nursing care of patients with peripheral nervous system disorders n.
Skip this Video
Loading SlideShow in 5 Seconds..
Nursing Care of Patients with Peripheral Nervous System Disorders PowerPoint Presentation
Download Presentation
Nursing Care of Patients with Peripheral Nervous System Disorders

Loading in 2 Seconds...

play fullscreen
1 / 49

Nursing Care of Patients with Peripheral Nervous System Disorders - PowerPoint PPT Presentation

  • Uploaded on

Nursing Care of Patients with Peripheral Nervous System Disorders . Rita Carey-Nita . Neuromuscular Disorders . Neuromuscular Disorders involve a disruption of the transmission of impulses between neurons and the muscles they innervate They include: Multiple Sclerosis Myasthenia Gravis

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Nursing Care of Patients with Peripheral Nervous System Disorders' - quant

Download Now An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
neuromuscular disorders
Neuromuscular Disorders

Neuromuscular Disorders involve a disruption of the transmission of impulses between neurons and the muscles they innervate

They include:

  • Multiple Sclerosis
  • Myasthenia Gravis
  • Amyotrophic Lateral Sclerosis
multiple sclerosis
Multiple Sclerosis


  • MS is a chronic progressive degenerative disease that affects the myelin sheath of the neurons in the CNS
  • The myelin sheath begins to break down as a result of the activation of the immune system
  • The nerve becomes inflamed and edematous
  • Nerve impulse slows
  • With progression of disease scarring or sclerosis of nerve occurs
  • Nerve impulse become blocked causing permanent muscle function loss
  • Unknown

May be:

  • Autoimmune process
  • May be result of viral infection
  • Hereditary
  • Environmental triggers

Onset is usually between 20-50 years old

Women twice as often than men

May be mild or may be permanently debilitating


Symptoms may begin slowly over long period of time or suddenly & progressive faster

Characterized by remissions and exacerbations


  • Extreme heat or cold
  • Fatigue
  • Infection
  • Physical or emotional stress
  • Hormonal changes as in pregnancy
signs symptoms
Signs & Symptoms
  • Muscle weakness/paralysis of limbs, trunk or dead
  • Ataxia
    • Results in falls & accidents
  • Tingling sensation
  • Numbness
  • forgetfulness/difficulty concentrating
  • Visual disturbances
    • One eye at a time
    • May have pain on eye movement
    • Diplopia
    • Blurred vision
    • Patchy blindness
signs symptoms1
Signs & Symptoms
  • Fatigue
  • Muscle spasticity
  • Bowel or bladder dysfunction
  • Dysarthria
  • Dizziness/vertigo
  • Impaired hearing
    • Tinnitus
  • Constipation
  • Spastic bladder
  • Sexual dysfunction
  • Anger—depression—euphoria
diagnostic tests
Diagnostic Tests
  • History and Physical
  • Signs & Symptoms
  • CSF fluid may show increase in oligoclonalimmunoglobin G
  • MRI shows sclerotic plaques
therapeutic interventions
Therapeutic Interventions
  • No cure
  • Interferon treatment reduces exacerbations
    • Betaseron—Avonex
  • Steroids decrease inflammation and edema of neuron
    • Adrenocorticotropic—prednisone—corticotropics
  • Immunosuppresant depress immune response
    • Imuran—Cytoxan
  • Anticonvulsants decrease neuropathic pain
    • Dilantin—Tegretol
  • Parasympathetic agents help with bladder issues
    • Urecholine—Ditropan
  • Muscle spasm may be controlled with
    • Valium—Liorseal—Zanaflex
  • Fatigue is treated with antidepressants or Symmetrel (antiviral)
therapeutic interventions1
Therapeutic Interventions
  • Rehabilitation
    • PT
    • OT
    • ST
  • Plasmaphersis
    • Removes plasma portion of whole blood and replaces it with fresh plasma
    • Removes antibodies that may be attacking the myelin sheath
    • Hope is to suppress the immune response and inflammtion
nursing interventions
Nursing Interventions
  • Teach to avoid triggers that can cause exacerbation
  • Rest—exercise—stress reduction or avoidance—balanced diet
  • Monitor airway due to muscle weakness
      • Resp rate—depth—oxygen saturation—cough & deep breathe—suction
  • Monitor for dysphagia
      • HOB elevated—monitor cough & gag reflex—ST—swallowing precautions—soft diet—thickened liquids
  • Mobility
      • AROM & PROM—PT—OT—reposition frequently if immobile
myasthenia gravis
Myasthenia Gravis
  • Myasthenia Gravis is weakness of the voluntary muscles of the body
  • Disease of the neuromuscular junction
  • The neuron release the neurotransmitter acetycholine across the synaptic cleft which cause muscle contraction
  • With MG antibodies attack and destroy acetycholine receptors sites at the neuromuscular junction
  • Result is inability to stimulate muscle contraction and therefore loss of voluntary muscle strength
signs symptoms2
Signs & Symptoms
  • Progressive extreme weakness
    • Hallmark sign—increase weakness with activity with improved strength with rest
  • Affects eye and eyelid movement
    • Ptosis
  • Chewing
  • Swallowing
  • Breathing
  • Masklike expression
  • Voice fades with long conversation

Exacerbations & Remissions

  • Triggers
    • Emotional & physical stress
    • Pregnancy
    • Illness
    • Trauma
    • Extreme temperatures
    • Surgery
    • Medications that block action at neuromuscular junction
    • Electrolyte imbalance
  • Aspiration
  • Respiratory infection
  • Respiratory failure
  • Mysathnic crisis
    • Not enough medication
    • Results in
      • Ptosis—dysphagia—dysarthria—dyspnea—weakness
  • Cholinergic crisis
    • Overmedication with anticholinesterase
    • Results in
        • Increased muscle weakness—dyspnea—nausea & vomiting—salivation—abd cramping—sweating—increased bronchial secretions—miosis
diagnostic test
Diagnostic Test
  • Diagnosis based on history & physical
  • Patient looks up for 2-3 minutes—ptosis will occur with MG
    • With rest eyelids open without difficulty
  • IV Tensilon given—if muscle strength improves dramatically MG diagnosed
  • EMG to rule out other causes of symptoms
  • PFT’s to determine to predict myasthenic crisis leading to respiratory failure
therapeutic intervention
Therapeutic Intervention
  • No Cure
  • Treatment aimed at control symptoms
  • Thymectomy to decrease the production of Ach receptor antibodies and decrease symptoms
  • Anticholinesterase drugs destroys acetycholinesterase that breaks down ACh allowing for ACh to attach to muscles causing contraction therefore strength increases
    • Prostigmin—Mestinon
  • Steroids suppress immune response
    • Prednisone—Prednisolone
  • Plasmapheresis to remove antibodies from plasma
nursing care
Nursing Care
  • Monitor & teach patient signs of
    • Myasthenic crisis
    • Cholinergic crisis
  • Schedule anticholinesterase medication to peak during times of most activity
  • Teach
    • patient importance of well balance diet
    • How to conserve energy with daily activities
    • Avoidance of persons with infections
    • Teach patient to avoid medications that will exacerbate weakness
      • Beta-blockers—calcium channel blockers—quinine—quinidine—procainamide—D penicillamine—alpha-interferon—botulinum toxin—neuromuscular blocking agents
amyotrophic lateral sclerosis
Amyotrophic Lateral Sclerosis

ALS also called Lou Gehrig’s disease

  • Progressive degenerative neuromuscular condition
  • Affects motor neurons responsible for voluntary muscles
  • Upper and lower motor neurons begin to degenerate and form scar tissue or die blocking nerve impulses from brain and spinal cord
  • Muscle tissue atrophy occurs decreasing muscle strength and coordination
  • With progression more muscle groups are affected
  • Unable to breathe and swallow
  • Cognitive function remains unaffected
  • Occurs at any age
  • No known cause
  • Genetic tendency in some cases
  • Onset between 40-70 years
  • More often in men than women
signs symptoms3
Signs & Symptoms
  • Progressive muscle weakness leads to complete immobility
  • Decreased coordination of arms—legs—trunk
  • Atrophy of muscles
  • Fasciculations
  • Muscle spasms that cause pain
  • Difficulty chewing & dysphagia lead to aspiration
  • Inappropriate emotional outbursts
  • Dysarthria—progresses to complete inability to speak
  • Constipation
  • Urinary urgency—hesitancy—frequency
  • Malnutrition
  • Falls
  • PE
  • CHF
  • Death related to respiratory complications
    • Atelectasis—pneumonia—respiratory failure—ventilator dependence
  • Death occurs within 3-5 years of diagnosis usually due to respiratory failure
  • Only 10% live 10 years or more
diagnostic tests1
Diagnostic Tests
  • CSF analysis
  • EEG
  • EMG
  • Blood enzymes increase with muscle atrophy
therapeutic interventions2
Therapeutic Interventions
  • Maintain function
  • Emotional support to patient & family
  • Baclofen—Diazepam for muscle spasms
  • Quinine for muscle cramps
  • Riluzole to reduce damage to motor neurons & prolong life
  • PT—OT
  • ST
    • AAC such as laptop computer
  • Massage
  • Position change & skin care
  • Enteral feedings
  • Prevention of infection
  • Support Groups
  • Counseling
guillain barre syndrome
Guillain-Barre Syndrome

GBS is also called acute inflammatory polyneuropathy

  • Inflammatory disorder characterized by abrupt onset of symmetrical paresis that progress to paralysis
  • Destruction of myelin sheath of spinal and cranial nerves occurs due to the diffuse inflammatory reaction
  • Peripheral nerves are infiltrated with lymphocytes leading to edema and inflammation
  • Segmental demyelination cause axonal atrophy slowing or blocking nerve conduction
  • Begins distal and ascends manner
  • Remyelination slowly occurs in a descending manner with resolution of symptoms
guillain barre syndrome1
Guillain-Barre Syndrome
  • Ascending GBS
    • Progressive weakness and numbness beginning in legs and ascending up the body
    • Numbness mild but muscle weakness leads to paralysis
    • Ascends all the way to cranial nerves
    • Deep tendon reflexes depressed or absent
    • Respiratory function impaired 50% of time
  • Descending GBS
    • Less common
    • Affects cranial nerves that originate in brain stem
    • Dysarthria
    • Dysphagia
    • Respiratory function impairment rapid
    • Numbness more in hands than feet
    • Diminshed or absent reflexes
guillain barre syndrome2
Guillain-Barre Syndrome
  • Miller Fisher syndrome
    • Rare
    • No respiratory compromise or sensory loss
    • Profound ataxia
    • Absence of reflexes
    • Paralysis of extraocular muscles
  • Pure motor GBS
    • Milder form
    • Mimics ascending GBS
    • Does not have numbness or paresthesias
  • Exact cause unknown
  • Possible autoimmune response to viral infection or vaccination
  • Viral illness noted within 2 weeks prior to onset of symptoms
  • Usually occurs between 20-50 years old
    • 45 or older more often
  • Affects men and women equally
  • 50% higher incidence in Caucasians than African Americans
signs symptoms4
Signs & Symptoms

Three stages

  • Stage One
    • Start with onset of symptoms and lasts until progression stops
    • 24 hours to 3 weeks
    • Abrupt onset of muscle weakness and paralysis
    • Little or no muscle atrophy
    • Recent history of viral illness or vaccination
    • Extent of respiratory impairment is dependent on type of GBS
      • May require intubation and mechanical ventilation
    • Labile blood pressure—cardiac dysrhythmias—urinary retention—paralytic ileus—numbness—cramping—pain
guillain barre syndrome3
Guillain-Barre Syndrome
  • Stage two
    • Symptoms most severe but progression has stopped
    • 2-14 days
  • Stage three
    • Recovery stage
    • Axonal regeneration and remyelination occurs
    • 6 – 24 months
    • Symptoms improve slowly
    • Takes months to a year to recover
  • Few patients suffer chronic disability
  • Respiratory Failure
  • Infection
  • Depression
  • Pneumonia
  • UTI
  • Complications of immobility
    • PE—DVT—Impaired skin intergrity—muscle atrophy
diagnostic tests2
Diagnostic Tests
  • Lumbar puncture to obtain CSF
    • Elevated protein
  • EMG
  • Nerve Conduction Velocity tests
  • PFT’s
therapeutic interventions3
Therapeutic Interventions

First stage

  • Complete care
  • Oxygen & mechanical ventilation
  • Plasmapheresis within 7-14 days of onset

Second phase—plateau phase

  • Emotional support

Third phase—recovery phase

  • Intensive rehabilitation
nursing care1
Nursing Care


  • Monitor respiratory function
  • Monitor swallowing
  • Pain management
  • Enteral feedings
  • Communication board
  • Diversional activity during recovery phase
patient education
Patient Education
  • Explain all procedures
  • Disease process—sign & symptoms—recovery
  • Discuss need for intubation as respiratory function may be impaired
postpolio syndrome
Postpolio Syndrome

Postpolio Syndrome

  • Condition that affects survivors of polio 10-40 years after recovering from infection of poliomyelitis virus
  • Severity depends on degree of residual weakness and disability from initial illness
signs symptoms5
Signs & Symptoms
  • Further weakness of muscles that were affected initially with polio virus
  • Fatigue to progressive weakness to atrophy
  • Sleeping difficulties
  • Joint pain
  • Scoliosis
  • Respiratory compromise

Symptoms vary from mild to debilitating

postpolio syndrome1
Postpolio Syndrome

Diagnostic Tests

  • History and Physical Exam

Therapeutic Interventions

  • None other than rest and moderate exercise

Review Table 50.4 Summary of PNS Disorders

  • Review Box 50.3 Nursing Care Plan for Patients with Progressive Neuromuscular Disorder
cranial nerve disorders1
Cranial Nerve Disorders
  • There are 12 pairs of cranial nerves that originate in the brain
  • They innervate the head—neck—special sensory organs
  • Cranial nerve disorders are classified as peripheral neuropathies
  • Disorders affect sensory—motor—or both of a single nerve
  • Cause can be unknown or may include:
    • Tumors—infection—inflammation—trauma
  • Two common cranial nerve disorders are
    • Trigeminal neuralgia
    • Bell’s palsy
trigeminal neuralgia
Trigeminal Neuralgia

Trigeminal Neuralgia is also called tic douloureux

  • Affects 5th cranial nerve—trigeminal nerve
    • Has 3 branches that have both sensory & motor function
    • Innervates the forehead—nose—cheek—gums—jaw
  • TN only affects the sensory portion of nerve
  • Irritation or chronic compression of nerve initiates symptoms
  • Seen more often in women between 50-60 years old
trigeminal neuralgia1
Trigeminal Neuralgia

Signs & Symptoms

  • Intense recurring pain in the skin of one side of the face
    • Sudden jabbing, burning, knifelike pain
  • Onset begins & ends suddenly lasting a few seconds to minutes
  • Occurs in clusters that can be many times or few
  • Slight touch—cold breeze—talking—chewing are triggers
  • Trigger zones include:
    • Lips—upper & lower gums—cheeks—forehead—side of nose
  • Sleep provides relief
  • Frequent blinking and tearing of eye on affected side
trigeminal neuralgia2
Trigeminal Neuralgia

Therapeutic Intervention

  • Anticonvulsants reduce nerve impulses
    • Dilantin—Tegretol
  • Baclofen—clonazepam—gabapentin—valproic acid
    • Help control symptoms
    • May cause bone marrow suppression so need routine CBC
  • Nerve block with local anesthetic
    • 6-8 months relief
  • Surgery if all else fails
    • Radio frequency ablation to destroy some nerve branches
    • Results are anesthesia of area
  • Gamma Knife radiosurgery
    • Creates lesion on nerve which blocks pain signal
trigeminal neuralgia3
Trigeminal Neuralgia

Patient Education

  • Eye (cornea) on affected side needs to be protected from injury due to loss of sensation
    • Goggles—sunglasses—eye patch at night
    • Artificial tears
bell s palsy
Bell’s Palsy


  • Affects cranial nerve VII—facial nerve
  • Inflammation and edema of nerve causes interruption of nerve impulse
  • Loss of motor control on one side results
  • Contracture of facial muscle can occur if slow recovery


  • Nerve trauma by viral or bacterial infection
  • May be autoimmune
  • Affects men and women equally
  • Affects all ages
  • Any time of year
  • More common in:
    • 3rd trimester of pregnancy—immunocompromised—diabetics
bell s palsy1
Bell’s Palsy

Signs & Symptoms

  • Onset abrupt & progresses over 2-5 days
  • Pain behind ear may precede onset of facial paralysis
  • Dry eye
  • Tingling around lips
  • Inability to close eyelid—wrinkle forehead—smile—close lip
  • Mouth pulled to unaffected side
  • Drooling on affected side
  • Constant tearing of affected eye
  • Loss of taste on anterior 2/3 of tongue
  • Dysarthria
  • Severity of paralysis peaks within several days of onset
bell s palsy2
Bell’s Palsy

Diagnostic Tests

  • 50 % of patients recover completely in short time
  • 35% within one year
  • History & Physical
    • Need to rule out CVA

Therapeutic Interventions

  • Prevention of complications
    • Protect cornea eye on affected side
  • Prednisone for 7-10 days to decrease edema
  • Antiviral medication
  • Moist heat
  • Gentle massage
  • Facial sling

Review the Nursing Diagnosis on 1140

  • Review table 50.5 to summarize Cranial Nerve Disorders