NUR 317 - Neurological Disorders

Mutiple sclerosis etiology and pathophysiology

• Destroyed or damaged myelin leads to scarring (sclerosis)

• Autoimmune process

• Activated T cells migrate to CNS, disrupting blood-brain barrier

  • Likely the initial event in development of MS

• Subsequent antigen-antibody reaction leads to demyelination of axons

Multiple sclerosis progression

• Onset insidious, gradual

  • Vague symptoms

  • Diagnosis long after 1st symptom

• Rapid progression vs exacerbations and remissions

• Life expectancy after diagnosis is 25+ years

Multiple sclerosis 1st symptoms

• 1st symptoms may include:

  • Vision changes

  • Color distortions

  • Blindness in one eye

Multiple sclerosis common symptoms

• Symptoms vary based on area of CNS affected

• Other common symptoms include

  • Extremity weakness

  • Loss of coordination and balance

  • Sensory problems (numbness and tingling, Lhermitte’s sign)

  • Emotional problems (depression, anger, anxiety)

  • Speech impairment, dysarthria, dysphagia

  • Hearing loss

  • Fatigue

Multiple sclerosis bowel and bladder functions

• May be impaired

  • Constipation

  • Variable urinary problems

    • Spastic bladder

    • Flaccid bladder

Multiple sclerosis sexual dysfunction

• Can occur in MS

  • Erectile dysfunction

  • Decreased libido

  • Difficulty with orgasmic response

  • Painful intercourse

  • Decreased lubrication

Multiple sclerosis cognitive issues

• Short-term memory

• Concentration

• Information processing (speed)

• Multi-tasking

• Visual perception

• Word finding

Multiple sclerosis manifestations

• Early warning signs

  • Vision problems

  • Numbness/tingling

  • Dizziness/balance issues

• Common manifestations

  • Weakness

  • Cognitive impairment – 50%

  • Bladder dysfunction – 80%

• Don’t Ignore...

  • Depression

  • Irritability

  • Mood swings

  • Sexual dysfunction

Multiple sclerosis diagnostic studies

• Definitive diagnostic test for MS

  • Based primarily on history, clinical manifestations, and results of certain diagnostic tests

  • MRI of brain and spinal cord may show presence of plaques, inflammation, atrophy, and tissue breakdown and destruction

• MS diagnosis based on:

  • Evidence of at least 2 inflammatory demyelinating lesions in at least 2 different locations within the CNS

  • Damage or an attack occurring at different times (usually 1 month or more apart)

  • All other possible diagnoses ruled out

Multiple sclerosis drug therapy

• No cure for MS

  • Treat the disease process/provide symptomatic relief

  • Tailored therapy

  • Early intervention is most effective

Slowing progression of multiple sclerosis

• Immunosuppressants

  • Suppress strength of immune system

• Immunomodulators

  • Includes, amplifies, or inhibits components of the immune system

• Adrenocorticotropic hormone (ACTH)

  • From the anterior pituitary gland – regulates cortisol

Mulltiple sclerosis immunomodulator drug therapy

• Begin with Immunomodulator drugs

  • Interferon β-1a (SQ Rebif and Plegridy; IM Avonex)

  • Interferon β-1b (SQ Betaseron and Extavia)

  • SQ Glatiramer acetate (Copaxone)

• Patients need:

  • To be able to self administer medications and rotate injection sites

  • Use NSAID or acetaminophen

  • To wear sunscreen / protective clothing

    • More sensitive to sun

Drug therapy for relapsing forms of multiple sclerosis

• Teriflunomide (Aubagio)

  • Immunomadulatory agent with antiinflammatory properties

  • May cause severe liver disease

• Fingolimod (Gilenya)

  • Prevents lymphocytes from reaching the CNS and causing damage

  • Regular monitoring of BP and HR

Drug therapy for more active and aggressive forms of multiple sclerosis

• Natalizumab (Tysabri)

  • Used when other medications ineffective

  • Risk of fatal brain infection

• Alemtuzumab (Lemtrada)

  • Used when ineffective response to 2 or more medications

• Ocrelizumab (Ocrevus)

  • Increases risk of infection and breast cancer

Multiple sclerosis disease modifying therapy considerations

• Patients need to report side effects of medications

• Patients need to talk to provider before taking over the counter medications

• Avoid pregnancy with most medications

• Assess for depression, suicidal ideation

• All immunosuppressants put patient at risk for infection

  • Avoid large crowds, people who have infections

Multiple sclerosis drug therapy

• Muscle relaxant – spasticity

• CNS stimulant

• Anticholinergics – bladder symptoms

• Tricyclic antidepressants – chronic pain

• Antiseizure drugs – chronic pain

• Selective potassium channel blocker – improves nerve conduction in damaged nerve segments

Multiple sclerosis nursing interventions and care

• Avoid and identify triggers

  • Climate change or hot/cold extremes

  • Infection

  • Stress

• Build general resistance to illness

  • Exercise

  • Rest

  • Healthy diet

• Reassurance

  • Tests

  • Procedures

• Education

  • Support groups/resources

  • Medication

  • Treatment plans

Multiple sclerosis symptom management

• Fatigue – schedule activities and rest periods

• Limited mobility – walking aids, promote and maintain mobility, avoid injury

• Bowel and bladder dysfunction – bladder training, intermittent cathing, external catheter, adequate fiber and fluids

End stage multiple sclerosis

• Symptoms increase in severity, may see more symptoms at one time, or symptoms may be come permanent

• May not be able to live independently/function independently

• May see serious complications

• Palliative care may be helpful

Parkinson’s disease

• Chronic, progressive neurodegenerative disorder characterized by

  • Bradykinesia

  • Rigidity

  • Gait disturbance

Parkinsonism

• Mimics PD but often resolves after removal of the cause

• Causes of Parkinsonism:

  • Medications - metoclopramide (Reglan), reserpine, methyldopa, lithium, haloperidol (Haldol), and chlorpromazine

  • Amphetamine or methamphetamine

  • Hydrocephalus, stroke, trauma, infection, hypoparathyroidism

Parkinson’s lack of dopamine

• Degeneration of dopamine-producing neurons in substantia nigra of midbrain

• Lose 80% of dopamine before symptoms are seen

Parkinson’s etiology and pathophysiology

• Unusual clumps of protein deposited inside neurons

  • Unknown cause

• Lewy bodies

  • Found in brains of patients with PD

  • Presence indicates abnormal brain functioning

Lewy body dementia

• Can be misdiagnosed as PD

  • Sleep

  • Behavior changes

Parkinson’s clinical manifestations

• Onset is gradual and insidious with ongoing progression

• Just one side may be affected at first

• TRAP

  • Tremor

  • Rigidity

  • Akinesia

  • Postural instability

• Speech impairments

Parkinson’s - tremor

• Often first sign

• Initially minimal

• More prominent at rest

• Aggravated by

  • Emotional stress

  • ↑ Concentration

Parkinson’s - rigidity

• ↑ Resistance to passive motion when limbs are moved through their ROM

• Cogwheel rigidity

  • Jerky quality

  • Like intermittent catches in passive movement of a joint

• Occurs due to sustained muscle contraction

  • Muscle soreness

  • Tired/achy

  • Slow movements

Parkinson’s - akinesia

• Absence or loss of control of voluntary muscle movements

• “Freezing”

  • Distinct, rigid gait

  • Expressionless

Parkinson’s - bradykinesia

• Slowness of movement

• Particularly evident in the loss of automatic movements

Parkinson’s - postural instability

• Propulsion or retropulsion (forward and backward movement) is common

• Pull test

Parkinson’s - nonmotor symptoms

• Depression and anxiety

• Apathy

• Fatigue

• Pain

• Urinary retention and constipation

• Erectile dysfunction

• Memory changes

• Sleep disturbances

Parkinson’s complications

• Swallowing difficulties increase -

  • Malnutrition

  • Aspiration

• General debilitation, increasing weakness -

  • Pneumonia

  • UTIs

  • Skin breakdown

• Orthostatic hypotension is common -

  • ↑ Risk for falls and injuries

Parkinson’s disease progression

• Complications increase

  • Motor symptoms

  • Weakness

  • Akinesia

  • Neurologic problems

  • Neuropsychiatric problems

• Dementia often results

  • Associated with ↑ mortality

Parkinson’s diagnostic tests

• No specific tests exist

• Diagnosis based on history and clinical features

  • Requires presence of:

    • Asymmetric onset

    • Confirmation is a positive response to antiparkinsonian drugs

Parkinson’s drug therapy

• No cure for PD, care aimed at symptom management

• Drug therapy should correct imbalances of neurotransmitters within the CNS

• Antiparkinsonian drugs either

  • Enhance the release or supply of DA (dopaminergic)

  • Antagonize or block the effects of overactive cholinergic neurons in the striatum (anticholinergic)

PD - Dopamine agonists drugs

• Amantadine

• Apomorphine (Apokyn)

• Pramipexole (Mirapex)

• Ropinirole (Requip)

Amantadine

• PD treatment

• Antiviral agent

• ↑ Dopamine release; blocks reuptake

• May be useful early on, but used with levodopa in later stages

Apomorphine (Apokyn)

• PD treatment

• Injection

• Take with antiemetic (but not ondansetron)

Pramipexole (Mirapex)

• PD treatment

• Also used for restless leg

• Side effects vary based on early or late stages of PD

• Filtered through kidneys - considerations with kidney impairment

Ropinirole (Requip)

• PD treatment

• Also used for restless leg

• Side effect considerations

  • Nausea, fatigue, dyskinesia, dry mouth (common in many PD meds)

PD - MAO-B inhibitors drugs

• Selegiline

• Rasagiline

• Safinamide (Xadago)

MAO-B inhibitors actions

• ↑ Levels of dopamine

• May be used in combo with Levodopa

• When used with other medications, may minimize “off” times and extend “on” times

PD - Levodopa drugs

• Increases avaliable dopamine

• Levodopa, Sinemet (levodopa with carbidopa)

• Carbidopa, levodopa, entacapone (Stalevo)

Sinemet (levodopa with carbidopa)

• PD treatment

• Levodopa converts to DA in the basal ganglia

• Carbidopa inhibits an enzyme that breaks down levodopa before it reaches brain

• Carbidopa combining with levodopa reduces chance of side effects from levodopa

Stalevo (carbidopa, levodopa, entacapone)

• PD treatment

• For “off” episodes

• Advanced PD

PD - Levodopa/carbidopa considerations

• Sinemet is added when moderate to severe symptoms develop

• Effectiveness of Sinemet could wear off after a few years of therapy

  • Some HCPs initiate therapy with a DA receptor agonist

    • Ropinirole (Requip), pramipexole (Mirapex), rotigotine (Neupro)

  • Add Sinemet when moderate to severe symptoms develop

When taking Sinemet:

• Monitor for dyskinesia

• Report uncontrolled movements (eyes, face, extremities), difficulty urinating, mental changes, palpitations

• Monitor for nausea, vomiting, light-headedness (short term side effects)

• Do not give with food (protein inhibits drug absorption)

PD - Anticholinergic drugs

• Bentyl

• Scopolamine

• Benztropine (Cogentin)

Anticholinergic actions

• Help blocks acetylcholine

• Decrease involuntary muscle movements

• Potential adverse effects include blurred vision, dry mouth, constipation and urinary retention

Parkinson’s drug therapy things to note

• Use of only one drug is preferred

  • Fewer side effects

  • Dosages are easier to adjust

• Combination therapy often required as disease progresses

  • As “off” episodes occur

    • Often occur within 3-5 years

PD - Antiemetic drug therapy

• Ondansetron (Zofran) drug of choice

• Avoid metoclopramide (Reglan) and promethazine (Phenergan)

PD - Antipsychotic drug therapy

• Exacerbate symptoms

• Olanzapine (Zyprexa), quetiapine (Seroquel), risperidone (Risperdal)

PD - Dopaminergic drug therapy

Excessive use can lead to paradoxic intoxication

Parkinson’s interprofessional care

• Surgical therapy – for patients

  • Unresponsive to drug therapy

  • Have developed severe motor complications

• DBS – Deep brain stimulation - delivers current to the targeted brain location)

• Ablation – destruction of tissue that produces abnormal chemical or electrical impulses leading to tremors or other symptoms

• Duopa - stoma created, gel containing carbidopa/levodopa is injected directly (through a pump) and into small bowel through PEG tube

• Transplantation

Deep brain stimulation

• Parkinson’s treatment

• Most common surgical treatment

• Reversible and programmable

• ↓ Increased neuronal activity produced by DA depletion

  • Improves motor function

  • Reduces dyskinesia and medications

Parkinson’s nursing management

• Promote well balanced diet

  • Malnutrition and constipation can be serious consequences

  • Adequate fiber and fruit

  • Need to consider diet of patients with dysphagia and bradykinesia

• Promote physical exercise

  • Exercise limits consequences from decreased mobility - contractures, constipation, muscle atrophy

  • Physical therapy

  • Occupational therapy

• Educate/promote sleep hygiene

For patients who are at risk of falls or “freeze”...have patient

• Consciously thinking about stepping over a line on the floor

• Lifting toes when stepping

• One step back and . . .two steps forward

• Rock side to side before stepping forward

Parkinson’s promoting independence and self-care

• Get out of a chair by using arms and placing the back legs on small blocks

• Remove rugs and excess furniture

• Simplify clothing (no buttons or hooks)

• Use elevated toilet seats

• Use an ottoman to elevate legs

Parkinson’s resources and support

• As disease progresses

  • End stage – around the clock care, wheelchair or bedridden, hallucinations/delusions

• Emotional support - depression, anxiety

• Family