Experimental hydrocephalus and hydromyelia: A new insight in mechanism of their development

Abstract

One group of cats had an acrylic screw implanted into the adqueduct of Sylvius, while the other group of animals received a solution of kaolin into the cisterna magna. Three weeks later the dye phenolsulphonphthalein was instilled into the lateral ventricle to ascertain communication between CSF compartments, and thereafter the brain was perfused with formalin. As shown by planimetry of brain ventricles both groups of experimental animals developed hydrocephalus, i.e., coronal surface of brain ventricles was about 10 times larger in kaolin and about 3 times in aqueductal screw experiments than in the controls, respectively. In aqueductal screw experiments communication of CSF between lateral ventricle and subarachnoid spaces was not blocked but only restricted, i.e., an aqueductal stenosis was produced. In kaolin experiments communication of CSF between lateral ventricles and spinal subarachnoid space was blocked by thick meningeal adhesions in the upper cervical region, while the central spinal canal was dilated (hydromyelia) with enhanced CSF communication between it and the lumbar subarachnoid space. We assume that during systolic expansion of brain the CSF is displaced from the cranial cavity toward the spinal subarachnoid space which accommodates an additional volume of CSF primarily due to compliance of the spinal dural sac, while during diastole CSF recoils in the opposite direction. Thus, in case of aqueductal stenosis the undisplaced volume of CSF from the ventricles can be accommodated due to diminution of cerebral blood volume and brain parenchyma so that hydrocephalus develops over time. Since the cervical subarachnoid space is blocked in kaolin experiments the systolic brain expansion forces CSF from basal cisterns via the fourth ventricle into the aqueduct and central canal with consequent development of hydrocephalus and hydromyelia.

Development of hydrocephalus and classical hypothesis of cerebrospinal fluid hydrodynamics: Facts and illusions

“…This consideration is supported by the observations that in patients with communicative and non-communicative hydrocephalus, transmantle pressure is absent (Stephensen et al, 2002). All of the evidence supports the idea that the transmantle pressure gradient may not be necessary or instrumental for the development of hydrocephalus, and that some other factors such as an increase in the ventricular CSF pulse pressure without affecting the CSF pressure (Di Rocco et al, 1978), an impairment of systolic-diastolic displacement of the CSF with the development of periventricular ischemia (Miše et al 1996), changes in the arterial pulsations (Greitz, 2004 and, an increase in ventricular CSF osmolarity without affecting the CSF pressure (Krishnamuthy et al, 2009), and venous compliance (Bateman, 2000 and2003) may play an important role in the development of that pathological process (see Section 8. -Mechanisms of hydrocephalus development which are not in accordance with the classical hypothesis of CSF hydrodynamics).…”

“…The increase in systolic pressure in the brain should distend the brain toward the skull and simultaneously compress the periventricular region of the brain against the ventricles, with the final result being the enlargement of the ventricles and the narrowing of the subarachnoid space. The fact that systolic pressure could be involved in the pathogenesis of hydrocephalus was elaborated in experiments on cats (Miše et al 1996) in which the importance of systolic craniospinal displacement was suggested as the reason for the hydrocephalus development.…”

The formation of cerebrospinal fluid: Nearly a hundred years of interpretations and misinterpretations

“…It was shown in cats that 3 weeks after the application of kaolin in the cisterna magna with the obstruction of cervical subarachnoid space, or the stenosis of the aqueduct with a plastic screw, dilatation of ventricles is developed without a rise in the ventricular CSF pressure (Miše et al 1996). The acute experiments show that an occlusion of the aqueduct itself does not cause the rise of CSF pressure in isolated ventricles and their dilatation .…”

“…For example, some other factors, such as an increase in the ventricular CSF pulse pressure (Di Rocco et al, 1978), an impairment of systolic-diastolic displacement of the CSF with the development of periventricular ischemia (Miše et al, 1996), cardiac disease (Luciano and Dombrowski, 2007), changes in arterial pulsations (Greitz, 2004 and and venous compliance (Bateman, 2000 and2003) may play an important role in the development of that pathological process.…”

New experimental model of acute aqueductal blockage in cats: Effects on cerebrospinal fluid pressure and the size of brain ventricles

“…However, a drawback of this surgical approach was the CSF leakage from the subarachnoid space, as the closing of the surgical wound could not be prevented. To prevent the CSF leakage, a different surgical approach to the aqueduct was used in these experiments, as described in detail in our previous paper (Miše et al, 1996). In short, a burr hole (10 mm in diameter) was made in the midline of the occipital bone and the exposed dura was incised.…”