Spontaneous spinal cerebrospinal fluid venous-fistula treated with transvenous embolization: A case report

Background: Spinal cerebrospinal fluid venous fistula (CVF) is a recognized cause of chronic positional headache and spontaneous intracranial hypotension (SIH). It occurs due to an aberrant connection formed between the spinal subarachnoid space and an adjacent spinal epidural vein. The diagnosis of CVF can be difficult to establish but can be documented utilizing advanced imaging techniques (e.g., enhanced MR myelography/digital subtraction myelography). Their treatment involves surgical ligation of the involved nerve root, imaging-guided epidural blood patching, and/or endovascular embolization. Here, we report a 40-year-old male who presented with a symptomatic lumbar CVF successfully treated with transvenous embolization. Case Description: A 40-year-old male presented with several months of positional headaches. The MRI of the brain showed diffuse pachymeningeal enhancement consistent with the diagnosis of SIH. Although the MR of the lumbar spine was unremarkable, the MR myelogram with digital subtraction imaging showed a CVF at the L2 level. Following transvenous embolization (i.e., through the Azygous vein), the patient’s symptoms fully resolved. Conclusion: Spinal CVF are rare and may cause chronic headaches and symptoms/signs of SIH. In this case, an MR myelogram with digital subtraction images demonstrated the anomalous connection between the spinal subarachnoid space and an adjacent spinal epidural vein at the L2 level. Although open surgical ablation of this connection may be feasible, less invasive techniques such as endovascular embolization should become the treatment of choice for the future management of CVF.

Altered Cerebrospinal Fluid Clearance and Increased Intracranial Pressure in Rats 18 h After Experimental Cortical Ischaemia

Oedema-independent intracranial pressure (ICP) rise peaks 20–22-h post-stroke in rats and may explain early neurological deterioration. Cerebrospinal fluid (CSF) volume changes may be involved. Cranial CSF clearance primarily occurs via the cervical lymphatics and movement into the spinal portion of the cranio-spinal compartment. We explored whether impaired CSF clearance at these sites could explain ICP rise after stroke. We recorded ICP at baseline and 18-h post-stroke, when we expect changes contributing to peak ICP to be present. CSF clearance was assessed in rats receiving photothrombotic stroke or sham surgery by intraventricular tracer infusion. Tracer concentration was quantified in the deep cervical lymph nodes ex vivo and tracer transit to the spinal subarachnoid space was imaged in vivo. ICP rose significantly from baseline to 18-h post-stroke in stroke vs. sham rats [median = 5 mmHg, interquartile range (IQR) = 0.1–9.43, n = 12, vs. −0.3 mmHg, IQR = −1.9–1.7, n = 10], p = 0.03. There was a bimodal distribution of rats with and without ICP rise. Tracer in the deep cervical lymph nodes was significantly lower in stroke with ICP rise (0 μg/mL, IQR = 0–0.11) and without ICP rise (0 μg/mL, IQR = 0–4.47) compared with sham rats (4.17 μg/mL, IQR = 0.74–8.51), p = 0.02. ICP rise was inversely correlated with faster CSF transit to the spinal subarachnoid space (R = −0.59, p = 0.006, Spearman’s correlation). These data suggest that reduced cranial clearance of CSF via cervical lymphatics may contribute to post-stroke ICP rise, partially compensated via increased spinal CSF outflow.

Case Report: A Rare Case of Fourth Ventricle to Spinal Subarachnoid Space Shunt Migration: Surgical Pearl and Literature Review

Background: In the event of syringomyelia communicating with the fourth ventricle, a fourth ventricle to cervical subarachnoid space shunting could be proposed.Case Report: In this review article, we describe the case of a 40-year-old woman who had a previously implanted fourth ventricle to spinal subarachnoid space shunt for the treatment of syringomyelia in the context of Chiari syndrome. The catheter migrated intradurally to the lumbosacral space, but in the absence of neurological repercussions, we decided to leave it in place.Conclusions: To the best of our knowledge, this is the first case described in the literature review of a catheter migration in the subarachnoid space from occipitocervical to lumbosacral level.

A history of the path towards imaging of the brain: From skull radiography through cerebral angiography

This publication reviews the steps in the path towards obtaining a complete image of the brain. Up to the 1920s, plain X-ray films could demonstrate only calcified tumors, shifts in midline position of a calcified pineal gland due to a mass in the cranium, or foreign metallic objects within the skull. Walter Dandy reported in 1918 that he visualized cerebral ventricles by introducing air as a contrast agent through a trocar into one of the occipital lobes or the right frontal horn of the ventricular system. Dandy localized lesions that distorted or shifted the ventricles. In 1920, Dandy placed air by lumbar puncture into the spinal subarachnoid space that could visualize the brain and entire ventricles. Antonio Egas Moniz with the assistance of his neurosurgeon colleague, Almeida Lima, obtained X-ray images of cerebral arteries of dogs and decapitated human heads from corpses after injecting strontium bromide into their carotid arteries. Satisfied by these experiments, Moniz injected strontium bromide directly into carotid arteries of five patients which failed to show intracranial vessels. In the sixth patient, intracranial arteries were outlined but that patient died of cerebral thrombosis presumably due to the hyper- osmolality of that contrast agent. Finally, on June 18, 1927, Moniz injected 22% sodium iodine into a 20-year-old man and obtained clear visualization of his carotid artery and intracerebral branches after temporarily occluding the artery with a ligature.

Cerebrospinal fluid drainage kinetics across the cribriform plate are reduced with aging

Background Continuous circulation and drainage of cerebrospinal fluid (CSF) are essential for the elimination of CSF-borne metabolic products and neuronal function. While multiple CSF drainage pathways have been identified, the significance of each to normal drainage and whether there are differential changes at CSF outflow regions in the aging brain are unclear. Methods Dynamic in vivo imaging of near infrared fluorescently-labeled albumin was used to simultaneously visualize the flow of CSF at outflow regions on the dorsal side (transcranial and -spinal) of the central nervous system. This was followed by kinetic analysis, which included the elimination rate constants for these regions. In addition, tracer distribution in ex vivo tissues were assessed, including the nasal/cribriform region, dorsal and ventral surfaces of the brain, spinal cord, cranial dura, skull base, optic and trigeminal nerves and cervical lymph nodes. Results Based on the in vivo data, there was evidence of CSF elimination, as determined by the rate of clearance, from the nasal route across the cribriform plate and spinal subarachnoid space, but not from the dorsal dural regions. Using ex vivo tissue samples, the presence of tracer was confirmed in the cribriform area and olfactory regions, around pial blood vessels, spinal subarachnoid space, spinal cord and cervical lymph nodes but not for the dorsal dura, skull base or the other cranial nerves. Also, ex vivo tissues showed retention of tracer along brain fissures and regions associated with cisterns on the brain surfaces, but not in the brain parenchyma. Aging reduced CSF elimination across the cribriform plate but not that from the spinal SAS nor retention on the brain surfaces. Conclusions Collectively, these data show that the main CSF outflow sites were the nasal region across the cribriform plate and from the spinal regions in mice. In young adult mice, the contribution of the nasal and cribriform route to outflow was much higher than from the spinal regions. In older mice, the contribution of the nasal route to CSF outflow was reduced significantly but not for the spinal routes. This kinetic approach may have significance in determining early changes in CSF drainage in neurological disorder, age-related cognitive decline and brain diseases.

Spinal cerebrospinal fluid flow is increased in rats with elevated intracranial pressure 18 hours after cortical ischaemic stroke

Background A dramatic oedema-independent intracranial pressure (ICP) rise occurs 24 hours post-stroke in rats and may explain infarct expansion. Underlying mechanisms of this rise are unknown but evidence suggests cerebrospinal fluid (CSF) dynamics are involved. Methods We investigated how CSF flow changes post-stroke and how this relates to ICP by infusing CSF tracer into the lateral ventricles of rats and assessing transport time and total tracer transport to the spinal subarachnoid space over a 90 minute period. Results Stroke animals with ICP rise had faster tracer transit when compared with stroke animals without ICP rise (27.6 ± 4, n = 6, vs 48.6 ± 4.5 mins, n = 6) or animals subjected to a sham procedure (47.9 ± 4 mins, n = 8), F(2,17) = 0.1, p≤0.01. There was a correlation between tracer transit time and ΔICP (R = -0.52, p=0.02) and infarct volume (R = -0.6, p=0.04). There was no difference in total tracer observed. Conclusions Faster tracer transit in stroke animals may be explained by impairment of other CSF outflow pathways, whereby, spinal drainage acts as a compensatory mechanism. Investigation into the disruption of other CSF drainage routes post-stroke may offer insight into the underlying mechanisms of infarct expansion post-stroke.

In vitro and Numerical Simulation of Blood Removal from Cerebrospinal Fluid: Comparison of Lumbar Drain to Neurapheresis Therapy

Background: Blood removal from cerebrospinal fluid (CSF) in post-subarachnoid hemorrhage patients may reduce the risk of related secondary brain injury. We formulated a computational fluid dynamics (CFD) model to investigate the impact of a dual-lumen catheter-based CSF filtration system, called Neurapheresis TM therapy, on blood removal from CSF compared to lumbar drain. Methods: A subject-specific multiphase CFD model of CSF system-wide solute transport was constructed based on MRI measurements. The Neurapheresis catheter geometry was added to the model within the spinal subarachnoid space. Neurapheresis flow aspiration and return rate was 2.0 and 1.8 (mL/min), versus 0.2 (mL/min) drainage for lumbar drain. Blood was modeled as a bulk fluid phase within CSF with a 10% initial tracer concentration and identical viscosity and density as CSF. Subject-specific oscillatory CSF flow was applied at the model inlet. The dura and spinal cord geometry were considered to be stationary. Spatial-temporal tracer concentration was quantified based on time-average steady-streaming velocities throughout the domain under Neurapheresis therapy and lumbar drain. To help verify CFD results, an optically clear in vitro CSF model was constructed with fluorescein used as a blood surrogate. Quantitative comparison of numerical and in vitro results was performed by linear regression of spatial-temporal tracer concentration over 24-hours. Results: After 24-hours, tracer concentration was reduced to 4.9% under Neurapheresis therapy compared to 6.5% under lumbar drain. Tracer clearance was most rapid between the catheter aspiration and return ports. Neurapheresis therapy was found to have a greater impact on steady-streaming compared to lumbar drain. Steady-streaming in the cranial SAS was ~50X smaller than in the spinal subarachnoid space for both cases. CFD results were strongly correlated with the in vitro spatial-temporal tracer concentration under Neurapheresis therapy (R 2 =0.89 with +2.13% and -1.93% tracer concentration confidence interval). Conclusion: A subject-specific CFD model of CSF system-wide solute transport was used to investigate the impact of Neurapheresis therapy on tracer removal from CSF compared to lumbar drain over a 24-hour period. Neurapheresis therapy was found to substantially increase tracer clearance compared to lumbar drain. The multiphase CFD results were verified by in vitro fluorescein tracer experiments.