Oscillations of Subarachnoid Space Width as a Potential Marker of Cerebrospinal Fluid Pulsatility

Author(s):  
Marcin Gruszecki ◽  
Magdalena K. Nuckowska ◽  
Arkadiusz Szarmach ◽  
Marek Radkowski ◽  
Dominika Szalewska ◽  
...  
2020 ◽  
pp. 088307382097799
Author(s):  
Ke Yu ◽  
Minggang Yi ◽  
Ruodi Cui ◽  
Tao Gong ◽  
Chunhua Dong ◽  
...  

A widened subarachnoid space might be pathologic, potentially pathologic, or simply a normal developmental variant. However, the definition of a normal subarachnoid space width in infants remains unclear, especially on computed tomography (CT) images. To determine the physiological subarachnoid space width among infants aged 1-24 months, its upper limit, and changes with age, we measured the cerebrospinal fluid width on 538 CT images. Measurements were obtained at fixed planes and fixed positions to prevent variance and increase comparability between patients. We observed an asymmetry in the cerebrospinal fluid width of the temporal region. The width increased in all positions until 4-6 months of age, after which it began to decrease, reaching a relatively stable range in infants aged 13-24 months. We suggest considering the 95th percentile of the cerebrospinal fluid width as the upper limit. The correlation between age and the subarachnoid space width should be considered during clinical diagnosing.


2021 ◽  
pp. 1-8
Author(s):  
Paul Theo Zebhauser ◽  
Achim Berthele ◽  
Marie-Sophie Franz ◽  
Oliver Goldhardt ◽  
Janine Diehl-Schmid ◽  
...  

Background: Tau proteins are established biomarkers of neuroaxonal damage in a wide range of neurodegenerative conditions. Although measurement of total-Tau in the cerebrospinal fluid is widely used in research and clinical settings, the relationship between age and total-Tau in the cerebrospinal fluid is yet to be fully understood. While past studies reported a correlation between age and total-Tau in the cerebrospinal fluid of healthy adults, in clinical practice the same cut-off value is used independently of patient’s age. Objective: To further explore the relationship between age and total-Tau and to disentangle neurodegenerative from drainage-dependent effects. Methods: We analyzed cerebrospinal fluid samples of 76 carefully selected cognitively healthy adults and included amyloid-β 1–40 as a potential marker of drainage from the brain’s interstitial system. Results: We found a significant correlation of total-Tau and age, which was no longer present when correcting total-Tau for amyloid-β 1–40 concentrations. These findings were replicated under varied inclusion criteria. Conclusion: Results call into question the association of age and total-Tau in the cerebrospinal fluid. Furthermore, they suggest diagnostic utility of amyloid-β 1–40 as a possible proxy for drainage-mechanisms into the cerebrospinal fluid when interpreting biomarker concentrations for neurodegenerative diseases.


1981 ◽  
Vol 240 (4) ◽  
pp. F329-F336 ◽  
Author(s):  
M. W. Bradbury ◽  
H. F. Cserr ◽  
R. J. Westrop

Lymph from the jugular lymph trunks of anesthetized rabbits has been continuously collected and radioiodinated albumin (RISA) therein estimated after microinjection of 1 microliter of 131I-albumin into the caudate nucleus, after single intraventricular injections, and during intraventricular infusions. Comparison of lymph at 7 and 25 h after intracerebral microinjection with efflux of radioactivity from whole brain suggests that about 50% of cleared radioactivity goes through lymph. Concentrations, normalized to cerebrospinal fluid (CSF), were much higher in lymph and retropharyngeal nodes after brain injection than after CSF injection or infusion. Also after brain injection, lymph and nodes contained more activity on injected side in contrast to lack of laterality after CSF administration. Calculation suggests that less than 30% of RISA cleared from brain can do so via a pool of well-mixed CSF. Analysis of tissues is compatible with much RISA draining by bulk flow via cerebral perivascular spaces plus passage from subarachnoid space of olfactory lobes into submucous spaces of nose and thus to lymph.


1982 ◽  
Vol 52 (1) ◽  
pp. 231-235 ◽  
Author(s):  
J. M. Luce ◽  
J. S. Huseby ◽  
W. Kirk ◽  
J. Butler

We investigated possible mechanisms by which positive end-expiratory pressure (PEEP) increased cerebrospinal fluid pressure (PCSF) in anesthetized mechanically ventilated dogs. In part I of the study, PEEP was applied in 5 cmH2O increments each lasting 1–2 min, before and after a snare separated the spinal from the cerebral subarachnoid space in each animal. Next, with the spinal cord still ligated, the dogs were ventilated without PEEP while superior vena cava pressure (PSVC) was raised in 5 cmH2O increments by means of a fluid reservoir connected with the superior vena cava. Cerebrospinal fluid pressure in the cisterna magna increased immediately and in parallel with PEEP before and after the spinal subarachnoid space was occluded and also increased when PSVC was raised independently; in all circumstances the increase in PCSF correlated closely with PSVC (r = 0.926). In part II of the study, arterial blood gases were drawn before and after PEEP was applied in the same increments and for the same duration as in part I. Cerebrospinal fluid pressure measured with a hollow skull screw again rose in parallel with PEEP, whereas arterial carbon dioxide tension rose only slightly at 60 s. In part III of the study, mean arterial pressure (Pa) was allowed to decrease with PEEP or was held constant by distal aortic obstruction and volume infusion. Cerebrospinal fluid pressure increased regardless of Pa, but the increase was greater when Pa was held constant than when it fell with PEEP. We conclude that PEEP increases PCSF primarily by increasing PSVC and decreasing cerebral venous outflow. This effect is augmented if cerebral arterial inflow is increased as well.


1981 ◽  
Vol 2 (9) ◽  
pp. 269-276
Author(s):  
John F. Griffith ◽  
Jimmy C. Brasfield

The infant or child with increasing pressure within the cranial cavity must be identified early and treated promptly in order to prevent serious complications or death. When the pressure elevation is gradual it is frequently well tolerated, and the patient may seem deceptively well. There is a critical point, however, beyond which any further increase in pressure leads to a catastrophic deterioration in the patient's condition.1 When this occurs, the outlook for quality survival is poor despite the best therapy. Unfortunately, this can occur when the underlying process is benign and would have been reversible if recognized and treated promptly. For prompt recognition and treatment, the physician must be familiar with the pathophysiology of raised intracranial pressure. PATHOPHYSIOLOGY The intracranial compartment contains blood vessels, cerebrospinal fluid (CSF), brain, and leptomeninges which include the rigid dural membranes forming the falx and tentorium. Whenever there is an increase in the volume of any one of these intracranial components (brain, CSF, blood) there must be a corresponding reduction in the size of the others in order for the intracranial pressure to remain normal. This type of compensation or buffering capacity is particularly important in the early stages of intracranial disease. As the pressure mounts from any type of mass lesion, the CSF is displaced caudally into the spinal subarachnoid space and there is a corresponding increase in the rate of absorption of CSF.2


1929 ◽  
Vol 22 (5) ◽  
pp. 673-686
Author(s):  
G. J. Jenkins

(1) Meningitis: two groups of cases. (2) A method of washing out the subarachnoid space in cases of septic meningitis secondary to infection of the ear. (3) Discussion on the value of maintaining a positive pressure of the cerebrospinal fluid when operating on a septic region communicating with the subarachnoid space. (4) Leaking cerebrospinal fluid from the region of the ear: operative treatment.


2019 ◽  
Vol 216 (11) ◽  
pp. 2492-2502 ◽  
Author(s):  
Qiaoli Ma ◽  
Yann Decker ◽  
Andreas Müller ◽  
Benjamin V. Ineichen ◽  
Steven T. Proulx

The pathways of circulation and clearance of cerebrospinal fluid (CSF) in the spine have yet to be elucidated. We have recently shown with dynamic in vivo imaging that routes of outflow of CSF in mice occur along cranial nerves to extracranial lymphatic vessels. Here, we use near-infrared and magnetic resonance imaging to demonstrate the flow of CSF tracers within the spinal column and reveal the major spinal pathways for outflow to lymphatic vessels in mice. We found that after intraventricular injection, a spread of CSF tracers occurs within both the central canal and the spinal subarachnoid space toward the caudal end of the spine. Outflow of CSF tracers from the spinal subarachnoid space occurred predominantly from intravertebral regions of the sacral spine to lymphatic vessels, leading to sacral and iliac LNs. Clearance of CSF from the spine to lymphatic vessels may have significance for many conditions, including multiple sclerosis and spinal cord injury.


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