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.

Alteplase (tpa) is an effective medication for acute ischemic stroke. When given within 3 hours, treatment with tpa significantly improves the probability of a favourable outcome versus treatment with placebo.

The outcome of brain ischemia is influenced by the quality of subsequent supportive care. Systemic blood pressure (or slightly above) should be maintained so that cerebral blood flow is restored. Also, hypoxaemia and hypercapnia should be avoided. Seizures can induce more damage; accordingly, anticonvulsants should be prescribed and should a seizure occur, aggressive treatment should be undertaken. Hyperglycaemia should also be avoided during brain ischemia.

When someone presents with an ischemic event, treatment of the underlying cause is critical for prevention of further episodes.

Anticoagulation with warfarin or heparin may be used if the patient has atrial fibrillation.

Operative procedures such as carotid endarterectomy and carotid stenting may be performed if the patient has a significant amount of plaque in the carotid arteries associated with the local ischemic events.

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.

Treatment for cerebrovascular disease may include medication, lifestyle changes and/or surgery, depending on the cause.

Examples of medications are:

- antiplatelets (aspirin, clopidogrel)

- blood thinners (heparin, warfarin)

- antihypertensives (ACE inhibitors, beta blockers)

- anti-diabetic medications.

Surgical procedures include:

- endovascular surgery and vascular surgery (for future stroke prevention).

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.

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.

Prevention of PTE involves preventing brain trauma in general; protective measures include bicycle helmets and child safety seats. No specific treatment exists to prevent the development of epilepsy after TBI occurs. In the past, antiepileptic drugs were used with the intent of preventing the development of PTE. However, while antiepileptic drugs can prevent early PTS, clinical studies have failed to show that prophylactic use of antiepileptic drugs prevents the development of PTE. Why antiepileptic drugs in clinical trials have failed to stop PTE from developing is not clear, but several explanations have been offered. The drugs may simply not be capable of preventing epilepsy, or the drug trials may have been set up in a way that did not allow a benefit of the drugs to be found (e.g. drugs may have been given too late or in inadequate doses). Animal studies have similarly failed to show much protective effect of the most commonly used seizure medications in PTE trials, such as phenytoin and carbamazepine. Antiepileptic drugs are recommended to prevent late seizures only for people in whom PTE has already been diagnosed, not as a preventative measure. On the basis of the aforementioned studies, no treatment is widely accepted to prevent the development of epilepsy. However, it has been proposed that a narrow window of about one hour after TBI may exist during which administration of antiepileptics could prevent epileptogenesis (the development of epilepsy).

Corticosteroids have also been investigated for the prevention of PTE, but clinical trials revealed that the drugs did not reduce late PTS and were actually linked to an increase in the number of early PTS.

Antiepileptic drugs may be given to prevent further seizures; these drugs completely eliminate seizures for about 35% of people with PTE. However, antiepileptics only prevent seizures while they are being taken; they do not reduce the occurrence once the patient stops taking the drugs. Medication may be stopped after seizures have been controlled for two years. PTE is commonly difficult to treat with drug therapy, and antiepileptic drugs may be associated with side effects. The antiepileptics carbamazepine and valproate are the most common drugs used to treat PTE; phenytoin may also be used but may increase risk of cognitive side effects such as impaired thinking. Other drugs commonly used to treat PTE include clonazepam, phenobarbitol, primidone, gabapentin, and ethosuximide. Among antiepileptic drugs tested for seizure prevention after TBI (phenytoin, sodium valproate, carbamazepine, phenobarbital), no evidence from randomized controlled trials has shown superiority of one over another.

People whose PTE does not respond to medication may undergo surgery to remove the epileptogenic focus, the part of the brain that is causing the seizures. However surgery for PTE may be more difficult than it is for epilepsy due to other causes, and is less likely to be helpful in PTE than in other forms of epilepsy. It can be particularly difficult in PTE to localize the epileptic focus, in part because TBI may affect diffuse areas of the brain. Difficulty locating the seizure focus is seen as a deterrent to surgery. However, for people with sclerosis in the mesial temporal lobe (in the inner aspect of the temporal lobe), who comprise about one third of people with intractable PTE, surgery is likely to have good outcome. When there are multiple epileptic foci or the focus cannot be localized, and drug therapy is not effective, vagus nerve stimulation is another option for treating PTE.

People with PTE have follow-up visits, in which health care providers monitor neurological and neuropsychological function and assess the efficacy and side effects of medications. As with sufferers of other types of epilepsy, PTE sufferers are advised to exercise caution when performing activities for which seizures could be particularly risky, such as rock climbing.

Prognostics factors:

Lower Glasgow coma scale score, higher pulse rate, higher respiratory rate and lower arterial oxygen saturation level is prognostic features of in-hospital mortality rate in acute ischemic stroke.

The natural history of this disorder is not well known. The long term outlook for patients with treated moyamoya seems to be good. While symptoms may seem to improve almost immediately after the in-direct EDAS, EMS, and multiple burr holes surgeries, it will take probably 6–12 months before new vessels can develop to give a sufficient blood supply. With the direct STA-MCA surgery, increased blood supply is immediate.

Once major stroke or bleeding take place, even with treatment, the patient may be left with permanent loss of function so it is very important to treat this condition promptly.

Dr. Michael Scott, MD discusses the success rate for Moyamoya surgery in

There is no cure for this disease. Drugs such as antiplatelet agents (including aspirin) are usually given to prevent clots, but surgery is usually recommended. Since moyamoya tends to affect only the internal carotid artery and nearby sections of the adjacent anterior and middle cerebral arteries, surgeons can direct other arteries, such as the external carotid artery or the superficial temporal artery to replace its circulation. The arteries are either sewn directly into the brain circulation, or placed on the surface of the brain to reestablish new circulation after a few weeks.

There are many operations that have been developed for the condition, but currently the most favored are the in-direct procedures EDAS, EMS, and multiple burr holes and the direct procedure STA-MCA. Direct superficial temporal artery (STA) to middle cerebral artery (MCA) bypass is considered the treatment of choice, although its efficacy, particularly for hemorrhagic disease, remains uncertain. Multiple burr holes have been used in frontal and parietal lobes with good neovascularisation achieved.

The EDAS (encephaloduroarteriosynangiosis) procedure is a synangiosis procedure that requires dissection of a scalp artery over a course of several centimeters and then making a small temporary opening in the skull directly beneath the artery. The artery is then sutured to a branch of the middle cerebral artery on the surface of the brain and the bone is replaced.

In the EMS (encephalomyosynangiosis) procedure, the temporalis muscle, which is in the temple region of the forehead, is dissected and through an opening in the skull placed onto the surface of the brain.

In the multiple burr holes procedure, multiple small holes (burr holes) are placed in the skull to allow for growth of new vessels into the brain from the scalp.

In the STA-MCA procedure, the scalp artery (superficial temporal artery or STA) is directly sutured to an artery on the surface of the brain (middle cerebral artery or MCA). This procedure is also commonly referred to as an EC-IC (External Carotid-Internal Carotid) bypass.

All of these operations have in common the concept of a blood and oxygen "starved" brain reaching out to grasp and develop new and more efficient means of bringing blood to the brain and bypassing the areas of blockage. The modified direct anastomosis and encephalo-myo-arterio-synangiosis play a role in this improvement by increasing cerebral blood flow (CBF) after the operation. A significant correlation is found between the postoperative effect and the stages of preoperative angiograms. It is crucial for surgery that the anesthesiologist have experience in managing children being treated for moyamoya, as the type of anesthesia they require is very different from the standard anesthetic children get for almost any other type of neurosurgical procedure.

Some of the most up to date treatments for Moyamoya are explained by top rated surgeons at Boston Children's Hospital in Massachusetts in these

Pediatric FMD medical and surgical treatments or interventions are available. Treatment is determined by factors such as age and disease location but routinely involve controlling hypertension, re-establishing vascular flow, clot prevention, and improving lifestyle such as diet, exercise and smoking cessation.

Medical therapy for pediatric population may involve the use of angiotensin-converting enzyme inhibitor (ACE inhibitors) and/or angiotensin II receptor blockers, multiple anti-hypertensive medications, diuretics, calcium channel blockers, and beta-blockers. Prevention of thrombosis of affected arteries may be taken through administration of an antiplatelet medication such as aspirin.

Percutaneous transluminal renal angioplasty (PTRA) remains the gold standard for renal-artery FMD. This treatment is useful when hypertension is difficult to control; patient is intolerant to the anti-hypertensive medications, non-complainant to medication regime and patient loss of renal volume due to ischemia. PTRA can also aide in preventing a lifelong dependency on a medication for such a young patient. According to Meyers, “effective PTRAs result in cured or controlled blood pressure, which is often signified by reductions in plasma renin activity and angiotensin II levels, and when compared with surgery, percutaneous balloon angioplasty is less costly, able to be performed on an outpatient basis, results in lower morbidity, and the use of stenting is not primarily necessary.” However, there is a subset of the pediatric population that are resistant to PTRA. Adverse events may include, “recurrent stenosis, arterial occlusion with renal loss, and arterial rupture with extravasations and pseudo aneurysm formation and may require surgical intervention.

There is no known cure for FMD. However, treatment focuses on relieving symptoms associated with it. Medical management is the most common form of treatment. The best approach to medically managing these patients is constantly being reevaluated as more information is learned about the disease.

Treatment varies with the type of vascular disease; in the case of renal artery disease, information from a meta-analysis indicated that balloon angioplasty results in improvement of diastolic blood pressure and a reduction in antihypertensive drug requirements. In the case of peripheral artery disease, preventing complications is important; without treatment, sores or gangrene (tissue death) may occur. Among the treatments are:

- Quitting smoking

- Lowering cholesterol

- Lower blood pressure

- Lower blood glucose

- Physical activity

Currently, there are no medications that have been approved specifically for prevention or treatment of vascular dementia. The use of medications for treatment of Alzheimer's dementia, such as cholinesterase inhibitors and memantine, has shown small improvement of cognition in vascular dementia. This is most likely due to the drugs' actions on co-existing AD-related pathology. Multiple studies found a small benefit in VaD treatment with: memantine, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist; cholinesterase inhibitors galantamine, donepezil, rivastigmine; and ginkgo biloba extract.

The general management of dementia includes referral to community services, aid with judgment and decision-making regarding legal and ethical issues (e.g., driving, capacity, advance directives), and consideration of caregiver stress.

Behavioral and affective symptoms deserve special consideration in this patient group. These problems tend to be resistant to conventional psychopharmacological treatment and often lead to hospital admission and placement in permanent care.

Cilostazol or pentoxifylline can improve symptoms in some. Cilostazol may improve walking distance for people who experience claudication due to peripheral artery disease, but there is no strong evidence to suggest that it improves the quality of life, decreases mortality, or decreases the risk of cardiovascular events.

Treatment with other drugs or vitamins are unsupported by clinical evidence, "but trials evaluating the effect of folate and vitamin B-12 on hyperhomocysteinemia, a putative vascular risk factor, are near completion".

A number of psychotherapy approaches have been designed with the treatment of trauma in mind—EMDR, progressive counting (PC), somatic experiencing, biofeedback, Internal Family Systems Therapy, and sensorimotor psychotherapy.

There is a large body of empirical support for the use of cognitive behavioral therapy for the treatment of trauma-related symptoms, including posttraumatic stress disorder. Institute of Medicine guidelines identify cognitive behavioral therapies as the most effective treatments for PTSD. Two of these cognitive behavioral therapies, prolonged exposure and cognitive processing therapy, are being disseminated nationally by the Department of Veterans Affairs for the treatment of PTSD. Recent studies show that a combination of treatments involving dialectical behavior therapy (DBT), often used for borderline personality disorder, and exposure therapy is highly effective in treating psychological trauma. If, however, psychological trauma has caused dissociative disorders or complex PTSD, the trauma model approach (also known as phase-oriented treatment of structural dissociation) has been proven to work better than simple cognitive approach. Studies funded by pharmaceuticals have also shown that medications such as the new anti-depressants are effective when used in combination with other psychological approaches.

Trauma therapy allows processing trauma-related memories and allows growth towards more adaptive psychological functioning. It helps to develop positive coping instead of negative coping and allows the individual to integrate upsetting-distressing material (thoughts, feelings and memories) resolve internally. It also aids in growth of personal skills like resilience, ego regulation, empathy...etc.

Process' involved in trauma therapy are:

- Psychoeducation: Information dissemination and educating in vulnerabilities and adoptable coping mechanisms.

- Emotional regulation: Identifying, countering discriminating, grounding thoughts and emotions from internal construction to an external representation.

- Cognitive processing: Transforming negative perceptions and beliefs to positive ones about self, others and environment through cognitive reconsideration or re-framing.

- Trauma processing: Systematic desensitization, response activation and counter-conditioning, titrated extinction of emotional response, deconstructing disparity (emotional vs. reality state), resolution of traumatic material (state in which triggers don't produce the harmful distress and able to express relief.)

- Emotional processing: Reconstructing perceptions, beliefs and erroneous expectations like trauma-related fears are auto-activated and habituated in new life contexts, providing crisis cards with coded emotions and appropriate cognition's. (This stage is only initiated in pre-termination phase from clinical assessment & judgement of the mental health professional.)

- Experiential processing: Visualization of achieved relief state and relaxation methods.

When there is no pancreatic duct injury, typically hemostasis and surgical drainage are the main form of treatment. Surgical repair is undertaken when there is evidence or suspicion of ductal injury. The type of surgery depends on the degree of the injury and its proximity to the mesenteric blood vessels that serve the pancreas. When injuries are not close to the mesenteric vessels, a distal pancreatectomy may be done; this procedure preserves much of the pancreas and usually avoids loss of its endocrine and exocrine functions. In severe cases of pancreaticoduodenal injury, a pancreaticoduodenectomy can be used. Common complications after surgery include pancreatitis, pancreatic fistula, abscess, and pseudocyst formation. Initial management of hemorrhage includes controlling it by packing the wound.

After a trial of the best medical treatment outline above, if symptoms persist, patients may be referred to a vascular or endovascular surgeon. The benefit of revascularization is thought to correspond to the severity of ischemia and the presence of other risk factors for limb loss such as wound and infection severity.

- Angioplasty (PTA, or percutaneous transluminal angioplasty) can be done on solitary lesions in large arteries, such as the femoral artery, but angioplasty may not have sustained benefits. Patency rates following angioplasty are highest for iliac arteries, and decrease with arteries towards the toes. Other criteria that affect outcome following revascularization are length of lesion, and number of lesions. There does not appear to be long term advantages or sustained benefit to placing a stent following angioplasty in order to hold the narrowing of the superficial femoral artery open.

- Atherectomy, in which the plaque is scraped off of the inside of the vessel wall (albeit with no better results than angioplasty).

- Vascular bypass grafting can be performed to circumvent a diseased area of the arterial vasculature. The great saphenous vein is used as a conduit if available, although artificial (Gore-Tex or PTFE) material is often used for long grafts when adequate venous conduit is unavailable.

- When gangrene has set in, amputation is required to prevent infected tissues from causing sepsis a life-threatening illness.

- Thrombolysis and thrombectomy are used in cases of arterial thrombosis or embolism.

Birth trauma (BT) refers to damage of the tissues and organs of a newly delivered child, often as a result of physical pressure or trauma during childbirth. The term also encompasses the long term consequences, often of a cognitive nature, of damage to the brain or cranium. Medical study of birth trauma dates to the 16th century, and the morphological consequences of mishandled delivery are described in Renaissance-era medical literature. Birth injury occupies a unique area of concern and study in the medical canon. In ICD-10 "birth trauma" occupied 49 individual codes (P10-Р15).

However, there are often clear distinctions to be made between brain damage caused by birth trauma and that induced by intrauterine asphyxia. It is also crucial to distinguish between "birth trauma" and "birth injury". Birth injuries encompass any systemic damages incurred during delivery (hypoxic, toxic, biochemical, infection factors, etc.), but "birth trauma" focuses largely on mechanical damage. Caput succedaneum, subcutaneous hemorrhages, small subperiostal hemorrhages, hemorrhages along the displacements of cranial bones, intradural bleedings, subcapsular haematomas of liver, are among the more commonly reported birth injuries. Birth trauma, on the other hand, encompasses the enduring side effects of physical birth injuries, including the ensuing compensatory and adaptive mechanisms and the development of pathological processes (pathogenesis) after the damage.

Early detection and accurate diagnosis are important, as vascular dementia is at least partially preventable. Ischemic changes in the brain are irreversible, but the patient with vascular dementia can demonstrate periods of stability or even mild improvement.

Since stroke is an essential part of vascular dementia, the goal is to prevent new strokes. This is attempted through reduction of stroke risk factors, such as high blood pressure, high blood lipid levels, atrial fibrillation, or diabetes mellitus. Meta-analyses have found that medications for high blood pressure are effective at prevention of pre-stroke dementia, which means that high blood pressure treatment should be started early. These medications include angiotensin converting enzyme inhibitors, diuretics, calcium channel blockers, sympathetic nerve inhibitors, angiotensin II receptor antagonists or adrenergic antagonists. Elevated lipid levels, including HDL, were found to increase risk of vascular dementia. However, four large recent reviews showed that therapy with statin drugs was ineffective in treatment or prevention of this dementia. Aspirin is a medication that is commonly prescribed for prevention of strokes and heart attacks; it is also frequently given to patients with dementia. However, its efficacy in slowing progression of dementia or improving cognition has not been supported by studies. Smoking cessation and Mediterranean diet have not been found to help patients with cognitive impairment, however physical activity was consistently the most effective method of preventing cognitive decline.

Quick determination of the cause may lead to urgent measures to save the eye and life of the patient. High clinical suspicion should be kept for painless vision loss in patients with atherosclerosis, deep venous thrombosis, atrial fibrillation, pulmonary thromboembolism or other previous embolic episodes. Those caused by a carotid artery embolism or occlusion have the potential for further stroke by detachment of embolus and migration to an end-artery of the brain. Hence, proper steps to prevent such an eventuality need to be taken.

Retinal arterial occlusion is an ophthalmic emergency, and prompt treatment is essential. Completely anoxic retina in animal models causes irreversible damage in about 90 minutes. Nonspecific methods to increase blood flow and dislodge emboli include digital massage, 500 mg IV acetazolamide and 100 mg IV methylprednisolone (for possible arteritis). Additional measures include paracentesis of aqueous humor to decrease IOP acutely. An ESR should be drawn to detect possible giant cell arteritis. Improvement can be determined by visual acuity, visual field testing, and by ophthalmoscopic examination.

At a later stage, pan-retinal photocoagulation (PRP) with an argon laser appears effective in reducing the neovascular components and their sequelae.

The visual prognosis for ocular ischemic syndrome varies from usually poor to fair, depending on speed and effectiveness of the intervention. However, prompt diagnosis is crucial as the condition may be a presenting sign of serious cerebrovascular and ischemic heart diseases.

In 2009, the Undersea and Hyperbaric Medical Society added "central retinal artery occlusion" to their list of approved indications for hyperbaric oxygen (HBO). When used as an adjunctive therapy, the edema reducing properties of HBO, along with down regulation of inflammatory cytokines may contribute to the improvement in vision. Prevention of vision loss requires that certain conditions be met: the treatment be started before irreversible damage has occurred (over 24 hours), the occlusion must not also occur at the ophthalmic artery, and treatment must continue until the inner layers of the retina are again oxygenated by the retinal arteries.

An immediate need in treatment is to ensure that the airway is open and not threatened (for example by tissues or foreign objects), because airway compromisation can occur rapidly and insidiously, and is potentially deadly. Material in the mouth that threatens the airway can be removed manually or using a suction tool for that purpose, and supplemental oxygen can be provided. Facial fractures that threaten to interfere with the airway can be reduced by moving the bones back into place; this both reduces bleeding and moves the bone out of the way of the airway. Tracheal intubation (inserting a tube into the airway to assist breathing) may be difficult or impossible due to swelling. Nasal intubation, inserting an endotracheal tube through the nose, may be contraindicated in the presence of facial trauma because if there is an undiscovered fracture at the base of the skull, the tube could be forced through it and into the brain. If facial injuries prevent oraotracheal or nasotracheal intubation, a surgical airway can be placed to provide an adequate airway. Although cricothyrotomy and tracheostomy can secure an airway when other methods fail, they are used only as a last resort because of potential complications and the difficulty of the procedures.

A dressing can be placed over wounds to keep them clean and to facilitate healing, and antibiotics may be used in cases where infection is likely. People with contaminated wounds who have not been immunized against tetanus within five years may be given a tetanus vaccination. Lacerations may require stitches to stop bleeding and facilitate wound healing with as little scarring as possible. Although it is not common for bleeding from the maxillofacial region to be profuse enough to be life-threatening, it is still necessary to control such bleeding. Severe bleeding occurs as the result of facial trauma in 1–11% of patients, and the origin of this bleeding can be difficult to locate. Nasal packing can be used to control nose bleeds and hematomas that may form on the septum between the nostrils. Such hematomas need to be drained. Mild nasal fractures need nothing more than ice and pain killers, while breaks with severe deformities or associated lacerations may need further treatment, such as moving the bones back into alignment and antibiotic treatment.

Treatment aims to repair the face's natural bony architecture and to leave as little apparent trace of the injury as possible. Fractures may be repaired with metal plates and screws. They may also be wired into place. Bone grafting is another option to repair the bone's architecture, to fill out missing sections, and to provide structural support. Medical literature suggests that early repair of facial injuries, within hours or days, results in better outcomes for function and appearance.

Surgical specialists who commonly treat specific aspects of facial trauma are oral and maxillofacial surgeons. These surgeons are trained in the comprehensive management of trauma to the lower, middle and upper face and have to take written and oral board examinations covering the management of facial injuries.

The application of MRI plays a significant role in the early diagnosis and treatment of SCIWORA in children and adults. Recently, systematic reviews on SCIWORA described the clinical and radiological patterns and correlations with neurological outcome.C.K. Boese und P. Lechler: "Spinal cord injury without radiologic abnormalities in adults: a systematic review." In: "Journal of Trauma and Acute Care Surgery." 78, 2015, S. 320-330 .Boese CK, Oppermann J, Siewe J, Eysel P, Scheyerer MJ, Lechler P.: "Spinal cord injury without radiologic abnormality in children: a systematic review and meta-analysis." In: "Journal of Trauma and Acute Care Surgery." 75, 2013. Boese and Lechler proposed a MRI-based classification for SCIWORA which correlated with the neurological outcome: