Myasthenia Gravis (MG)

Myasthenia Gravis-QR


Thanks to Dr. Mark Tarnopolsky, MD, PhD, FRCPC, Professor of Pediatrics (Neuromuscular and Neurometabolic Disease), Hamilton Health Sciences-McMaster Children’s Hospital, McMaster University, Hamilton, ON Canada, and Sadie Sattan, RN, BScN, MN, School of Nursing, Faculty of Health Sciences, McMaster University/Mohawk College, Hamilton, ON Canada for their expertise with the initial review of this topic.


A neuromuscular disorder arising from autoimmune-mediated injury of the post-synaptic neuromuscular junction and characterized by fluctuating skeletal muscle weakness and fatigability, usually affecting ophthalmic and bulbar muscles.


  • Thymus gland dysfunction: Both thymic hyperplasia and thymoma, have been implicated in the formation of autoantibodies through abnormal antigen presentation via MHC class II molecules
  • There are two recognized pathogenic neuromuscular junction (NMJ) autoantibodies:
    • Anti-nicotinic acetylcholine receptors (AchR) antibodies
    • Anti-Muscle-Specific receptor tyrosine kinase (MuSK)
  • Seronegative MG: Term used for the ~15 % patients who have symptoms of MG and are negative for both anti-AchR and anti-MuSK antibodies (often older adults with primarily ocular MG). Approximately 15% patients have symptoms of MG and negative for both anti-AChR and anti-MuSK antibodies
  • Other antibodies found in association with MG include:
    • Anti-lipoprotein-related protein 4 (LRP4) antibodies
    • Anti-striated muscle antibodies (StrAbs)
    • Anti-titin and ryanodine receptor (RyR) antibodies
    • Anti-ryanodine antibodies also detectable
  • Genetic predisposition


  • Female: male (overall 2:1), but ~3:1 (F: M) in younger and 1:1 in older adults
  • Age of onset: Women are typically affected younger (< 40 years; range 18-25 years) as compared to men (> 60 years)
  • Incidence is 3-30 cases per million per year
  • Prevalence is 14-40 per 100,000 population in the US (MG Foundation of America)

Types Of Myasthenia Gravis

Myasthenia Gravis is classified according to the involvement of skeletal muscles.

  • Generalized: Diffuse weakness in the trunk, arms, and legs (usually within 1 year of commencement of symptoms) affects ~80% of patients with early-onset of age (<50 years) versus ~60 % of patients with late-onset (>50 years)
  • Ocular: Weakness primarily affecting muscles that control eye movements. About 20% of early-onset of age (<50 years) and ~40% of late-onset (>50 years) patients will have restricted ocular MG, whereas most ( >90%) of patients will have ocular and/or bulbar symptoms at some time during the course of the disorder
  • Congenital MG: Inherited heterogeneous group of diseases caused by genetic defects of the NMJ, which may be presynaptic, synaptic, or postsynaptic. Generalized symptoms manifest at or shortly after birth and may cause generalized symptoms but most patients will have bulbar (feeding difficulty) and/or ocular (ptosis) findings
  • Transient neonatal myasthenia gravis: Observed in ~10-20% of infants born to mothers with MG. Mechanism related to transplacental transfer of circulating maternal antibodies (IgG). Symptoms dissipate over a few weeks as the levels of circulating offending antibodies decline
  • The Myasthenia Gravis Foundation of America has a classification scheme with increasing severity of symptoms:
    • Class I: Restricted to ocular muscles
    • Class II: Ocular and mild weakness in muscles other than ocular
    • Class III: Moderate weakness outside of ocular, may have ocular as well
    • Class IV: Severe weakness of muscles outside of ocular, may have ocular as well
    • Class V: Intubation

Ref: Myasthenia gravis: Recommendations for clinical research standards Neurology. 2000;55:16-23.


Normal NMJ function:

Arrival of an action potential at the presynaptic terminal of the NMJ results in the release of ACh within the synaptic cleft → binding of ACh to the post-synaptic nicotinic AChR → endplate/ muscle membrane depolarisation → DHP/ryanodine receptor interaction in t-tubule → muscle contraction. Acetylcholine esterase present within the synaptic cleft degrades Ach to choline and acetyl-CoA and prevents overstimulation of postsynaptic AChR.

Impact of Anti-AChR antibodies on NMJ function:

Anti-AChR antibodies (possible pathogenic mechanisms):

  • Block ACh from binding to the AChR, thereby disrupting/reducing post-synaptic transmission
  • Downregulation of AChR via cross-linking of surface ACh receptors followed by accelerated endocytosis and degradation. This results in less functional surface receptors available for interaction with ACh
  • Promotes local inflammation and complement-mediated damage and remodeling of the post-synaptic membrane leading to less post-synaptic folds and less AChR. This also eventually results in less functional surface receptors available for interaction with Ach

The combination of these factors leads to muscle weakness, fatigability, and disease progression over time.

Clinical Manifestations:

Depends on the muscles involved

General muscular symptoms

  • Fluctuating weakness and fatigue
    • Affects various groups of skeletal muscles
    • Weakness may fluctuate throughout the day
    • Worsens with activity
    • Transiently improves with rest
    • More evident later in day/evenings
    • Less evident/ absent upon awakening in the morning
  • May manifest as difficulty with:
    • Rising from a seated position
    • Ambulation/ ascending stairs
    • Maintaining muscular contraction (holding arms outstretched, lifting, gripping objects)

Ocular symptoms

  • Ptosis – unilateral or bilateral; heightened with sustained upgaze
  • Binocular diplopia due to weakened extraocular muscles (gaze may be disconjugate at rest)
  • Pupils are not affected

Bulbar symptoms

  • Dysarthria (often very nasal sounding)
  • Dysphagia
  • Fatigue with chewing
  • Hypophonia
  • Palatal muscle weakness may lead to nasal regurgitation

Involvement of neck muscles

  • Weakness of neck extensors more than flexors causes drooping of head usually late in the day (more common in older patients)
  • Muscular pain due to holding of head with weak muscles (may present as a tension-type headache)

Involvement of respiratory muscles

  • Difficulty breathing
  • Shortness of breath on exertion
  • Respiratory insufficiency/ failure

Facial muscle involvement

  • Bilateral facial weakness
  • Loss of facial expressions/ weak or absent smile
  • In-coordinated lip movements

Myasthenic crises:

Life-threatening condition stemming from severe weakness/failure of respiratory and oropharyngeal muscles. Intubation and ICU intervention often required with nasogastric feeds.

Usual precipitating factors:

  • Tapering of immunosuppressive medications
  • Concurrent infection
  • Surgery
  • Pregnancy/ childbirth

Cholinergic crises:

Very rare occurrence caused by overmedication with cholinesterase inhibitors leading to bradycardia and/or respiratory distress. Atropine alleviates symptoms.


  • Active: Fluctuating symptoms with increased severity within 5-7 years of disease onset
  • Stable: Symptoms persist but stable. May worsen with stressors (e.g. infection) or medication adjustments
  • Remission: Relatively symptom free on immunotherapy ±thymectomy. With prolonged stability, medications might be tapered/stopped (as tolerated)

Workup and Diagnosis


  • Weakness (duration, fatigability, exacerbating factors)
  • Family history of MG or other autoimmune disorders (weak association)
  • Medication use, occupational hazards (potential toxin exposure)

Physical: Requires a neurological examination that should include assessment of:

  • Gaze induced ptosis and diplopia: May be evident during sustained upwards or horizontal gaze for 30-60 sec. Assess for ptosis and/or abnormal extra-ocular eye movements
  • Coggan’s twitch: Upon rapid up-gaze, the eye lids lift fully and then rapidly drop down; appearing to “twitch”.
  • Weakness: Strength of limbs or neck (weakness in extension > flexion) assessed at rest and after repetitive movement to reproduce/ induce fatigue. Manoeuvres to induce fatigue might include: Prolonged shoulder abduction or neck flexion against resistance; holding arms stretched; ascending a flight of stairs, deep knee bends, walking on toes or heels

Tensilon (Edrophonium) test:

  • Short acting, rapid onset acetylcholinesterase inhibitor, edrophonium can improve strength in patients impaired neuromuscular junction transmission
  • The test may be useful in cases where the weakness is readily apparent as with ptosis and/or opthalmoparesis but less useful with generalized weakness
  • A test dose of 2 mg of Edrophonium is given intravenously and repeated after 1 minute with 8 mg
    • Onset of action 30-45 seconds, lasts for ~4 minutes
    • Patients must be warned that they may experience an increase in cholinergic effects (tearing, cough, and increased saliva)
    • It is important to have atropine readily available in rare cases of severe bradycardia (0.6 mg)
  • Contraindications to IV edrophonium:
    • Include heart disease
    • Bradycardia
    • First degree heart block
    • Bronchial asthma

Note: Agents with longer duration of action than Edrophonium, e.g. neostigmine (IM) or pyridostigmine (PO) may provide a better assessment in situations where it may be difficult to fully appreciate or quantify the brief response to edrophonium, e.g. infants and children. Often a trial for a week on and a week off of a trial dose of pyridostigmine with a symptom log is very helpful to determine if there is a positive response to acetylcholinesterase blockade.

Serology: Antibodies in Myasthenia Gravis

  • Acetylcholine receptor antibodies are detected in
    • Approximately 45% of patients with generalized myasthenia and
    • Approximately 40% of those with ocular myasthenia
    • The serum concentration of anti-AChR antibody does not correlate with disease severity
  • Anti-MuSK antibodies
    • Detected in about 40% of MG patients who are seronegative for AChR antibodies
  • Antibodies are diagnostic of MG; there absence does not preclude the diagnosis

Note: While elevated serum concentrations of anti-AChR binding and anti-MuSK antibodies are diagnostic of MG, there absence does not preclude the diagnosis (i.e. these are specific but not sensitive tests).

Electrodiagnostic studies

Single fiber electromyography (SFEMG)

  • Most sensitive clinical test of neuromuscular transmission

Repetitive nerve stimulation (RNS)

  • A compound muscle action potential (CMAP) can be generated by inserting a needle electrode over the muscle endplate and stimulating the motor nerve


Chest CT or MRI can be used to assess for thymic abnormalities (thymic hyperplasia or thymoma).

RN/Medical Management:


  • Individualized and based on the extent of functional impairment, age, and sex
  • Reduction/treatment of stressors (infections, physical and emotional stress) may improve symptoms
  • Fifteen percent of MG patients can have thyroid abnormalities (i.e. Hashimoto’s thyroiditis) as co-existent conditions; consequently, it is important to check TSH for hypothyroidism symptoms can mimic MG

Note: In the early stages of MG, remissions and spontaneous improvement can occur without any specific therapy.

– Cholinesterase inhibitors

  • Often used initially as a diagnostic and therapeutic trial
  • May be discontinued when immunological control of disease is achieved
  • Blocks acetylcholine esterase within the synaptic cleft and prolongs the action of ACh
  • Daily requirements may vary depending on the extent of fluctuations/exacerbations
  • In general limb and bulbar symptoms respond better than do ocular symptoms (diplopia is particularly resistant)
  • Pyridostigmine: Acts within 15-30 minutes, peaks in 2 hours and lasts for 3-4 hours
  • Dose: 30 mg TID and increased as required and as tolerated to a usual dose of 180-360 mg/day. Long-acting forms are available for long -term use (180 mg dose-sometimes helpful as an overnight dose in those symptomatic later in the evening)
  • Neostigmine: 15 mg/dose every 3-4 hr. Increase as tolerated; Max daily dose: 375 mg (divided)

Common adverse effects:


  • Nausea, vomiting, abdominal cramps, loose stools, and diarrhea


  • Increased oral and bronchial secretions, sweating, bradycardia

Cholinergic crisis:

  • Results from over-stimulation of NMJ due to an excess ACh (acetylcholinesterase inhibition)
  • Increased sweating, salivation, bronchial secretions
  • Dysphagia, miosis, flaccid paralysis, respiratory failure-paradoxical worsening weakness
  • Treatment:
    • Discontinue cholinergic agent
    • Respiratory support (intubation and ventilation as required)
    • Antimuscarinic drugs (e.g. atropine)
    • Resume cholinergic therapy once patient stabilized and use lower doses



  • Refractory or progressive MG
  • Inadequate response or side effects with cholinesterase inhibitors
  • Increasing disability
  • One approach is to start all symptomatic proven patients with cholinesterase inhibitors and prednisone and once the disease is under control to stop the cholinesterase inhibitors (should not need them when the disease is under control) and slowly taper the prednisone

– Corticosteroids (prednisone):

  • Often improves strength within days to weeks (usually 2-3 weeks) after initiation
  • Approximately 1/3 of patients temporarily deteriorate within a week of initiating prednisone; which lasts for ~ 5-6 days (rare if the starting dose is low)
  • Always start at low dose (≤20 mg) and titrate upwards after ~2 weeks by 5 mg/week increments according to clinical response (max = 40 mg/d)
  • When adjuvant immunotherapy is added, prednisone may be tapered to the lowest effective dose after the adequate time of onset for a clinical response from added immunotherapy has been achieved; subsequently, pyridostigmine tapering may be tried

Common side effects:

  • Hypertension, glucose intolerance, osteoporosis (long term), weight gain, cushingoid features, mood changes/psychosis
  • If the patient has significant side effects or cannot get to a dose of <10 mg/prednisone/day, then one should consider alternative disease-modifying agents (see below)


  • Starting Dose: Variable; one approach is to begin with 10-20 mg PO daily; increase by 5 mg per week monitoring clinical response
  • Once stabilized may begin an alternate day regimen, by reducing the dose every other day OR taper the dose very slowly to the minimal effective dose using an alternate day drop with a fixed daily dose (e.g. 20 mg/d then 20/17.5 mg alt days, 17.5 mg/d, then 17.5/15 mg alt days, etc. The time interval for any of these dose changes is variable and dependent on patient response and tolerance to dose changes

– Azathioprine

  • Used as steroid-sparing therapy or adjunct to steroids
  • Often initiated in combination with steroids as a response to azathioprine is often delayed by 4-8 months
  • Steroids can then be weaned off or reduced depending on the response to azathioprine
  • Effective, but relapses may recur 2-3 months after the drug is discontinued or reduced below therapeutic levels

Side Effects: Discontinue use if

  • Acute flu-like illness (~5%) → stop and do not use
  • Chronic elevation of GGT in (~7%), elevation of bilirubin 3 times than the upper limit of normal, or neutropenia/ severe lymphopenia seen in ~5%

Note: MCV elevation is expected and indicative of the drug having a biochemical effect → not an indication to stop therapy


  • Start at 1.0 mg/kg/d and increase over ~30 days to 2 mg/kg/d and re-check GGT, bilirubin, and CBC
  • If no response in ~4 months may increase dose to a maximum of 3 mg/kg per day
  • Most can take the medication once per day but if they have gastrointestinal upset, it may be divided as a TID dosing
  • Follow CBC, bilirubin, and GGT every 2 months while on therapy

– Cyclosporine A

  • Long-term immunosuppression (steroid-sparing)
  • Improvement may be detected 1 to 2 months after initiating treatment
  • Benefits disappear when treatment is stopped or reduced below therapeutic levels

Side effects:

  • Renal toxicity and hypertension [monitor plasma creatinine, blood pressure and plasma trough cyclosporine levels (some use peak levels)]


  • Start at 50 mg BID and increase to a maximum of 2.5 mg/kg twice a day adjusted according to levels, tolerance and renal function (creatinine)

– Mycophenolate Mofetil (MMF)

  • Corticosteroid-sparing agent that may be considered for adjunctive or primary therapy in refractory MG
  • Faster onset of action than azathioprine but generally less consistently effective

Side effects:

  • Liver toxicity but considered somewhat less toxic vs azathioprine-follow similar monitoring as per azathioprine


  • Start at 500 mg twice daily and increase as tolerated to 1 g BID

– Cyclophosphamide

  • Alternative therapy to other immunosuppressive agents
  • Good response in >50% of patients

Side effects:

  • Potential for life-threatening infections (watch WBC count and neutrophils), hemorrhagic cystitis, do not use if not familiar with the use of the drug and seek local expertise


  • 150-200 mg/day PO



  • Acute exacerbations
  • Myasthenic crises
  • As part of pre-surgical treatment to boost strength and improve respiratory status
  • Intermittent therapy for those sub-optimally controlled with other treatments
  • Bridging therapy until the response to immunotherapy is apparent

– Plasmapheresis:

  • Use of plasma exchange determined by the clinical scenario
  • Rapid action-benefits may be seen after one exchange
  • Usually 5 exchanges can be done over 10-14 days
  • Short term benefit (4-6 weeks)
  • Risks: Hypotension, thromboembolism, metabolic disturbances

– Human immune globulin (IVIG):

  • Improvement usually occurs within 1 week and may last for months
  • Patients with more severe symptoms seem to have a better response to therapy
  • May be used monthly as bridge therapy in patients who cannot tolerate corticosteroids, until immunotherapy takes effect

Side effects:

  • Mild headache is common
  • Allergy: Approximately 1/1,000, check IgA levels and do not use if IgA deficient without consulting haematologist
  • Shaking/chills: Use Benadryl and/or Demerol as a pre-medication
  • Rarely severe headache

Note: Often a pre-dose of methyl-prednisolone is given that may lessen side effects and enhance efficacy (low dose <125 mg NOT 1 g dose).


  • 2 g/kg given over 3-5 days (can be used as 1 g/kg/d X 2 Or 0.4 g/kg X 5 doses)



  • Considered in most patients with MG
  • Thymectomy is not indicated for anti-AchR Ab-negative patients even if anti-MuSK Ab is positive
  • Some anti-MuSK Ab-negative patients may still be covered for the procedure
  • However, advancing age, mild or limited MG (e.g primarily ocular) and/or other significant co-morbidities might preclude thymic excision
  • Variable post-surgical clinical course; may take months or years to see the benefit (due to persistence of antibody-producing plasma cells)
  • Younger patients early in the disease course may have the best response
  • Older (>60 years) patients, show little or no benefit
  • Paradoxically, patients with thymomas do not respond as well to thymectomy as do patients without thymoma, but thymoma can locally or distantly metastasize and all suspected thymomas should be removed

Procedure: Removal of thymus and tissue mediastinal and cervical adipose as these may contain ectopic thymic tissue. Transcervical and thoracoscopic approaches have been used but there is a concern about residual thymic tissue to remain and most consider a full sternal split thymectomy to be the “gold standard”.

Potential complications: Risk of injury to recurrent laryngeal, vagus, and phrenic nerves.


May occur with both Myasthenic and Cholinergic crises; respiratory muscle and bulbar weakness resulting in compromised respiratory function. Treatment includes:

  • Vital signs
  • Assessment of respiratory status including oximetry and arterial blood gases
  • Positive pressure ventilation or endotracheal intubation (as required)
  • Plasmapheresis or IVIG treatment is employed
  • Discontinue cholinesterase inhibitor; restart once the patient stabilizes and begins to improve
  • Avoid magnesium therapy, aminoglycoside antibiotics as well as muscle blocking agents

Acetylcholinesterase inhibitor

  • Pyridostigmine
  • Neostigmine


  • Reversibly inhibits cholinesterase
  • Thus facilitates the transmission of impulses across NMJ




  • Start with 30-60 mg PO TID; may increase dose gradually at intervals of ≥48 hrs, as needed; usual dose range 180-360 mg/day in 3-6 divided doses (i.e. 120 mg every 3-4h). Max dose 540 mg/day total dose (including long-acting forms)
  • If excessive muscarinic side effects occur (GI cramps, diarrhea, salivation, increased bronchial secretions, nausea, sweating, bradycardia), then anticholinergic (e.g. glycopyrrolate 1 mg) can be taken with each pyridostigmine dose
  • Dosing is individualized; patients who do well until midday may take 60 mg at lunch and 90 mg 4-8 h later; patients with dysphagia may benefit from taking dose 30 minutes before meals


  • 180 mg once or twice daily; should have at least 8 hours gap in between doses

Note: It may be used at bedtime if severe persistent weakness occurs upon awakening; not preferred choices during daytime use, due to variable release and delayed absorption, resulting in inconsistent control of symptoms



  • 15 mg PO every 3-4h; may increase dose gradually at intervals of ≥48 hours, as needed; usual maintenance dose 15-375 mg/day


  • 0.5-2.5 mg IM/ IV/ SC every 1-3 hours, as needed and tolerated; Max. 10 mg/24 hours

Renal impairment: Clcr 10-50 mL/minute: Administer 50% of normal dose; Clcr <10 mL/minute: Administer 25% of normal dose


  • Administer atropine sulfate 0.6-1.2 mg IV at the same time with large parenteral neostigmine doses to counteract adverse muscarinic effects
  • Atropine and epinephrine may be required to treat hypersensitivity reactions.



  • Prednisone

Use: Acute exacerbations


  • Decreases inflammation and the normal immune response through multiple mechanisms, also suppresses adrenal function in higher doses


  • Start 10-20 mg daily; increase gradually by 5 increments every 7 days as tolerated up to maximum of 40 mg/d. Once stabilized may begin an alternate day regimen, by reducing dose every other day or taper the dose very slowly to the minimal effective dose using an alternate day drop with a fixed daily dose (e.g. 20 mg/d, followed by 20/17.5 mg alt days, then 17.5 mg/d, followed by 17.5/15 mg alt. days, etc.

Tumor necrosis factor (TNF) blocker

  • Azathioprine

Use: Immunosuppressant therapy


  • Complete mechanism of immunosuppression is not fully known
  • It antagonizes purine metabolism and may inhibit synthesis of DNA, RNA, and proteins
  • May also interfere with cellular metabolism and inhibit mitosis


  • Begin 50 mg PO daily; titrated by 50 mg every week to therapeutic dose achieved; usual therapeutic dose range 2-3.5 mg/kg/day (typically 150-200 mg/day)

Monitor: CBC every other week while adjusting dose; then monthly; LFTs

Calcineurin inhibitor, Immunosuppressant agent

  • Cyclosporine A


  • Exact mechanism of action is not known
  • Inhibits production and release of interleukin II and also inhibits interleukin II-induced activation of resting T-lymphocytes


  • Start at 50 mg BID and increase to a maximum of 2.5 mg/kg twice a day, doses 12 hours apart; after ~4 weeks adjust the dose according to serum cyclosporine concentration of 100-150 ng/ml, tolerance and renal function (creatinine). Take consistently with regard to time of day and meals


  • Measure serum creatinine every month
  • Measure serum cyclosporine concentration every 2-3 months (to monitor for toxicity in all patients; and efficacy in transplant patients)
  • IV to oral conversion is 1:3 (300 mg per day PO = 100 mg per day IV)

Renal impairment:

  • If serum creatinine levels increase to ≥25% above pre-treatment levels: Decrease dose by 25% to 50%
  • Monitor: Creatinine, lipids, K, Mg, uric acid, BP, liver function

Antineoplastic agent, Alkylating agent; Antirheumatic

  • Cyclophosphamide

Use: Immunosuppressant


  • An alkylating agent that prevents cell division by cross-linking DNA strands and inhibiting DNA synthesis
  • Interferes with DNA replication and RNA transcription
  • It is a cell cycle phase nonspecific agent and potent immunosuppressive agent


  • 150-200 mg/day PO


  • Mycophenolate mofetil


  • Mycophenolate mofetil hydrolyzed to form mycophenolic acid (MPA), a reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH) in the purine biosynthesis pathway
  • Inhibition of IMPDH results in depletion of guanosine triphosphate and deoxyguanosine triphosphate
  • Thus selectively inhibits the proliferation of activated B and T lymphocytes
  • It also suppresses the formation of antibodies active in complement-dependent lysis and antibody-dependent, cell-mediated cytotoxicity


  • Start at 500 mg twice daily and increase as tolerated to 1 g PO BID; range 1-3 g/day
  • Divided doses may reduce abdominal pain and gastritis


  • Pregnancy test prior to treatment
  • CBC, ANC (absolute neutrophil count) every week x 4; then every 2 weeks x 4 then monthly

Immune globulin/ Blood product derivative

  • Immune globulin (IVIG)


  • Exact mechanism of action unknown
  • Probably facilitates immune-regulation through down-regulation of offending antibodies


  • 2 gm/kg given IV over 2-5 days (can also be used as 1 g/kg/d for 2 days Or 0.4 g/kg/day for 5 days)
Diagnosis and Goals:


  • Fatigue related to muscle weakness (disease process)
  • Risk for aspiration related to muscle weakness of face and tongue
  • Social isolation related to diminished speech capabilities and increased secretions


  • Develop energy conserving strategies to relieve fatigue and provide rest
  • Preventing aspiration by closely monitoring the patients
  • Maintaining social interactions
Nursing Intervention:

Minimizing fatigue:

  • Determine the duration of energy peaks and the plan exercise, meals, and other activity of daily living (ADLs) with a frequent short period of rest to regain energy
  • Advise to take medications 30 minutes before meals to facilitate chewing and swallowing
  • Obtain assistive devices to support weak muscles, to help the patient perform ADLs (as required)
  • Provide an eye patch to the patient with diplopia, and advise to use the patch on alternate eyes to rest the eyes, and allow safe participation in activity

Preventing aspiration:

  • Advise patient to slightly flex the head position during eating to prevent aspiration of food
  • Evaluation and assessment of oral motor strength is essential prior to each meal
  • Advise to select the best suited textured diet for e.g soft, solid foods instead of liquid to reduce the risk of aspiration, and facilitate chewing without exhausting the muscles during mealtime
  • Have suction available which patient can operate
  • Administer IV fluids and nasogastric tube feedings to the patient in crisis or with impaired swallowing; head end of the bed should be elevated after feeding
  • In cases where the patient is intubated:
    • Frequent suction may be required
    • Assessment of breath sounds and chest X-ray reports follow-ups required since aspiration is common

Maintaining social interactions:

  • Develop strategies and alternate communication methods such as flashcards or letter board, if speech is affected
  • Speech therapist referral (as required)
  • Advise to speak in a slow manner to avoid voice strain
  • Supporting the lower jaw by cupping the chin in the hands, help assist with speech
  • Patient with bulbar weakness have weak cough or gag reflexes, which can cause problems in clearing their respiratory secretions, advised to sit with their head tilted and ask to carry a handkerchief to manage secretions in public
  • Patients may be directed to the Myasthenia Gravis Foundations/Societies in order to meet other patients with the disease and participate in support groups

Community and home care considerations:

  • Regular follow-up and compliance with the treatment regimen is necessary to lead a productive life
  • Referrals are given when needed to community agencies, such as home respiratory care, physical therapy, nutritional services
  • Frequent assessments are required to determine fluctuations in the patient’s condition and inform caregivers as needed
  • Teach patient and family how to use home suction in case of aspiration. Make sure everyone in the household knows Heimlich maneuver

Patient education and health maintenance:

  • Patient and family should recognize the symptoms of the crisis
  • For patients on anticholinesterase therapy:
    • Maintain accurate dosage and times (30mins prior meals)
    • Avoid taking medication with fruit, coffee, tomato juice, or other medications
    • Adherence to the therapy is expected and always advised
    • GI distress is a common complaint in patients receiving therapy
  • Short intervals of rest periods are advised before fatigue ensues
  • Teach the patient ways to prevent crisis and aggravation of symptoms
    • Avoid exposure to flu, colds, and infections
    • Avoid extreme hot or cold environment
    • Agents which have neuromuscular blocking effect, like procaine (often used by the dentists as a nerve-blocking agent in procedures), should not be used in patients with MG, because they are not well tolerated. The patient should always ask and should be able to provide the history to caregiver whenever seeing one for any reason
  • Medic Alert bracelet is advised to be worn by the patient
  • Stress importance of adequate nutrition; instruct to chew food thoroughly and eat slowly
  • Advise patient to avoid tranquilizers, sedatives, alcohol
  • Refer patient/family for more information to:
    • Myasthenia Gravis Association of B.C.:
    • The Myasthenia Gravis Foundation of America:
Nursing Alerts:
  • Many medications can exacerbate the weakness experienced by the patient with myasthenia, including some antibiotics, antiarrhythmics, local and general anesthetics, muscle relaxants, and analgesics. Assess function after administering any new drug, and report deterioration in the condition
  • It is necessary to maintain the blood adequate blood levels of anticholinesterase medication to avoid weakness. Medications should be given on time. Delays may lead to muscle weakness, including swallowing difficulty, which may pose further problems with taking orally administered medications


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  • Rowland LP and Pedley TA, eds. Merritt’s Neurology. 12th ed. Philadelphia: Lippincott Williams and Wilkins; 2010
  • Skidmore-Roth L. ed. Mosby’s drug guide for nurses. 9th ed. St. Louis: Elsevier-Mosby; 2011
  • Skidmore-Roth L, ed. Mosby’s nursing drug reference. 24th ed. St. Louis: Elsevier-Mosby; 2011
  • Online Resources:
    • National Guideline Clearinghouse (NGC)-Guidelines for treatment of autoimmune neuromuscular transmission disorders

Online Pharmacological Resources:

  • e-Therapeutics
  • Lexicomp
  • RxList
  • Epocrates

Journals/Clinical Trials:

  • Barber C. Diagnosis and management of myasthenia gravis. Nurs Stand. 2017;31(43):42-47. doi:10.7748/ns.2017.e10434
  • Benatar M, Burns T, Anthony V. Serological, pharmacological and electrophysiological tests for the diagnosis of myasthenia gravis. Published Online: 2010. doi: 10.1002/14651858.CD008904
  • Daniel Hantaı D, Richard P, Koeniga J and Eymard B. Congenital myasthenic syndromes 2004 Curr Opin Neurol 17:539-551
  • Gajdos P, Chevret S, Toyka KV. Intravenous immunoglobulin for myasthenia gravis. Cochrane Database of Systematic Reviews 2012, Issue 12. Art. No.: CD002277. doi: 10.1002/14651858.CD002277.pub4
  • Gajdos P, Chevret S, Toyka KV. Plasma exchange for generalized myasthenia gravis. Cochrane Database of Systematic Reviews. 2002, Issue 4. Art. No.: CD002275. doi: 10.1002/14651858.CD002275
  • Gomez AM, Van Den Broeck J, Vrolix K, Antibody effector mechanisms in myasthenia gravis-pathogenesis at the neuromuscular junction. Autoimmunity. 2010:5-6:353-70
  • Kołtuniuk A, Rozensztrauch A, Beniak M, et al. Nursing Care of Patients with Myasthenia Gravis — Case Report. The Journal of Neurological and Neurosurgical Nursing. 2017;6:88-97. doi:10.15225/PNN.2017.6.2.6
  • Meriggioli MN. Myasthenia gravis with anti-acetylcholine receptor antibodies 2009; 26:94-108
  • Mehndiratta MM, Pandey S, Kuntzer T. Acetylcholinesterase inhibitor treatment for myasthenia gravis. Cochrane Database of Systematic Reviews. 2011, Issue 2. Art. No.: CD006986. doi: 10.1002/14651858.CD006986.pub2
  • Okumura M, Inoue M, Kadota Y, et al. Biological implications of thymectomy for myasthenia gravis. Surg Today. 2010; 2:102-7
  • Sanders DB, Hart IK, Mantegazza R, et al. An international, phase III, randomized trial of mycophenolate mofetil in myasthenia gravis. Neurology.2008; 6:400-406
  • Schneider-Gold C, Gajdos P, Toyka KV, Hohlfeld RR. Corticosteroids for myasthenia gravis. Cochrane Database of Systematic Reviews 2005, Issue 2. Art. No.: CD002828. doi: 10.1002/14651858.CD002828.pub2
  • Skeie G. O., Lunde, P. K., Sejersted, O. M. Myasthenia gravis sera containing antiryanodine receptor antibodies inhibit binding of [3H]-ryanodine to sacroplasmic reticulum. Muscle Nerve, 1998, 21: 329-335
  • Vincent A, Leite MI Neuromuscular junction autoimmune disease: muscle specific kinase antibodies and treatments for myasthenia gravis. Curr Opin Neurol. 2005, 5:519-25
  • Yamamoto AM, Gajdos P, Eymard B et al. Anti-titin antibodies in myasthenia gravis: tight association with thymoma and heterogeneity of nonthymoma patients. Arch Neurol. 2001, 6:885-90