subarachnoid hemorrhage

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Subarachnoid Hemorrhage



A subarachnoid hemorrhage is an abnormal and very dangerous condition in which blood collects beneath the arachnoid mater, a membrane that covers the brain. This area, called the subarachnoid space, normally contains cerebrospinal fluid. The accumulation of blood in the subarachnoid space can lead to stroke, seizures, and other complications. Additionally, subarachnoid hemorrhages may cause permanent brain damage and a number of harmful biochemical events in the brain. A subarachnoid hemorrhage and the related problems are frequently fatal.


Subarachnoid hemorrhages are classified into two general categories: traumatic and spontaneous. Traumatic refers to brain injury that might be sustained in an accident or a fall. Spontaneous subarachnoid hemorrhages occur with little or no warning and are frequently caused by ruptured aneurysms or blood vessel abnormalities in the brain.
Traumatic brain injury is a critical problem in the United States. According to annual figures compiled by the Brain Injury Association, approximately 373,000 people are hospitalized, more than 56,000 people die, and 99,000 survive with permanent disabilities due to traumatic brain injuries. The leading causes of injury are bicycle, motorcycle, and automobile accidents, with a significant minority due to accidental falls, and sports and recreation mishaps.
Exact statistics are not available on traumatic subarachnoid hemorrhages, but several large clinical studies have found an incidence of 23-39% in relation to severe head injury. Furthermore, subarachnoid hemorrhages have been described in the medical literature as the most common brain injury found during autopsy investigations of head trauma.
Spontaneous subarachnoid hemorrhages are often due to an aneurysm (a bulge or sac-like projection from a blood vessel) which bursts. Arteriovenous malformations (AVMs), which are abnormal interfaces between arteries and veins, may also rupture and release blood into the subarachnoid space. Both aneurysms and AVMs are associated with weak spots in the walls of blood vessels and account for approximately 60% of all spontaneous subarachnoid hemorrhages. The rest may be attributed to other causes, such as cancer or infection, or are of unknown origin.
In industrialized countries, it is estimated that there are 6.5-26.4 cases of spontaneous subarachnoid hemorrhage per 100,000 people annually. Certain factors raise the risk of suffering a hemorrhage. Aneurysms are acquired over a person's lifetime and are rarely a factor in subarachnoid hemorrhage before age 20. Conversely, AVMs are present at birth. In some cases, there may be a genetic predisposition for aneurysms or AVMs. Other factors that have been implicated, but not definitively linked to spontaneous subarachnoid hemorrhages, include atherosclerosis, cigarette use, extreme alcohol consumption, and the use of illegal drugs, such as cocaine. The exact role of high blood pressure is somewhat unclear, but since it does seem linked to the formation of aneurysms, it may be considered an indirect risk factor.
The immediate danger due to subarachnoid hemorrhage, whether traumatic or spontaneous, is ischemia. Ischemia refers to tissue damage caused by restricted or blocked blood flow. The areas of the brain that do not receive adequate blood and oxygen can suffer irreparable injury, leading to permanent brain damage or death. An individual who survives the initial hemorrhage is susceptible to a number of complications in the following hours, days, and weeks.
The most common complications are intracranial hypertension, vasospasm, and hydrocephalus. Intracranial hypertension, or high pressure within the brain, can lead to further bleeding from damaged blood vessels; a complication associated with a 70% fatality rate. Vasospasm, or blood vessel constriction, is a principal cause of secondary ischemia. The blood vessels in the brain constrict in reaction to chemicals released by blood breaking down within the subarachnoid space. As the blood vessels become narrower, blood flow in the brain becomes increasingly restricted. Approximately one third of spontaneous subarachnoid hemorrhages and 30-60% of traumatic bleeds are followed by vasospasm. Hydrocephalus, an accumulation of fluid in the chambers of the brain (ventricles) due to restricted circulation of cerebrospinal fluid, follows approximately 15% of subarachnoid hemorrhages. Because cerebrospinal fluid cannot drain properly, pressure accumulates on the brain, possibly prompting further ischemic complications.

Causes and symptoms

Whether through trauma or disease, subarachnoid hemorrhages are caused by blood being released by a damaged blood vessel and accumulating in the subarachnoid space. Symptoms associated with traumatic subarachnoid hemorrhage may or may not resemble those associated with spontaneous hemorrhage, as trauma can involve multiple injuries with overlapping symptoms.
Typically, a spontaneous subarachnoid hemorrhage is indicated by a sudden, severe headache. Nausea, vomiting, and dizziness frequently accompany the pain. Loss of consciousness occurs in about half the cases of spontaneous hemorrhage. A coma, usually brief, may occur. A stiff neck, fever, and aversion to light may appear following the hemorrhage. Neurologic symptoms may include partial paralysis, loss of vision, seizures, and speech difficulties.
Spontaneous subarachnoid hemorrhages may be preceded by warning signs prior to the initial bleed. Sentinel, or warning, headaches may be present in the days or weeks before an aneurysm or AVM ruptures. These headaches can be accompanied by dizziness, nausea, and vomiting, and possibly neurologic symptoms. Approximately 50% of AVMs are discovered before they bleed significantly; however, most aneurysms are not diagnosed before they rupture.


To make a diagnosis, a health-care provider takes a detailed history of the symptoms and does a physical examination. The symptoms may mimic other disorders and diagnosis can be complicated, especially if the individual is unconscious. The sudden, severe headache can fuel suspicion of a subarachnoid hemorrhage or similar event, and a computed tomography scan (CT scan) or magnetic resonance imaging (MRI) scan is considered essential to a quick diagnosis. The MRI is less sensitive than the CT in detecting acute subarachnoid bleeding, but more sensitive in diagnosing AVM or aneurysm.
A CT scan reveals blood that has escaped into the subarachnoid space. For the best results, the scan should be done within 12 hours of the hemorrhage. If this is not possible, lumbar puncture and examination of the cerebrospinal fluid is advised. Lumbar puncture is also done in cases in which the CT scan doesn't reveal a hemorrhage, but there is a high suspicion that one has occurred. In subarachnoid hemorrhage, cerebrospinal fluid shows red blood cells and/or xanthochromia, a yellowish tinge caused by blood breakdown products. Xanthochromia first appears six to 12 hours after subarachnoid hemorrhage, making it advisable to delay lumbar puncture until at least 12 hours after the onset of symptoms for a more definite diagnosis.
Once a hemorrhage, AVM, or aneurysm has been diagnosed, further tests are done to pinpoint the damage. The CT scan may be useful in giving the general location, but cerebral angiography maps out the exact details. This procedure involves injecting a special dye into the blood stream. This dye makes blood vessels visible in x rays of the area.


The initial course of treatment focuses on stabilizing the hemorrhage victim. Depending on the individual's condition, this may involve intubation and mechanical ventilation, supplemental oxygen, intravenous fluids, and close monitoring of vital signs. If the person suffers seizures, an anticonvulsant, such as phenytoin (Dilantin), is administered. Nimodipine, a calcium channel blocker, may be given to prevent vasospasm and its complications. Sedatives and medications for pain, nausea, and vomiting are administered as needed.
Once the individual is stabilized, cerebral angiography is done to locate the damaged blood vessel. This information and the individual's condition are considered before attempting surgical treatment. Surgery is necessary to remove the damaged area of the blood vessel and prevent a second hemorrhage. The specific neurosurgical procedures depend on the location and type of blood vessel damage. Typically, clip ligation is the preferred means of treating an aneurysm, and surgical excision, radiosurgery, or endovascular embolization are used to manage an AVM.


Individuals who are conscious and demonstrate few neurologic symptoms when they reach medical help have the best prognosis. However, the overall prospects for subarachnoid hemorrhage patients are generally not good. Of the individuals who suffer an aneurysmal hemorrhage, approximately 15% do not live long enough to get medical treatment. Another 20-40% will not survive the complications caused by the hemorrhage, and approximately 12% of the survivors will experience permanent neurologic disability. Neurologic disabilities may include partial paralysis, weakened or numbed areas of the body, cognitive or speech difficulties, and vision problems. Individuals whose subarachnoid hemorrhages occur as a result of AVMs have a slightly better prognosis, although the risk of death is approximately 10-15% for each hemorrhage.
Subarachnoid hemorrhage associated with traumatic brain injury has a poor prognosis. In clinical studies, 46-78% of head injury cases involving subarachnoid hemorrhage resulted in severe disability, vegetative survival, or death. Furthermore, it is possible that traumatic subarachnoid hemorrhages are accompanied by additional injuries, which would further diminish survival and recovery rates.


Traumatic brain injury is the leading cause of subarachnoid hemorrhages, so it follows that efforts to prevent head injury would prevent these hemorrhages. Since accidents cannot always be prevented, measures to minimize potential damage are always advisable. Use of activity-appropriate protective gear, such as bicycle helmets, motorcycle helmets, and sports head gear, is strongly encouraged and promoted by medical associations, consumer organizations, advocacy groups, and health-care professionals. These same groups also advise using seat belts in automobiles.
Spontaneous subarachnoid hemorrhages are more difficult to prevent. Since there may be a genetic component to aneurysms and AVMs, close relatives to individuals with these conditions may consider being screened to assess their own status. Quitting smoking and keeping blood pressure within normal limits may also reduce the risk of suffering a spontaneous subarachnoid hemorrhage.

Key terms

Aneurysm — A weak point in a blood vessel where the pressure of the blood causes the vessel wall to bulge outwards. An aneurysm may also appear as a sac-like projection from the blood vessel wall.
Arachnoid mater — One of three membranes that encase the brain and spinal cord. The arachnoid mater is the middle membrane.
Arteriovenous malformation — An abnormal tangle of arteries and veins in which the arteries feed directly into the veins without a normal intervening capillary bed.
Atherosclerosis — An abnormal condition in which lipids, or fats, form deposits on the inside walls of blood vessels.
Cerebral angiography — A medical test in which an x-ray visible dye is injected into blood vessels to allow them to be imaged on an x ray.
Cerebrospinal fluid — The clear, normally colorless fluid found within the subarachnoid space.
Computerized tomography (CT) scan — Cross-sectional x rays of the body compiled to create a three-dimensional image of the body's internal structures.
Hemorrhage — The escape of blood from blood vessels.
Hydrocephalus — Englargement of the chambers in the brain (ventricles) caused by an accumulation of cerebrospinal fluid.
Intracranial hypertension — Abnormally high pressure within the brain.
Ischemia — A condition in which blood flow is cut off or restricted from a particular area. The tissue becomes starved of oxygen and nutrients, resulting in tissue death.
Ischemic — Referring to ischemia.
Lumbar puncture — A diagnostic procedure in which a needle is inserted into the lower spine to withdraw a small amount of cerebrospinal fluid. This fluid is examined to assess trauma to the brain.
Subarachnoid — Referring to the space underneath the arachnoid mater.
Vasospasm — The constriction or narrowing of blood vessels. In cases of hemorrhage, the constriction is prompted by chemical signals from the escaped blood as it breaks down.



Brain Injury Association of America. 105 North Alfred St., Alexandria, VA 22314. (800) 444-6443.
National Stroke Association. 9707 E. Easter Lane, Englewood, Co. 80112. (800) 787-6537.

sub·a·rach·noid hem·or·rhage

extravasation of blood into the subarachnoid space, often due to aneurysm rupture and usually spreading throughout the cerebrospinal fluid pathways.

subarachnoid hemorrhage (SaH, SAH)

an intracranial hemorrhage into the cerebrospinal fluid-filled space between the arachnoid and pial membranes on the surface of the brain. The hemorrhage may extend into the brain if the force of the bleeding from the broken vessel is sudden and severe. The cause may be trauma, rupture of an aneurysm, or an arteriovenous anomaly.
observations The first symptom of a subarachnoid hemorrhage is a sudden, extremely severe headache that begins in one localized area and then spreads, becoming dull and throbbing. It is frequently described by patients as "the worst headache of my life." The localized pain results from vascular distortion and injury. The generalized ache is the result of meningeal irritation by blood in the subarachnoid space. Other characteristics of subarachnoid hemorrhage can include dizziness, rigidity of the neck, pupillary inequality, vomiting, seizures, drowsiness, sweating and chills, stupor, and loss of consciousness. A brief period of unconsciousness immediately after the rupture is common; severe hemorrhage may result in continued unconsciousness, coma, and death. Delirium and confusion often persist through the first weeks of recovery, and permanent brain damage is common.

subarachnoid hemorrhage

Neurology A severe intracerebral hemorrhage in the subarachnoid space, often due to a ruptured intracranial aneurysm Clinical Abrupt severe headache, loss of consciousness, vomiting Etiology Ruptured cerebral aneurysm, AV malformation, idiopathic Risk factors Aneurysms, polycystic kidney disease; fibromuscular dysplasia, HTN Management Ventilation, oxgenation, fluid, tissue dehydration–eg, mannitol; surgical evacuation; bed rest, sedation, analgesia, anti-seizures. See Warning leak. Cf Intracerebral hemorrhage.

sub·a·rach·noid hem·or·rhage

(sŭb'ă-rak'noyd hem'ŏr-ăj)
Bleeding between the middle membrane covering of the brain and the brain itself; 5-10% of strokes are caused by subarachnoid hemorrhage. Most common in people 20-60 years old; female predilection.
Synonym(s): subarachnoid bleed, subarachnoid haemorrhage.

Subarachnoid Hemorrhage

DRG Category:26
Mean LOS:6.8 days
Description:SURGICAL: Craniotomy and Endovascular Intracranial Procedures With CC
DRG Category:70
Mean LOS:6.8 days
Description:MEDICAL: Nonspecific Cerebrovascular Disorders With Major CC

Subarachnoid hemorrhage (SAH) is the direct hemorrhage of arterial blood into the subarachnoid space. Immediately after rupture, intracranial pressure (ICP) rises, resulting in a fall in cerebral perfusion pressure (CPP  =  mean arterial pressure  −  ICP). The expanding hematoma acts as a space-occupying lesion as it compresses or displaces brain tissue. Blood in the subarachnoid space may impede the flow and reabsorption of cerebrospinal fluid (CSF), resulting in hydrocephalus. The bleeding ceases with the formation of a fibrin-platelet plug at the point of the rupture and by tissue compression. As the clot, which forms initially to seal the rupture site, undergoes normal lysis or dissolution, the risk of rebleeding increases. More than 30,000 people in the United States have a ruptured intracranial aneurysm each year, although the annual incidence is probably underestimated because death is attributed to other reasons.

Cerebral vasospasm, or narrowing of the vessel lumen, is another common complication of SAH; it occurs in 35% to 49% of individuals. The pathophysiology of vasospasms is not clearly understood, but it is believed that they are precipitated by certain vasoactive substances (e.g., prostaglandins, serotonin, and catecholamines), which are released by the blood into the subarachnoid space. When vasospasm develops, it may last for several days or even several weeks. By decreasing cerebral blood flow, a vasospasm produces further neurological deterioration, cerebral ischemia, and cerebral infarction.


SAH typically results from cerebral aneurysm rupture (70%), which occurs when the blood vessel wall becomes so thin that it can no longer withstand the surrounding arterial pressure. Because aneurysm-forming vessels usually lie in the space between the arachnoid and the brain, hemorrhage from an aneurysm usually occurs in the subarachnoid space. Another less common cause of SAH is arteriovenous malformation.

Genetic considerations

SAH appears to cluster in families independent of environmental factors, as does the propensity to have vasospasm following surgery. One case study of 1,150 SAH patients reported a 10% incidence of familial SAH among all cases. Risk-associated regions have been mapped to 7q11 and 5q31, although no gene has been definitively identified. Patients with the APOE-e4 allele have demonstrated poorer outcomes after aneurysmal SAH than those with other variants of this gene even though an association between APOE and incidence of SAH has not been well documented. The autosomal dominantly transmitted disorder, polycystic kidney disease (ADPKD), has also been associated with an increased incidence of SAH.

Gender, ethnic/racial, and life span considerations

The peak incidence of aneurysm rupture is between ages 40 and 65. Under age 40, SAH occurs more commonly in men, but after age 50, it is more common in women. Few aneurysms rupture in persons younger than 20. Pregnancy creates a significant risk of SAH, which is higher in the third trimester of pregnancy and a leading cause of maternal mortality. The peak incidence of SAH from arteriovenous malformation is between ages 30 and 40. In the United States, people with African American ancestry have a greater risk for SAH than people with white/European ancestry.

Global health considerations

SAH occurs around the world, with reported rates varying widely between 5 to 30 cases per 100,000 individuals. The Middle East, China, and India have low reported rates, which may partly be due to the low rates of cardiovascular disease for people living in these regions.



Ask if the patient has had a sudden brief loss of consciousness followed by a severe headache; this sign has been reported by 45% of patients who survive SAH. Many also report a severe headache associated with exertion but no loss of consciousness. Establish any recent history of vomiting, stiff neck, photophobia, seizure, or partial paralysis. Establish any history of cerebral aneurysms.

Physical examination

The most common symptoms are neck pain, neck stiffness, loss of consciousness, severe headache, and limited neck flexion. Observe the patient for signs and symptoms of cranial nerve deficits, especially cranial nerves III, IV, and VI. Meningeal irritation may lead to nausea, vomiting, stiff neck, pain in the neck and back, and possible blurred vision or photophobia. Examine for symptoms of stroke syndrome, such as hemiparesis, hemiplegia, aphasia, and cognitive deficits. Cerebral edema, increased ICP, and seizures may also occur. Assess the vital signs for bradycardia, hypertension, and a widened pulse pressure. Other symptoms may result from pituitary dysfunction, caused by irritation or edema, leading to diabetes insipidus (excessive urinary output, hypernatremia) or hyponatremia.

SAHs are graded as follows:

  • Grade I: Mild headache with or without meningeal irritation
  • Grade II: Severe headache and a nonfocal examination, with or without mydriasis
  • Grade III: Mild alteration in neurological examination, including mental status
  • Grade IV: Obviously depressed level of consciousness or focal deficit
  • Grade V: Patient either posturing or comatose


Provide emotional support for the patient and family. Encourage the patient to verbalize his or her fears of death, disability, dependency, and becoming a burden. Answer the patient’s and family’s questions and involve both the patient and the family or the significant others in all aspects of planning care. If necessary, make home health referrals before the patient’s discharge.

Diagnostic highlights

TestNormal ResultAbnormality With ConditionExplanation
Computed tomography scan without contract (urgent)Normal brain and supporting structuresBlood collection in subarachnoid space often in the cisterns or sylvian fissureIdentifies areas of bleeding

Other Tests: Lumbar puncture, complete blood count, coagulation studies, cerebral angiogram, arterial blood gases, serum electrolytes, magnetic resonance imaging if no lesion is found on angiogram

Primary nursing diagnosis


Alteration in tissue perfusion (cerebral) related to interruption in cerebral blood flow or increased ICP


Circulation status; Cognitive ability; Neurological status; Tissue perfusion: Peripheral; Communication: Expressive ability; Communication: Receptive ability


Cerebral perfusion promotion; Circulatory care; ICP monitoring; Neurological monitoring; Peripheral sensation management; Circulatory precautions; Hypovolemia management; Vital signs monitoring; Emergency care; Medication management

Planning and implementation


Surgery is the treatment of choice for a cerebral aneurysm that has ruptured into the subarachnoid space. Until a decision about surgery is made, however, the management of the patient is focused on preventing secondary injury and relieving symptoms.

Monitor ICP to detect brain swelling and hydrocephalus. Maintain fluid volume within a normal range because dehydration increases hemoconcentration, which may increase the incidence of vasospasm. If cerebral edema is present, maintain moderate fluid restriction and administer prescribed steroids; dexamethasone (Decadron) and methylprednisolone (Solu-Medrol) are the drugs of choice. Steroid therapy is continued for at least 1 week postoperatively. Pharmacologic management is also used to control hypertension to prevent rebleeding. The goal of therapy is to maintain the systolic blood pressure at 150 mm Hg. Hypotension must be avoided at all costs because it worsens ischemic deficits. Assess the intravascular volume status with either a central venous access monitor or pulmonary artery catheter, depending on the patient’s condition.

Complications during the immediate postoperative period include brain swelling, bleeding at the operative site, fluid and electrolyte disturbances, hydrocephalus, and the onset of cerebral vasospasm. If an intracranial monitoring system is in place, report ICP rises over 15 mm Hg. Calculate the CPP and maintain the CPP greater than 50 mm Hg. Goals of medication management include control of blood pressure, prevention of seizures, treatment of symptoms (pain, nausea), maintenance of cerebral perfusion, and prevention of elevated intracranial pressure and vasospasm.

Pharmacologic highlights

Medication or Drug ClassDosageDescriptionRationale
Nimodipine60 mg PO q 4 hrCalcium channel blockerReduces venospasm and cerebral ischemia
AntihypertensivesVaries by drugNitroprusside; propranolol; hydralazine; labetalolLower blood pressure (BP), but used only with extreme hypertension (when diastolic BP > 130 mm Hg)

Other Drugs: Mannitol (osmotic diuretic) may be ordered to decrease cerebral edema, stool softeners, sedatives may be used to induce rest, anticonvulsants, analgesics (acetaminophen or codeine) to control headache, antiemetics, anticonvulsants


Accurate, detailed, and serial assessments are essential. Frequently, the first signs of rebleeding and vasospasm are evidenced through subtle changes in the neurological examination. At any time during the course of SAH, maintenance of airway, breathing, and circulation is the top priority. In the postoperative period, unless otherwise indicated, maintain the bed at an elevation of 30 to 40 degrees. Prevent flexion of the head and maintain proper alignment of the head and neck with towel rolls or sandbags. Avoid hip flexion greater than 90 degrees. Suction the patient as needed to keep the airway open. If deep endotracheal suctioning is indicated, hyperventilate and hyperoxygenate the patient before suctioning and limit suctioning to less than 30 seconds.

To prevent complications from postoperative immobility, turn the patient often and provide skin care. Perform active or passive range-of-motion exercises and encourage deep-breathing exercises when the patient is able. Space all nursing care activities to maintain ICP less than 15 mm Hg. Allow ICP to drop between all activities. Encourage other departments to space x-rays, therapies, and interviews to allow adequate rest and to avoid ICP elevations. Avoid conversations at the bedside that might be disturbing to the patient. Explain all procedures even if the patient does not appear to respond. Use soft restraints only when absolutely necessary; fighting restraints raises ICPs and thereby impedes venous outflow from the brain.

After surgery, monitor the dressing for bleeding or CSF leakage. If either occurs, notify the physician and reinforce the dressing. Inspect the surgical site with all dressing changes for redness, drainage, poor wound healing, and swelling.

Evidence-Based Practice and Health Policy

De Marchis, G.M., Lantigua, H., Schmidt, J.M., Lord, A.S., Velander, A.J., Fernandez, A., …Mayer, S.A. (2014). Impact of premorbid hypertension on haemorrhage severity and aneurysm rebleeding risk after subarachnoid haemorrhage. Journal of Neurology, Neurosurgery, and Psychiatry, 85(1), 56–59.

  • In a retrospective cohort study among 1,312 patients treated for subarachnoid hemorrhage, 49% of patients had hypertension, which was associated with a 1.58 times increased risk of mortality at 3 months (95% CI, 1.04 to 2.41; p = 0.03). In this study, 23.8% of patients with hypertension died within 3 months of the initial hemorrhage compared to 11.5% of patients without hypertension (p < 0.001).
  • Patients with hypertension presented more frequently with Grade 4 or 5 subarachnoid hemorrhage (42.6% versus 28.2%; p < 0.001). Hypertensive patients were also 1.67 times more likely to have an episode of rebleeding (95% CI, 1.02 to 2.74; p = 0.04) and 4.95 times more likely to develop renal failure while hospitalized (95% CI, 2.19 to 11.2; p < 0.001).

Documentation guidelines

  • Neurological findings: Level of consciousness; pupillary size, shape, and reaction to light; motor function of extremities; other cranial nerve deficits (blurred vision, extraocular movement deficits, drooping eyelids, facial weakness); speech loss; headache and facial pain; photophobia; and stiff or painful neck; deterioration of neurological status

Discharge and home healthcare guidelines

Prepare the patient and family for the possible need for rehabilitation after the acute care phase of hospitalization. Instruct the patient to report any deterioration in neurological status to the physician. Teach the patient signs and symptoms of deterioration in neurological status. Stress the importance of follow-up visits with the physician. If the patient has had surgery, teach the patient or caregiver to notify the physician for any signs of wound infection or poor incisional healing. Be sure the patient understands all medications, including dosage, route, action, adverse effects, and the need for routine laboratory monitoring for anticonvulsants.

sub·a·rach·noid hem·or·rhage

(sŭb'ă-rak'noyd hem'ŏr-ăj)
Extravasation of blood into subarachnoid space.
Synonym(s): subarachnoid haemmorhage.

subarachnoid hemorrhage (SAH),

n an intracranial hemorrhage into the cerebrospinal fluid.