A 1994 community-based study indicated that two out of every 100,000 people suffered from SCSFLS, while a 2004 emergency room-based study indicated five per 100,000. SCSFLS generally affects the young and middle aged; the average age for onset is 42.3 years, but onset can range from ages 22 to 61. In an 11-year study women were found to be twice as likely to be affected as men.

Studies have shown that SCSFLS runs in families and it is suspected that genetic similarity in families includes weakness in the dura mater, which leads to SCSFLS. Large scale population-based studies have not yet been conducted. While a majority of SCSFLS cases continue to be undiagnosed or misdiagnosed, an actual increase in occurrence is unlikely.

Final outcomes for people with SCSFLS remain poorly studied. Symptoms may resolve in as little as two weeks, or persist for months. Less commonly, patients may suffer from unremitting symptoms for many years. People with chronic SCSFLS may be disabled and unable to work. Recurrent CSF leak at an alternate site after recent repair is common.

A cerebrospinal fluid leak (CSFL) is a medical condition where the cerebrospinal fluid(CSF) in the brain leaks out of the dura mater. This can be due to a spontaneous cerebrospinal fluid leak or result from different causes such as a lumbar puncture or physical trauma. While high CSF pressure can make lying down unbearable, low CSF pressure due to a leak can be relieved by lying flat on the back.

The most common symptoms of a CSFL is extremely high pressure in the head when sitting, standing, or bending down which can be lessened by laying down flat.

A myelogram can be used to help identify a CSFL by injecting a dye to further enhance the imaging allowing the location of the leak to be found. If it is a slow leak it may not appear on a single myelogram so more than one may be needed. Due to the ease of the procedure no anesthesia is used however a local anesthetic is given.

An epidural blood patch is the normal treatment for a CSFL, the patient's blood is drawn and it is then injected into the lumbar spine. Patients are told to lie flat without moving from 2 to 24 hours after the blood patch is done. A blood patch can be used to patch a CSFL in the cervical neck although it is rare for it to be done in that location, though it may take more than one blood patch to fully close the leak. Anesthesia is also uncommon for blood patch procedures. If you have a low pain tolerance it would be a good idea to have anesthesia for all of the procedures.

If the leak is strong or fast, the loss of CSF fluid can cause the brain to drop inside the skull due to the body's inability to replenish the CSF fluid at a quick enough pace, which would show up on a MRI of the brain. This is called a Chiari malformation where the brain is lower in the skull almost in the spinal canal.

According to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000 annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.

Although the group of people at risk for SAH is younger than the population usually affected by stroke, the risk still increases with age. Young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have a subarachnoid hemorrhage. The risk continues to rise with age and is 60 percent higher in the very elderly (over 85) than in those between 45 and 55. Risk of SAH is about 25 percent higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause, such as a decrease in estrogen levels.

Genetics may play a role in a person's disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid hemorrhage. However, lifestyle factors are more important in determining overall risk. These risk factors are smoking, hypertension (high blood pressure), and excessive alcohol consumption. Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked. Some protection of uncertain significance is conferred by caucasian ethnicity, hormone replacement therapy, and diabetes mellitus. There is likely an inverse relationship between total serum cholesterol and the risk of non-traumatic SAH, though confirmation of this association is hindered by a lack of studies. Approximately 4 percent of aneurysmal bleeds occur after sexual intercourse and 10 percent of people with SAH are bending over or lifting heavy objects at the onset of their symptoms.

Overall, about 1 percent of all people have one or more cerebral aneurysms. Most of these, however, are small and unlikely to rupture.

Prognosis is also very poor when IVH results from intracerebral hemorrhage related to high blood pressure and is even worse when hydrocephalus follows. It can result in dangerous increases in ICP and can cause potentially fatal brain herniation. Even independently, IVH can cause morbidity and mortality. First, intraventricular blood can lead to a clot in the CSF conduits blocking its flow and leading to obstructive hydrocephalus which may quickly result in increased intracranial pressure and death. Second, the breakdown products from the blood clot may generate an inflammatory response that damages the arachnoid granulations, inhibiting the regular reabsorption of CSF and resulting in permanent communicating hydrocephalus.

Factors increasing the risk of a subdural hematoma include very young or very old age. As the brain shrinks with age, the subdural space enlarges and the veins that traverse the space must travel over a wider distance, making them more vulnerable to tears. This and the fact that the elderly have more brittle veins make chronic subdural bleeds more common in older patients. Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults. For this reason, subdural hematoma is a common finding in shaken baby syndrome. In juveniles, an arachnoid cyst is a risk factor for a subdural hematoma.

Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, dementia, and the presence of a cerebrospinal fluid leak.

SAH is often associated with a poor outcome. The death rate (mortality) for SAH is between 40 and 50 percent, but trends for survival are improving. Of those that survive hospitalization, more than a quarter have significant restrictions in their lifestyle, and less than a fifth have no residual symptoms whatsoever. Delay in diagnosis of minor SAH (mistaking the sudden headache for migraine) contributes to poor outcome. Factors found on admission that are associated with poorer outcome include poorer neurological grade; systolic hypertension; a previous diagnosis of heart attack or SAH; liver disease; more blood and larger aneurysm on the initial CT scan; location of an aneurysm in the posterior circulation; and higher age. Factors that carry a worse prognosis during the hospital stay include occurrence of delayed ischemia resulting from vasospasm, development of intracerebral hematoma, or intraventricular hemorrhage (bleeding into the ventricles of the brain) and presence of fever on the eighth day of admission.

So-called "angiogram-negative subarachnoid hemorrhage", SAH that does not show an aneurysm with four-vessel angiography, carries a better prognosis than SAH with aneurysm; however, it is still associated with a risk of ischemia, rebleeding, and hydrocephalus. Perimesencephalic SAH (bleeding around the mesencephalon in the brain), however, has a very low rate of rebleeding or delayed ischemia, and the prognosis of this subtype is excellent.

The prognosis of head trauma is thought to be influenced in part by the location and amount of subarachnoid bleeding. It is difficult to isolate the effects of SAH from those of other aspects of traumatic brain injury; it is unknown whether the presence of subarachnoid blood actually worsens the prognosis or whether it is merely a sign that a significant trauma has occurred. People with moderate and severe traumatic brain injury who have SAH when admitted to a hospital have as much as twice the risk of dying as those who do not. They also have a higher risk of severe disability and persistent vegetative state, and traumatic SAH has been correlated with other markers of poor outcome such as post traumatic epilepsy, hydrocephalus, and longer stays in the intensive care unit. However, more than 90 percent of people with traumatic subarachnoid bleeding and a Glasgow Coma Score over 12 have a good outcome.

There is also modest evidence that genetic factors influence the prognosis in SAH. For example, having two copies of ApoE4 (a variant of the gene encoding apolipoprotein E that also plays a role in Alzheimer's disease) seems to increase risk for delayed ischemia and a worse outcome. The occurrence of hyperglycemia (high blood sugars) after an episode of SAH confers a higher risk of poor outcome.

Brain contusions and subarachnoid hemorrhages are commonly associated with IVH. The bleeding can involve the anterior communicating artery or the posterior communicating artery.

In both adults and infants, IVH can cause dangerous increases in ICP, damage to the brain tissue, and hydrocephalus.

Most subdural hygromas are small and clinically insignificant. Larger hygromas may cause secondary localized mass effects on the adjacent brain parenchyma, enough to cause a neurologic deficit or other symptoms. Acute subdural hygromas can be a potential neurosurgical emergency, requiring decompression. Acute hygromas are typically a result of head trauma—they are a relatively common posttraumatic lesion—but can also develop following neurosurgical procedures, and have also been associated with a variety of conditions, including dehydration in the elderly, lymphoma and connective tissue diseases.

Subdural hematomas are most often caused by head injury, when rapidly changing velocities within the skull may stretch and tear small bridging veins. Subdural hematomas due to head injury are described as traumatic. Much more common than epidural hemorrhages, subdural hemorrhages generally result from shearing injuries due to various rotational or linear forces. Subdural hemorrhage is a classic finding in shaken baby syndrome, in which similar shearing forces classically cause intra- and pre-retinal hemorrhages. Subdural hematoma is also commonly seen in the elderly and in alcoholics, who have evidence of cerebral atrophy. Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear. It is also more common in patients on anticoagulants or antiplatelet drugs, such as warfarin and aspirin. Patients on these medications can have a subdural hematoma after a relatively minor traumatic event.

A further cause can be a reduction in cerebral spinal fluid pressure which can create a low pressure in the subarachnoid space, pulling the arachnoid away from the dura mater and leading to a rupture of the blood vessels.

A subdural hygroma is a collection of cerebrospinal fluid (CSF), without blood, located under the dural membrane. Most hygromas are believed to be derived from chronic subdural hematomas. They are commonly seen in elderly patients after minor trauma but can also be seen in children after an infection. One of the common causes of subdural hygroma is a sudden decrease in pressure as a result of placing a ventricular shunt. This can lead to leakage of CSF into the subdural space especially in cases with moderate to severe brain atrophy. In these cases the symptoms such as mild fever, headache, drowsiness and confusion can be seen, which are relieved by draining this subdural fluid.

A pseudomeningocele is an abnormal collection of cerebrospinal fluid (CSF) that communicates with the CSF space around the brain or spinal cord. In contrast to a meningocele, in which the fluid is surrounded and confined by dura mater, in a pseudomeningocele, the fluid has no surrounding membrane, but is contained in a cavity within the soft tissues.

Pseudomeningocele may result after brain surgery, spine surgery, or brachial plexus avulsion injury.

Treatment for pseudomeningocele is conservative or may involve neurosurgical repair.

Cerebrospinal fluid, which fills the subarachnoid space between the arachnoid membrane and the pia mater surrounding the brain, is normally clear and colorless. When there has been bleeding into the subarachnoid space, the initial appearance of the cerebrospinal fluid can range from barely tinged with blood to frankly bloody, depending on the extent of bleeding. Within several hours, the red blood cells in the cerebrospinal fluid are destroyed, releasing their oxygen-carrying molecule heme, which is then metabolized by enzymes to bilirubin, a yellow pigment. The most common cause for bleeding into the subarachnoid space is a subarachnoid hemorrhage from a ruptured cerebral aneurysm.

The most frequently employed initial test for subarachnoid hemorrhage is a computed tomography scan of the head, but it detects only 98% of cases in the first 12 hours after the onset of symptoms, and becomes less useful afterwards. Therefore, a lumbar puncture ("spinal tap") is recommended to obtain cerebrospinal fluid if someone has symptoms of a subarachnoid hemorrhage (e.g., a thunderclap headache, vomiting, dizziness, new-onset seizures, confusion, a decreased level of consciousness or coma, neck stiffness or other signs of meningismus, and signs of sudden elevated intracranial pressure), but no blood is visible on the CT scan. According to one article, a spinal tap is not necessary if no blood is seen on a CT scan done using a third generation scanner within six hours of the onset of the symptoms. However, this is not standard of care.

Heme from red blood cells that are in the cerebrospinal fluid because a blood vessel was nicked during the lumbar puncture (a "traumatic tap") has no time to be metabolized, and therefore no bilirubin is present.

After the cerebrospinal fluid is obtained, a variety of its parameters can be checked, including the presence of xanthochromia. If the cerebrospinal fluid is bloody, it is centrifuged to determine its color.

Many laboratories rely on only the color of the cerebrospinal fluid to determine the presence or absence of xanthochromia. However, recent guidelines suggest that spectrophotometry should be performed. Spectrophotometry relies on the different transmittance, or conversely, absorbance, of light by different substances or materials, including solutes. Bilirubin absorbs light at wavelengths between 450–460 nm. Spectrophotometry can also detect the presence of oxyhemoglobin and methemoglobin, which absorb light at 410-418 nm and 403-410 nm, respectively, and also may indicate that bleeding has occurred; to identify substances in cerebrospinal fluid that absorb light at other wavelengths but are not due to bleeding, such as carotenoids; and to detect very small amounts of yellow color saturation (about 0.62%) which may be missed by visual inspection, especially when the cerebrospinal fluid has been examined under incandescent lighting or a tungsten desk lamp (corresponding to International Commission on Illumination standard illuminant A).

Visual inspection is the most frequent method used in the United States to assess cerebrospinal fluid for xanthochromia, while spectrophotometry is used on up to 94% of specimens in the United Kingdom. There is still disagreement about whether or not to routinely use spectrophotometry or whether visual inspection is adequate, and one group of authors has even advocated measuring bilirubin levels.

CSF rhinorrhoea refers to the drainage of cerebrospinal fluid through the nose. Measures of CSF components such as glucose have been used in the past, but are neither sensitive nor specific; beta-2 transferrin, however, has been shown to have a high positive predictive value. It has also been noted to be characterized by unilateral discharge.

It is a sign of basal skull fracture. Management includes watchful waiting - leaks often stop spontaneously; if this does not occur then neurosurgical closure is necessary to prevent the spread of infection to the meninges.

Other signs of basal skull fracture includes CSF otorrhoea (drainage of CSF through the ear). It can have devastating complications in some patients, as the communication between the nasal cavity and the cerebrospinal fluid and CNS can result in bacterial infections of the CNS that can have catastrophic effects on the patient.

CSF rhinorrhoea can also be a symptom of a pituitary adenoma.

Spontaneous CSF rhinorrhea. The most common congenital or acquired defect in the skull base bones (anterior cranial fossa) at the spontaneous nasal liquorrhea localized in following formation:

- sphenoid sinus (43%)

- ethmoid bone (29%)

- cribriform plate (29%)

Traumatic pneumorrhachis is a medical condition in which air has entered the spinal canal.

Traumatic pneumorrhachis is very rare phenomenon. Only eight cases with pneumorrhachis extending to more than one spinal region had been reported in the literature. Gordon had initially described the phenomenon of intraspinal air. The term "pneumorrhachis" was used for the first time by Newbold et al. The two subtypes of pneumorrhachis, which includes epidural or subarachnoid, are difficult to distinguish even with CT scanning. However, the presence of pneumocephalus goes more in favor of subarachnoid subtype. Goh and Yeo in their study have reported that the epidural pneumorrhachis is self-limited, whereas the more common subarachnoid pneumorrhachis type may be complicated by tension pneumocephalus and meningitis. Traumatic subarachnoid pneumorrhachis is almost always secondary to major trauma and is a marker of a severe injury. The pathophysiology described for it states that the penetrated air, which had led to the formation of pneumocephalus might have been forced caudally due to the raised intracranial pressure as a consequence of severe brain injury and patient's horizontal position allowing the entrapped air to pass through the foramen magnum into the spinal canal. Due to its rareness, asymptomatic presentation and myriad etiologies, no guidelines for its treatment or care has been described. Pneumorrhachis typically resolves spontaneously but occasionally it can have serious complications. Patient with subarachnoid pneumorrhachis should be treated meticulously and a temporary lumbar drainage may be required if they have concomitant cerebro-spinal fluid leak.

Froin's syndrome – coexistence of xanthochromia, high protein level and marked coagulation of cerebrospinal fluid (CSF). It is caused by meningeal irritation (e.g. during spinal meningitis) and CSF flow blockage by tumour mass or abscess. Stagnation of the CSF within the thecal sac facilitates exudation from the tumour itself and activation of coagulation factors. A clinical test formerly used for evaluation of spinal stenosis is Queckenstedt's maneuver. Nowadays, a magnetic resonance imaging is used for identification of CSF flow obstruction. It often shows the prolongation of T1 and T2 signal in CSF caudal to a level of block. This phenomenon is named after Georges Froin (1874–1932), a French physician who first described it.

Arachnoid cysts are seen in up to 1.1% of the population with a gender distribution of 2:1 male:female Only 20% of these have symptoms, usually from secondary hydrocephalus.

A study that looked at 2,536 healthy young males found a prevalence of 1.7% (95% CI 1.2 to 2.3%). Only a small percentage of the detected abnormalities require urgent medical attention.

Subdural effusion refers to an effusion in the subdural space, usually of cerebrospinal fluid.

It is sometimes treated with surgery.

The exact cause of arachnoid cysts is not known. Researchers believe that most cases of arachnoid cysts are developmental malformations that arise from the unexplained splitting or tearing of the arachnoid membrane.

In some cases, arachnoid cysts occurring in the middle fossa are accompanied by underdevelopment (hypoplasia) or compression of the temporal lobe. The exact role that temporal lobe abnormalities play in the development of middle fossa arachnoid cysts is unknown.

There are some cases where hereditary disorders have been connected with arachnoid cysts.

Some complications of arachnoid cysts can occur when a cyst is damaged because of minor head trauma. Trauma can cause the fluid within a cyst to leak into other areas (e.g., subarachnoid space). Blood vessels on the surface of a cyst may tear and bleed into the cyst (intracystic hemorrhage), increasing its size. If a blood vessel bleeds on the outside of a cyst, a collection of blood (hematoma) may result. In the cases of intracystic hemorrhage and hematoma, the individual may have symptoms of increased pressure within the cranium and signs of compression of nearby nerve (neural) tissue.

Some scientists debate whether arachnoid cysts are a true congenite condition or if this should be separated from secondary cysts. A recent study shows differences in communication between the arachnoid cyst and the subarachnoid space by CT cisternography

. A comparison of arachnoid cyst fluid and CSF in a series of patients show differences in chemical composition.

Arachnoid cysts can also occur secondary to other disorders such as Marfan syndrome, arachnoiditis, or agenesis of the corpus callosum.

The incidence of RCVS is unknown, but it is believed to be "not uncommon", and likely under-diagnosed. One small, possibly biased study found that the condition was eventually diagnosed in 45% of outpatients with sudden headache, and 46% of outpatients with thunderclap headache.

The average age of onset is 42, but RCVS has been observed in patients aged from 19 months to 70 years. Children are rarely affected. It is more common in females, with a female-to-male ratio of 2.4:1.

Genetic counseling is often recommended to provide more information about fetal CPCs, to answer questions and concerns, and to outline available options such as amniocentesis or a blood test from the mother. There is a possible association between ultrasound-detected fetal CPCs and Trisomy 18. It is not correlated to the presence of Trisomy 21 (Down syndrome).

Generally the risks are very low if there are no other risk factors. If no additional abnormalities are detected by a thorough "level II" ultrasound, the likelihood the fetus has trisomy 18 is very low.

A meta-analysis of 8 studies between 1990 and 2000 with choroid plexus cysts that were identified in second-trimester (an incidence of 1.2%). The incidence of the cysts in women younger than 35 was 1% (n=1017). The study found no cases of trisomy 18 in fetuses with cysts whose mother was younger than 35. The study concluded that "there is no evidence that detection of isolated choroid plexus cyst in women who are <35 years of age increases the risk of trisomy 18".

Other factors which may have a bearing on the baby's chances of developing chromosome problems include:

- mother's age at the expected date of delivery

- the results of serum screening; XAFP triple testing or quad screening

- evidence of other "fetal findings" seen at the time of the ultrasound that may suggest a chromosome problem

When Tarlov cysts are ruptured or drained they cause leakage of cerebrospinal fluid (CSF). Ruptures of Tarlov cysts have been reported associated with communicating aneurysms and from fracture in the proximity of the cysts. An undetected rupture can cause intracranial hypotension, including orthostatic neurological symptoms along with headache, nausea, and vomiting that improve when supine. The ruptured cysts can be patched either with a biosynthetic dural patch or using a blood patch to stem the flow of CSF.

Because of the unclear pathogenesis and pathophysiology of Tarlov cysts, there is no consensus on the optimal treatment of symptomatic sacral perineural cysts. Patients often choose to pursue treatment when the progression of neurological deficits seriously impacts their quality of life.

Since cysts are innervated, microfenestration and surgical sleeving of the cysts to diminish the amount of accumulated cerebrospinal fluid and decrease compression of the spine and spinal nerves has been successful in a number of patients. The cysts are carefully separated enough from surrounding tissue to be wrapped with fatty tissue or pericardial biomaterial to excise the fluid from the cyst. If the cyst does not drain spontaneously, then it is drained and patched using a biosynthetic dural patch.

The use of this technique is done in the U.S. and is spreading in Europe but recovery is generally extensive. Microfenestration alone has been done with some success in Asia.

A biopolymer plate is also being used experimentally to strengthen a sacrum thinned by cystic erosion by Dr. Frank Feigenbaum.

The risks of CSF leakage are higher on patients that have bilateral cysts on the same spinal level or clusters of cysts along multiple vertebrae, but immediate recognition of the leakage and repair can mitigate that risk.

Various treatment methods have been tried in the past, including the extraction of cerebrospinal fluids from the cyst, fibrin glue injection and the complete or partial removal of cyst. Epidurals can provide temporary relief but are not generally recommended as they can cause cysts to enlarge. Extraction of fluid can provide limited or no relief depending on rate the cysts refill and the need to repeat the procedure. Removal of the cyst results in irreversible damage to the intersecting spinal nerve.

Although fibrin-glue therapy initially had been thought to be a promising therapy in the treatment of these cysts, there have been multiple problems associated with the fibrin glue therapy including seepage of fibrin. It is no longer recommended for use at present by the Health Department in some countries and neurosurgeons previously performing the procedures.

Nevertheless, all types of surgical treatment pose common risks, including neurological deficits, infection and inflammation, spinal headache, urinary disturbances, and leakage of cerebrospinal fluids.

Here is an article for treatment of meningeal diverticulum. Feigenbaum F1, Henderson FC. Giant sacral meningeal diverticula: surgical implications of the "thecal tip" sign. Report of two cases. J Neurosurg Spine. 2006 Nov;5(5):443-6.

The direct cause of the symptoms is believed to be either constriction or dilation of blood vessels in the brain. The pathogenesis is not known definitively, and the condition is likely to result from multiple different disease processes.

Up to two-thirds of RCVS cases are associated with an underlying condition or exposure, particularly vasoactive or recreational drug use, complications of pregnancy (eclampsia and pre-eclampsia), and the adjustment period following childbirth called "puerperium". Vasoactive drug use is found in about 50% of cases. Implicated drugs include selective serotonin reuptake inhibitors, weight-loss pills such as Hydroxycut, alpha-sympathomimetic decongestants, acute migraine medications, pseudoephedrine, epinephrine, cocaine, and cannabis, among many others. It sometimes follows blood transfusions, certain surgical procedures, swimming, bathing, high altitude experiences, sexual activity, exercise, or coughing. Symptoms can take days or a few months to manifest after a trigger.

Following a study and publication in 2007, it is also thought SSRIs, uncontrolled hypertension, endocrine abnormality, and neurosurgical trauma are indicated to potentially cause vasospasm.