Bulbar Palsy as the Initial Manifestation of Multiple Myeloma: A Case Report.

Multiple Myeloma (MM) is a neoplastic disorder derived from the malignant proliferation of monoclonal plasma cells. It is characterized by the overproduction of immunoglobulins (Ig). We report a rare case in which bulbar palsy was the initial manifestation of IgG-MM. A 66-year-old woman initially presented with progressive dysphagia and dysarthria for half a year. Physical examination demonstrated a deviation of the uvula, difficulty in protruding tongue, and bilateral tongue atrophy. Laboratory assessments revealed anemia and prominent monoclonal elevation of IgG levels both in serum and cerebrospinal fluid (CSF). The diagnosis of IgG-MM was confirmed by the identification of plasmacytosis in bone marrow aspiration and biopsy and elevation of γ-M protein in serum protein electrophoresis (SPEP). Therefore, the patient began to receive the chemotherapy with PAD (bortezomib-doxorubicin-dexamethasone) regimen. Her condition had been under control. MM as a hematological malignancy can affect cranial nerves and present as chronic progressive bulbar palsy.

dl-3-n-butylphthalide preserves white matter integrity and alleviates cognitive impairment in mice with chronic cerebral hypoperfusion.

AIMS: Effects of dl-3-n-butylphthalide (NBP) on white matter damage and cognitive impairment in vascular cognitive impairment (VCI) have not been well studied. This study aimed to investigate the effects of NBP treatment on chronic cerebral hypoperfusion-induced white matter lesions and cognitive dysfunction in mice. METHODS: Mice were subjected to bilateral common carotid artery stenosis (BCAS) for over 30 days. The cerebral blood flow was detected using a laser Doppler flowmetry. Cognitive functions were assessed by several behavioral tests. We also evaluated the effects of NBP on the blood-brain barrier (BBB) disruption and reactive astrogliosis, using Evans Blue extravasation, Western blot, CBA, and immunofluorescence in BCAS mice and cultured astrocytes. RESULTS: The results indicated that NBP treatment attenuated spatial memory dysfunction while promoted cerebral perfusion and white matter integrity in BCAS mice. Moreover, NBP treatment prevented BBB leakage and damage of endothelial cells, as well as disruption of endothelial tight junctions. Furthermore, NBP administration effectively decreased the number of activated astrocytes and pro-inflammatory cytokines, as well as the production of MMPs, in BCAS-induced mice and LPS-stimulated astrocytes. CONCLUSION: Our results indicated that NBP represents a promising therapy for chronic cerebral hypoperfusion-induced white matter damage and cognitive impairment.

The initial glycemic variability is associated with early neurological deterioration in diabetic patients with acute ischemic stroke.

The association between glycemic variability and early neurological deterioration (END) in acute ischemic stroke remains unclear. This study attempted to explore whether initial glycemic variability increases END in diabetic patients with acute ischemic stroke. We enrolled type 2 diabetic patients undergoing acute ischemic stroke from November 2015 to November 2016. A total of 336 patients within 72 h from stroke onset were included. The serum glucose levels were checked four times per day during the initial 3 hospital days. The standard deviation of blood glucose (SDBG) values and the mean amplitude of glycemic excursions (MAGE) were calculated for glycemic variability. END was defined as an increase in the National Institutes of Health Stroke Scale (NIHSS) ≥ 2 points between hospital days 0 and 5. The frequencies of END and HbA1c were significantly different in subjects grouped according to tertiles of MAGE (9.09, 12.07 and 50.00%, p < 0.001 for END; 7.36 ± 1.91, 7.83 ± 1.93 and 8.56 ± 1.79, p < 0.001 for HbA1c). Compared to patients without END, patients with END had significantly higher HbA1c levels (8.30 ± 1.92 vs 7.80 ± 1.93, p = 0.043), increased SDBG (3.42 ± 1.14 vs 2.60 ± 0.96, p < 0.001), and increased MAGE (6.46 ± 2.09 vs 4.59 ± 1.91, p < 0.001). In a multivariable logistic regression, stroke etiology (OR 0.675; 95% CI 0.485-0.940, p = 0.020), baseline NIHSS (OR 1.086; 95% CI 1.004-1.175, p = 0.040), and MAGE (OR 1.479; 95% CI 1.162-1.882, p = 0.001) were significantly associated with END. Initial glycemic variability is associated with END in diabetic patients with acute ischemic stroke.

Crosstalk between microglia and T cells contributes to brain damage and recovery after ischemic stroke.

OBJECTIVES: To summarize available knowledge regarding the crosstalk, thereby providing a more detailed explanation for the mechanism of brain damage and recovery after ischemic stroke. METHODS: An extensive review of the literature on the crosstalk between microglia and T cells in ischemic stroke was performed. We review the relevant publications in PubMed database. RESULTS: After cerebral ischemia, microglia are activated and peripheral T cells infiltrated into the brain. The crosstalk between microglia and T cells has both pro-inflammatory and anti-inflammatory effects in the inflammation after stroke. The crosstalk between M1 and Th1/Th17 cells promotes immune response after stroke and contributes to brain damage, while the crosstalk between M2 and Th2/Treg cells plays an anti-inflammatory role and contributes to brain recovery. Meanwhile, the crosstalk can be regulated by many factors, in both contact dependent and non-contact dependent way. CONCLUSION: Inflammation mediated by microglia crosstalking to T cells contributes to brain damage and recovery after ischemic stroke. Extensive evidence supports a critical role for the crosstalk of microglia and T cells in the prognosis of brain injury after ischemic stroke. The regulation of the crosstalk may provide a potential therapeutic target for improving the ischemic brain damage.