

Unilateral (affects one side of face only)
Sudden, intense, sharp - described as shooting, stabbing, electric shock-like, or burning
Brief episodes - lasting seconds to 2 minutes
Excruciating intensity - one of the most severe pains known to medicine
Paroxysmal - comes in sudden attacks with pain-free intervals

Distribution: Follows one or more branches of trigeminal nerve

V2 (maxillary): Upper lip, upper teeth, cheek, lower eyelid
V3 (mandibular): Lower lip, lower teeth, chin, jaw
V1 (ophthalmic): Forehead, eye, upper eyelid (least common)

Trigger Zones & Activities

Paroxysms can be triggered by stimulation of nerve branch terminals:

Facial Touch

Light touch to face, cheek, or lips. Even a breeze can trigger attacks.

Oral Activities

Chewing, talking, swallowing, brushing teeth.

Facial Movements

Smiling, grimacing, washing face, applying makeup.

Temperature

Cold air, hot or cold foods/beverages.

Patients often develop adaptive behaviors to avoid triggers: eating on unaffected side, not washing face, letting beard grow, avoiding conversation. Weight loss is common due to fear of triggering pain while eating.

Impact on Quality of Life

Fear and anxiety: Constant worry about when next attack will occur
Social isolation: Avoiding activities that might trigger pain
Depression: Common due to chronic pain and lifestyle limitations
Malnutrition: Avoiding eating to prevent triggering pain
Poor oral hygiene: Fear of brushing teeth

Diagnostic Studies

Clinical diagnosis: Based primarily on characteristic pain description and pattern
MRI with contrast: Rule out structural causes (tumor, MS plaques, vascular compression)
MR angiography: Identify vascular compression
Neurological examination: Usually normal between attacks; no sensory deficits

Medical Management

TREATMENT GOAL

Achieve pain control while minimizing medication side effects and improving quality of life. Medical management is always tried first; surgery reserved for medication failures or intolerable side effects.

Pharmacologic Management

FIRST-LINE MEDICATION

Carbamazepine (Tegretol) - Anticonvulsant

Mechanism: Blocks sodium channels, reducing nerve excitability
Effectiveness: 70-80% of patients achieve initial pain relief
Dosing: Start low (100-200 mg twice daily), gradually increase to effective dose (usually 600-1200 mg/day divided)
CRITICAL: Must be taken with food to minimize GI upset and enhance absorption
Side effects: Dizziness, drowsiness, ataxia, nausea, diplopia
Monitoring: CBC, liver function, serum sodium (risk of hyponatremia), therapeutic drug levels
Warning: Risk of aplastic anemia, agranulocytosis, Stevens-Johnson syndrome (rare but serious)

Alternative Medications

Medication	Dosing	Notes
Gabapentin	900-3600 mg/day divided	Fewer side effects than carbamazepine; useful for neuropathic pain
Baclofen	40-80 mg/day divided	Muscle relaxant; can be used alone or with carbamazepine
Phenytoin	300-400 mg/day	Alternative anticonvulsant if carbamazepine not tolerated
Oxcarbazepine	600-1800 mg/day divided	Similar to carbamazepine but better tolerated; fewer drug interactions
Lamotrigine	200-400 mg/day	Useful adjunct; slow titration required to prevent rash

Surgical Management

Indications for surgery:

Medication failure or intolerable side effects
Patient preference for definitive treatment
Younger patients seeking long-term solution

Microvascular Decompression (MVD)

Most effective long-term solution

Surgical procedure to move or cushion blood vessel compressing nerve
Success rate: 80-90% pain relief
Durability: 70-80% remain pain-free at 10 years
Risks: Hearing loss, facial weakness, CSF leak, stroke (rare)

Percutaneous Procedures

Less invasive alternatives

Radiofrequency thermal coagulation: Heat lesions nerve
Balloon microcompression: Compresses nerve with inflated balloon
Glycerol injection: Chemical lesioning
Stereotactic radiosurgery (Gamma Knife): Focused radiation
Lower success rates but fewer risks than MVD

Nursing Management

PAIN PREVENTION STRATEGIES

Personal Hygiene Modifications

Provide cotton pads and room temperature water for washing face (avoid extremes)
Use soft, small toothbrush or recommend mouthwash if brushing triggers pain
Encourage oral hygiene during pain-free intervals
Suggest electric razor to avoid face touching (for men)

Dietary Modifications

Serve foods and fluids at room temperature (avoid hot/cold extremes)
Provide soft, easy-to-chew foods that require minimal jaw movement
Encourage patient to chew on unaffected side
Small, frequent meals rather than large meals requiring prolonged chewing
Use straw for liquids if it doesn't trigger pain
High-calorie, nutrient-dense foods to prevent weight loss

Environmental Modifications

Protect face from cold air and wind
Keep room at comfortable, stable temperature
Avoid drafts and air conditioning blowing directly on face

Psychosocial Support

Anxiety Management

Address fear of next attack. Teach relaxation techniques. Consider referral to counseling.

Depression Screening

Assess for signs of depression. Discuss treatment options. Provide mental health resources.

Insomnia Support

Pain can disrupt sleep. Address sleep hygiene. Discuss medication timing to optimize rest.

Support Groups

Connect with Trigeminal Neuralgia Association. Share coping strategies with others who understand.

Postoperative Care (After Surgical Procedures)

POST-SURGICAL NURSING CARE

Neurological assessment: Monitor for changes in level of consciousness, pupil response, motor/sensory function
Cranial nerve function: Assess all cranial nerves, particularly facial nerve (CN VII) and vestibulocochlear nerve (CN VIII)
Swallowing and chewing assessment: Observe for difficulties; test swallow before oral intake
Pain assessment: Evaluate for relief of trigeminal pain; assess surgical site pain
Monitor for complications: CSF leak, meningitis, facial numbness, hearing loss
Wound care: Keep incision clean and dry; monitor for infection

After percutaneous procedures, patients often experience facial numbness or decreased sensation. While this may be concerning, it often improves over time. Educate patients about protecting numb areas from injury (burns, trauma) and the importance of good oral hygiene despite altered sensation.

Bell's Palsy

PATHOPHYSIOLOGY

Bell's Palsy (also called "idiopathic facial paralysis") is an acute, unilateral inflammation and paralysis of the facial nerve (Cranial Nerve VII). The exact cause is unknown, but it is believed to result from reactivation of dormant viral infections (particularly herpes simplex virus or varicella-zoster virus) or autoimmune processes that cause inflammation and swelling of the facial nerve within the narrow bony canal (facial canal).

The inflammation leads to compression of the nerve, disrupting nerve signal transmission and causing temporary facial paralysis. Most cases recover spontaneously, but early treatment can improve outcomes.

Epidemiology & Risk Factors

Age: Can occur at any age, but most common in individuals 15-45 years old
Incidence: Most common cause of acute facial paralysis (60-75% of cases)
Risk factors:
- Pregnancy (especially third trimester)
- Diabetes mellitus
- Upper respiratory infections
- Family history
Recurrence: 7-12% of patients experience recurrence, sometimes affecting the opposite side

Clinical Manifestations

CHARACTERISTIC PRESENTATION

Onset: Sudden, typically developing over 24-48 hours; patient often wakes with facial weakness

Facial Distortion (Unilateral):

Inability to close eye on affected side (lagophthalmos)
Drooping of mouth and corner of mouth
Flattening of nasolabial fold
Loss of forehead wrinkles (cannot raise eyebrow)
Asymmetric smile - mouth pulls to unaffected side
Drooling from affected side

Associated Symptoms:

Excessive lacrimation (tearing) or paradoxical dry eye
Painful sensations in face, behind ear, or in the eye
Hyperacusis (increased sensitivity to sound on affected side)
Loss of taste on anterior two-thirds of tongue
Decreased saliva production on affected side

Key Differential Feature: Bell's palsy affects BOTH upper and lower face (cannot close eye, cannot raise eyebrow). In stroke, the forehead is typically spared (can raise eyebrow, wrinkle forehead) because upper face has bilateral innervation. If patient can wrinkle forehead on affected side, suspect stroke!

Speech Difficulties

Difficulty articulating labial sounds (p, b, m)
Speech may sound slurred or distorted
Difficulty drinking from cup or straw (leakage)
Food collecting in cheek on affected side

Diagnostic Evaluation

Bell's palsy is primarily a clinical diagnosis based on sudden onset unilateral facial weakness with involvement of forehead.

Neurological examination: Assess all cranial nerves; rule out other neurological deficits
Exclude other causes: Lyme disease, stroke, tumor, trauma, Ramsay Hunt syndrome
- Ramsay Hunt syndrome: Herpes zoster of geniculate ganglion; presents with vesicles in ear canal, more severe pain, worse prognosis
MRI: Not routinely needed; used if atypical features, bilateral involvement, or no improvement
Electromyography (EMG): May be used after 2 weeks to assess nerve damage and prognosis

Medical Management

TREATMENT GOAL

Reduce inflammation, maintain muscle tone, prevent denervation, protect the eye, and support recovery. Most patients (70-80%) recover spontaneously, but treatment can improve outcomes, especially if started early.

Pharmacologic Management

MEDICATION THERAPY

Corticosteroids (MOST IMPORTANT)

Prednisone: 60-80 mg daily for 5-7 days, then taper
Mechanism: Reduce inflammation and nerve swelling
Timing critical: Most effective when started within 72 hours of symptom onset
Evidence: Significantly improves likelihood of complete recovery

Antiviral Medications (Controversial)

Acyclovir or Valacyclovir: May be added to steroids if viral etiology suspected
Evidence mixed on benefit when used alone; may provide small benefit when combined with steroids
Consider in severe cases or if vesicles present (Ramsay Hunt syndrome)

Analgesics

For pain behind ear or facial pain
NSAIDs, acetaminophen, or opioids for severe pain

Electrical Stimulation

May help maintain muscle tone during recovery
Prevents muscle atrophy
Physical therapy can guide appropriate exercises

Recovery & Prognosis

Typical recovery time: 3-5 weeks for most patients
Complete recovery: 70-80% of patients recover fully
Partial recovery: 15-20% have residual weakness
No recovery: <5% have permanent facial paralysis
Poor prognostic signs: Complete paralysis, no improvement by 3 weeks, age >60, diabetes, severe pain, hyperacusis
Synkinesis: Abnormal facial movements may develop during recovery (involuntary movement when trying to move another facial muscle)

Nursing Management

PRIORITY NURSING CARE

Eye Protection (HIGHEST PRIORITY)

Inability to close eye can lead to corneal drying, abrasion, ulceration, and permanent vision loss! Eye protection is the most critical nursing intervention.

Protective shield at night: Cover eye with shield or patch to prevent corneal abrasion during sleep
Moisturizing eye drops during day: Artificial tears every 1-2 hours while awake
Lubricating eye ointment at night: Apply before bed; provides longer-lasting protection
Wraparound sunglasses and goggles: Protect from wind, dust, debris outdoors
Gentle eye closure: Manually close eyelid periodically throughout day
Avoid eye strain: Limit reading, computer use, bright lights
Monitor for complications: Redness, pain, discharge, vision changes (report immediately)

Facial Muscle Care

Facial Massage

Gentle massage if decreased sensitivity. Upward motion following muscle fibers. Maintain muscle tone and blood flow.

Facial Exercises

Start after acute phase. Practice facial expressions in mirror. Smile, frown, raise eyebrows, pucker lips.

Moist Heat

Apply warm, moist compresses to face. Promotes comfort and circulation. 15-20 minutes several times daily.

Positioning

Support affected side of face when lying down. Prevents stretching of weak muscles.

Nutrition & Oral Care

Soft diet: Easier to chew; less likely to collect in cheek
Small bites: Easier to manage with facial weakness
Chew on unaffected side
Check affected side: Food may collect in cheek; remove with finger or rinse
Avoid hot foods: Decreased sensation increases burn risk
Use straw if possible: May reduce drooling
Oral hygiene: Meticulous care; food particles trapped more easily

Communication Support

Speak slowly and allow time for patient to respond
Provide paper and pen or communication board if speech significantly affected
Encourage patient to communicate; speech intelligibility usually maintained
Reassure that speech clarity will improve as facial function returns

Psychosocial Support

EMOTIONAL CARE

Acknowledge distress: Facial paralysis is emotionally traumatic; validate patient's feelings
Provide reassurance: Most patients recover completely; emphasize positive prognosis
Body image concerns: Address fears about appearance; offer strategies for managing in public
Social support: Encourage family support; consider support groups
Screen for depression: Prolonged recovery or poor prognosis can lead to depression
Return to work/school: Discuss timing and accommodations needed

The psychological impact of Bell's palsy is often underestimated. Sudden facial asymmetry affects self-image, social interactions, and emotional well-being. Provide empathy, reassurance, and hope. Remind patients that recovery is expected and facial appearance will improve.

Amyotrophic Lateral Sclerosis (ALS)

PATHOPHYSIOLOGY

Amyotrophic Lateral Sclerosis (also known as "Lou Gehrig's Disease") is a progressive, fatal neurodegenerative disorder characterized by the loss of motor neurons in the anterior horns of the spinal cord and the motor nuclei of the lower brainstem. The disease causes progressive muscle weakness, atrophy, and paralysis while sparing sensory function, cognition (initially), and autonomic functions like bladder and bowel control.

"Amyotrophic" refers to muscle atrophy from denervation; "lateral sclerosis" refers to hardening of the lateral corticospinal tracts in the spinal cord. The disease affects both upper motor neurons (brain and brainstem) and lower motor neurons (spinal cord).

Epidemiology & Risk Factors

Age

Typically affects individuals 40-60 years old. Average age of onset: 55 years.

Gender

Slightly more common in men (1.5:1 ratio).

Genetics

90-95% sporadic (no family history). 5-10% familial (inherited mutations, often SOD1 gene).

Risk Factors

Military service, smoking, environmental toxin exposure, autoimmune diseases (possible associations).

CRITICAL DISTINCTION: In ALS, anal and bladder sphincter function remains intact throughout the disease course. This differentiates ALS from other motor neuron diseases and helps with diagnosis.

Clinical Manifestations

Early Symptoms

INITIAL PRESENTATION

Onset is typically insidious and asymmetric. Early symptoms vary depending on which motor neurons are affected first:

Limb-Onset ALS (70% of cases):

Focal weakness: One hand, arm, or leg
Muscle cramps and fasciculations (visible muscle twitching)
Difficulty with fine motor tasks: Buttoning clothes, writing, turning keys
Foot drop: Tripping, stumbling, difficulty walking
Hand weakness: Dropping objects, difficulty with grip

Bulbar-Onset ALS (25% of cases):

Dysarthria: Slurred speech, difficulty articulating
Dysphagia: Difficulty swallowing, choking
Excessive drooling
Tongue weakness and atrophy
Poorer prognosis than limb-onset

Progressive Symptoms

Muscle Weakness

Progressive, eventually affecting all voluntary muscles. Weakness spreads from initial site to adjacent regions.

Muscle Atrophy

Visible wasting of muscles due to denervation. Particularly noticeable in hands, arms, legs.

Spasticity

Increased muscle tone from upper motor neuron involvement. Can cause painful muscle cramps and stiffness.

Fasciculations

Spontaneous muscle twitching visible under skin. Result of dying motor neurons firing irregularly.

Fatigue

Overwhelming tiredness from muscle weakness and increased effort for all movements.

Hyperreflexia

Exaggerated deep tendon reflexes from upper motor neuron damage. Reflexes become brisk and overactive.

Bulbar Symptoms (Eventually Affect Most Patients)

Difficulty swallowing (dysphagia): Increased risk of aspiration, choking, weight loss
Difficulty chewing: Jaw weakness makes eating exhausting
Difficulty speaking (dysarthria): Progresses to anarthria (inability to speak)
Excessive saliva: Actually normal saliva production but difficulty swallowing it
Pseudobulbar affect: Inappropriate laughing or crying (emotional lability)

Respiratory Symptoms

Respiratory compromise is the leading cause of death in ALS. Progressive weakness of diaphragm and intercostal muscles leads to respiratory failure.

Dyspnea: Shortness of breath, especially when lying flat
Weak cough: Difficulty clearing secretions; increased pneumonia risk
Sleep disturbances: Sleep apnea, morning headaches from CO2 retention
Use of accessory muscles
Paradoxical breathing: Abdomen moves inward with inspiration

Cognitive Impairment

Frontotemporal dementia: Develops in ~15% of ALS patients
Executive dysfunction: Planning, organization, decision-making difficulties
Language difficulties: Word-finding problems
Behavioral changes: Apathy, disinhibition, loss of empathy

Preserved Functions in ALS: Eye movements (usually spared until late), bladder and bowel control, sensory function, sexual function. These preserved functions distinguish ALS from other neurological disorders.

Diagnostic Studies

No single definitive test for ALS; diagnosis based on clinical presentation and ruling out other conditions.

DIAGNOSTIC WORKUP

Electromyography (EMG)

Shows denervation in multiple body regions
Fibrillations, positive sharp waves, fasciculations
Evidence of both acute and chronic denervation

Nerve Conduction Studies

Usually normal or mildly reduced
Helps rule out peripheral neuropathy

MRI

Rule out structural lesions (tumors, spinal stenosis)
May show signal changes in corticospinal tracts (not diagnostic)

Laboratory Tests

Rule out mimics: Heavy metal toxicity, Lyme disease, HIV, thyroid disorders
Creatine kinase (CK) often mildly elevated

Muscle Biopsy

Shows denervation atrophy
Not routinely performed

Neuropsychological Testing

Assess for cognitive impairment and frontotemporal dementia
Important for care planning and advance directives

Medical Management

TREATMENT GOALS

ALS is incurable and fatal. Treatment focuses on slowing disease progression, managing symptoms, maintaining quality of life, and providing supportive care. Multidisciplinary care is essential.

Disease-Modifying Medications

Medication	Mechanism	Benefit & Notes
Riluzole	Glutamate antagonist; reduces excitotoxicity	Extends survival by 2-3 months. Must be taken on empty stomach. Monitor LFTs.
Edaravone	Free radical scavenger; antioxidant	May slow functional decline in early-stage ALS. Given IV. Expensive.

Note: These medications provide modest benefit and do not cure or reverse the disease.

Symptom Management Medications

Spasticity

Baclofen: First-line
Tizanidine
Dantrolene sodium
Diazepam: Also helps anxiety

Fatigue

Modafinil: Wakefulness-promoting
Energy conservation strategies

Depression/Anxiety

SSRIs: Sertraline, citalopram
Tricyclics: Also helps with pseudobulbar affect
Counseling and support

Excessive Saliva

Anticholinergics: Glycopyrrolate
Botulinum toxin: Salivary gland injections
Suction devices

Respiratory Management

RESPIRATORY SUPPORT

Non-Invasive Ventilation (NIV)

BiPAP: Started when symptoms of respiratory insufficiency develop
Improves quality of life and may extend survival
Initially used at night, then may progress to continuous use
Most patients tolerate well

Mechanical Ventilation

Via tracheostomy when NIV insufficient or not tolerated
Major decision requiring discussion of goals of care
Can prolong life significantly but requires 24/7 care
Patient may become "locked-in" (conscious but unable to move or communicate)
Requires early discussion as part of advance care planning

Cough Assist Devices

Mechanical insufflation-exsufflation helps clear secretions
Prevents pneumonia in patients with weak cough

Nutritional Support

FEEDING OPTIONS

Dietary Modifications

Soft, moist foods easier to swallow
Thickened liquids to prevent aspiration
High-calorie, nutrient-dense foods
Small, frequent meals

Enteral Feeding (PEG Tube)

Indications: Significant dysphagia, aspiration risk, weight loss >10%
Placed before respiratory function declines significantly (FVC >50%)
Improves nutrition, reduces aspiration risk
Does NOT prevent all aspiration (saliva can still be aspirated)
Patients can still eat small amounts for pleasure if safe

Advance Care Planning

Early discussion of advance directives is ESSENTIAL. Patients must make decisions about ventilation, feeding tubes, and end-of-life care while they can still communicate their wishes.

Advance directives: Living will, healthcare proxy
Goals of care discussion: What level of intervention desired?
Ventilation preferences: NIV? Tracheostomy and mechanical ventilation?
Feeding tube preferences
Hospice care planning
POLST forms (Physician Orders for Life-Sustaining Treatment)

Reasons for Hospitalization

ALS patients may require hospitalization for:

Respiratory failure: Most common reason for admission
Pneumonia: Aspiration or ventilator-associated
Malnutrition/Dehydration: Severe dysphagia, inadequate intake
Falls and injuries: From progressive weakness
Equipment management: BiPAP adjustments, ventilator setup

Nursing Management

PRIORITY NURSING CARE

Respiratory Assessment & Support

Monitor respiratory rate, pattern, oxygen saturation continuously
Assess vital capacity regularly
Position patient for optimal breathing (head of bed elevated)
Assist with cough, suction secretions as needed
Ensure BiPAP mask fits properly and patient tolerates well
Monitor for signs of respiratory distress

Nutrition & Swallowing

Assess swallowing ability before meals
Position upright for meals and 30 minutes after
Monitor for signs of aspiration (coughing, choking, wet voice)
Provide modified diet as ordered (soft, thickened liquids)
Allow adequate time for meals; patient will tire easily
Monitor weight weekly
PEG tube care if present

Mobility & Safety

Assess fall risk; implement fall precautions
Assist with transfers and ambulation as needed
Encourage use of assistive devices (walker, wheelchair)
Perform passive range of motion to prevent contractures
Reposition every 2 hours to prevent pressure injuries
Monitor skin integrity closely

Communication Support

Early Stage

Speech may be slurred but intelligible. Allow extra time for responses. Reduce background noise.

Moderate Stage

Speech therapy for strategies. Amplification devices. Write/type messages. Communication boards.

Advanced Stage

Eye-gaze technology. Computer systems with eye tracking. Yes/no signals (eye blinks). Letter boards.

Augmentative Devices

Speech-generating devices. Introduce early to allow learning. Arrange speech therapy consult.

Psychosocial & Emotional Support

EMOTIONAL CARE

Acknowledge grief: Validate feelings about losses and disease progression
Provide hope: Focus on quality of life, maintaining dignity, meaningful moments
Screen for depression: Very common; offer treatment
Support family/caregivers: Caregiver burden is enormous; provide respite resources
Facilitate communication: Help family members express fears and concerns
Spiritual support: Arrange chaplain visits if desired
Support groups: Connect with ALS Association for patient and caregiver support
Normalize emotions: Anger, fear, sadness are all expected and valid

ALS is devastating for patients and families. Despite physical limitations, patients often remain cognitively intact and fully aware of their decline. Preserve dignity, provide compassionate care, and support quality of life. Focus on what CAN be done rather than losses. Small acts of kindness and maintaining human connection are profoundly important.

End-of-Life Care

Hospice referral: Appropriate when curative treatments exhausted or patient chooses comfort-focused care
Symptom management: Pain, dyspnea, anxiety, excessive secretions
Comfort measures: Positioning, massage, music, presence
Family support: Prepare family for dying process; provide bereavement resources
Respect wishes: Honor advance directives and patient/family preferences

Prognosis

Median survival: 3-5 years from symptom onset
Range: Some survive 10+ years; others decline rapidly within 1-2 years
Poor prognostic factors: Bulbar onset, older age, rapid progression, low FVC
Better prognosis: Limb onset, younger age, familial ALS (paradoxically)
Cause of death: Usually respiratory failure or pneumonia
5% of patients (particularly those with SOD1 mutations) survive >10 years

MOVEMENT DISORDER

Parkinson's Disease

PATHOPHYSIOLOGY

Parkinson's Disease: A progressive neurodegenerative disorder characterized by the loss of dopamine-producing cells in the substantia nigra of the brain. This results in NOT ENOUGH dopamine, leading to the characteristic movement difficulties.

Key mechanism: The butterfly-shaped area in the brain (ventricles with dopamine receptors) begins to diminish, reducing dopamine production and affecting motor control.

TRAP MNEMONIC - CRITICAL FOR EXAMS

Classic Clinical Features of Parkinson's Disease:

T = TREMORS (pill rolling motion with hands)
R = RIGIDITY (stiff muscles)
A = AKINESIA / BRADYKINESIA (slow movement, difficulty initiating movement)
P = POSTURAL INSTABILITY (balance problems)

Etiology and Risk Factors

Genetics: One of the biggest risk factors
Aging: The other biggest determining factor
Substantia nigra damage: Dopamine-producing cells diminish over time
Environmental factors may play a role

Clinical Manifestations

Tremors

Pill Rolling Tremor: A characteristic repetitive hand movement that looks like the person is rolling a small pill between their thumb and fingers. This is one of the most recognizable signs of Parkinson's disease.

Rigidity

Stiff, rigid muscles make movement difficult and slow
Due to lack of dopamine needed for smooth muscle movements
Contributes to bradykinesia and posture problems

Bradykinesia / Akinesia

Bradykinesia: Slow, jerky movements caused by rigid muscles and insufficient dopamine
Akinesia: Difficulty initiating movement - hard to start moving
Movements are not smooth due to dopamine deficiency

Postural Instability

Results from combination of all symptoms (tremors, rigidity, slow movement)
Parkinson's Shuffle: Feet barely lift off ground, patient shuffles forward instead of taking normal steps
Normal walking: one foot in front of the other with heel-toe gait
Parkinson's walking: feet slide along ground in shuffling motion

WALKING ASSISTANCE

Help patients maintain cadence: Encourage them to find a song or rhythm to walk to. This helps keep their brain active and maintains a steady rhythm. Example: Walking to the beat of "They Not Like Us" or any favorite song helps prevent the irregular shuffling pattern.

Equipment: Patients often use shopping carts or walkers for stabilization and support.

Stages of Parkinson's Disease

Early Stages

Stage 1: Mild symptoms, still upright and walking, symptoms manageable
Stage 2: Tremors increase, cane is appropriate assistive device

Advanced Stages

Stage 3: Bradykinesia really kicks in, movement significantly slowed, WALKER needed
Stage 4: Severe difficulty with movement, wheelchair often needed for safety (still encourage walker use at home)

Safety Measures and Assistive Devices

⭐ ELEVATED TOILET SEAT - VERY IMPORTANT ⭐

An elevated toilet seat makes sitting down and standing up MUCH easier and significantly prevents falls. This is a critical safety device that is often overlooked but makes a huge difference in patient safety and independence.

Mobility Assistive Devices

Walker

For moderate symptoms (stage 3) when stability becomes an issue

Cane

For mild symptoms (stage 2) to provide additional support

Shoehorn

Long stick that helps put on shoes without bending over - prevents falls

Special Silverware

Larger handles allow fist grip instead of pinch grip, making eating easier

Bathroom Grab Bars

Provide support for transfers and balance in bathroom

Elevated Toilet Seat

CRITICAL DEVICE - easier sitting/standing, prevents falls

Home Safety Modifications

Remove ALL rugs and carpets - tripping hazards
Clear pathways - no clutter anywhere
Well-lit areas - adequate lighting throughout home
Avoid stairs if possible, or add railings
Declutter hospital rooms - helps with stress and safety

Therapy and Ongoing Care

Physical Therapy: Maintains mobility and strength
Occupational Therapy: Helps with ADLs and adaptive equipment
Continue ADLs as long as possible: CRITICAL to prevent contractures
Contractures CANNOT be reversed once developed - prevention is key!

Pharmacological Management

Pramipexole (Mirapex)

EARLY STAGE MEDICATION

Use: Given in early stages of Parkinson's disease, typically before levodopa-carbidopa

Side Effects:

Sleep attacks: Sudden onset of sleep
Hallucinations: Visual or auditory disturbances
Compulsive behaviors: Gambling, online scams, shopping
- Why this happens: Patient feels better from medication + understands their prognosis = living life to fullest
- Educate patient and listen to family concerns about behavior changes

Levodopa-Carbidopa (Sinemet)

PRIMARY MEDICATION FOR TREMORS

Mechanism:

Levodopa: Crosses the blood-brain barrier to increase dopamine
Carbidopa: Acts as a vehicle to help levodopa cross the blood-brain barrier
Combination therapy is essential - carbidopa allows levodopa to work

Administration:

Take with LOW PROTEIN or small protein snack for better absorption
Timing is important for optimal effect

Side Effects (Carbidopa causes these):

⭐ Orthostatic Hypotension (PRIMARY) - see teaching section below
Nausea
Dizziness
Dyskinesia: Abnormal involuntary movements
- Can cause TOO MUCH dopamine → Huntington's-like symptoms (chorea movements)
- Monitor patient for irregular movements
- Report to provider if dyskinesia develops
Impotence: Expected side effect - discuss options with patient (Viagra, etc.)

⚠️ CRITICAL CONTRAINDICATIONS:

NO MAOIs with levodopa - causes HYPERTENSIVE CRISIS risk
MAOIs already carry high risk for hypertensive crisis
Combined with levodopa = MUCH WORSE risk
DO NOT STOP ABRUPTLY - must taper

Orthostatic Hypotension Teaching

CRITICAL PATIENT EDUCATION

Why it happens: Dopamine agonists cause vasodilation → blood pressure drops, especially with position changes

Patient Teaching:

Rise SLOWLY
Sit at edge of bed before standing
Dangle feet for a moment
Take time moving from: Lying → Sitting → Standing
High fall risk due to sudden blood pressure drops

Educate patients: These side effects are EXPECTED. Orthostatic hypotension and potential impotence are known effects of the medication. Have open conversations about management strategies.

Nursing Delegation for Parkinson's Patients

WHAT RN CAN DELEGATE TO LPN:

✓ Established medication administration (if patient already taking the medication)
✓ Basic care tasks
✓ Vital signs

WHAT RN CANNOT DELEGATE TO LPN:

✗ Narcotics
✗ Opioids

IMPORTANT CONSIDERATIONS:

RN must assess parameters FIRST (e.g., check blood pressure before delegating BP medication administration)
RN can delegate the "passing" (giving) of meds but NOT the "assessing"
If handoff report states "client has been taking this medication reliably," LPN can administer
If parameters are involved: RN assesses → confirms parameters are met → then delegates administration

Nursing Priorities

Fall prevention: #1 safety concern
Medication management: Precise timing, monitor for side effects
Maintain independence: Encourage ADLs to prevent contractures
Nutrition support: Balanced diet, adequate hydration
Dysphagia screening: Aspiration risk increases as disease progresses
Emotional support: Depression and anxiety common

MOVEMENT DISORDER

Huntington's Disease

PATHOPHYSIOLOGY

Huntington's Disease: A progressive neurodegenerative genetic disorder that is THE OPPOSITE of Parkinson's Disease. In Huntington's, there is TOO MUCH dopamine, resulting in characteristic involuntary movements called chorea.

Mechanism: The ventricles in the brain atrophy and close down, which squeezes the dopamine-producing cells. When you squeeze them (like squeezing a lemon for more juice), they produce MORE dopamine, leading to excessive dopamine levels.

Chorea - Defining Feature

CHOREA DEFINITION

Chorea: Rapid, involuntary, jerky, non-patterned, semi-purposeful movements

CRITICAL DIFFERENCE FROM TREMORS:

Tremors (Parkinson's): Small, repeated movements - patient can still function and grab objects
Chorea (Huntington's): CANNOT control movements to grab things - involuntary and jerky throughout entire body
Chorea affects entire body including head, face, limbs
Movements are unpredictable and interfere with voluntary actions

Genetics and Diagnosis

Strong genetic component: Autosomal dominant inheritance
Genetic testing recommended especially if patient is young and planning a family
Diagnosis: Brain imaging shows atrophy in ventricles
Typically develops in mid-30s to 40s but can occur earlier or later

TOP Nursing Priority - NUTRITION

⭐⭐⭐ #1 PRIORITY: HIGH CALORIE DIET ⭐⭐⭐

Why high calorie diet is CRITICAL:

Patient is moving CONSTANTLY due to chorea
Burning MANY more calories than average person
Risk for cachexia (muscle wasting) if caloric needs not met
Weight loss can be rapid and severe

Diet Specifics:

HIGH CALORIE, small frequent meals
If they want cheesecake with caramel sauce and whipped cream → LET THEM EAT IT!
Goal: Meet caloric intake to prevent muscle wasting
Monitor weight closely - trending is important
Nutritionist determines basal metabolic rate and specific calorie needs

CONTRAST WITH PARKINSON'S:

Parkinson's: Balanced, regular diet
Huntington's: HIGH CALORIE diet

Dysphagia Management

Jerky movements affect head, mouth, throat - swallowing becomes difficult:

Thickened liquids: Prevent aspiration
Aspiration pneumonia prevention: Top complication to watch for
Appropriate food choices:
- NOT small items (e.g., pigs in blanket = choking hazard)
- Foods that are easy to swallow and won't break into small pieces
Positioning: Sit UPRIGHT, keep esophagus straight
Timing: DO NOT rush eating - takes a long time
- Use warming tray to keep food warm
- Make eating experience pleasurable, not stressful
Feeding approach: Let patient feed themselves as much as possible
- Help ONLY when patient becomes frustrated
- Don't force or rush
- Maintain dignity and independence

Communication Support

Challenge: Jerky movements affect speech and ability to communicate verbally
Solutions:
- iPad with communication apps
- Writing board
- Button/switch communication devices
- Any adaptive communication method that works for the patient
Speech therapy consultation important

Fall Prevention and Safety

Same safety measures as Parkinson's disease:
Assistive devices (walker, cane as appropriate)
Clear pathways, remove rugs
Well-lit areas
Close supervision due to unpredictable movements

Pharmacological Management

Tetrabenazine (Xenazine)

PRIMARY MEDICATION FOR CHOREA

Purpose: Main medication to reduce involuntary chorea movements

Side Effects:

Sedation
Dizziness
Xerostomia (dry mouth)
- Management: Sugar-free hard candies
- Encourage adequate hydration
- Sugar-free gum can also help

Psychiatric Medications

Mood and Behavior Management:

SSRIs (Fluoxetine, etc.): First-line for mood control
- Use BEFORE needing antipsychotics
- Helps manage depression and anxiety
- Jerky movements can cause frustration and psychological distress
Antipsychotics: May be needed if SSRIs insufficient
- Constant involuntary movement can lead to psychosis or severe frustration
- Use lowest effective dose

Bromocriptine

HOMEWORK ASSIGNMENT

Student Assignment: Look up Bromocriptine and research:

What condition does it treat?
What are the common side effects?
How does it work?

This medication is important to know for your studies and may appear on exams.

Huntington's vs. Parkinson's - Quick Comparison

Feature	Parkinson's Disease	Huntington's Disease
Dopamine Level	NOT ENOUGH	TOO MUCH
Movement Type	Slow, rigid (bradykinesia)	Rapid, jerky (chorea)
Tremors	Yes (pill rolling)	No (chorea instead)
Diet	Balanced, regular	HIGH CALORIE
Top Priority	Safety, mobility	NUTRITION
Both Have	Dysphagia risk, aspiration pneumonia prevention priority, fall risk, need assistive devices

Nursing Priorities

⭐ #1: NUTRITION - Prevent cachexia with high-calorie diet
Dysphagia management: Aspiration pneumonia prevention
Fall prevention: Due to unpredictable movements
Communication support: Maintain patient's ability to express needs
Psychological support: Depression, anxiety, frustration common
Family education: Genetic counseling, disease progression, caregiver support
Quality of life: Maintain dignity and independence as long as possible

Key Takeaways & Nursing Priorities

ESSENTIAL CONCEPTS

Neurological disorders present unique challenges requiring comprehensive, individualized nursing care. Understanding the pathophysiology, recognizing clinical manifestations early, and implementing appropriate interventions are crucial for optimizing patient outcomes and quality of life.

Critical Nursing Priorities Across All Neurological Disorders

Respiratory Monitoring

For MG, GBS, and ALS: Respiratory failure is life-threatening. Continuous assessment is essential.

Safety & Fall Prevention

For MS, MG, GBS, ALS: Progressive weakness increases fall risk. Implement precautions early.

Medication Management

Precise timing and dosing crucial for MG and MS. Educate about adherence and side effects.

Nutrition Support

Dysphagia common in MG, GBS, ALS, Bell's Palsy. Prevent aspiration and maintain nutrition.

Eye Protection

For Bell's Palsy and MG: Prevent corneal damage from inability to close eye completely.

Pain Management

For trigeminal neuralgia: Prevent trigger-induced pain. For MS and ALS: Manage neuropathic pain.

Psychosocial Support

All disorders: Depression, anxiety common. Provide emotional support and mental health resources.

Patient Education

Empower patients and families with knowledge about disease management and self-care.

Disease-Specific Priorities

Disorder	TOP Priority	Key Intervention
Multiple Sclerosis	Symptom management & complication prevention	Energy conservation, heat avoidance, bladder/bowel program
Myasthenia Gravis	Respiratory monitoring & medication timing	Watch for crisis; precise medication scheduling
Guillain-Barré	Respiratory support & complication prevention	Close monitoring, early ventilation if needed, DVT prophylaxis
Trigeminal Neuralgia	Pain control & trigger avoidance	Medication adherence, dietary/hygiene modifications
Bell's Palsy	Eye protection	Eye lubricants, protective shield, monitor for corneal damage
ALS	Respiratory support & advance care planning	Early discussions about goals of care, ventilation decisions

Commonalities Across Neurological Disorders

Shared Challenges

Progressive functional decline
Impact on independence and ADLs
Psychological and emotional burden
Caregiver stress and burden
Need for multidisciplinary care
Importance of rehabilitation
Quality of life concerns

Universal Nursing Roles

Patient and family educator
Care coordinator
Advocate for patient needs
Emotional support provider
Monitor for complications
Promote independence and dignity
Facilitate advance care planning

Study Tips for Exam Success

EXAM PREPARATION

Focus on These High-Yield Topics:

Pathophysiology differences: MS (demyelinating CNS), MG (neuromuscular junction), GBS (peripheral nerve myelin), ALS (motor neurons)
Crisis recognition: Myasthenic vs. cholinergic crisis; respiratory failure in GBS and ALS
Medication specifics: Carbamazepine with food, pyridostigmine timing, when to stop anticholinesterase
Priority assessments: Respiratory function in MG/GBS/ALS, eye protection in Bell's Palsy
Disease trajectories: MS exacerbations/remissions, GBS phases (progression-plateau-recovery), ALS terminal

Key Distinguishing Features:

Sensation: MG and GBS have NO sensory loss; MS has sensory changes
Cognition: Intact in MG and GBS; may be affected in MS and ALS (late)
Symmetry: MS and MG often asymmetric initially; GBS symmetric ascending; Trigeminal neuralgia and Bell's Palsy unilateral
Reversibility: GBS and Bell's Palsy often reversible; MS has exacerbations/remissions; MG controlled with meds; ALS always progressive

Test-Taking Strategy: When answering NCLEX-style questions, always consider safety first. Respiratory compromise, aspiration risk, and fall prevention are high-priority concerns across multiple neurological disorders. If the question involves a crisis situation (myasthenic, cholinergic, respiratory failure), airway and breathing are ALWAYS the priority.

Additional Resources

Textbook: Brunner & Suddarth's Textbook of Medical-Surgical Nursing (15th ed.), Chapters 64 & 65
National MS Society: www.nationalmssociety.org
Myasthenia Gravis Foundation of America: www.myasthenia.org
GBS/CIDP Foundation International: www.gbs-cidp.org
Facial Pain Association: www.facialpaincourage.org
ALS Association: www.als.org

Adult Health II - Exam 3 Study Guide
Neurological Disorders: Comprehensive Nursing Care
Reference: Brunner & Suddarth's Textbook of Medical-Surgical Nursing (15th ed.), Chapters 64 & 65