O.016 Resonance and intracranial pressure pulsations: An experimental study

Abstract

s of the Hydrocephalus 2008 Congress / Clinical Neurology and Neurosurgery 110S (2008), S1–S41 S5 O.015 New model of cervical stenosis in cats: Effects on size of brain ventricles and cerebrospinal fluid pressure M. Klarica1 , I. Jurjevic1 , T. Jukic2, D. Oreskovic3, M. Bulat 1 1Department of Pharmacology and Croatian Institute for Brain Research, School of Medcine University of Zagreb, Zagreb, Croatia; 2Department of Ophtalmology, Clinical Hospital center Rebro, Zagreb, Croatia; 3Rudjer Boskovic Institute, Zagreb, Croatia It was shown that cervical obstruction of physiological cranio-spinal displacement of cerebrospinal fluid (CSF), which is developed during inflammating process after kaolin application, may lead to development of hydrocephalus and hydromyelia. We have tested this hypothesis on new experimental model of cervical stenosis without inflammation. Acute and subacute experiments were performed in cats in which plastic semiring was positioned in epidural space at C2 vertebrae separating spinal from cranial cerebrospinal fluid. CSF pressures were recorded in lateral ventricle (LV) and lumbar subarahnoid space (LSS). Size of both the brain ventricles and central canal was determined by planimetric method. In all experiments the CSF pressures were normal. However, in acute experiments with infusion of artificial CSF, the transmission of the increased CSF pressure from LV to LSS was limited. After 3 or 6 weeks, an atrophy of spinal cord was observed at the site of cervical stenosis and pressure transmission from LV to LSS was improved. Planimetric measurement of surface of coronal brain slice and ventricles showed that ventricular surface was 0.6±;0.1% (n=5) in control and 1.6±;0.2% (n=4) in animals with cervical stenosis (p<0.002). Change in size of central canal was not detected. These results support the hypothesis claiming that impairment of cranio-spinal displacement of CSF volume can lead to development of hydrocephalus. However, changes in size of brain ventricle and central canal are relatively limited, probably due to atrophy of spinal cord at the stenosis site, and improvement of physiological CSF cranio-spinal displacement. O.016 Resonance and intracranial pressure pulsations: An experimental study M.E. Wagshul1,2,3, M.R. Egnor 2, E.J. Kelly4, H.J. Yu3 1Department of Radiology, 2Department of Neurosurgery, 3Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY, USA; 4Toshiba Medical Systems, Tustin, CA, USA While the existence of a coupling between intravascular and intraparenchymal pressure is undisputed, the nature of this coupling and how it changes under conditions of decreased intracranial compliance has not been carefully investigated. We used transfer function analysis between the intracarotid and intraparenchymal pulse pressure waveforms in twelve healthy mongrel dogs, under conditions of normal and decreased intracranial compliance, to characterize the relationship between arterial and intracranial pulsations. Compliance was manipulated via infusions of isotonic saline into the spinal subarachnoid space. We find that under normal conditions, the intracranial pressure wave leads the arterial wave and there is a relative minimum in the intracranial pulse pressure amplitude near the frequency of the heart rate. Under conditions of decreased intracranial compliance, the intracranial pressure wave begins to lag behind the arterial wave and increases significantly in amplitude. Most interestingly, in many animals the pulse pressure exhibits a minimum in amplitude at a particular mean pressure which coincides with the transition from a leading to lagging ICP wave. This transfer function behavior is characteristic of a resonant notch system, in which the portion of the arterial pulsations near the heart rate are optimally dissipated, and may explain the importance of altered pulse pressure in the pathophysiology of hydrocephalus. New models of intracranial dynamics are needed to explain these results and may open the path for development of new therapies geared toward addressing the pulsation dysfunction in hydrocephalus. Session 2A 10:30–12:30, Room A