SciCombinator

Postdural puncture headache (PDPH) is a common complication after inadvertent dural puncture. Risks factors include female sex, young age, pregnancy, vaginal delivery, low body mass index, and being a non-smoker. Needle size, design, and the technique used also affect the risk. Because PDPH can be incapacitating, prompt diagnosis and treatment are mandatory. A diagnostic hallmark of PDPH is a postural headache that worsens with sitting or standing, and improves with lying down. Conservative therapies such as bed rest, hydration, and caffeine are commonly used as prophylaxis and treatment for this condition; however, no substantial evidence supports routine bed rest and aggressive hydration. An epidural blood patch is the most effective treatment option for patients with unsuccessful conservative management. Various other prophylactic and treatment interventions have been suggested. However, due to a lack of conclusive evidence supporting their use, the potential benefits of such interventions should be weighed carefully against the risks. This article reviews the current literature on the diagnosis, risk factors, pathophysiology, prevention, and treatment of PDPH.

Spontaneous subarachnoid hemorrhage (SAH) is a rare, but serious etiology of headache. The diagnosis of SAH is especially challenging in alert, neurologically intact patients, as missed or delayed diagnosis can be catastrophic.

Tuberculous meningitis (TBM) comprises a significant proportion of TB cases globally and causes substantial morbidity and mortality, especially in children and HIV-infected patients. It is a challenging condition to diagnose due to its non-specific clinical presentation and the limited sensitivity of existing laboratory techniques. Smear microscopy and culture are the most widely available diagnostic tools yet are negative in a significant proportion of TBM cases. Simplified and more affordable nucleic acid amplification tests (NAATs) are increasing in use in resource-limited settings but have not been optimised for cerebrospinal fluid (CSF) samples. Novel diagnostic methods such as CSF interferon-gamma release assays and various biomarkers have been developed but require further evaluation to establish their utility as diagnostic tools. There is an urgent need for further research into optimal diagnostic strategies to decrease the morbidity and mortality as a result of delayed or missed diagnosis of TBM. In this review, we discuss current and novel diagnostic tests in TBM and areas where future research should be prioritised.

Fusobacterium necrophorum causes various clinical syndromes, ranging from otitis media to life-threatening Lemierre’s syndrome. The purpose of this study was to review our experience with pediatric Fusobacterium infections. The medical records of all children aged 0 to 18 years who were diagnosed between 1999 and 2011 with Fusobacterium infection were reviewed. Fusobacterium was isolated from clinical samples of 27 children: blood cultures (n = 16), abscesses (n = 8), joint fluids (n = 2), and cerebrospinal fluid (n = 1). The median age at admission was 3.5 years (range, 7 months to 17 years). Eight children (30 %) had seizures at presentation. Ten children (37 %) underwent lumbar puncture. Fifteen children (56 %) underwent brain imaging, and in seven of these children, a thrombus was identified either in a sinus vein or in an internal jugular vein. The most common source of infection was otogenic in 19 (70 %) of the children. Six of the children presented in 2011. All patients recovered. Conclusions: Neurologic manifestations are common at presentation of children with Fusobacterium infections. In young children, the most common source of infection is otogenic. Thrombotic complications are common, and imaging should be considered in all children with Fusobacterium infections arising from the head or neck region. There was a recent increase in the isolation of this bacterium, either because of better culturing techniques and increased awareness to this entity or a true increase in infections due to this organism.

Post-dural puncture headaches (PDPHs) present an important clinical problem. We assessed methods to decrease accidental dural punctures (ADPs) and interventions to reduce PDPH following ADP. Multiple electronic databases were searched for randomised clinical trials (RCTs) of parturients having labour epidurals, in which the studied intervention could plausibly affect ADP or PDPH, and the incidence of at least one of these was recorded. Forty RCTs (n = 11,536 epidural insertions) were included, studying combined spinal-epidurals (CSEs), loss of resistance medium, prophylactic epidural blood patches, needle bevel orientation, ultrasound-guided insertion, epidural morphine, Special Sprotte needles, acoustic-guided insertion, administration of cosyntropin, and continuous spinal analgesia. The RCTs for CSE, loss of resistance medium, and prophylactic epidural blood patches were meta-analysed. Five methods reduced PDPH: prophylactic epidural blood patch {four trials, median quality score = 2, risk difference = -0.48 [95% confidence interval (CI): -0.88 to -0.086]}, lateral positioning of the epidural needle bevel upon insertion (one trial, quality score = 1), Special Sprotte needles [one trial, quality score = 5, risk difference = -0.44 (95% CI: -0.67 to -0.21)], epidural morphine [one trial, quality score = 4, risk difference = -0.36 (95% CI -0.59 to -0.13)], and cosyntropin [one trial, quality score = 5, risk difference = -0.36 (95% CI -0.55 to -0.16)]. Several methods potentially reduce PDPH. Special Sprotte needles, epidural morphine, and cosyntropin are thus far each supported by a single, albeit good quality trial. Prophylactic blood patches are supported by three trials, but these had flawed methodology. Mostly, trials were of limited quality, and further well-conducted, large studies are needed.

PURPOSE: To study the incidence and clinical characteristics of delayed cerebral thrombosis in bacterial meningitis patients. METHODS: We assessed the incidence and clinical characteristics of delayed cerebral thrombosis in adults with cerebrospinal fluid (CSF) culture-proven community-acquired bacterial meningitis included in a prospective nationwide study in The Netherlands performed from 2006 to 2012. RESULTS: Delayed cerebral thrombosis occurred in 11 of 1,032 episodes (1.1 %). CSF culture yielded Streptococcus pneumoniae in ten patients and Listeria monocytogenes in one. Adjunctive dexamethasone therapy was administered before or with the first dose of antibiotics in 9 of 11 patients; two patients were initially not treated with dexamethasone. All patients made good initial recovery, followed by sudden deterioration after 7-42 days. Cranial imaging studies showed multiple cerebral infarctions in all patients. The outcome was unfavorable in all but one patient. In an explorative analysis, patients with delayed cerebral thrombosis had eightfold higher complement C5a CSF concentrations on the diagnostic lumbar puncture as compared in those without delayed cerebral thrombosis (p = 0.04). CONCLUSION: Delayed cerebral thrombosis is a rare but devastating complication of bacterial meningitis. Adjunctive dexamethasone therapy seems to predispose patients with bacterial meningitis to this complication. We found some evidence that this thrombotic complication is associated with activation of the complement system.

Postdural puncture headache (PDPH) is a relatively common complication after lumbar punctures (LP). If conservative treatment is not sufficient within a few days and the symptoms are severe, an epidural blood patch (EBP) may be performed.

BACKGROUND: Spontaneous intracranial hypotension has become a well-recognized cause of headaches and a wide variety of other manifestations have been reported. Recently, several patients with asymptomatic spontaneous intracranial hypotension were reported. I now report two patients with spontaneous intracranial hypotension who developed multiple arterial strokes associated with death in one patient, illustrating the spectrum of disease severity in spontaneous intracranial hypotension. METHODS: Medical records and radiologic imaging of the two patients were reviewed. RESULTS: Case 1. A 45-year-old man presented with an orthostatic headache. Neurologic examination was normal. MRI showed bilateral subdural fluid collections, brain sagging, and pachymeningeal enhancement. At lumbar puncture, the opening pressure was too low to record. He underwent two epidural blood patches with transient improvement of symptoms. His headaches progressed and a CT-myelogram showed a lower cervical CSF leak. Subsequently, periodic lethargy and confusion was noted and he then rapidly deteriorated. Examination showed coma (GCS: 4 [E1, M2, V1]), a fixed and dilated right pupil, and decerebrate posturing. Bilateral craniotomies were performed for the evacuation of chronic subdural hematomas. Immediate postoperative CT showed bilateral posterior cerebral artery infarcts and a recurrent right subdural hematoma, requiring re-evacuation. Postoperative examination was consistent with brain death and support was withdrawn.  Case 2. A 42-year-old man presented with a non-positional headache. Neurologic examination was normal. CT showed bilateral acute on chronic subdural hematomas and effacement of the basilar cisterns. MRI showed brain sagging, bilateral subdural hematomas, and pachymeningeal enhancement. Bilateral craniotomies were performed and subdural hematomas were evacuated. Postoperatively, the patient became progressively lethargic (GCS: 8 [E2, M4, V2]) and variable degrees of pupillary asymmetry and quadriparesis were noted. MRI now also showed multiple areas of restricted diffusion in the pons and midbrain, consistent with multiple infarcts. CT showed worsening subdural fluid collections with midline shift and increased effacement of the basilar cisterns. Repeat bilateral craniotomies were performed for evacuation of the subdural fluid collections. Neurologic examination was then noted to be fluctuating but clearly improved when lying flat (GCS: 10T [E4, M6, VT]). CT-myelography demonstrated an extensive cervico-thoracic CSF leak. An epidural blood patch was performed. The patient made a good, but incomplete, recovery with residual quadriparesis and dysphagia. CONCLUSIONS: Arterial cerebral infarcts are rare, but potentially life-threatening complications of spontaneous intracranial hypotension. The strokes are due to downward displacement of the brain and can be precipitated by craniotomy for evacuation of associated subdural hematomas.

The spinal canal is frequently a source of difficulties, traps and diagnostic errors. Pitfalls related to artifacts are resolved by using appropriate sequences. Good knowledge of the appearance of certain particular anatomical structures (the cauda equina roots, the radicular veins of the lumbar spine and conus medullaris, the dorsal root ganglion) and of frequent variants (fibrolipoma of the filum terminale, common root sheaths, root cysts) will avoid a good many errors. Dilatation of epidural veins in intracranial hypotension can simulate the contrast enhancement of a tumour. An increase in epidural fat can induce pathogenic stenosis of the dural sheath.

A simple, reproducible and chronic technique of cerebrospinal fluid (CSF) collection in rats was developed by direct cisterna magna (CM) puncture utilizing stereotaxic apparatus. CSF collection apparatus was constructed using 1mL syringe, silicone tubing, 21G disposable needle and water. Animal was placed on an elevated platform over stereotaxic apparatus base and puncture site was identified with the aid of stereotaxic co-ordinates. The volume of CSF collected varied from 100 to 180μL with mean CSF volume of 150μL. Neurological deficits were recorded according to the modified Bederson’s scoring system 24h post CSF collection and differential cell count in CSF samples was performed. Animals continued to be normal with regular feed intake and gained body weight (∼24%) even after repeated sampling for four weeks and showed no severe neurological deficits (mean Bederson score<1 for four weeks). Neuropharmacokinetic data for Phenytoin sodium, MS 275 and Valproic acid (VPA) demonstrated CSF uptake with CSF(AUC)/plasma(AUC) ratio (K(p,CSF)) of 0.09, 0.01 and 0.33, respectively. This model exemplifies the 3R's of animal use and has been successfully implemented at Orchid Chemicals and Pharmaceuticals Limited for lead optimization of CNS penetrating HDAC inhibitors.