The role of NLRP3 inflammasome in stroke and central poststroke pain.

BACKGROUND: NLRP3 inflammasome plays a prominent role in the pathogenesis and progression of many diseases, such as type 2 diabetes mellitus, obesity, atherosclerosis, and Alzheimer's disease. However, little knowledge is known about the role of NLRP3 inflammasome in central post-stroke pain (CPSP). METHODS: We selected relevant studies by searching PubMed, Embase, and Medline from inception through February, 2018. We systematically reviewed available publications according to the terms "NLRP3 inflammasome" and "stroke" or "central post-stroke pain" in the title/abstract field. RESULTS: We reviewed the articles and put forward two possible ways for NLRP3 inflammasome in CPSP. One way is that NLRP3 activation causes cerebral cortex injure, decreasing descending projection fiber to thalamus. Such condition may let GABAergic releases reduce, making the ventral basal (VB) neurons excitability increased. Finally, CPSP occur. Another way is that NLRP3 inflammasome leads to thalamic lesion and strengthens inflammatory response of microglia at the same time. Persistent inflammation causes GABAergic alteration in thalamus reticular neurons (TRN) to restrain VB interneurons functions, contributing to CPSP. CONCLUSIONS: These possible mechanisms will help become knowledgeable about the occurrence CPSP and provide potential therapy for CPSP.

A 58-Year Old Male with Cognitive Deteriorations Caused by Septum Pellucidum Cyst: A Case Report.

Dementia is known to be induced by vascular dementia and certain neurodegenerative diseases. The presenting features of disordered memory, intellect and personality often result in referral to a neurologist initially. Septum pellucidum cyst (SPC) is a rare clinical finding and defined as a cystic structure between the lateral ventricles. SPC induced memory disorder and dementia has been seldom reported in which the clinical features are atypical and can be misdiagnosed. The main difficulty is to establish a correlation between symptoms and the cyst. When indicated, the treatment is essentially surgical and the ideal operative technique is also a matter of debate. Here, we reported a 58-year-male Chinese patient who presented with memory impairment 1 year ago. Both the physical and laboratory examinations were performed to evaluate the general conditions of the patient. Brain magnetic resonance imaging (MRI) was applied to observe SPC and the neighboring brain structures. Mini-Mental State Exam (MMSE) and Montreal Cognitive Assessment (MoCA) were used to assess cognitive function. The results of the patient's laboratory examinations were normal. However, the patient exhibited severe sleeplessness along with cognitive deteriorations despite short-term (less than 2 weeks) use of benzodiazepines with regular dose. MRI fulfills the consensus criteria for clinical diagnosis of SPC. Furthermore, the results of MMSE and MoCA were showed mild cognitive impairment (MCI) before the treatment of SPC. After neuroendoscopic fenestration of SPC, the patient's syndromes were disappeared, and his cognitive function was improved. In conclusion, the patient's symptoms were due to a secondary lesion attributed to the cyst. Comprehensive clinical evaluation and MRI help diagnose SPC induced dementia.