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Original Article

Assessment of cognitive function in patients

with myasthenia gravis

1
1
1
Sherifa A. Hamed , Ahmad H. Youssef , Mohamad A. Abd ElHameed , Mohamed F. Mohamed ,
1
Amal M. Elattar 2
1 Department of Neurology and Psychiatry, Assiut University Hospital, Assiut 71516, Assiut, Egypt.
2 Department of ENT, Audiology Unit, Assiut University Hospital, Assiut 71516, Assiut, Egypt.
ABSTRA CT

Aim: During the past decade, there has been an increasing interest in the evaluation of cognitive function in myasthenia gravis (MG),
neuromuscular transmission disorder caused by acetylcholine receptor auto‑antibodies. However, the results of previous studies
on cognition and MG are inconsistent and controversial. This study aimed to evaluate cognition in patients with mild/moderate
grades of MG. Methods: This study included 20 patients with MG with a mean age of 28.45 ± 8.89 years and duration of illness of
3.52 ± 1.15 years. Cognition was tested using a sensitive battery of psychometric testing (Mini‑mental State Examination [MMSE],
Stanford‑Binet Intelligence Scale 4 edition [SBIS] and Wechsler Memory Scale‑Revised [WMS‑R]) and by recording P300
th
component of event‑related potentials (ERPs), a neurophysiological analog for cognitive function. Results: Compared with
healthy subjects (n = 20), patients had lower total scores of cognitive testing (MMSE, SBIS and WMS‑R) (P = 0.001), higher Beck
nd
Depression Inventory 2 edition scores (P = 0.0001) and prolonged latencies (P = 0.01) and reduced amplitudes (P = 0.001) of
P300 component of ERPs. Correlations were identified between total scores of cognitive testing and age (r = ‑0.470, P = 0.010),
duration of illness (r = ‑0.788, P = 0.001) and depression scores (r = ‑0.323, P = 0.045). Using linear regression analysis and after
controlling for age and depression scores, a significant correlation was identified between total scores of cognitive testing and duration
of illness (β = ‑0.305, P = 0.045). Conclusion: Patients with mild/moderate MG may have cognitive dysfunction. This is important
to determine prognosis and managing patients.

Key words: Cognition, myasthenia gravis, nicotinic acetylcholine receptors

INTRODUCTION to the bulbar and limb muscles. Approximately, 85% of
patients develop generalized weakness. Many patients
Myasthenia gravis (MG) is an autoimmune disease progress from mild to severe disease, and if weakness
caused mainly by auto‑antibodies against skeletal of respiratory muscles becomes severe enough to
muscle nicotinic acetylcholine receptors (nAChRs) at require mechanical ventilation, the patient is said
[3]
the postsynaptic membrane resulting in depletion of to be in crisis. Spontaneous remissions are very
ACh at the neuromuscular junction. MG is uncommon rare and last for varying periods that mostly occur
[1]
[4]
with a prevalence of (25‑125)/10 . The disease tends during the first 3 years of the disease. In adults, the
6
to affect women more often than men (3:2) in their thymus gland is abnormal in up to 90% of people with
[2]
second and third decades. The cardinal symptoms MG with approximately 70% of them have thymic
hyperplasia while 10‑20% have benign thymic tumors
of MG are fatigue and weakness of skeletal muscles or thymoma. The currently used treatment modalities
[5]
with repeated or sustained exertion in the course of for MG include acetyl choline esterase inhibitors
the day but improved by rest. Ocular muscles are (AChE‑Is) (as pyridostigmine), immunopharmacologic
[6]
initially involved in about 2/3 of patients then spread drugs (as prednisone, azathioprine, cyclosporine,
[9]
[7]
[8]
mycophenolate mofetil, [10] cyclophosphamide, [11]
Access this article online
tacrolimus [12] and rituximab [13] ) plasmapharesis, [14]
Quick Response Code: intravenous immunoglobulins (IVIGs) [15] and
Website: [16]
www.nnjournal.net thymectomy.
DOI: Subjective impairments of memory and other cognitive
10.4103/2347-8659.143671 functions are very frequent in patients with MG,
however, previous studies, which investigated cognitive

Corresponding Author: Dr. Sherifa A. Hamed, Department of Neurology and Psychiatry, Floor No. 7, Room No. 4, Hospital of
Neurology and Psychiatry, Assiut University Hospital, Assiut 71516, Assiut, Egypt. E-mail: hamed_sherifa@yahoo.com

Neuroimmunol Neuroinflammation | Volume 1 | Issue 3 | December 2014 141