Neurophysiology in neurotrauma
Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor in Essentials of Anesthesia for Neurotrauma, 2018
CSF is produced by specific capillary networks in cerebral ventricles known as choroid plexus at a relatively constant rate of 0.35 mL/min in adults and approximately 0.40 mL/min in children.3 The total CSF volume equals 100 to 150 mL in adults; the majority of that volume remains in the cerebral subarachnoid space and major cisterns of the brain. A relatively minor volume of CSF occupies cerebral ventricles and the spinal subarachnoid space and spinal canal.4 CSF formation is constant when continuous absorption occurs through specialized structures called arachnoid villi (small protrusions of the thin, second layer covering the brain) and granulations. Arachnoid granulations are herniations of arachnoid membrane through the dura mater into cerebral venous sinuses. Arachnoid granulations function as one-way valves permitting all CSF components to flow in the same direction into the cerebral venous blood.4
Meningioma
Dongyou Liu in Tumors and Cancers, 2017
As the membranous coverings of the brain and spinal cord, the meninges are composed of three layers: the dura mater, arachnoid mater, and pia mater. The dura mater (or the pachymeninges) is the outermost, thick, tough, and inextensible layer situated beneath the bones of the skull and vertebral column. The arachnoid mater is the middle layer lying underneath the dura mater. Small projections of the arachnoid mater into the dura (known as arachnoid granulations) allow cerebrospinal fluid (CSF) contained in the subarachnoid space to reenter the circulation via the dural venous sinuses. The pia mater is the inner layer that lies below the subarachnoid space. As the only covering to follow the contours of the brain (the gyri and fissures), the pia mater is very thin, vascular, and fibrous and adheres tightly to the surface of the brain and spinal cord. Collectively, the arachnoid mater and the pia mater are often referred to as the leptomeninges.
Anatomy of the head and neck
Helen Whitwell, Christopher Milroy, Daniel du Plessis in Forensic Neuropathology, 2021
The dura mater has two distinct layers, an outer layer that is fused to the periosteum lining the inner surface of the skull and an inner fibrous layer. Consequently, no epidural space exists superficial to this layer, unlike the situation found within the spinal canal of the vertebral column. However, there is a potential space, termed the ‘extradural space’, present that can serve as a reservoir for blood if the meningeal vessels become ruptured by trauma. The tightly adherent skull-dura layers serve to prevent spread of blood. Both layers of dura are separated by a thin gap layer, in which are found the major blood sinuses and other blood vessels. Arachnoid granulations project through the dura into the venous sinuses and serve to absorb CSF back into the venous system. All the venous sinuses drain eventually into the internal jugular veins of the neck.
Dural venous sinus stenting in patients with idiopathic intracranial hypertension: report of outcomes from a single-center prospective database and literature review
Published in Expert Review of Ophthalmology, 2022
Matthew J Kole, Juan Carlos Martinez-Gutierrez, Francisio Sanchez, Rosa Tang, Peng Roc Chen
Weight loss is always recommended in patients with IIH. The process of weight loss and its benefits are not immediate and as such it remains a secondary treatment while other treatments are pursued. The exact pathophysiologic mechanism linking body weight to IIH is not understood. It is speculated that increased body weight and the associated increase in intra-abdominal pressure is transmitted into the central venous system, which is in turn transmitted to the cerebral venous system. This increase in cerebral venous pressure inhibits bulk transport of CSF by the arachnoid granulations, and thus may increase intracranial pressure [72–74]. Weight loss has been demonstrated to improve IIH symptoms including improvement in intracranial pressure, papilledema, and visual loss [75,76]. Case series of bariatric surgery mediated weight loss interventions in IIH have replicated the improvements seen in diet-based weight reduction techniques [77,78]. Moreover, the role of weight loss in recurrence prevention cannot be overstated with a mere 6% weight gain being associated with recurrence [79]. Weight loss for patient with obesity and IIH is important and can result in added long-term health benefits so should be universally recommended once acute symptoms are improved to facilitate this lifestyle modification.
Fluid–structure interaction analysis of cerebrospinal fluid with a comprehensive head model subject to a rapid acceleration and deceleration
Published in Brain Injury, 2018
Milan Toma, Paul D.H. Nguyen
The anatomical features missing in the head model include the skin, arachnoid granulations, spinal cord, vasculature and meninges. Skin is irrelevant for our objectives. The arachnoid granulations are negligible due to the relatively slow CSF flow. To make the simulation less computationally expensive, the spinal cord, vasculature and meninges are omitted at this stage but may be considered in future studies. The omission of cerebral vasculature is considered to be a major uncertainty in the proposed predictions and therefore it is to be integrated in the next stage. Subsequently, the displacement of CSF into the spinal subarachnoid space is to be implemented. The final goal is to simulate a closed model of the entire CSF space (37). Natural CSF pulsation may be too slow to affect brain dynamics in high acceleration head injury. However, the displacement of CSF into the spinal subarachnoid space might occur at much higher wave speeds due to the near incompressibility of the CSF. The plan is to include the complete CSF system dynamics in the future head injury models (12). Another limitation of this study is that the brain is modelled as isotropic. The brain is anisotropic and especially white matter fibre tracts have strong axial stiffness compared to the ability to transmit radial stresses (38). This, too, will be addressed in the future studies.
Post-traumatic hydrocephalus: unknown knowns and known unknowns
Published in British Journal of Neurosurgery, 2022
Ashwin Kumaria, Christos M. Tolias
All the same, the exact pathophysiology of PTH remains a mystery – another known unknown. As a communicating hydrocephalus, disordered CSF reabsorption appears to be culpable and arachnoid granulations are implicated: indeed this is measurable as the resistance to CSF outflow.27 Arachnoid granulation fibrosis, mechanical blockage or inflammation as a result of trauma and associated debris have been put forth as mechanisms to explain PTH.28 However, aspects of the pre-existing understanding of CSF flow have recently been challenged.29,30 In particular, too much emphasis has been placed on the bulk flow theory of active production of CSF in the choroid plexus and its passive absorption via arachnoid granulations, first described by Dandy following experiments on a canine model.29,31 Indeed, perhaps the most obvious critique of our contemporary understanding of CSF physiology is overreliance on animal models – principally dogs, cats and rodents – when a multitude of anatomical and physiological differences are known to exist.32 Furthermore, while arachnoid granulations and villi have been implicated in CSF reabsorption, this has recently been challenged with advanced neuroimaging. Arachnoid granulations are absent in the vast majority of children below the age of 2 and in up to a third of adults, suggesting arachnoid granulations do not play an essential role in CSF absorption as it is generally accepted.33,34 Accordingly, an updated pathophysiology for PTH is sought.
Related Knowledge Centers
- Arachnoid Mater
- Cerebrospinal Fluid
- Meninges
- Skull
- Superior Sagittal Sinus
- Vacuole
- Vein
- Endothelium
- Dura Mater
- Dural Venous Sinuses