Relapsing MOG-IgG-associated diseases coexisting with anti-NMDAR encephalitis: a case report and literature review.

BACKGROUND: In recent years, an overlapping syndrome, MNOS, of MOG encephalomyelitis and NMDARE has been clinically identified. In these diseases, both MOG-Ab and NMDAR-Ab are positive. Previous studies were almost case reports and incomprehensive which focused on this kind of overlapping syndrome in adults. METHODS: We reported a rare case of MNOS. In addition, we reviewed the clinical characteristics, diagnosis, and treatment of MNOS in adults by consulting relevant literature. RESULTS: The patient initially presented with CNS demyelination symptoms followed by recurrent encephalitis, concomitant anti-MOG, and NMDAR antibodies. His symptoms improved significantly after initiating hormonal therapy. We searched previous MNOS case reports and 17 adult MNOS cases were retrieved. The previous history of all patients was unremarkable. Most of these patients (72.2%, 13/18) first developed NMDR encephalitis-related symptoms, such as cognitive behavior abnormalities, cognitive decline, and epilepsy. Some patients (16.7%, 3/18) first developed MOG-related demyelinating symptoms, such as visual deterioration, walking instability, and dizziness. The most common site of new brain lesions was the supratentorial region. In the acute phase, MNOS patients were sensitive to hormone therapy. During the follow-up, 72.2% (13/18) of the patients relapsed, with a median interval of 12.25 months. Immunotherapy was still effective after recurrence, and no deaths were reported. CONCLUSIONS: (1) The clinical manifestations of MNOS are atypical, sometimes like MOG encephalomyelitis, sometimes like NMDARE, sometimes both of the characteristic clinical manifestations are present. (2) Immunotherapy is the primary treatment of patients with MNOS. (3) MNOS are prone to recurrence, and serum MOG and tumor markers should be monitored.

Usefulness of ECG to differentiate apical hypertrophic cardiomyopathy from non-ST elevation acute coronary syndrome.

BACKGROUND: Apical hypertrophic cardiomyopathy (ApHCM) is a phenotypic variant of nonobstructive HCM. ApHCM is characterized by left ventricular hypertrophy involve the distal apex. The electrocardiographic character of ApHCM can mimic non-ST elevation acute coronary syndrome (NSTEACS), triggering a series of studies and treatments that may be unnecessary. This study aimed to clarify the electrocardiogram (ECG) differences between the two diseases. METHODS: Initial ECG recordings of 41 patients with ApHCM and 72 patients with NSTEACS were analyzed retrospectively. We analyzed the voltage of negative T (neg T) and R wave, the change of ST-segment as well as the number of leads with neg T wave in the 12-lead ECGs. RESULTS: Across the 12-lead ECGs, the magnitude of R wave significantly differed between ApHCM and NSTEACS in 10 leads excluding leads aVR and V1. ApHCM was associated with a greater maximal amplitude of R wave in lead V5 (3.13 ± 1.08 vs. 1.38 ± 0.73 mV, P <  0.001). The magnitude of T wave significantly differed between ApHCM and NSTEACS in 10 leads excluding leads II and V1. ApHCM was associated with a greater maximal amplitude of neg T wave in lead V4 (0.85 ± 0.69 vs. 0.35 ± 0.23 mV, P <  0.001). The frequency of giant neg T (1mv or more) wave was higher in ApHCM (36.5% vs. 0%, P <  0.001). The magnitude of ST-segment deviation significantly differed between ApHCM and NSTEACS in 10 leads excluding leads aVF and V2. ApHCM was associated with a greater maximal amplitude of ST-segment depression in lead V5 (0.19 ± 0.07 vs. 0.03 ± 0.06 mV, P <  0.001). The number of leads with neg T wave also differed between ApHCM and NSTEACS (6.75 ± 1.42 vs. 6.08 ± 1.51, P = 0.046). The sum of R wave in lead V5, neg T wave in lead V6 and ST-segment depression in lead V4 > 2.585 mV identified ApHCM with 90.2% sensibility and 87.5% specificity, representing the highest diagnostic accuracy. CONCLUSIONS: Compared with NSTEACS patients, ApHCM patients presented higher R and neg T wave voltage as well as a greater ST-segment depression in the 12-lead ECG. The ECG characteristics can help to differentiate ApHCM from NSTEACS in clinical setting.