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function in such patients showed contradictory results. Table 1: Demographic, clinical and laboratory
Some reported memory difficulties and other cognitive characteristics of the studied groups
dysfunction [17‑21] and electroencephalographic (EEG) Demographic and clinical Patients Control P
abnormalities. [22‑24] In contrast, others reported lack of characteristics (n = 20) subjects
(%)
neuropsychological impairments, normal intelligence, Male/female 4/16 (n = 20) (%) ‑
10/10
attention, memory and motor performance with Age (years) 16‑50 20‑50 ‑
MG. [25‑27] 28.45 ± 8.89 30.22 ± 5.76 0.380
Duration of illness (years) 1‑4 ‑ ‑
3.52 ± 1.15
The exact mechanisms of the co‑morbid cognitive Clinical grade
dysfunction in patients with MG are unknown. The I 0 ‑ ‑
most likely suggested mechanism is central cholinergic IIa/IIb 2/10 ‑ ‑
deficiency due to the involvement of central neuronal IIIa/IIIb 8/0 ‑ ‑ ‑ ‑
IVa/IVb
0
nAChRs and other cholinergic nervous systems V 0 ‑ ‑
and pathways by the immune‑mediated processes Thymic pathology
of MG. [20,28‑30] However, controversial views suggest Normal 5 (25) ‑ ‑ ‑ ‑
Hyperplasia
8 (40)
that the co‑morbid nervous system manifestations Thymoma 7 (35) ‑ ‑
with MG may result from nonspecific mechanisms Previous treatment (single or
as complications of MG, which include respiratory combination of the followings) 20 (100) ‑ ‑
Acetyl choline esterase
impairment, sleep apnea and hypoxia, [31‑33] mental inhibitors
fatigue, [26,27,34] adverse effects from medications used Prednisolone 20 (100) ‑ ‑
for treatment of MG and mood disorder. [35,36] Azathioprine 8 (40) ‑ ‑ ‑ ‑
9 (45)
Plasmapharesis
Thymectomy 7 (25) ‑ ‑
This study aimed to investigate cognitive function in Data are expressed as range, mean ± SD, n (%). SD: standard deviation
adults with mild/moderate MG. Cognitive functions
were assessed using a battery of sensitive psychometric they were free of clinical manifestations (i.e. after
testing in addition to recording event‑related resolution of active stage of the disease for at least
potentials (ERPs), a neurophysiological analog of 3 months) and were on maintenance treatment with
cognitive function. low doses of AChE‑Is and/or steroids. Twenty healthy
subjects matched for age, sex and socioeconomic status
METHODS were included in this study for statistical comparisons.
Control subjects were recruited from the general
Subjects population. This study was accepted by the regional
This study included 20 patients (males = 6, females = 14) Ethical Committee. Detailed information on the study
diagnosed clinically and electrophysiologically as MG. was given to all patients, and control subjects, and all
Their age ranged from 16 to 50 years, and duration gave their written consent to attend the study.
of illness ranged from 1 to 4 years. Clinical grading
of the patients was done based on the medical, We excluded subjects (patients and controls)
scientific advisory board of MG Foundation of America with: (1) respiratory involvement or in
classification. [37] Patients grading was based on their crisis (i.e. severe stages of the disease); (2) history
histories and diagnoses shown in their medical of other primary neurological (e.g. transient
records. Patients reported histories of weakness ischemic attacks, cerebrovascular stroke or
of ocular muscles (ptosis) (class I), of mild and epilepsy), psychiatric (e.g. major depression) or
predominant weakness of the limb muscles (class II a) medical (e.g. diabetes mellitus) diseases which are known
or oropharyngeal muscles (class II b), or with moderate to affect cognition; (3) previous serious head injury; (4)
and predominant weakness of the limb muscles (class III any sensory or motor disorder that would preclude
a). Before the presentation, all patients were treated psychological testing (as blindness or deafness); and (5)
with AChE‑Is (pyridostigmine bromide or mestinon regular treatment with medications (other than those
in a dose of 60 mg/4 h during the daytime and 60 mg used for treatment of MG) which may alter cognitive
at night time), immunotherapy with prednisolone testing (e.g. as benzodiazepines, beta‑adrenoceptor
and/or azathioprine (imuran) or plasmapharesis. antagonists, major tranquillizers and antidepressants).
Thymectomies were performed to the seven patients
with thymoma. Table 1 shows the demographic and Electroencephalographic recording
clinical characteristics of the studied group. Patients Electroencephalographic was done using the eight
were recruited from the Out‑patient Clinic of the channels Nihon Kohden machine (4217), employing
Department of Neurology, Assiut University Hospital, scalp electrodes placed according to the international
Assiut, Egypt during their follow‑up visits in which 10‑20 system with bipolar and referential montages.

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