My AChR antibody test was negative. Can I still have myasthenia gravis?

Yes. About 15% of patients with generalised MG are AChR-antibody negative. In these patients, MuSK antibody testing is the next step, and LRP4 antibodies are tested in selected double-seronegative cases. Repetitive nerve stimulation and the clinical pattern of fatigable weakness remain central to the diagnosis. A negative AChR test does not exclude MG.

Why do I need a CT scan of my chest?

Because approximately 10–15% of people with MG have a thymoma — a tumour of the thymus gland, which sits in the chest behind the breastbone. Finding it matters both for the tumour itself and because removing the thymus (thymectomy) is an important part of MG treatment. Every patient diagnosed with MG at KIMS has a CT chest.

Are there medicines I should avoid with myasthenia gravis?

Several medications can worsen MG, including certain antibiotics (fluoroquinolones and aminoglycosides), some anaesthetic agents, magnesium given intravenously, and some heart and blood pressure medications. Always tell any doctor, dentist, or anaesthetist that you have MG before a new medicine or procedure, and carry a note of your diagnosis.

EMERGENCY:Difficulty breathing, inability to swallow, or rapidly worsening weakness in a patient with myasthenia gravis (possible myasthenic crisis) —call040-46324365immediately — 24 hours, 7 days— 24/7

NEUROMUSCULAR DISORDERS

Myasthenia Gravis (MG): Weakness That Worsens With Use and Recovers With Rest

The most common neuromuscular junction disorder — an autoimmune condition producing fatigable weakness of the eyes, face, throat, and limbs. Antibody testing, repetitive nerve stimulation, CT chest for thymoma, immunotherapy, thymectomy, and 24-hour neuro-ICU care for myasthenic crisis at KIMS Neuroscience, Secunderabad, Hyderabad.

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ICD-10

G70.0

AChR-Positive (Indian Series)

84.7%

Thymoma in MG

10–15%

Crisis Care

Neuro-ICU 24/7

Myasthenia gravis (MG) is the most common disorder of the neuromuscular junction — the specialised synapse where a motor nerve meets the muscle it controls. In MG, autoantibodies against the acetylcholine receptor (AChR), muscle-specific kinase (MuSK), or LRP4 disrupt nerve-to-muscle signal transmission. The result is fatigable weakness: muscles weaken with sustained or repeated use and recover with rest, so symptoms fluctuate within a day and between days. MG classically affects the eye muscles (drooping eyelids and double vision), the face and throat (difficulty swallowing and slurred speech), and the proximal limbs. In the largest Indian series of acquired MG, 84.7% of patients were AChR-antibody positive. A thymoma is present in approximately 10–15% of MG patients, which is why CT chest is part of every diagnosis. Myasthenic crisis — respiratory failure from MG — is a neurological emergency requiring neuro-ICU care.

What it is: An autoimmune neuromuscular junction disorder in which AChR, MuSK, or LRP4 antibodies disrupt nerve-to-muscle transmission, producing fatigable weakness that is worse with use and better with rest.
Typical symptoms: Drooping eyelids (ptosis) · Double vision (diplopia) · Difficulty swallowing and chewing · Slurred or nasal speech · Proximal limb weakness · Symptoms worse in the evening and after exertion.
Diagnosis at KIMS: AChR antibody (positive in ~85% of generalised MG) · MuSK antibody in seronegative patients · Repetitive nerve stimulation (decremental response) · CT chest for thymoma in every new diagnosis.
Treatment: Pyridostigmine (symptomatic) · Corticosteroids · Azathioprine · Mycophenolate · Rituximab · Eculizumab · Thymectomy in appropriate patients · IVIG or plasmapheresis for crisis.
Myasthenic crisis: Respiratory muscle weakness severe enough to threaten breathing. Triggers include infection, missed medication, certain antibiotics (quinolones, aminoglycosides), and early steroid worsening. Requires neuro-ICU, ventilatory support, and IVIG or plasmapheresis.
Contact KIMS: Outpatient: 040-44885000 · Emergency (breathing or swallowing difficulty): 040-46324365 · No referral required.

Fact	Details
Condition	Myasthenia Gravis (MG)
ICD-10	G70.0
Mechanism	Autoantibodies against AChR, MuSK, or LRP4 at the neuromuscular junction
Hallmark	Fatigable weakness — worse with sustained use, better after rest · Fluctuates within and across days
Antibody positivity	AChR antibodies in approximately 85% of generalised MG (84.7% in the largest Indian series) · MuSK antibodies in a proportion of AChR-negative patients
Electrodiagnosis	Repetitive nerve stimulation shows a decremental response
Thymus	Thymoma in approximately 10–15% of MG patients · CT chest mandatory at diagnosis · Thymectomy improves long-term outcomes in appropriate patients
Treatment	Pyridostigmine · Corticosteroids · Azathioprine · Mycophenolate · Rituximab · Eculizumab · Thymectomy
Emergency	Myasthenic crisis = neuro-ICU, ventilatory support, IVIG or plasmapheresis · Call 040-46324365

About This Condition

The Question That Changes Everything

A 42-year-old woman in Hyderabad has been told by three different doctors over two years that her weakness is due to anaemia, thyroid disease, and stress. None of her blood tests were clearly abnormal. None of her doctors asked one specific question: does your weakness get worse as the day goes on, and does it improve after rest? None of them noticed that her left eyelid was very slightly drooping.

At KIMS Neuroscience, the answer to that question — yes, the weakness is worst in the evening, and yes, it improves after rest — changes everything. This is fatigable weakness, the hallmark of myasthenia gravis: a neuromuscular junction disorder that responds well to treatment but requires specific diagnosis before that treatment can begin.

At the neuromuscular junction, the nerve releases acetylcholine, which crosses a tiny gap and binds to receptors on the muscle surface to trigger contraction. In MG, antibodies block or destroy those receptors, so each nerve impulse produces a weaker response — and with repeated firing, the response fades further. That is why the weakness builds with use and recovers with rest.

Indian MG patients tend to present younger on average than Western cohorts. Because ptosis and swallowing difficulty can be mistaken for a stroke, and generalised fatigable weakness for anaemia or anxiety, diagnostic delay is common — and it matters, because untreated MG can progress to myasthenic crisis.

Book a Consultation

Speak directly with our neuromuscular team — AChR and MuSK antibody testing, repetitive nerve stimulation, CT chest for thymoma, immunotherapy, thymectomy coordinated with cardiothoracic surgery, and 24-hour neuro-ICU crisis care. No referral required. Monday to Saturday.

040-44885000Emergency line: 040-46324365

Recognising the Condition

How Myasthenia Gravis Presents

The defining feature is not weakness alone but its behaviour: it fluctuates, it builds with use, and it recovers with rest.

Ocular symptoms

Drooping of one or both eyelids (ptosis) and double vision (diplopia) are the most common first symptoms. They are often asymmetric and characteristically worse in the evening, after reading, or after prolonged screen use. In some patients MG remains confined to the eyes (ocular MG).

Bulbar symptoms

Weakness of the face, jaw, and throat produces difficulty chewing (particularly towards the end of a meal), difficulty swallowing, nasal or slurred speech, and a flattened smile. Bulbar weakness is important because it can progress to aspiration and respiratory compromise.

Limb and neck weakness

Proximal limb weakness — difficulty lifting the arms above the head, climbing stairs, or rising from a chair — and neck weakness, with difficulty holding the head up. The weakness worsens with repeated effort and improves after rest.

Fluctuation

Symptoms vary within a day and from day to day. Heat, infection, emotional stress, and physical exertion commonly worsen them. This variability is the single most important clinical clue and the reason MG is so often missed at a single examination.

Myasthenic crisis

A life-threatening worsening in which the respiratory muscles become too weak to sustain breathing. Triggers include infection, missed medication, certain antibiotics (quinolones, aminoglycosides), surgery, and initial steroid worsening. It requires immediate neuro-ICU care.

Thymus involvement

The thymus gland is abnormal in many MG patients, and approximately 10–15% have a thymoma — a tumour of the thymus. This is why every patient diagnosed with MG at KIMS undergoes CT of the chest.

Diagnosis at KIMS

1

Clinical assessment of fatigability

A focused history of the pattern of weakness through the day, followed by examination designed to provoke fatigue — sustained upgaze to reveal ptosis, sustained arm abduction, and repeated counting to test bulbar endurance.

2

Antibody testing

AChR antibody is the specific marker for MG and is positive in approximately 85% of generalised MG. MuSK antibody is tested in AChR-negative patients; LRP4 antibody in selected double-seronegative cases.

3

Repetitive nerve stimulation (RNS)

Repeated stimulation of a motor nerve produces a characteristic decremental response in MG — the muscle response becomes progressively smaller with each stimulus. This distinguishes MG from Lambert-Eaton syndrome, where high-frequency stimulation produces an incremental response.

4

CT chest for the thymus

Every patient diagnosed with MG at KIMS undergoes CT of the chest to assess the thymus. A thymoma is present in approximately 10–15% of MG patients, and its surgical removal is an important component of management.

5

Screening before immunotherapy

Thyroid function (autoimmune thyroid disease frequently coexists), blood sugar and bone health before corticosteroids, and baseline tests before steroid-sparing immunosuppression.

Treatment

Treatment of Myasthenia Gravis

MG is highly treatable. Most patients achieve good control with a combination of symptomatic medication, immunotherapy, and — where appropriate — thymectomy.

Symptomatic

Pyridostigmine

An acetylcholinesterase inhibitor that increases the amount of acetylcholine available at the neuromuscular junction, improving strength within hours.

It treats symptoms rather than the underlying autoimmune process and is usually combined with immunotherapy in generalised MG.

Immunotherapy

Corticosteroids and Steroid-Sparing Agents

Corticosteroids are the mainstay of immunotherapy. They are started carefully because a temporary worsening can occur in the first weeks.

Azathioprine and mycophenolate are used as steroid-sparing agents for long-term control; rituximab and eculizumab are used in refractory disease.

Surgery

Thymectomy

Removal of the thymus is indicated in all patients with a thymoma and improves long-term outcomes in appropriate patients with generalised AChR-positive MG.

Thymectomy at KIMS is coordinated with cardiothoracic surgery.

Crisis Care

IVIG, Plasmapheresis, and Neuro-ICU

Myasthenic crisis is treated with respiratory monitoring and ventilatory support, IVIG or plasmapheresis to rapidly reduce circulating antibodies, and identification of the triggering cause.

KIMS has dedicated neuromuscular ICU protocols available 24 hours, 7 days. Emergency line: 040-46324365.

Related Conditions

Myasthenia gravis is one of the neuromuscular junction disorders evaluated and managed at KIMS Neuroscience:

Lambert-Eaton Myasthenic Syndrome Congenital Myasthenic Syndrome Neuromuscular Disorders (Master)

FAQs

Frequently Asked Questions

Drooping eyelids combined with swallowing difficulty, in the absence of other stroke signs, is far more suggestive of a neuromuscular junction disorder — particularly myasthenia gravis — than a stroke. In MG these symptoms characteristically fluctuate: worse in the evening, better after rest, and often triggered by activity, heat, or infection. Please come to KIMS urgently — call 040-44885000. An AChR antibody test, repetitive nerve stimulation study, and CT chest will be performed. If swallowing is severely affected or breathing is laboured, call 040-46324365 immediately, as this may represent a myasthenic crisis.

A myasthenic crisis is a life-threatening worsening of MG in which the respiratory muscles become too weak to sustain adequate breathing. Triggers include infection, missed medication, certain antibiotics (quinolones, aminoglycosides), and initial steroid worsening. Treatment at KIMS includes respiratory monitoring and ventilatory support, immediate IVIG or plasmapheresis to rapidly reduce circulating antibodies, and identification of the triggering cause. Myasthenic crisis carries significant mortality if managed without neuro-ICU capability — call 040-46324365.

Eyelids that droop by evening. Swallowing that tires halfway through a meal. Weakness that recovers with rest. Myasthenia gravis is diagnosable and highly treatable at KIMS Neuroscience, Hyderabad.

At KIMS Neuroscience, Secunderabad, Hyderabad, myasthenia gravis is diagnosed with AChR and MuSK antibody testing, repetitive nerve stimulation, and CT chest for thymoma — then treated with pyridostigmine, corticosteroids and steroid-sparing immunotherapy, rituximab or eculizumab for refractory disease, thymectomy where appropriate, and 24-hour neuro-ICU care with IVIG and plasmapheresis for myasthenic crisis. Outpatient 040-44885000 · Emergency 040-46324365.

040-44885000

International enquiries: info@kimsneurosciences.com