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Anatomy of the head and neck
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, 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.
Tumors of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
CT of the brain is often used in the emergency department setting to detect initially the presence of tumor and hemorrhage in patients presenting with acute neurologic illness. On CT, metastases are typically hypodense to normal brain on noncontrast imaging, with disproportionate hypodense vasogenic edema surrounding them. Mass effect is almost always present, and 70% are multiple. Meningeal metastases may be very difficult to detect on CT. Communicating hydrocephalus is often present due to obstruction of the arachnoid granulation.
Neurophysiology in neurotrauma
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, 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
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.
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.
Choroid plexus and CSF: an updated review
Published in British Journal of Neurosurgery, 2022
Dana Hutton, Mohammed Gadoora Fadelalla, Avinash Kumar Kanodia, Kismet Hossain-Ibrahim
NPH is a condition clinically characterised by the triad of: dementia, gait disturbance, and urinary incontinence. It presents similarly to other dementias, however brain imaging reveals ventriculomegaly without concomitant cerebral atrophy.33 NPH has been assumed to result from insufficient CSF reabsorption of the arachnoid granulations. This can occur secondary to thickening of the arachnoid mater from previous subarachnoid haemorrhage or meningitis. However, in most cases the cause remains uncertain – idiopathic NPH (INPH). Whatever the cause of NPH, slight transmantle pressure gradients arise, and cause hyperdynamic CSF flow through the aqueduct. NPH can still be termed ‘normal’ pressure despite being at a new, higher level, as over time CSF formation is dampened to achieve a stable state.33 CT features of NPH have been demonstrated in Figure 3.