Brain death-like changes: A case report of anti-GQ1b antibody syndrome.

RATIONALE: Anti-GQ1b antibody syndrome originates in the peripheral nervous system or the central nervous system. Various overlapping syndromes and atypical manifestations are also seen in clinic. It is rare to see multiple sites (almost all targets) of central and peripheral damage at the same time, resulting in brain death-like changes in patient. PATIENT CONCERNS: This is a 55-year-old female patient, with a history of prodromal upper respiratory tract infection, began with headache, quickly developed body paralysis, eye paralysis, disturbance of consciousness, apnea, and tested positive for anti-GQ1b antibody. The patient is diagnosed clearly, the disease progresses rapidly, and almost all GQ1b sites in the central nervous system and peripheral nervous system are involved, which is rare. DIAGNOSES: Anti-GQ1b antibody syndrome. INTERVENTIONS AND OUTCOMES: The patient was treated with tracheal intubation, ventilator assisted breathing, and immunoglobulin. The patient recovered quickly and was discharged after about 30 days in hospital. LESSONS: The concept of anti-GQ1b antibody syndrome is not only beneficial for clinical diagnosis, but also beneficial for understanding the continuous disease spectrum with the same etiology and different clinical manifestations. The pathogenesis of each subtype has not been fully defined. There are mild patients with isolated syndromes and severe patients with multiple subtypes overlapping. Encounter severe patients but also active response, the general prognosis is good.

Ginsenoside Rb1 Promotes Motor Functional Recovery and Axonal Regeneration in Post-stroke Mice through cAMP/PKA/CREB Signaling Pathway.

The central nervous system (CNS) has a poor self-repairing capability after injury because of the inhibition of axonal regeneration by many myelin-associated inhibitory factors. Therefore, ischemic stroke usually leads to disability. Previous studies reported that Ginsenoside Rb1 (GRb1) plays a role in neuronal protection in acute phase after ischemic stroke, but its efficacy in post-stroke and the underlying mechanism are not clear. Recent evidences demonstrated GRb1 promotes neurotransmitter release through the cAMP-depend protein kinase A (PKA) pathway, which is related to axonal regeneration. The present study aimed to determine whether GRb1 improves long-term motor functional recovery and promotes cortical axon regeneration in post-stroke. Adult male C57BL/6 mice were subjected to distal middle cerebral artery occlusion (dMCAO). GRb1 solution (5 mg/ml) or equal volume of normal saline was injected intraperitoneally for the first time at 24 h after surgery, and then daily injected until day 14. Day 3, 7, 14 and 28 after dMCAO were used as observation time points. Motor functional recovery was assessed with Rota-rod test and grid walking task. The expression of growth-associated protein 43 (GAP43) and biotinylated dextran amine (BDA) was measured to evaluate axonal regeneration. The levels of cyclic AMP (cAMP) and PKA were measured by Elisa, PKAc and phosphorylated cAMP response element protein (pCREB) were determined by western blot. Our results shown that GRb1 treatment improved motor function and increased the expression of GAP43 and BDA in ipsilesional and contralateral cortex. GRb1 significantly elevated cAMP and PKA, increased the protein expression of PKAc and pCREB. However, the effects of GRb1 were eliminated by H89 intervention (a PKA inhibitor). These results suggested that GRb1 improved functional recovery in post-stroke by stimulating axonal regeneration and brain repair. The underlying mechanism might be up-regulating the expression of cAMP/PKA/CREB pathway.