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Table 2: Comparison between patients and controls in   DISCUSSION
           scores of cognitive functions and depression
           Variable             Patients    Controls   P      The results of this study indicate that patients with
                                 (n = 20)   (n = 20)          mild/moderate MG may experience significant
           MMSE                23.25 ± 2.35  27.56 ± 1.45 0.036  manifestations of cognitive impairment in the absence
           SBST                                               of disease activity and despite the short duration
            Vocabulary         36.33 ± 5.45  50.45 ± 3.88 0.042
            Comprehension      35.46 ± 9.07  49.76 ± 7.56 0.007  of illness. Patients with MG may experience poor
            Total verbal reasoning   75.32 ± 8.85  96.82 ± 16.25 0.0001  performance in different cognitive tasks indicating
            score                                             central or brain involvement. These included deficits
            Visual reasoning   36.63 ± 4.64  48.68 ± 5.04 0.0001
            Total visual reasoning   68.43 ± 8.09  88.33 ± 14.70 0.0001  in verbal relations, comprehension, visual reasoning,
            score                                             pattern analysis, quantitation, bead memory, short‑term
            Quantitative test  36.57 ± 6.54  45.30 ± 5.43 0.0001  memory  and  memory  for  sentences,  digit  forward,
            Total quantitative   75.53 ± 8.67  96.65 ± 9.57 0.0001
            reasoning score                                   digit backward, mental control, logical memory, and
            Bead memory        45.30 ± 7.28  60.50 ± 10.08 0.0001  associate learning. In the agreement with our findings,
            Memory for sentences  44.72 ± 6.34  65.56 ± 8.57 0.0001  patients with MG commonly reported subjective
            Total score for    85.65 ± 9.66  150.25 ± 25.26 0.0001
            short‑term memory                                 cognitive complaints. In patients with MG, several
            Total score of SBST  289.56 ± 55.48 360.34 ± 50.04 0.0001  previous studies reported memory difficulties [17,18]  and
            IQ                 78.53 ± 6.46  95.35 ± 8.73 0.0001
           WMS‑R                                              impaired performance on varieties of cognitive tests as
            Digit forward       4.56 ± 1.01  6.64 ± 0.88  0.035  MMSE and memory tests, [19]  the Boston Naming Test,
            Digit backward      2.23 ± 0.25  5.58 ± 0.45  0.010  the Logical Memory and Design Reproduction portions
            Mental control      3.57 ± 1.45  5.89 ± 1.06  0.042  of the WMS, Rey Auditory Verbal Learning Test, [17]  and
            Logical memory     10.65 ± 1.30  14.83 ± 2.45 0.007
            Associate learning  8.52 ± 2.04  12.06 ± 2.24 0.005  measures of response fluency, information processing
            Total scores of cognitive  76.54 ± 8.35  96.54 ± 6.28 0.0001  and verbal and visual learning. [20,21,47]  In additions, the
            testing (MMSE, SBST                               detected abnormalities in P300 component of ERPs
            and WMS‑R)
            Depression scores  20.64 ± 6.24  8.65 ± 3.55  0.0001  also suggest the central or brain involvement in MG.
           Data are expressed as mean ± SD. SBST: stanford Binet subtests testing,   In fact, abnormal evoked potential responses were
           MMSE: mini‑mental state examination, WMS‑R: wechsler memory scale‑revised,   noted in patients with MG. [48‑50]  In contrast, several
           SD: standard deviation, IQ: intelligence quotient
                                                              studies reported normal IQ, memory, attention and
                                                              motor performance and normal ERPs in MG. [25‑27]  We
           Table 3: Comparison between patients and controls in   believe that such discrepancies could be explained
           event‑related potentials
           Variable       Patients (n = 20) Controls (n = 20)  P  by differences in methodologies, small sample size,
           P  latency (ms)                                    different lists of inclusion and exclusion criteria and
            300
            Right sided    250.00‑450.00  285.00‑353.00  ‑    lack of control for potential confounding variables.
                           350.80 ± 35.88  320.88 ± 25.75  0.010
            Left sided     270.00‑450.00  250.00‑350.00  ‑    Several mechanisms have been hypothesized as
                           355.60 ± 33.08  325.45 ± 20.45  0.010
           P  amplitude (mv)                                  etiologies of cognitive impairment in patients with MG.
            300
            Right sided     2.20‑20.25     6.88‑20.54   ‑     The central cholinergic deficiency due to the involvement
                            7.55 ± 2.45   12.45 ± 2.84  0.001  of the central nAChRs and central cholinergic pathways
            Left sided      2.55‑18.09     6.80‑22.25   ‑
                            6.67 ± 3.23   12.63 ± 2.56  0.001  by the disease process of MG have been suggested as the
           Data are expressed as range, mean ± SD. SD: standard deviation  high likely mechanisms. [20,28‑30]  This hypothesis is based
                                                              on the fact that there are structural identities between
           Table 4: Pearson’s correlation (r and P value) between   different muscle and neuronal nAChRs subunits with
           total scores of cognitive testing and clinical variables, lab   the possibility of cross‑reactivity between different
           variables, depression scores and ERPs variables    nAChRs antibodies. [51‑53]  The hippocampus, a cerebral
           Variables                  Total scores of cognitive   structure highly involved in learning and memory,
                                     testing (MMSE, SBST and   has abundant cholinergic innervation and enriched
                                            WMS‑R)            in nAChRs that modulate synaptic plasticity via
                                       r                P     mechanisms involved in long‑term potentiation. [54]
           P  latency                ‑0.650           0.001
            300
           P  amplitude              0.557            0.001   Few suggested that cognitive dysfunction co‑morbidity
            300
           Age                       ‑0.470           0.010   may  be  due  to  the  immune  responses  driven  by
           Duration of illness       ‑0.788           0.0001  muscle and neuronal nAChRs antibodies expressed
           Depression scores         ‑0.323           0.045
           ERPs: event‑related potentials, MMSE: mini‑mental state examination,   by cancer  (e.g.  thymoma)  (i.e.  paraneoplastic
           SBST: stanford Binet subtests testing, WMS‑R: wechsler memory scale‑revised  syndrome). [55,56]  Others suggested that it might be a
                                                              nonspecific autoimmune response in presence or
           total scores of cognitive testing  (MMSE, SBIS and   absence of tumor. [57]  This it further supported by an
           WMS‑R) and duration of illness (β = ‑0.305, P = 0.045).  association of MG with other nonnervous system medical



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