The traditional theory of communicating hydrocephalus has implicated the bulk flow component of CSF motion; that is, hydrocephalus is generally understood as an imbalance between CSF formation and absorption. The theory that the cause of communicating hydrocephalus is malabsorption of CSF at the arachnoid villi is not substantiated by experimental evidence or by physical reasoning. Flow-sensitive MRI has shown that nearly all CSF motion is pulsatile, and there is substantial evidence that hyperdynamic choroid plexus pulsations are necessary and sufficient for ventricular dilation in communicating hydrocephalus. We have developed a model of intracranial pulsations based on the analogy between the pulsatile motion of electrons in an electrical circuit and the pulsatile motion of blood and CSF in the cranium. Increased impedance to the flow of CSF pulsations in the subarachnoid space redistributes the flow of pulsations into the ventricular CSF and into the capillary and venous circulation. The salient features of communicating hydrocephalus, such as ventricular dilation, intracranial pressure waves, narrowing of the CSF-venous pressure gradient, diminished cerebral blood flow, elevated resistive index and malabsorption of CSF, emerge naturally from the model. We propose that communicating hydrocephalus is the result of a redistribution of CSF pulsations in the cranium.
The acute traumatic central cord syndrome (ATCCS) is commonly stated to result from an injury which affects primarily the center of the spinal cord and is frequently hemorrhagic. To test the validity of this widely disseminated hypothesis, the magnetic resonance images [MRI] of 11 consecutive cases of ATCCS caused by closed injury to the spine were analyzed and correlated with the gross pathological and histological features of 3 cervical spinal cords obtained at post mortem from patients with ATCCS, including 2 of patients studied by MRI. The MRI studies were performed acutely (18 h to 2 days after injury) in 7 patients and subacutely (3-10 days after injury) in 4. Ten of the 11 patients had pre-existing spondylosis and/or canal stenosis. The 11th suffered a cervical fracture. All patients exhibited hyperintense signal within the parenchyma of the cervical spinal cord on gradient echo MRI. None showed MRI features characteristic of hemorrhage on T1-weighted spin echo or T2-weighted gradient echo studies. Gross and histological examination of the necropsy specimens showed no evidence of blood or blood products within the cord parenchyma: the primary finding was diffuse disruption of axons, especially within the lateral columns of the cervical cord in the region occupied by the corticospinal tracts. The central gray matter was intact. In patients with ATCCS, the predominant loss of motor function in the distal muscles of the upper limbs may reflect the importance of the corticospinal tract for hand and finger function in the primate. In this study, the MRI and pathological observations indicate that ATCCS is predominantly a white matter injury and that intramedullary hemorrhage is not a necessary feature of the syndrome; indeed, it is probably an uncommon event in ATCCS. We suggest that the most common mechanism of injury in ATCCS may be direct compression of the cervical spinal cord by buckling of the ligamenta flava into an already narrowed cervical spinal canal; this would explain the predominance of axonal injury in the white matter of the lateral columns.
Under normal conditions, pulsatile ventricular CSF flow is a small fraction of the net pulsatile CSF flow in the cranium. A thorough review of the literature supports the view that modified intracranial compliance can lead to redistribution of pulsations and increased intraventricular pulsations. The phase of CSF flow may also reflect the local and global compliance of the brain.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.