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Onset age for Parkinson’s disease
>= 50
Who does Parkinson’s disease affect more? Men or women?
Men
Etiology of Parkinson’s Disease
Unknown
Genetic and environmental influences
In Parkinson’s, what is the imbalance between?
Dopamine and acetylcholine levels (ACh)
What is Parkinson’s disease?
Chronic, progressive neurodegenerative disease
What is Parkinson’s characterized by?
TRAP:
Tremors
Rigidity
Akinesia/Bradycardia
Postural disturbance
What are other non-motor symptoms
Depression
Psychosis
Dementia
Sleep disturbances
Autonomic dysfunction
Medications for Mild symptoms (Parkinson’s Disease):
MAO-B inhibitors
Anticholinergics
Medications for Mild-to-Moderate symptoms (Parkinson’s):
Dopamine releaser
Dopamine agonists
Medications for severe symptoms (Parkinson’s):
Levodopa/carbidopa
Adjunct medication: COMT inhibitors
Dopamine agonists, dopamine releaser
Levodopa-Carbidopa side effects
Nausea and vomiting
Dyskinesia
Change in behavior, personality, psychosis
Postural hypotension and dysthymias
Hypertensive crisis and non-selective MAO inhibitor
Dyskinesia vs. Dystonia
Dyskinesia: involuntary movements
Dystonia: Painful muscle contractures, abnormal postures, involuntary twisting
What is the On-Off phenomena:
On period: Levodopa-carbidopa working well, symptoms controlled
Off-period: Acute loss of levodopa-carbidopa effects
On-off phenomena are possibly due to:
Issues with absorption/distribution or adaptive mechanisms of brain
When does Levodopa wear off?
May occur near end of dosing interval or randomly
What do you do when Levodopa wears off?
Increase dose
Decrease dosing interval
Administer COMT inhibitor to prolong levodopa ½ life
Surgical Treatment for Parkinson’s Disease":
Thalamotomy and pallidotomy
Deep brain stimulator
What is Multiple Sclerosis?
Chronic autoimmune disease affecting the myelin sheath and conduction pathway of the CNS (brain, optic nerve, spinal cord)
What happens during Multiple Sclerosis?
Demyelination: Immune mediated inflammatory response that destroys the myelin sheath
What is MS characterized by?
Periods of remission and exacerbation
What age range is MS the leading cause of neurologic disability?
20-30
Who does MS effect the most? Men or women?
Women
What triggers the inflammatory response for MS?
Genetic predisposition and environmental factor trigger an autoimmune inflammatory response
What happens when there’s a loss of myelin in CNS (loss of oligodendrocytes)?
Plaques form causing axonal scarring which disrupts nerve conduction
Disease course for: Relapsing remitting, Secondary and Primary progressive, Progressive relapsing
Relapsing remitting: 85-90%
Secondary progressive: 40%
Primary progressive: 10%
Progressive relapsing: 5%
MS Manifestations: General
Fatigue
Pain
“Brain Fog”
MS Manifestations: Eyes
Diplopia (Double vision)
Blurry vision
Visual clouding
Partial loss of visual field (scotoma)
Nystagmus (involuntary, rapid, repetitive movement of one or both eyes
Orbital pain
MS Manifestations: Ears
Tinnitus (ringing in ears)
Vertigo (feeling of spinning)
Hearing loss
MS Manifestations: Mouth
Dysphagia
Changes in speech
MS Manifestations: Motor
Fatigue/Stiffness of extremities
Unsteady gait
Weakness
Flexor spasms at night
Hyperactive, deep tendon reflexes
MS Manifestations: Cerebellar
Loss of balance, poor coordination
Intention tremor
Clumsy motor movement
MS Manifestations: Sensory changes
Paresthesia: Numbness, tingling, burning of face or involved extremities
Lhermitte sign
Decreased temperature perception
Bowel/Bladder dysfunction
Alterations in sexuality
What is the goal of MS treatment?
Delay disease course, treat exacerbations
Symptom: Management only, no cure exists
Modalities of MS treatment:
Corticosteroids — flares
Immunomodulators — first line treatment
Immunosuppressants: Used when interferon-beta fails to suppress symptoms/disease progression
Antispasmodic drugs: Reduce spasms, contractures
Mechanism of Action for Corticosteroids
Anti-inflammatory
Suppress immune system
Absorption methods of Corticosteroids
Rapid orally
IM
IV
Side effects of Corticosteroids
Hyperglycemia
Hypokalemia
Adrenal insufficiency
Osteoporosis
Infection
Peptic ulcer disease
Cataracts and glaucoma
Nursing considerations for Corticosteroids
Monitor serum electrolytes
Close monitoring for infection
Assess muscle strength
Monitor skin integrity
Monitor for dyspepsia, melena
Assess visual acuity
Safety precautions
Assess for psychosocial manifestations
What is Amyotrophic Lateral Sclerosis (ALS) also known as?
Lou Gehrig disease: a progressive and degenerative disease that involves the motor system
Early symptoms of Amyotrophic Lateral Sclerosis
Fatigue while talking
Tongue atrophy
Dysphagia
Weakness of hands and arms
Amyotrophic Lateral Sclerosis pathophysiology
Loss of upper motor neurons —> Spasticity
Loss of lower motor neurons —> Muscle weakness, atrophy paralysis, and death
Amyotrophic Lateral Sclerosis clinical manifestations
Extremity weakness
Dysphagia (aspirations)
Fatigue while talking
Respiratory muscle weakness —> respiratory failure —> death
Intellect, eye movements and sensory system are spared
Amyotrophic Lateral Sclerosis treatment
No cure, supportive care only
What is Guillain-Barre Syndrome?
Acute, life-threatening disorder: Auto-immune attack of peripheral nerve myelin causing rapid demyelination, slowing conduction
What does the Guillain-Barre Syndrome follow?
A viral GI or respiratory infection
EBV
CMV
Mycoplasma pneumoniae
Guillain-Barre Syndrome Manifestations
Hyporeflexia —> Paresis —> Quadriplegia
Respiratory compromise (30%)
Autonomic dysfunction
Postural hypotension
Arrhythmias
Facial flushing
Decreased sweating/salivation
Urinary retention
GBS stages
Acute/Initial period
1-4 weeks
Plateau Period
Days to weeks
Recovery phase
4-6 months up to 2 years
Remyelination and axonal regeneration
GBS Treatment
High-dose IVIG therapy, Plasmapheresis
Neutralizes and removes antibodies causing myelin destruction
What is Myasthenia gravis?
Autoimmune disorder affecting acetylcholine receptors at the neuromuscular junction
What percentage of patients have thymus dysfunction (thymoma)?
75%
Myasthenia Gravis is characterized by:
Weakness primarily in muscles innervated by cranial nerves, and in skeletal and respiratory muscles
Myasthenia Gravis: Clinical Manifestations
Ocular signs
Ptosis (eyelid droop)
Diplopia (Double vision)
Respiratory compromise, SOB
Rapid onset fatigue
Muscle weakness
Facial weakness
Dysphagia
Dysarthria
Unstable, wadding gait
Myasthenia Gravis Pharmacotherapy
Acetylcholinesterase inhibitor drugs
Corticosteroids, Immunosuppressant medications
Use if poor response
Emergency Crisis of Myasthenia Gravis
Myasthenic Crisis
Cholinergic Crisis
Myasthenic Crisis
An exacerbation of the myasthenic symptoms caused by stressors, undermedication, or spontaneous occurrence
Cholinergic Crisis
An acute exacerbation of muscle weakness caused by overmedication with cholinergic (anticholinesterase) drugs
What test is used to distinguish between Myasthenic and Cholinergic Crisis?
Tensilon test
Myasthenic Crisis symptoms
Increased pulse, RR, BP
Bowel and bladder incontinence
Extreme muscle weakness can result in death
Nursing Management of Myasthenic Crisis
Priority is to maintain respiratory function
Ventilator support
Administer neostigmine, immunosuppressants
Cholinergic Crisis symptoms
Acute exacerbation of muscle weakness/paralysis
Muscarinic stimulation
SLUDGE” — Salivation, Lacrimation, Urination, Defecation, Gastrointestinal Distress and Emesis
What is withheld in Cholinergic Crisis?
Anticholinesterases drugs are withheld while client is maintained on a ventilator
What medication can be given for Cholinergic Crisis?
Atropine may be given and repeated if necessary
Displaces acetylcholine, decreases SLUDE symptoms
What is the antidote for Tensilon complications?
Atropine sulfate