Subdural hematoma (SDH) following labor epidural analgesia is a rare neurological complication. SDH is a late complication of this procedure; it is caused by a leak of cerebrospinal fluid that may damage the vascular structures of the brain. Persistent headache in the days after labor epidural analgesia is a nonspecific clinical symptom caused by hematoma. Preexisting vascular malformations can be a concomitant cause of headache. Clinical cases have been reported even after epidural anesthesia. The differential diagnosis includes unspecified headache, sinusitis headache, drug-induced headache, cortical vein thrombosis, fistula of the dura mater, and bacterial, viral, and aseptic meningitis.

After a 34-year-old female developed a headache and high fever, she was diagnosed with aseptic meningitis. On admission, neurological examinations revealed cerebellar limb ataxia, horizontal gaze paretic nystagmus, and pyramidal tract signs. Laboratory tests showed hyponatremia (129 mEq/l). Five days after admission, convulsions in the upper limbs due to the severe hyponatremia (108 mEq/l) were noted. In addition, serum antidiuretic hormone levels were markedly increased to 18.5 pg/ml. Brain MRI showed multiple small inflammatory lesions in the subcortical cerebral white matter, thalamus, and around the third ventricular diencephalic regions. Pulse corticosteroid treatment promptly improved her symptoms. Although tests for serum anti-aquaporin 4, anti-myelin oligodendrocyte glycoprotein, and anti-voltage-gated potassium channel antibodies were negative, cerebrospinal fluid samples tested positive for anti-N-methyl-D-aspartate (NMDA) receptor antibodies. Oral prednisolone administration was continued, but she developed paresthesia in her upper and lower extremities and gaze-evoked nystagmus three months after the first attack. MRI showed that the previously observed high-intensity regions were decreased, but a new area of high intensity was observed in ventral regions through the lower midbrain to the pons. Because pulse corticosteroid treatment was again effective, we continued the oral prednisolone treatment. This case presented none of the characteristic symptoms of anti-NMDA receptor antibody encephalitis during the clinical course other than repeated demyelinating encephalitis and severe syndrome of inappropriate antidiuretic hormone secretion (SIADH). Additional clinical observations are needed to better understand the underlying pathology of the NMDA receptor antibodies in the cerebrospinal fluid in this case.

Early diagnosis and initial therapy are important to reduce the complications of bacterial meningitis. We aimed to evaluate the diagnostic value of serum procalcitonin in children with acute meningitis. We included 40 children (4 months-14 years) suspected to have acute meningitis in our study. Based on the clinical scenario, physical examination and complete analysis of cerebrospinal fluid, patients were assigned into two groups: bacterial meningitis group (24 patients) and aseptic meningitis group (16 patients). Twenty-five apparently healthy children of matched age and sex served as a control group. Procalcitonin, C-reactive protein, and leukocyte count were measured initially at the time of admission and again after 72 h. Initially, patients with bacterial meningitis showed statistically significant higher values of serum procalcitonin than both patients with aseptic meningitis and the control groups (p < 0.001). After 72 h of treatment, patients of bacterial meningitis group showed statistically significant lower values of serum procalcitonin than their initial values (P < 0.05). The cutoff point of procalcitonin needed for early diagnosis of bacterial meningitis was >10 ng/ml at the time of admission. However, values of procalcitonin >2 ng/ml had 100% sensitivity. Whereas, the specificity, negative predictive value and positive predictive value of procalcitonin were 63%, 100%, and 67% respectively. Serum Procalcitonin can be used as an early diagnostic marker of acute bacterial meningitis and its differentiation from aseptic meningitis. In acute bacterial meningitis, it can be used to follow the response to antibiotic therapy.

We describe a man presenting with unusual neurological manifestations of systemic lupus erythematosus (SLE) including pachymeningitis, aseptic meningitis and encephalitis with grossly elevated cerebrospinal fluid protein, responding to immunosuppression. Initially he had intermittent dysarthria, dysphasia and unilateral upper limb weakness. One month later he experienced dysphasia, right-sided hemiparesis and confusion. Cerebrospinal fluid (CSF) analysis showed a white cell count of 70 x 106/litre and an unusually elevated protein level of 5.39 g/litre. An MRI brain showed dural and leptomeningeal enhancement compatible with a meningitic process. He improved with cefotaxime and aciclovir. On day seven of antimicrobials he developed left-sided weakness, sensory inattention and a left homonymous hemianopia. He responded well to intravenous methylprednisolone. On switching to oral prednisolone he developed expressive dysphasia, a right inferior quadrantanopia and seizures. His bloods were suggestive of macrophage activation syndrome. The patient improved with methylprednisolone and intravenous immunoglobulins, and the improvement was sustained on switching back to oral prednisolone. The prevalence of neuropsychiatric manifestations of SLE varies between 14 and 80% and according to the American College of Rheumatology includes 19 conditions. This case is unique because although some features were in keeping with aseptic meningitis the MRI appearances were also suggestive of pachymeningitis.

Background The differential diagnosis between postneurosurgical bacterial meningitis and aseptic meningitis remains challenging both for the clinician and the laboratory. Combinations of markers, as opposed to single ones, may improve diagnosis and thereby survival. Methods This prospective cohort study included patients with suspected bacterial meningitis after neurosurgery. The patients were divided into two groups according to the diagnostic criteria of meningitis involving a postneurosurgical bacterial meningitis group and a postneurosurgical aseptic meningitis group. Four biomarkers, including cerebrospinal fluid procalcitonin, lactate, interleukin-8 and interleukin-10 were assayed separately, and three algorithms were constructed using a linear combination. The area under the receiver operating characteristic curve was used to compare their performances. Results A cohort of 112 patients was enrolled in our study. Forty-three patients were diagnosed with postneurosurgical bacterial meningitis, and the cerebrospinal fluid values of their biomarkers were higher in patients with postneurosurgical bacterial meningitis than with postneurosurgical aseptic meningitis. The area under the receiver operating characteristic curves for the detection of postneurosurgical bacterial meningitis were 0.803 (95% confidence interval [CI], 0.724-0.883) for procalcitonin; 0.936 (95% CI, 0.895-0.977) for lactate; 0.771 (95% CI, 0.683-0.860) for interleukin-8; 0.860 (95% CI, 0.797-0.929) for interleukin-10; 0.937 (95% CI, 0.897-0.977) for the composite two-marker test; 0.945 (95% CI, 0.908-0.982) for the composite three-marker test and 0.954 (95% CI, 0.922-0.989) for the composite of all tests. The area under the receiver operating characteristic curves of the combination tests were greater than those of the single markers. Conclusions Combining information from several markers improved the diagnostic accuracy in detecting postneurosurgical bacterial meningitis.

In viral meningitis, proinflammatory cytokines were detected at higher levels in the cerebrospinal fluid (CSF) and might play an important role in the inflammatory process. Our goal was to compare the cytokine profiles in the CSF of children of enteroviral meningitis (EVM) with versus without CSF pleocytosis. In total, 158 patients were enrolled in this prospective cohort study and were classified as EVM (group-A, n = 101), nonenteroviral aseptic meningitis (group-B, n = 27), and control (group-C, n = 30) groups. Of the 101 children with EVM, 71 had CSF pleocytosis (group-A1) and 30 had CSF nonpleocytosis (group-A2). Fifteen cytokines/chemokines in the CSF were measured simultaneously by immunoassay. Significant differences were found in interleukin (IL)-2, IL-6, and IL-8 levels in the CSF across the 3 groups, with the highest levels in group-A, followed by group-B and group-C. The levels of IL-1β, IL-2, IL-6, IL8, IL-10, interferon-γ, and tumor necrosis factor-α were significantly higher in the CSF of group-A1 than in that of group-A2. Group-A2 was significantly younger than group-A1 (3.4 ± 2.8 years versus 5.5 ± 3.2 years, P = 0.016). Significant differences between CSF pleocytosis and nonpleocytosis in EVM appear to be associated with distinct levels of CSF cytokines.