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Background: Rickettsias cause a wide spectrum of tick-, flea-, or mite-borne infections. Rickettsial infections have no classical manifestations and can often lead to encephalitis, which can be fatal if improperly diagnosed.Case Presentation: A 74-year-old male farmer was admitted to the hospital with fevers and a headache that had lasted for 10 days, followed by 4 days of unconsciousness, and his condition continued to deteriorate. Images showed multiple acute lesions in the brain stem, and bilateral cerebral and cerebellar hemispheres. He was finally diagnosed with endemic typhus and treated with antibiotics that resulted in improvement.Conclusion: The present report describes a patient with a rickettsial infection and subsequent deterioration to coma because of an initial misdiagnosis. Because of the similarity to other infectious diseases, physicians should be more vigilant towards the history and radiologic results to ensure early detection and avoid complications which may prove to be fatal. [ABSTRACT FROM AUTHOR]

Background: Hyponatremia is the most common electrolyte abnormality encountered in hospitalized patients, resulting from a varied spectrum of conditions. Both the primary disturbance and its correction can result in life-threatening neurological consequences. Extrapontine myelinolysis is one such complication that is associated with the rapid correction of hyponatremia. Here we describe a patient who developed extrapontine myelinolysis unexpectedly after the correction of hyponatremia, which involved the drug pituitrin.Case Presentation: A 24-year-old Chinese woman was transferred to our neurology department with the symptoms of dysarthria and quadriparesis developing one day after the correction of hyponatremia (from 118 mmol/L to 140 mmol/L), which followed with a continuous intravenous drip of pituitrin used to control hemoptysis in the emergency room. During the course, she developed involuntary movement. Magnetic resonance imaging changes were consistent with extrapontine myelinolysis.Conclusion: This present case describes the mechanism of profound hyponatremia involving pituitrin, and the subsequent development of extrapontine myelinolysis. Physicians may approach effective clinical management of patients through awareness of the adverse effect of pituitrin on serum sodium levels, and avoid rapid correction of hyponatremia in clinical practice. [ABSTRACT FROM AUTHOR]

Background: Ischemic stroke and glioblastoma multiforme have similar features on anatomic magnetic resonance imaging (MRI) and thus may require a surgical biopsy for a definitive diagnosis., Case Presentation: A 55-year-old male complained of dysphasia for 4 weeks and continuous deterioration for 5 days. Cerebral infarction was considered based on MRI, which showed hyperintensity at the border zone of the left hemisphere, and computed tomography angiography (CTA) showed left carotid artery severe stenosis. The patient underwent placement of a left carotid artery stent, and his symptoms recurred 2 months after carotid artery stent (CAS). MRI showed multiple ring-enhanced lesions in the left temporal, parietal, and occipital lobes accompanied by massive brain edema. The final pathologic diagnosis was glioblastoma multiforme., Conclusion: Although there is no evidence that stent therapy for carotid artery stenosis will worsen an ipsilateral glioblastoma, we should be careful to perform surgeries involving carotid artery stents when the patient has a glioblastoma.

Background: Reversible cerebral vasoconstriction syndrome (RCVS) is an infrequent disease characterized by severe headaches with or without focal neurological deficits or seizures and a reversible vasoconstriction of cerebral arteries. The Orpha number for RCVS is ORPHA284388. However, RCVS triggered by blood transfusion is rare. Here we provided the clinical, neuroimaging and outcome data of patients diagnosed with RCVS resulting from red blood cells transfusion., Methods: We retrospectively identified 7 patients presenting with RCVS after red blood cells transfusion from January 2010 to May 2014. The information on clinical features, neuroimaging and outcome were collected and analyzed., Results: All 7 patients were Chinese women, with a mean age of 42 years (38-46). All the patients had severe anemia (Hb level < 6 g/dl) caused by primary menorrhagia due to uterine myoma (n = 5) or end-stage renal disease (n = 2) and severe anemia persisted for a average period of 4 months (2-6). Each patient received packed red blood cells transfusion (average: 1580 ml) over a period of 2-5 days. Blood transfusion increased the hemoglobin level by at least 4.5 g/dL from baseline. The neurological symptoms appeared a mean of 6.3 days (2-13) after the last blood transfusion. Headache was the most frequent symptom and seizure, transient or persistent neurological disorders were observed. Neuroimaging showed cortical subarachnoid hemorrhage (n = 2), focal intracerebral hemorrhage (n = 2), localized brain edema (n = 3), cerebral infarction (n = 1), and posterior reversible encephalopathy syndrome (n = 2). Cerebral vasoconstrictions were demonstrated by magnetic resonance angiography or cerebral angiography. Arterial constriction reversed in all patients within 1 to 3 months of follow-up after disease onset and no relapse was observed up to a mean of 17.1 ± 4.8 months of follow-up., Conclusions: RCVS is a rare complication as a result of blood transfusion in patients with chronic severe anemia and should be considered in patients who show severe headache or neurologic deficits after transfusion.

Sneddon's syndrome (SS) is a rare non-inflammatory thrombotic vasculopathy characterized by the combination of cerebrovascular disease with livedo racemosa(LR). The Orpha number for SS is ORPHA820. It has been estimated that the incidence of SS is 4 per 1 million per annum in general population and generally occurs in women between the ages of 20 and 42 years. LR may precede the onset of stroke by years and the trunk and/or buttocks are involved in nearly all patients. The cerebrovascular manifestations are mostly secondary to ischemia (transient ischemic attacks and cerebral infarct). Other neurological symptoms range from headache, cerebral hemorrhage, seizures, cognitive and psychiatric disturbances. The involved internal organs include heart, kidney, and eyes. Histological findings of skin are characteristic and the involved vessels are small to medium-sized arteries at the border of dermis to subcutis with a distinct histopathological time course. The main diagnostic criteria are general LR with typical histopathological findings on skin biopsy and focal neurological deficits. The pathogenesis is related to hypercoagulable state and intrinsic small-vessel vasculopathy. The optimal management remains an unsolved problem and long-term anticoagulation have been recommended for cerebral ischemic events based on the presumed pathogenesis. There are controversial results in treatment of SS with immunomodulatory agents. The aim of this review is to comprehensively discuss this disease.

Background: Neuroinflammation plays an important role in cerebral ischemia/reperfusion (I/R) injury. The P2X7 receptor (P2X7R) has been reported to be involved in the inflammatory response of many central nervous system diseases. However, the role of P2X7Rs in transient global cerebral I/R injury remains unclear. The purpose of this study is to determine the effects of inhibiting the P2X7R in a rat model of transient global cerebral I/R injury, and then to explore the association between the P2X7R and neuroinflammation after transient global cerebral I/R injury., Methods: Immediately after infusion with the P2X7R antagonists Brilliant blue G (BBG), adenosine 5'-triphosphate-2',3'-dialdehyde (OxATP) or A-438079, 20 minutes of transient global cerebral I/R was induced using the four-vessel occlusion (4-VO) method in rats. Survival rate was calculated, neuronal death in the hippocampal CA1 region was observed using H & E staining, and DNA cleavage was observed by deoxynucleotidyl transferase-mediated UTP nick end labeling TUNEL). In addition, behavioral deficits were measured using the Morris water maze, and RT-PCR and immunohistochemical staining were performed to measure the expression of IL-1β, TNF-α and IL-6, and to identify activated microglia and astrocytes., Results: The P2X7R antagonists protected against transient global cerebral I/R injury in a dosage-dependent manner. A high dosage of BBG (10 μg) and A-0438079 (3 μg), and a low dosage of OxATP (1 μg) significantly increased survival rates, reduced I/R-induced learning memory deficit, and reduced I/R-induced neuronal death, DNA cleavage, and glial activation and inflammatory cytokine overexpression in the hippocampus., Conclusions: Our study indicates that inhibiting P2X7Rs protects against transient global cerebral I/R injury by reducing the I/R-induced inflammatory response, which suggests inhibition of P2X7Rs may be a promising therapeutic strategy for clinical treatment of transient global cerebral I/R injury.