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Understanding Brain Delivery
Published in Carla Vitorino, Andreia Jorge, Alberto Pais, Nanoparticles for Brain Drug Delivery, 2021
Joana Bicker, Ana Fortuna, Gilberto Alves, Amílcar Falcäo
As previously mentioned, about two-thirds of the CSF are secreted at high capacity by four choroid plexuses in the lateral right, lateral left, third and fourth brain ventricles [36, 37]. The CSF circulates from the lateral to the third ventricle via the interventricular foramina and then to the fourth ventricle through the cerebral aqueduct. Afterwards, it flows down the central canal of the spinal cord and circulates in the subarachnoid space, where it is reabsorbed by arachnoid villi or granulations, which are valve-like structures which enable the CSF to flow out into cerebral veins when its pressure is higher than venous pressure [36]. Lastly, the CSF is directed into the systemic venous circulation or to regional and cervical lymph nodes through cranial and spinal nerves [38, 39]. Regular CSF flow is critical for balanced cerebral metabolism and propelled by several mechanisms, including arterial pulsations in the choroid plexus, a hydrostatic pressure gradient from the CSF to venous blood and the movement of ciliary processes which extend from the apical surfaces of ependymal cells [24]. The rate of production and the composition of the CSF are altered by circadian oscillations [40, 41].
The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
The term hydrocephalus means an increased volume of CSF within the cranial cavity (Box 12.5). The most common cause of enlargement of the ventricles is hydrocephalus ex vacuo as a result of cerebral atrophy, with no increase in ICP. Acute hydrocephalus with increased ICP is most often due to obstruction to the free flow of CSF leading to ventricular enlargement and compression of the white matter in the cerebral hemispheres. In obstructive hydrocephalus it is the site of the lesion rather than its nature that is of importance. Thus, even a small lesion in a critical site adjacent to an interventricular foramen of Monro or the aqueduct in the midbrain will rapidly produce hydrocephalus. Any process resulting in the partial obliteration of the subarachnoid space will also obstruct the flow of CSF, such as previous meningitis or subarachnoid haemorrhage.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Most of the CSF is produced by the choroid plexus, which is situated in the lateral, third, and fourth ventricles. It flows between the lateral ventricles and third ventricle via the interventricular foramen (of Monro). The third and fourth ventricles communicate via the cerebral aqueduct (or aqueduct of Sylvius). The fourth ventricle communicates with the spinal cord by way of the single median foramen of Magendie and the two laterally placed foramina of Luschka. CSF is absorbed directly into the cerebral venous sinuses through the arachnoid villi, or granulations, by a process known as ‘mass or bulk flow’.
First reported case of hydrocephalus in jointly diagnosed bacterial meningitis and a colloid cyst: how Ockham’s razor became Hickam’s dictum
Published in British Journal of Neurosurgery, 2022
Gareth May, Simon Lammy, Aditaya Kumar, Ajay Hegde, Edward Jerome St. George
Cyst enlargement, haemorrhage and positional obstruction of the interventricular foramen of Munro can cause ventriculomegaly and raised intracranial pressure (ICP).2,3,9 Most symptomatic patients will present with signs and symptoms of raised ICP, e.g. non-specific headache, vomiting, and papilloedema.2 Due to a peduncular attachment to the roof of the third ventricle a colloid cyst can intermittently occlude the interventricular foramen of Munro (in a ball-valve mechanism). This can result in sudden onset headaches and loss of consciousness (or drop attacks).3 Irreversible obstruction to CSF flow results in obstructive hydrocephalus. Without prompt neurosurgical intervention death can occur.2 Risk factors for being symptomatic include: age <50 years, presence of headaches, cyst diameter >8 mm, large cyst volume and presence of ventriculomegaly.2
Pre-hospital mild therapeutic hypothermia for patients with severe traumatic brain injury
Published in Brain Injury, 2022
Wusi Qiu, Mingmin Chen, Xu Wang, Ws Qiu, Mm Chen, X Wang
The following parameters of patients in both groups were monitored at admission or after operation (1): Brain and rectal temperature: brain temperature was monitored using a semiconductor temperature probe aseptically inserted 10 mm into the brain parenchyma or residual cavity where intracranial hematoma were evacuated, and rectal temperature was measured using another monitor (15,16,20) (2); Intracranial pressure (ICP): Continuous recording of ICP was applied in all patients for 96 hours with the ICP monitor system (Camino-MPM1, Integra LifeSciences CO, Plainsboro, New Jersey, USA.). A drainage catheter was introduced about 5 cm or so into the right lateral ventricles via the anterior horn, with the intraventricular pressure probe at the level of interventricular foramen (15,16);To avoid the possible intracraninal infection, we always removed such intracranial devices as ICP probe 3 days after surgery (7). Heart rate, respiratory rate, blood pressure, and arterial oxygen saturation, using an multiparameter monitor(Model NO: 90309, Space Lab, Medical. Inc., Issaquah, Washington, USA) (21). Complications such as pneumonia, gastrointestinal bleeding, thrombocytopenia, and electrolyte disturbances; and (17) Glasgow Outcome Scale (GOS) score (1 = death, 2 = vegetative state, 3 = severe disability, 4 = moderate disability, 5 = mild or no disability), evaluated at 6 months of follow-up after TBI.
Thrombosed Fetal Dural Sinus Malformation: Correlation Between Prenatal Ultrasound and Autopsy Findings
Published in Fetal and Pediatric Pathology, 2018
Hwa Jin Cho, Eun Jung Jung, Jung Mi Byun, Dae Hoon Jeong, Kyung Bok Lee, Moon Su Sung, Young Nam Kim
Prenatal sonographic findings include a well-defined round or triangle anechoic collection in the occipital region as a dilated superior sagittal sinus and an echogenic structure within the collection, which represents the thrombus [2,9]. The sonographic appearance may vary with the size and change over time with the stage of thrombus evolution, as in our presented cases. The main differential prenatal sonographic diagnosis of thrombosed dural sinus malformation is based on space-occupying lesions in the posterior fossa, such as an intracranial tumor, a vein of Galen aneurysm, arachnoid cysts, and Dandy-Walker malformations [2,4]. Intracranial tumors of the posterior fossa typically are teratomas demonstrating heterogeneous echogenicity [2]. A vein of Galen aneurysm is located in front of the posterior fossa, involving the region of the choroidal fissure and extending from the interventricular foramen to the pineal gland. Additionally, these fetuses may present with hydrops. Color Doppler is helpful in differentiating a vein of Galen aneurysm from other masses, showing high-velocity turbulent flow within the cystic structure [2,10]. In the presented cases, color Doppler demonstrated interruption of blood flow at the level of the dilated sinus [2,6,9]. The arachnoid cyst appears as an anechoic mass with a thin wall with absence of blood flow on color Doppler and similar signal intensity of the cerebrospinal fluid [6]. Dandy-Walker malformation is characterized by agenesis or hypoplasia of the cerebellar vermis, enlarged cisterna magna, and upward location of tentorium cerebelli [2]. Sagittal views are helpful in demonstrating the enlargement of the cisterna magna and the level of the tentorium. In the present cases, we suspected thrombosed fetal dural sinus malformation with ultrasound based on location, the appearance of the lesion, and color Doppler. The clot displayed organized layering consistent with the progressive growth of the thrombus.