Treatment is often in the form of preventative measures of prophylaxis. Drug therapy for underlying conditions, such as drugs for the treatment of high cholesterol, drugs to treat high blood pressure (ACE inhibitors), and anti-coagulant drugs, are often prescribed to help prevent arteriosclerosis. Lifestyle changes such as increasing exercise, stopping smoking, and moderating alcohol intake are also advised. Experimental treatments include senolytic drugs, or drugs that selectively eliminate senescent cells, which enhance vascular reactivity and reduce vascular calcification in a mouse model of atherosclerosis, as well as improving cardiovascular function in old mice.

There are a variety of types of surgery:

- Angioplasty and stent placement: A catheter is first inserted into the blocked/narrowed part of your artery, followed by a second one with a deflated balloon which is passed through the catheter into the narrowed area. The balloon is then inflated, pushing the deposits back against the arterial walls, and then a mesh tube is usually left behind to prevent the artery from retightening.

- Coronary artery bypass surgery: This surgery creates a new pathway for blood to flow to the heart. Taking a healthy piece of vein, the surgeon attaches it to the coronary artery, just above and below the blockage to allow bypass.

- Endarterectomy: This is the general procedure for the surgical removal of plaque from the artery that has become narrowed, or blocked.

- Thrombolytic therapy: is a treatment used to break up masses of plaque inside the arteries via intravenous clot-dissolving medicine.

A major aim of treatment is to prevent, limit, or reverse target organ damage by lowering the person's high blood pressure to reduce the risk of cardiovascular disease and death. Treatment with antihypertensive medications may be required to control the high blood pressure.

Asymptomatic individuals with intracranial stenosis are typically told to take over the counter platelet inhibitors like aspirin whereas those with symptomatic presentation are prescribed anti-coagulation medications. For asymptomatic persons the idea is to stop the buildup of plaque from continuing. They are not experiencing symptoms; however if more build up occurs it is likely they will. For symptomatic individuals it is necessary to try and reduce the amount of stenosis. The anti-coagulation medications reduce the likelihood of further buildup while also trying to break down the current build up on the surface without an embolism forming. For those with severe stenosis that are at risk for impending stroke endovascular treatment is used. Depending on the individual and the location of the stenosis there are multiple treatments that can be undertaken. These include angioplasty, stent insertion, or bypass the blocked area.

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 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.

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.

Oxygen consumption of skeletal muscle is approximately 50 times larger while contracting than in the resting state. Thus, resting the affected limb should delay onset of infarction substantially after arterial occlusion.

Low molecular weight heparin is used to reduce or at least prevent enlargement of a thrombus, and is also indicated before any surgery. In the legs, below the inguinal ligament, percutaneous aspiration thrombectomy is a rapid and effective way of removing thromboembolic occlusions. Balloon thrombectomy using a Fogarty catheter may also be used. In the arms, balloon thrombectomy is an effective treatment for thromboemboli as well. However, local thrombi from atherosclerotic plaque are harder to treat than embolized ones. If results are not satisfying, another angiography should be performed.

Thrombolysis using analogs of tissue plasminogen activator (tPA) may be used as an alternative or complement to surgery. Where there is extensive vascular damage, bypass surgery of the vessels may be necessary to establish other ways to supply the affected parts.

Swelling of the limb may cause inhibited flow by increased pressure, and in the legs (but very rarely in the arms), this may indicate a fasciotomy, opening up all four leg compartments.

Because of the high recurrence rates of thromboembolism, it is necessary to administer anticoagulant therapy as well. Aspirin and low molecular weight heparin should be administered, and possibly warfarin as well. Follow-up includes checking peripheral pulses and the arm-leg blood pressure gradient.

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.

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 includes supportive care with analgesics and anti-inflammatory agents. Exercise should be limited as it increases pain and extends the area of infarction. Symptoms usually resolve in weeks to months, but fifty percent of sufferers will experience relapse in either leg.

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

Treatment depends substantially of the type of ICH. Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery.

- Tracheal intubation is indicated in people with decreased level of consciousness or other risk of airway obstruction.

- IV fluids are given to maintain fluid balance, using isotonic rather than hypotonic fluids.

If the diagnostic workup reveals a systemic disease process, directed therapies to treat that underlying cause should be initiated. If the amaurosis fugax is caused by an atherosclerotic lesion, aspirin is indicated, and a carotid endarterectomy considered based on the location and grade of the stenosis. Generally, if the carotid artery is still patent, the greater the stenosis, the greater the indication for endarterectomy. "Amaurosis fugax appears to be a particularly favorable indication for carotid endarterectomy. Left untreated, this event carries a high risk of stroke; after carotid endarterectomy, which has a low operative risk, there is a very low postoperative stroke rate." However, the rate of subsequent stroke after amaurosis is significantly less than after a hemispheric TIA, therefore there remains debate as to the precise indications for which a carotid endarterectomy should be performed. If the full diagnostic workup is completely normal, patient observation is recommended.

Arteriosclerosis is the thickening, hardening and loss of elasticity of the walls of arteries. This process gradually restricts the blood flow to one's organs and tissues and can lead to severe health risks brought on by atherosclerosis, which is a specific form of arteriosclerosis caused by the buildup of fatty plaques, cholesterol, and some other substances in and on the artery walls.

Cerebral atherosclerosis is a type of atherosclerosis where build-up of plaque in the blood vessels of the brain occurs. Some of the main components of the plaques are connective tissue, extracellular matrix, including collagen, proteoglycans, fibronectin, and elastic fibers; crystalline cholesterol, cholesteryl esters, and phospholipids; cells such as monocyte derived macrophages, T-lymphocytes, and smooth muscle cells. The plaque that builds up can lead to further complications such as stroke, as the plaque disrupts blood flow within the intracranial arterioles. This causes the downstream sections of the brain that would normally be supplied by the blocked artery to suffer from ischemia. Diagnosis of the disease is normally done through imaging technology such as angiograms or magnetic resonance imaging. The risk of cerebral atherosclerosis and its associated diseases appears to increase with increasing age; however there are numerous factors that can be controlled in attempt to lessen risk.

Surgery is required if the hematoma is greater than , if there is a structural vascular lesion or lobar hemorrhage in a young patient.

- A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures.

- Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited.

Type 1 and Type 2 FAD call for the same treatment: immediate surgery to replace the aorta. Surgery is required due to the high risk of mortality. Type 3 is less severe and requires the maintenance of blood pressure through diet and exercise. Upon diagnosing someone with FAD intravenous antihypertensive treatment is frequently used. Often intravenous sodium nitroprusside is used for its efficiency in lessening the pulsatile load thus reducing blood pressure. Reducing this force slows the progression of the dissection. Surgical success depends on age, severity of symptoms, postoperative organ dysfunction and stroke. Surgical intervention is always indicated in Type 1 cases. Aortic surgery is palliative, not curative. The goal is to merely to prevent rupture, restore blood flow, and fix any aortic valve dysfunction. Post operative protocols include frequent monitoring of the aorta diameter. Statins and beta blockers are also popular treatments used to reduce future plaque build up and blockage of epinephrine receptors as a way to control heart rate and blood pressure.

Long term treatment should also include regular check ups every 3 to 6 months. A CT scan or MRI is recommended, along with required chest x-rays. Antihypertensive therapy with beta adrenergic antagonists is required regardless of medical versus surgical treatment. Ten to twenty percent of those who choose surgical intervention are re-operated on due to compression, aneurysm development or blood leakage.

Several other diseases can result in retinopathy that can be confused with hypertensive retinopathy. These include diabetic retinopathy, retinopathy due to autoimmune disease, anemia, radiation retinopathy, and central retinal vein occlusion.

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.

Macrovascular disease is a disease of any large ("macro") blood vessels in the body. It is a disease of the large blood vessels, including the coronary arteries, the aorta, and the sizable arteries in the brain and in the limbs.

This sometimes occurs when a person has had diabetes for an extended period of time. Fat and blood clots build up in the large blood vessels and stick to the vessel walls.

Three common macrovascular diseases are coronary disease (in the heart), cerebrovascular disease (in the brain), and peripheral vascular disease (in the limbs)

Macrovascular disease (macroangiopathy) refers to atherosclerosis. Atherosclerosis is a form of arteriosclerosis (thickening and hardening of arterial walls), characterized by plaque deposits of lipids, fibrous connective tissue, calcium, and other blood substances. Atherosclerosis, by definition, affects only medium and large arteries (excluding arterioles).

Macrovascular disease is associated with the development of coronary artery disease, peripheral vascular disease, brain attack (stroke), and increased risk of infection. Type 2 diabetes is more closely associated with macrovascular diseases than type 1 diabetes. Peripheral vascular disease and increased risk of infection have important implications in the care of the acutely ill patient.

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.

Historically, papilledema was a potential contraindication to lumbar puncture, as it indicates a risk for tentorial herniation and subsequent death via cerebral herniation, however newer imaging techniques have been more useful at determining when and when not to conduct a lumbar puncture. Imaging by CT or MRI is usually performed to elicit whether there is a structural cause i.e., tumor. An MRA and MRV may also be ordered to rule out the possibility of stenosis or thrombosis of the arterial or venous systems.

The treatment depends largely on the underlying cause. However, the root cause of papilledema is the increased intracranial pressure (ICP). This is a dangerous sign, indicative of a brain tumor, CNS inflammation or idiopathic intracranial hypertension (IIH) that may become manifest in the near future.

Thus, a biopsy is routinely performed prior to the treatment in the initial stages of papilledema to detect whether a brain tumor is present. If detected, laser treatment, radiation and surgeries can be used to treat the tumor.

To decrease ICP, medications can be administered by increasing the absorption of Cerebrospinal fluid (CSF), or decreasing its production. Such medicines include diuretics like acetazolamide and furosemide. These diuretics, along with surgical interventions, can also treat IIH. In IIH, weight loss (even a loss of 10-15%) can lead to normalization of ICP.

Meanwhile, steroids can reduce inflammation (if this is a contributing factor to increased ICP), and may help to prevent vision loss. However, steroids have also been known to cause increased ICP, especially with a change in dosage. However, if a severe inflammatory condition exists, such as multiple sclerosis, steroids with anti-inflammatory effects such as Methylprednisolone and prednisone can help.

Other treatments include repeated lumbar punctures to remove excess spinal fluid in the cranium. The removal of potentially causative medicines including tetracyclines and vitamin A analogues may help decrease ICP; however, this is only necessary if the medication is truly felt to contribute to the ICP increase.

Arteriolosclerosis is a form of cardiovascular disease involving hardening and loss of elasticity of arterioles or small arteries and is most often associated with hypertension and diabetes mellitus.

Types include hyaline arteriolosclerosis and hyperplastic arteriolosclerosis, both involved with vessel wall thickening and luminal narrowing that may cause downstream ischemic injury.

The following two terms whilst similar, are distinct in both spelling and meaning and may easily be confused with arteriolosclerosis.

- Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries (from the Greek "arteria", meaning "artery", and "", meaning "hardening")

- Atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque. The term "atherogenic" is used for substances or processes that cause atherosclerosis.

Treatment of a subdural hematoma depends on its size and rate of growth. Some small subdural hematomas can be managed by careful monitoring until the body heals itself. Other small subdural hematomas can be managed by inserting a temporary small catheter through a hole drilled through the skull and sucking out the hematoma; this procedure can be done at the bedside. Large or symptomatic hematomas require a craniotomy, the surgical opening of the skull. A surgeon then opens the dura, removes the blood clot with suction or irrigation, and identifies and controls sites of bleeding. Postoperative complications include increased intracranial pressure, brain edema, new or recurrent bleeding, infection, and seizure. The injured vessels must be repaired.

Depending on the size and deterioration, age of the patient, and anaesthetic risk posed, subdural hematomas occasionally require craniotomy for evacuation; most frequently, simple burr holes for drainage; often conservative treatment; and rarely, palliative treatment in patients of extreme age or with no chance of recovery.

In those with a chronic subdural hematoma, but without a history of seizures, the evidence is unclear if using anticonvulsants is harmful or beneficial.

Mönckeberg's arteriosclerosis, or Mönckeberg's sclerosis, also called medial calcific sclerosis or Mönckeberg medial sclerosis, is a form of arteriosclerosis or vessel hardening, where calcium deposits are found in the muscular middle layer of the walls of arteries (the tunica media). It is an example of dystrophic calcification. This condition occurs as an age-related degenerative process. However, it can occur in pseudoxanthoma elasticum and idiopathic arterial calcification of infancy as a pathological condition, as well. Its clinical significance and cause are not well understood and its relationship to atherosclerosis and other forms of vascular calcification are the subject of disagreement.

Mönckeberg's arteriosclerosis is named after Johann Georg Mönckeberg, who first described it in 1903.