The symptomatic deposition of CSF inside the brain ventricles is known as hydrocephalus. This build-up could be caused by a blockage in the normal flow of CSF, issues with Pacchionian arachnoid granulations absorption further inside the venous system, or excessive cerebrospinal fluid production.
Around the early year 1913, Dandy suggested the classifications of communicative and obstructive (non-communicating) hydrocephalus, and ever since then, several other classifications have been developed. There are 4 forms of hydrocephalus in adults: communicative, obstructive, NPH (normal pressure hydrocephalus), and hypersecretory.
Hydrocephalus, whether developmental or congenital, is frequently present at birth and is frequently associated with a spinal dysraphism or genetic abnormality. The initial treatment option is surgical surgery with the insertion of a ventricular shunt.
In appropriate cases of hydrocephalus, choroid plexus cauterization and ETV (endoscopic third ventriculostomy) are viable treatments. Without timely treatment, acute hydrocephalus can lead to brain herniation and mortality. Hydrocephalus does have a fatality incidence of zero to three percent in children, based on the length of follow-up.
Epidemiology
The most prevalent causes of hydrocephalus in children are congenital abnormalities and intraventricular bleeding among premature neonates. It reaches a new high later in life as a result of NPH instances. The high incidence of hydrocephalus is estimated to be around 85 per 100,000 people, with a notable disparity between age categories: 88 per 100,000 in children and 11 per 100,000 in adulthood.
Due to the high frequency of NPH later on in life, the prevalence in the senior individuals is substantially greater, about 175 per 100,000, and over 400 per 100,000 for those over eighty years old. Hydrocephalus is more common in South America and Africa. The prevalence of infantile hydrocephalus ranges from 1 to 32 per 10,000 babies. Both sexes are often impacted equally.
Anatomy
Pathophysiology
The choroid plexus, which is found in the lateral, 3rd, and 4th ventricles, is the main producer of cerebrospinal fluid. It passes via the ventricular circulation through the foramen of Monro from the lateral ventricle to the 3rd ventricle, and by the aqueduct of Sylvius or the cerebral aqueduct from the 3rd to the 4th ventricle.
It enters basal cisterns by two lateral foramina of Luschka and a median foramen of Magendie from the fourth ventricle, and a portion of it proceeds to circulate all around the spinal column and even in the central canal. Arachnoid granulations that develop across dural venous sinuses, particularly the superior sagittal sinus, are the primary sources of cerebrospinal fluid absorption.
Cerebrospinal fluid is drawn into the dural venal sinuses and circulated throughout the body. The daily output of cerebrospinal fluid is roughly 500 ml, with an average volume of 150 ml. This implies that every twenty hours, the whole cerebrospinal fluid volume is refilled three times.
According to the “bulk flow” paradigm, cerebrospinal fluid moves slowly from the point of generation to the point of absorption. Hydrocephalus can be caused by any functional or physical restriction within the subarachnoid space, venous sinuses, or ventricular system. Cerebrospinal fluid flow inside the ventricular system might be blocked by obstructive gliosis or lesion.
Cerebrospinal fluid absorption into the systemic circulation can be hampered by scarring of the subarachnoid space or inflammation, as well as high venous pressure within the venous sinuses. The overall amount of the skull, cerebrospinal fluid, plus blood inside the skull is static and per the Monro-Kellie doctrine.
If the capacity of one compartment increases without the volume of another decreasing, the pressure inside the brain will rise, as it does in hydrocephalus. Transependymal extravasation of cerebrospinal fluid into brain tissue occurs when ICP rises, producing brain parenchyma and stress-induced atrophy.
Etiology
A blockage in CSF channels causes obstructed hydrocephalus. The foramina Monro, the foramen magnum, the aqueduct of Sylvius, and the fourth ventricle are the most common sites of obstruction. However, most lesions of sufficient size can impede cerebrospinal fluid routes at any point.
Ependymoma, choroid plexus papilloma, subependymal giant cell astrocytoma, pituitary adenoma, hypothalamic, craniopharyngioma, or hamartoma, optic nerve glioma, and disseminated cancers are among the most common tumors linked with hydrocephalus. Hydrocephalus is frequently related to malignancies of the posterior fossa.
Impaired cerebrospinal fluid absorption causes communicative hydrocephalus. Post-inflammatory or post-hemorrhagic alterations are the most typical causes. One-third of such instances are caused by subarachnoid hemorrhage, which prevents cerebrospinal fluid absorption there at arachnoid granulations.
Meningitis, particularly bacterial meningitis, can make hydrocephalus worse. Head injury in the workplace is a major contributor to adult-onset hydrocephalus. Overproduction of cerebrospinal fluid causes hypersecretory hydrocephalus, which is most commonly caused by plexus papilloma or, in rare cases, cancer. Children are more likely to get these tumors.
NPH (Normal-pressure hydrocephalus) is a kind of communicative hydrocephalus that occurs more frequently in elderly people and has a pathophysiology that is not fully understood. It is caused by a change in cerebrospinal fluid dynamics with little or no rise in ICP (intracranial pressure).
Hydrocephalus can be caused by prenatal bleeding or inflammation. Some inherited kinds of hydrocephalus aren’t visible until later in life. A brainstem abnormality with stenosis of the cerebral aqueduct accounts for nearly 10% of all occurrences of hydrocephalus in infants.
Throughout this age category, Dandy-Walker deformity will be the source of two to four percent of hydrocephalus. Agenesis of the foramen of Monro, Bickers-Adams syndrome, and Arnold-Chiari type 1 and type 2 are all prevalent disorders in babies with hydrocephalus.
Genetics
Prognostic Factors
The prognosis is heavily influenced by the source of hydrocephalus. Patients with significant intraventricular hemorrhage may demand definitive therapy in half of the cases. Approximately twenty percent of children will need irreversible shunting following posterior fossa surgery.
There are a variety of parameters used to forecast the effectiveness of shunting in patients with NPH, some of which are debatable. If a gait impairment occurs before a mental disturbance, shunting has a greater than seventy-seven percent likelihood of improving the situation. The response to a single lumbar puncture or external lumbar drain is another criterion.
Improvement in symptoms following a single lumbar puncture with 40-50 ml of CSF drained or following the lumbar drainage is regarded as a good prognosis for shunt efficacy. Over a seventy-five percent chance of symptom relief with shunt installation if there is persistent ventricular action 48 to 72 hours following isotope cisternography.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK560875/
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The symptomatic deposition of CSF inside the brain ventricles is known as hydrocephalus. This build-up could be caused by a blockage in the normal flow of CSF, issues with Pacchionian arachnoid granulations absorption further inside the venous system, or excessive cerebrospinal fluid production.
Around the early year 1913, Dandy suggested the classifications of communicative and obstructive (non-communicating) hydrocephalus, and ever since then, several other classifications have been developed. There are 4 forms of hydrocephalus in adults: communicative, obstructive, NPH (normal pressure hydrocephalus), and hypersecretory.
Hydrocephalus, whether developmental or congenital, is frequently present at birth and is frequently associated with a spinal dysraphism or genetic abnormality. The initial treatment option is surgical surgery with the insertion of a ventricular shunt.
In appropriate cases of hydrocephalus, choroid plexus cauterization and ETV (endoscopic third ventriculostomy) are viable treatments. Without timely treatment, acute hydrocephalus can lead to brain herniation and mortality. Hydrocephalus does have a fatality incidence of zero to three percent in children, based on the length of follow-up.
The most prevalent causes of hydrocephalus in children are congenital abnormalities and intraventricular bleeding among premature neonates. It reaches a new high later in life as a result of NPH instances. The high incidence of hydrocephalus is estimated to be around 85 per 100,000 people, with a notable disparity between age categories: 88 per 100,000 in children and 11 per 100,000 in adulthood.
Due to the high frequency of NPH later on in life, the prevalence in the senior individuals is substantially greater, about 175 per 100,000, and over 400 per 100,000 for those over eighty years old. Hydrocephalus is more common in South America and Africa. The prevalence of infantile hydrocephalus ranges from 1 to 32 per 10,000 babies. Both sexes are often impacted equally.
The choroid plexus, which is found in the lateral, 3rd, and 4th ventricles, is the main producer of cerebrospinal fluid. It passes via the ventricular circulation through the foramen of Monro from the lateral ventricle to the 3rd ventricle, and by the aqueduct of Sylvius or the cerebral aqueduct from the 3rd to the 4th ventricle.
It enters basal cisterns by two lateral foramina of Luschka and a median foramen of Magendie from the fourth ventricle, and a portion of it proceeds to circulate all around the spinal column and even in the central canal. Arachnoid granulations that develop across dural venous sinuses, particularly the superior sagittal sinus, are the primary sources of cerebrospinal fluid absorption.
Cerebrospinal fluid is drawn into the dural venal sinuses and circulated throughout the body. The daily output of cerebrospinal fluid is roughly 500 ml, with an average volume of 150 ml. This implies that every twenty hours, the whole cerebrospinal fluid volume is refilled three times.
According to the “bulk flow” paradigm, cerebrospinal fluid moves slowly from the point of generation to the point of absorption. Hydrocephalus can be caused by any functional or physical restriction within the subarachnoid space, venous sinuses, or ventricular system. Cerebrospinal fluid flow inside the ventricular system might be blocked by obstructive gliosis or lesion.
Cerebrospinal fluid absorption into the systemic circulation can be hampered by scarring of the subarachnoid space or inflammation, as well as high venous pressure within the venous sinuses. The overall amount of the skull, cerebrospinal fluid, plus blood inside the skull is static and per the Monro-Kellie doctrine.
If the capacity of one compartment increases without the volume of another decreasing, the pressure inside the brain will rise, as it does in hydrocephalus. Transependymal extravasation of cerebrospinal fluid into brain tissue occurs when ICP rises, producing brain parenchyma and stress-induced atrophy.
A blockage in CSF channels causes obstructed hydrocephalus. The foramina Monro, the foramen magnum, the aqueduct of Sylvius, and the fourth ventricle are the most common sites of obstruction. However, most lesions of sufficient size can impede cerebrospinal fluid routes at any point.
Ependymoma, choroid plexus papilloma, subependymal giant cell astrocytoma, pituitary adenoma, hypothalamic, craniopharyngioma, or hamartoma, optic nerve glioma, and disseminated cancers are among the most common tumors linked with hydrocephalus. Hydrocephalus is frequently related to malignancies of the posterior fossa.
Impaired cerebrospinal fluid absorption causes communicative hydrocephalus. Post-inflammatory or post-hemorrhagic alterations are the most typical causes. One-third of such instances are caused by subarachnoid hemorrhage, which prevents cerebrospinal fluid absorption there at arachnoid granulations.
Meningitis, particularly bacterial meningitis, can make hydrocephalus worse. Head injury in the workplace is a major contributor to adult-onset hydrocephalus. Overproduction of cerebrospinal fluid causes hypersecretory hydrocephalus, which is most commonly caused by plexus papilloma or, in rare cases, cancer. Children are more likely to get these tumors.
NPH (Normal-pressure hydrocephalus) is a kind of communicative hydrocephalus that occurs more frequently in elderly people and has a pathophysiology that is not fully understood. It is caused by a change in cerebrospinal fluid dynamics with little or no rise in ICP (intracranial pressure).
Hydrocephalus can be caused by prenatal bleeding or inflammation. Some inherited kinds of hydrocephalus aren’t visible until later in life. A brainstem abnormality with stenosis of the cerebral aqueduct accounts for nearly 10% of all occurrences of hydrocephalus in infants.
Throughout this age category, Dandy-Walker deformity will be the source of two to four percent of hydrocephalus. Agenesis of the foramen of Monro, Bickers-Adams syndrome, and Arnold-Chiari type 1 and type 2 are all prevalent disorders in babies with hydrocephalus.
The prognosis is heavily influenced by the source of hydrocephalus. Patients with significant intraventricular hemorrhage may demand definitive therapy in half of the cases. Approximately twenty percent of children will need irreversible shunting following posterior fossa surgery.
There are a variety of parameters used to forecast the effectiveness of shunting in patients with NPH, some of which are debatable. If a gait impairment occurs before a mental disturbance, shunting has a greater than seventy-seven percent likelihood of improving the situation. The response to a single lumbar puncture or external lumbar drain is another criterion.
Improvement in symptoms following a single lumbar puncture with 40-50 ml of CSF drained or following the lumbar drainage is regarded as a good prognosis for shunt efficacy. Over a seventy-five percent chance of symptom relief with shunt installation if there is persistent ventricular action 48 to 72 hours following isotope cisternography.
https://www.ncbi.nlm.nih.gov/books/NBK560875/
medtigo
Hydrocephalus
Updated :
June 21, 2022
The symptomatic deposition of CSF inside the brain ventricles is known as hydrocephalus. This build-up could be caused by a blockage in the normal flow of CSF, issues with Pacchionian arachnoid granulations absorption further inside the venous system, or excessive cerebrospinal fluid production.
Around the early year 1913, Dandy suggested the classifications of communicative and obstructive (non-communicating) hydrocephalus, and ever since then, several other classifications have been developed. There are 4 forms of hydrocephalus in adults: communicative, obstructive, NPH (normal pressure hydrocephalus), and hypersecretory.
Hydrocephalus, whether developmental or congenital, is frequently present at birth and is frequently associated with a spinal dysraphism or genetic abnormality. The initial treatment option is surgical surgery with the insertion of a ventricular shunt.
In appropriate cases of hydrocephalus, choroid plexus cauterization and ETV (endoscopic third ventriculostomy) are viable treatments. Without timely treatment, acute hydrocephalus can lead to brain herniation and mortality. Hydrocephalus does have a fatality incidence of zero to three percent in children, based on the length of follow-up.
The most prevalent causes of hydrocephalus in children are congenital abnormalities and intraventricular bleeding among premature neonates. It reaches a new high later in life as a result of NPH instances. The high incidence of hydrocephalus is estimated to be around 85 per 100,000 people, with a notable disparity between age categories: 88 per 100,000 in children and 11 per 100,000 in adulthood.
Due to the high frequency of NPH later on in life, the prevalence in the senior individuals is substantially greater, about 175 per 100,000, and over 400 per 100,000 for those over eighty years old. Hydrocephalus is more common in South America and Africa. The prevalence of infantile hydrocephalus ranges from 1 to 32 per 10,000 babies. Both sexes are often impacted equally.
The choroid plexus, which is found in the lateral, 3rd, and 4th ventricles, is the main producer of cerebrospinal fluid. It passes via the ventricular circulation through the foramen of Monro from the lateral ventricle to the 3rd ventricle, and by the aqueduct of Sylvius or the cerebral aqueduct from the 3rd to the 4th ventricle.
It enters basal cisterns by two lateral foramina of Luschka and a median foramen of Magendie from the fourth ventricle, and a portion of it proceeds to circulate all around the spinal column and even in the central canal. Arachnoid granulations that develop across dural venous sinuses, particularly the superior sagittal sinus, are the primary sources of cerebrospinal fluid absorption.
Cerebrospinal fluid is drawn into the dural venal sinuses and circulated throughout the body. The daily output of cerebrospinal fluid is roughly 500 ml, with an average volume of 150 ml. This implies that every twenty hours, the whole cerebrospinal fluid volume is refilled three times.
According to the “bulk flow” paradigm, cerebrospinal fluid moves slowly from the point of generation to the point of absorption. Hydrocephalus can be caused by any functional or physical restriction within the subarachnoid space, venous sinuses, or ventricular system. Cerebrospinal fluid flow inside the ventricular system might be blocked by obstructive gliosis or lesion.
Cerebrospinal fluid absorption into the systemic circulation can be hampered by scarring of the subarachnoid space or inflammation, as well as high venous pressure within the venous sinuses. The overall amount of the skull, cerebrospinal fluid, plus blood inside the skull is static and per the Monro-Kellie doctrine.
If the capacity of one compartment increases without the volume of another decreasing, the pressure inside the brain will rise, as it does in hydrocephalus. Transependymal extravasation of cerebrospinal fluid into brain tissue occurs when ICP rises, producing brain parenchyma and stress-induced atrophy.
A blockage in CSF channels causes obstructed hydrocephalus. The foramina Monro, the foramen magnum, the aqueduct of Sylvius, and the fourth ventricle are the most common sites of obstruction. However, most lesions of sufficient size can impede cerebrospinal fluid routes at any point.
Ependymoma, choroid plexus papilloma, subependymal giant cell astrocytoma, pituitary adenoma, hypothalamic, craniopharyngioma, or hamartoma, optic nerve glioma, and disseminated cancers are among the most common tumors linked with hydrocephalus. Hydrocephalus is frequently related to malignancies of the posterior fossa.
Impaired cerebrospinal fluid absorption causes communicative hydrocephalus. Post-inflammatory or post-hemorrhagic alterations are the most typical causes. One-third of such instances are caused by subarachnoid hemorrhage, which prevents cerebrospinal fluid absorption there at arachnoid granulations.
Meningitis, particularly bacterial meningitis, can make hydrocephalus worse. Head injury in the workplace is a major contributor to adult-onset hydrocephalus. Overproduction of cerebrospinal fluid causes hypersecretory hydrocephalus, which is most commonly caused by plexus papilloma or, in rare cases, cancer. Children are more likely to get these tumors.
NPH (Normal-pressure hydrocephalus) is a kind of communicative hydrocephalus that occurs more frequently in elderly people and has a pathophysiology that is not fully understood. It is caused by a change in cerebrospinal fluid dynamics with little or no rise in ICP (intracranial pressure).
Hydrocephalus can be caused by prenatal bleeding or inflammation. Some inherited kinds of hydrocephalus aren’t visible until later in life. A brainstem abnormality with stenosis of the cerebral aqueduct accounts for nearly 10% of all occurrences of hydrocephalus in infants.
Throughout this age category, Dandy-Walker deformity will be the source of two to four percent of hydrocephalus. Agenesis of the foramen of Monro, Bickers-Adams syndrome, and Arnold-Chiari type 1 and type 2 are all prevalent disorders in babies with hydrocephalus.
The prognosis is heavily influenced by the source of hydrocephalus. Patients with significant intraventricular hemorrhage may demand definitive therapy in half of the cases. Approximately twenty percent of children will need irreversible shunting following posterior fossa surgery.
There are a variety of parameters used to forecast the effectiveness of shunting in patients with NPH, some of which are debatable. If a gait impairment occurs before a mental disturbance, shunting has a greater than seventy-seven percent likelihood of improving the situation. The response to a single lumbar puncture or external lumbar drain is another criterion.
Improvement in symptoms following a single lumbar puncture with 40-50 ml of CSF drained or following the lumbar drainage is regarded as a good prognosis for shunt efficacy. Over a seventy-five percent chance of symptom relief with shunt installation if there is persistent ventricular action 48 to 72 hours following isotope cisternography.
https://www.ncbi.nlm.nih.gov/books/NBK560875/
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