Management involves general measures to stabilize the person while also using specific investigations and treatments. These include the prevention of rebleeding by obliterating the bleeding source, prevention of a phenomenon known as vasospasm, and prevention and treatment of complications.

Stabilizing the person is the first priority. Those with a depressed level of consciousness may need to be intubated and mechanically ventilated. Blood pressure, pulse, respiratory rate, and Glasgow Coma Scale are monitored frequently. Once the diagnosis is confirmed, admission to an intensive care unit may be preferable, especially since 15 percent may have further bleeding soon after admission. Nutrition is an early priority, with by mouth or nasogastric tube feeding being preferable over parenteral routes. In general, pain control is restricted to less-sedating agents such as codeine, as sedation may impact on the mental status and thus interfere with the ability to monitor the level of consciousness. Deep vein thrombosis is prevented with compression stockings, intermittent pneumatic compression of the calves, or both. A bladder catheter is usually inserted to monitor fluid balance. Benzodiazepines may be administered to help relieve distress. Antiemetic drugs should be given to awake persons.

People with poor clinical grade on admission, acute neurologic deterioration, or progressive enlargement of ventricles on CT scan are, in general, indications for the placement of an external ventricular drain by a neurosurgeon. The external ventricular drain may be inserted at the bedside or in the operating room. In either case, strict aseptic technique must be maintained during insertion. In people with aneurysmal subarachnoid hemorrhage the EVD is used to remove cerebrospinal fluid, blood, and blood byproducts that increase intracranial pressure and may increase the risk for cerebral vasospasm.

Vasospasm, in which the blood vessels constrict and thus restrict blood flow, is a serious complication of SAH. It can cause ischemic brain injury (referred to as "delayed ischemia") and permanent brain damage due to lack of oxygen in parts of the brain. It can be fatal if severe. Delayed ischemia is characterized by new neurological symptoms, and can be confirmed by transcranial doppler or cerebral angiography. About one third of people admitted with subarachnoid hemorrhage will have delayed ischemia, and half of those have permanent damage as a result. It is possible to screen for the development of vasospasm with transcranial Doppler every 24–48 hours. A blood flow velocity of more than 120 centimeters per second is suggestive of vasospasm.

The use of calcium channel blockers, thought to be able to prevent the spasm of blood vessels by preventing calcium from entering smooth muscle cells, has been proposed for prevention. The calcium channel blocker nimodipine when taken by mouth improves outcome if given between the fourth and twenty-first day after the bleeding, even if it does not reduce the amount of vasospasm detected on angiography. It is the only Food and Drug Administration (FDA) approved drug for treating cerebral vasospasm. In "traumatic" subarachnoid hemorrhage, nimodipine does not affect long-term outcome, and is not recommended. Other calcium channel blockers and magnesium sulfate have been studied, but are not presently recommended; neither is there any evidence that shows benefit if nimodipine is given intravenously.

Some older studies have suggested that statin therapy might reduce vasospasm, but a subsequent meta-analysis including further trials did not demonstrate benefit on either vasospasm or outcomes. While corticosteroids with mineralocorticoid activity may help prevent vasospasm their use does not appear to change outcomes.

A protocol referred to as "triple H" is often used as a measure to treat vasospasm when it causes symptoms; this is the use of intravenous fluids to achieve a state of hypertension (high blood pressure), hypervolemia (excess fluid in the circulation), and hemodilution (mild dilution of the blood). Evidence for this approach is inconclusive; no randomized controlled trials have been undertaken to demonstrate its effect.

If the symptoms of delayed ischemia do not improve with medical treatment, angiography may be attempted to identify the sites of vasospasms and administer vasodilator medication (drugs that relax the blood vessel wall) directly into the artery. Angioplasty (opening the constricted area with a balloon) may also be performed.

Hypothermia treatment induced by head cooling or systemic cooling administered within 6 hours of birth for 72 hours has proven beneficial in reducing death and neurological impairments at 18 months of age. This treatment does not completely protect the injured brain and may not improve the risk of death in the most severely hypoxic-ischemic neonates and has also not been proven beneficial in preterm infants. Combined therapies of hypothermia and pharmacological agents or growth factors to improve neurological outcomes are most likely the next direction for damaged neonatal brains, such as after a stroke.

Treatment remains controversial with regards to the risk/benefit ratio, which differs significantly from treatment of stroke in adults. Presence or possibility of organ or limb impairment and bleeding risks are possible with treatments using antithrombotic agents.

Various studies have investigated the use of anticoagulation to suppress blood clot formation in cerebral venous sinus thrombosis. Before these trials had been conducted, there had been a concern that small areas of hemorrhage in the brain would bleed further as a result of treatment; the studies showed that this concern was unfounded. Clinical practice guidelines now recommend heparin or low molecular weight heparin in the initial treatment, followed by warfarin, provided there are no other bleeding risks that would make these treatments unsuitable. Some experts discourage the use of anticoagulation if there is extensive hemorrhage; in that case, they recommend repeating the imaging after 7–10 days. If the hemorrhage has decreased in size, anticoagulants are started, while no anticoagulants are given if there is no reduction.

The duration of warfarin treatment depends on the circumstances and underlying causes of the condition. If the thrombosis developed under temporary circumstances (e.g. pregnancy), three months are regarded as sufficient. If the condition was unprovoked but there are no clear causes or a "mild" form of thrombophilia, 6 to 12 months is advised. If there is a severe underlying thrombosis disorder, warfarin treatment may need to continue indefinitely.

Thrombolysis (removal of the blood clot with "clot buster" medication) has been described, either systemically by injection into a vein or directly into the clot during angiography. The 2006 European Federation of Neurological Societies guideline recommends that thrombolysis is only used in patients who deteriorate despite adequate treatment, and other causes of deterioration have been eliminated. It is unclear which drug and which mode of administration is the most effective. Bleeding into the brain and in other sites of the body is a major concern in the use of thrombolysis. American guidelines make no recommendation with regards to thrombolysis, stating that more research is needed.

Raised intracranial pressure, if severe or threatening vision, may require therapeutic lumbar puncture (removal of excessive cerebrospinal fluid), medication (acetazolamide), or neurosurgical treatment (optic nerve sheath fenestration or shunting). In certain situations, anticonvulsants may be used to try to prevent seizures. These situations include focal neurological problems (e.g. inability to move a limb) and focal changes of the brain tissue on CT or MRI scan. Evidence to support or refute the use of antiepileptic drugs as a preventive measure, however, is lacking.

Treatment focuses on monitoring and should be accomplished with inpatient floor service for individuals responsive to commands or neurological ICU observation for those with impaired levels of consciousness. Extra attention should be placed on intracranial pressure (ICP) monitoring via an intraventricular catheter and medications to maintain ICP, blood pressure, and coagulation. In more severe cases an external ventricular drain may be required to maintain ICP and evacuate the hemorrhage, and in extreme cases an open craniotomy may be required. In cases of unilateral IVH with small intraparenchymal hemorrhage the combined method of stereotaxy and open craniotomy has produced promising results.

Initial measures can include rest, caffeine intake (via coffee or intravenous infusion), and hydration. Corticosteroids may provide transient relief for some patients. An abdominal binder — a type of garment that increases intracranial pressure by compressing the abdomen — can temporarily relieve symptoms for some people.

The best-studied medical treatment for intracranial hypertension is acetazolamide (Diamox), which acts by inhibiting the enzyme carbonic anhydrase, and it reduces CSF production by six to 57 percent. It can cause the symptoms of hypokalemia (low blood potassium levels), which include muscle weakness and tingling in the fingers. Acetazolamide cannot be used in pregnancy, since it has been shown to cause embryonic abnormalities in animal studies. Also, in human beings it has been shown to cause metabolic acidosis as well as disruptions in the blood electrolyte levels of newborn babies. The diuretic furosemide is sometimes used for a treatment if acetazolamide is not tolerated, but this drug sometimes has little effect on the ICP.

Various analgesics (painkillers) may be used in controlling the headaches of intracranial hypertension. In addition to conventional agents such as paracetamol, a low dose of the antidepressant amitriptyline or the anticonvulsant topiramate have shown some additional benefit for pain relief.

The use of steroids in the attempt to reduce the ICP is controversial. These may be used in severe papilledema, but otherwise their use is discouraged.

The treatment of choice for this condition is the surgical application of epidural blood patches, which has a higher success rate than conservative treatments of bed rest and hydration. Through the injection of a person's own blood into the area of the hole in the dura, an epidural blood patch uses blood's clotting factors to clot the sites of holes. The volume of autologous blood and number of patch attempts for patients is highly variable. One-quarter to one-third of SCSFLS patients do not have relief of symptoms from epidural blood patching.

The first step in symptom control is drainage of cerebrospinal fluid by lumbar puncture. If necessary, this may be performed at the same time as a diagnostic LP (such as done in search of a CSF infection). In some cases, this is sufficient to control the symptoms, and no further treatment is needed.

The procedure can be repeated if necessary, but this is generally taken as a clue that additional treatments may be required to control the symptoms and preserve vision. Repeated lumbar punctures are regarded as unpleasant by patients, and they present a danger of introducing spinal infections if done too often. Repeated lumbar punctures are sometimes needed to control the ICP urgently if the patient's vision deteriorates rapidly.

Management consists of vigilant observation over days to detect progression. The subgaleal space is capable of holding up to 50% of a newborn baby's blood and can therefore result in acute shock and death. Fluid bolus may be required if blood loss is significant and patient becomes tachycardic. Transfusion and phototherapy may be necessary. Investigation for coagulopathy may be indicated.

Treatment depends on whether the aneurysm is ruptured and may involve a combination of antimicrobial drugs, surgery and/or endovascular treatment.

The treatment includes lowering the increased intracranial pressure and starting intravenous antibiotics (and meanwhile identifying the causative organism mainly by blood culture studies).

Hyperbaric oxygen therapy (HBO2 or HBOT) is indicated as a primary and adjunct treatment which provides four primary functions.

Firstly, HBOT reduces intracranial pressure. Secondly, high partial pressures of oxygen act as a bactericide and thus inhibits the anaerobic and functionally anaerobic flora common in brain abscess. Third, HBOT optimizes the immune function thus enhancing the host defense mechanisms and fourth, HBOT has been found to be of benefit when brain abscess is concomitant with cranial osteomyleitis.

Secondary functions of HBOT include increased stem cell production and up-regulation of VEGF which aid in the healing and recovery process.

Surgical drainage of the abscess remains part of the standard management of bacterial brain abscesses. The location and treatment of the primary lesion also crucial, as is the removal of any foreign material (bone, dirt, bullets, and so forth).

There are few exceptions to this rule: "Haemophilus influenzae" meningitis is often associated with subdural effusions that are mistaken for subdural empyemas. These effusions resolve with antibiotics and require no surgical treatment. Tuberculosis can produce brain abscesses that look identical to conventional bacterial abscesses on CT imaging. Surgical drainage or aspiration is often necessary to identify "Mycobacterium tuberculosis", but once the diagnosis is made no further surgical intervention is necessary.

CT guided stereotactic aspiration is also indicated in the treatment of brain abscess.

IVH in the preterm brain usually arises from the germinal matrix whereas IVH in the term infants originates from the choroid plexus. However, it is particularly common in premature infants or those of very low birth weight. The cause of IVH in premature infants, unlike that in older infants, children or adults, is rarely due to trauma. Instead it is thought to result from changes in perfusion of the delicate cellular structures that are present in the growing brain, augmented by the immaturity of the cerebral circulatory system, which is especially vulnerable to hypoxic ischemic encephalopathy. The lack of blood flow results in cell death and subsequent breakdown of the blood vessel walls, leading to bleeding. While this bleeding can result in further injury, it is itself a marker for injury that has already occurred. Most intraventricular hemorrhages occur in the first 72 hours after birth. The risk is increased with use of extracorporeal membrane oxygenation in preterm infants. Congenital cytomegalovirus infection can be an important cause.

The amount of bleeding varies. IVH is often described in four grades:

- Grade I - bleeding occurs just in the germinal matrix

- Grade II - bleeding also occurs inside the ventricles, but they are not enlarged

- Grade III - ventricles are enlarged by the accumulated blood

- Grade IV - bleeding extends into the brain tissue around the ventricles

Grades I and II are most common, and often there are no further complications. Grades III and IV are the most serious and may result in long-term brain injury to the infant. After a grade III or IV IVH, blood clots may form which can block the flow of cerebrospinal fluid, leading to increased fluid in the brain (hydrocephalus).

There have been various therapies employed into preventing the high rates of morbidity and mortality, including diuretic therapy, repeated lumbar puncture, streptokinase therapy and most recently combination a novel intervention called DRIFT (drainage, irrigation and fibrinolytic therapy).

In 2002, a Dutch retrospective study analysed cases where neonatologists had intervened and drained CSF by lumbar or ventricular punctures if ventricular width (as shown on ultrasound) exceeded the 97th centile as opposed to the 97th centile plus 4 mm. Professors Whitelaw's original Cochrane review published in 2001 as well as evidence from previous randomised control trials indicated that interventions should be based on clinical signs and symptoms of ventricular dilatation. An international trial has instead looked an early (97th centile) versus late (97th centile plus 4 mm) for intervening and draining CSF.

DRIFT has been tested in an international randomised clinical trial; although it did not significantly lower the need for shunt surgery, severe cognitive disability at two years Bayley (MDI <55) was significantly reduced. Repeated lumbar punctures are used widely to reduce the effects in increased intracranial pressure and an alternative to ventriculoperitoneal (VP) shunt surgery that cannot be performed in case of intraventricular haemorrhage. The relative risk of repeated lumbar puncture is close to 1.0, therefore it is not statistically therapeutic when compared to conservative management and does raise the risk of subsequent CSF infection.

Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. Currently there are two treatment options for securing intracranial aneurysms: surgical clipping or endovascular coiling. If possible, either surgical clipping or endovascular coiling is usually performed within the first 24 hours after bleeding to occlude the ruptured aneurysm and reduce the risk of rebleeding.

While a large meta-analysis found the outcomes and risks of surgical clipping and endovascular coiling to be statistically similar, no consensus has been reached. In particular, the large randomised control trial International Subarachnoid Aneurysm Trial appears to indicate a higher rate of recurrence when intracerebral aneurysms are treated using endovascular coiling. Analysis of data from this trial has indicated a 7% lower eight-year mortality rate with coiling, a high rate of aneurysm recurrence in aneurysms treated with coiling—from 28.6-33.6% within a year, a 6.9 times greater rate of late retreatment for coiled aneurysms, and a rate of rebleeding 8 times higher than surgically-clipped aneurysms.

A "subarachnoid hemorrhage" is bleeding into the subarachnoid space—the area between the arachnoid membrane and the pia mater surrounding the brain. Besides from head injury, it may occur spontaneously, usually from a ruptured cerebral aneurysm. Symptoms of SAH include a severe headache with a rapid onset ("thunderclap headache"), vomiting, confusion or a lowered level of consciousness, and sometimes seizures. The diagnosis is generally confirmed with a CT scan of the head, or occasionally by lumbar puncture. Treatment is by prompt neurosurgery or radiologically guided interventions with medications and other treatments to help prevent recurrence of the bleeding and complications. Since the 1990s, many aneurysms are treated by a minimal invasive procedure called "coiling", which is carried out by instrumentation through large blood vessels. However, this procedure has higher recurrence rates than the more invasive craniotomy with clipping.

Aneurysms can be treated by clipping the base of the aneurysm with a specially-designed clip. Whilst this is typically carried out by craniotomy, a new endoscopic endonasal approach is being trialled. Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937

After clipping, a catheter angiogram or CTA can be performed to confirm complete clipping.

There are some preliminary studies that seem to indicate that treatment with hydrogen sulfide (HS) can have a protective effect against reperfusion injury.

Superoxide dismutase is an effective anti-oxidant enzyme which converts superoxide anions to water and hydrogen peroxide. Recent researches have shown significant therapeutic effects on pre-clinical models of reperfusion injury after ischemic stroke.

Intracranial hemorrhage is a serious medical emergency because the buildup of blood within the skull can lead to increases in intracranial pressure, which can crush delicate brain tissue or limit its blood supply. Severe increases in intracranial pressure (ICP) can cause brain herniation, in which parts of the brain are squeezed past structures in the skull.

If ongoing and rapid haemorrhage is occurring then immediate delivery of the foetus may be indicated if the fetus is sufficiently developed. If the haemorrhage has already occurred and now stopped, an inutero transfusion of red cells to the foetus may be recommended.

The treatment of PRES dependent on its cause. Anti-epileptic medication may also be appropriate.

The surgical treatment involves the resection of the extracranial venous package and ligation of the emissary communicating vein. In some cases of SP, surgical excision is performed for cosmetic reasons. The endovascular technique has been described by transvenous approach combined with direct puncture and the recently endovascular embolization with Onyx.

In 2004 the first adequately large scale study on the natural history and long-term prognosis of this condition was reported; this showed that at 16 months follow-up 57.1% of patients had full recovery, 29.5%/2.9%/2.2% had respectively minor/moderate/severe symptoms or impairments, and 8.3% had died. Severe impairment or death were more likely in those aged over 37 years, male, affected by coma, mental status disorder, intracerebral hemorrhage, thrombosis of the deep cerebral venous system, central nervous system infection and cancer. A subsequent systematic review of nineteen studies in 2006 showed that mortality is about 5.6% during hospitalisation and 9.4% in total, while of the survivors 88% make a total or near-total recovery. After several months, two thirds of the cases has resolution ("recanalisation") of the clot. The rate of recurrence was low (2.8%).

In children with CVST the risk of death is high. Poor outcome is more likely if a child with CVST develops seizures or has evidence of venous infarction on imaging.

Examples of possible complications include shunt malfunction, shunt failure, and shunt infection, along with infection of the shunt tract following surgery (the most common reason for shunt failure is infection of the shunt tract). Although a shunt generally works well, it may stop working if it disconnects, becomes blocked (clogged), infected, or it is outgrown. If this happens the cerebrospinal fluid will begin to accumulate again and a number of physical symptoms will develop (headaches, nausea, vomiting, photophobia/light sensitivity), some extremely serious, like seizures. The shunt failure rate is also relatively high (of the 40,000 surgeries performed annually to treat hydrocephalus, only 30% are a patient's first surgery) and it is not uncommon for patients to have multiple shunt revisions within their lifetime.

Another complication can occur when CSF drains more rapidly than it is produced by the choroid plexus, causing symptoms - listlessness, severe headaches, irritability, light sensitivity, auditory hyperesthesia (sound sensitivity), nausea, vomiting, dizziness, vertigo, migraines, seizures, a change in personality, weakness in the arms or legs, strabismus, and double vision - to appear when the patient is vertical. If the patient lies down, the symptoms usually vanish quickly. A CT scan may or may not show any change in ventricle size, particularly if the patient has a history of slit-like ventricles. Difficulty in diagnosing overdrainage can make treatment of this complication particularly frustrating for patients and their families. Resistance to traditional analgesic pharmacological therapy may also be a sign of shunt overdrainage "or" failure.

The diagnosis of cerebrospinal fluid buildup is complex and requires specialist expertise. Diagnosis of the particular complication usually depends on when the symptoms appear - that is, whether symptoms occur when the patient is upright or in a prone position, with the head at roughly the same level as the feet.