Ventricular dilation and elevated aqueductal pulsations in a new experimental model of communicating hydrocephalus

Wagshul, Mark E.; McAllister, James P.; Rashid, Shams; Li, J.; Egnor, Michael; Walker, Marion L.; Yu, Meichen; Smith, Shawna; Zhang, Guangxiang; Chen, J.J.; Benveniste, Helene

doi:10.1016/j.expneurol.2009.03.034

Cited by 42 publications

(44 citation statements)

References 31 publications

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“…No correlation was found between either VV or aqueductal CSF SV and PI, for either acute or chronic CH animals. Based on prior measurements of CSF SV in intact control animals (Wagshul et al, 2009), we can conclude that there is no increase in microvascular flow pulsatility, even in the presence of a 10-to 500-fold increase in ventricular CSF pulsatility as measured at the cerebral aqueduct.…”

Section: Capillary Pulsatilitymentioning

confidence: 73%

“…Hydrocephalus was characterized a few days before multiphoton microscopy by magnetic resonance imaging to quantify the volume of the cerebral ventricles and the stroke volume (SV) of pulsatile CSF flow at the cerebral aqueduct, as described previously (Wagshul et al, 2009). Animals with a ventricular volume (VV) > 30 mL were considered hydrocephalic; this criterion had been established in a previous study (Wagshul et al, 2009). Kaolin animals that failed to develop hydrocephalus by this criterion were excluded from the study.…”

Section: Communicating Hydrocephalus Induction and Study Designmentioning

confidence: 99%

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Neocortical Capillary Flow Pulsatility is Not Elevated in Experimental Communicating Hydrocephalus

Rashid

McAllister

et al. 2011

J Cereb Blood Flow Metab

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While communicating hydrocephalus (CH) is often characterized by increased pulsatile flow of cerebrospinal fluid (CSF) in the cerebral aqueduct, a clear-cut explanation for this phenomenon is lacking. Increased pulsatility of the entire cerebral vasculature including the cortical capillaries has been suggested as a causative mechanism. To test this theory, we used two-photon microscopy to measure flow pulsatility in neocortical capillaries 40 to 500 lm below the pial surface in adult rats with CH at 5 to 7 days (acute, n = 8) and 3 to 5 weeks (chronic, n = 5) after induction compared with intact controls (n = 9). Averaging over all cortical depths, no increase in capillary pulsatility occurred in acute (pulsatility index (PI): 0.15 ± 0.06) or chronic (0.14 ± 0.05) CH animals compared with controls (0.18±0.07; P = 0.07). More specifically, PI increased significantly with cortical depth in controls (r = 0.35, P < 0.001), but no such increase occurred in acute (r = 0.06, P = 0.3) or chronic (r = 0.05, P = 0.5) CH. Pulsatile CSF aqueductal flow, in contrast, was elevated 10-to 500-fold compared with controls. We conclude that even in the presence of markedly elevated pulsatile CSF flow in the aqueduct, there is no concurrent increase in microvascular pulsatile flow.

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Section: Capillary Pulsatilitymentioning

confidence: 73%

Section: Communicating Hydrocephalus Induction and Study Designmentioning

confidence: 99%

Neocortical Capillary Flow Pulsatility is Not Elevated in Experimental Communicating Hydrocephalus

Rashid

McAllister

et al. 2011

J Cereb Blood Flow Metab

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“…This hydraulic system, which behaves like a second-order low-pass filter, is a finely tuned mechanism that relies on the correct timing of the individual arterial, venous, and CSF pulses (28). Abnormalities in the cerebral arterial and venous pulses can greatly influence the performance of the hydraulic regulatory mechanism, (28,29) resulting in increased CSF pulsatility-something that has previously been implicated in a number of pathologies, including microvascular angiopathy, (30) communicating hydrocephalus (31), and leukoaraiosis (32).…”

Section: Discussionmentioning

confidence: 99%

Cine cerebrospinal fluid imaging in multiple sclerosis

Magnano

Schirda

Weinstock‐Guttman

et al. 2012

Magnetic Resonance Imaging

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Purpose: To investigate cerebrospinal fluid (CSF) dynamics in the aqueduct of Sylvius in multiple sclerosis (MS) patients and healthy controls (HC) using cine phase contrast imaging. Materials and Methods:In all, 67 MS patients (48 relapsing-remitting [RR] and 19 secondary-progressive [SP]), nine patients with clinically isolated syndrome (CIS), and 35 age-and sex-matched HC were examined. CSF flow and velocity measures were quantified using a semiautomated method and compared with clinical and magnetic resonance imaging (MRI) disease outcomes.Results: Significantly decreased CSF net flow was detected in MS patients compared to HC (À3.7 vs. À7.1 mL/beat, P ¼ 0.005). There was a trend for increased net positive flow between SP, RR, and CIS patients. Altered CSF flow and velocity measures were associated with more severe T1 and T2 lesion volumes, lateral and fourth ventricular volumes, and third ventricular width in MS and CIS patients (P < 0.01 for all). In CIS patients, conversion to clinically definite MS in the following year was related to decreased CSF net flow (P ¼ 0.007). There was a trend between increased annual relapse rate and altered CSF flow/velocity measures in RRMS patients (P < 0.05).Conclusion: CSF flow dynamics are altered in MS patients. More severe clinical and MRI outcomes in RRMS and CIS patients relate to altered CSF flow and velocity measures.

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“…Cerebrospinal fluid (CSF) dynamics are thought to be altered in many pathological conditions including hydrocephalus [1,2], idiopathic intracranial hypertension [3,4], intracerebral haemorrhage [5], subarachnoid haemorrhage [6,7], large hemispheric stroke [8,9], traumatic brain injury [10], and in the aging brain [11,12]. However, relatively little is known about the exact mechanisms of changes in CSF dynamics and drainage in these conditions due to difficulties in quantification.…”

Section: Introductionmentioning

confidence: 99%

Cerebrospinal fluid is drained primarily via the spinal canal and olfactory route in young and aged spontaneously hypertensive rats

Murtha

Yang

Parsons

et al. 2014

Fluids Barriers CNS

106

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BackgroundMany aspects of CSF dynamics are poorly understood due to the difficulties involved in quantification and visualization. In particular, there is debate surrounding the route of CSF drainage. Our aim was to quantify CSF flow, volume, and drainage route dynamics in vivo in young and aged spontaneously hypertensive rats (SHR) using a novel contrast-enhanced computed tomography (CT) method.MethodsICP was recorded in young (2–5 months) and aged (16 months) SHR. Contrast was administered into the lateral ventricles bilaterally and sequential CT imaging was used to visualize the entire intracranial CSF system and CSF drainage routes. A customized contrast decay software module was used to quantify CSF flow at multiple locations.ResultsICP was significantly higher in aged rats than in young rats (11.52 ± 2.36 mmHg, versus 7.04 ± 2.89 mmHg, p = 0.03). Contrast was observed throughout the entire intracranial CSF system and was seen to enter the spinal canal and cross the cribriform plate into the olfactory mucosa within 9.1 ± 6.1 and 22.2 ± 7.1 minutes, respectively. No contrast was observed adjacent to the sagittal sinus. There were no significant differences between young and aged rats in either contrast distribution times or CSF flow rates. Mean flow rates (combined young and aged) were 3.0 ± 1.5 μL/min at the cerebral aqueduct; 3.5 ± 1.4 μL/min at the 3rd ventricle; and 2.8 ± 0.9 μL/min at the 4th ventricle. Intracranial CSF volumes (and as percentage total brain volume) were 204 ± 97 μL (8.8 ± 4.3%) in the young and 275 ± 35 μL (10.8 ± 1.9%) in the aged animals (NS).ConclusionsWe have demonstrated a contrast-enhanced CT technique for measuring and visualising CSF dynamics in vivo. These results indicate substantial drainage of CSF via spinal and olfactory routes, but there was little evidence of drainage via sagittal sinus arachnoid granulations in either young or aged animals. The data suggests that spinal and olfactory routes are the primary routes of CSF drainage and that sagittal sinus arachnoid granulations play a minor role, even in aged rats with higher ICP.

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Ventricular dilation and elevated aqueductal pulsations in a new experimental model of communicating hydrocephalus

Cited by 42 publications

References 31 publications

Neocortical Capillary Flow Pulsatility is Not Elevated in Experimental Communicating Hydrocephalus

Neocortical Capillary Flow Pulsatility is Not Elevated in Experimental Communicating Hydrocephalus

Cine cerebrospinal fluid imaging in multiple sclerosis

Cerebrospinal fluid is drained primarily via the spinal canal and olfactory route in young and aged spontaneously hypertensive rats

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