Treatment varies according to the type and severity of the encephalopathy. Anticonvulsants may be prescribed to reduce or halt any seizures. Changes to diet and nutritional supplements may help some patients. In severe cases, dialysis or organ replacement surgery may be needed.

Sympathomimetic drugs can increase motivation, cognition, motor performance and alertness in patients with encephalopathy caused by brain injury, chronic infections, strokes, brain tumors.

Treatment is mainly for the symptoms that toxic encephalopathy brings upon victims, varying depending on how severe the case is. Diet changes and nutritional supplements may help some patients. To reduce or halt seizures, anticonvulsants may be prescribed. Dialysis or organ replacement surgery may be needed in some severe cases.

Management of affected individuals consists of immediate removal from exposure to the toxic substance(s), treatment of the common clinical manifestation of depression if present, and counselling for the provision of life strategies to help cope with the potentially debilitating condition.

Treating the underlying cause of the disorder may improve or reverse symptoms. However, in some cases, the encephalopathy may cause permanent structural changes and irreversible damage to the brain. These permanent deficits can be considered a form of stable dementia. Some encephalopathies can be fatal.

During the acute stage, treatment is aimed at reducing the inflammation. As in other inflammatory diseases, steroids may be used first of all, either as a short course of high-dose treatment, or in a lower dose for long-term treatment. Intravenous immunoglobulin is also effective both in the short term and in the long term, particularly in adults where it has been proposed as first-line treatment. Other similar treatments include plasmapheresis and tacrolimus, though there is less evidence for these. None of these treatments can prevent permanent disability from developing.

During the residual stage of the illness when there is no longer active inflammation, treatment is aimed at improving the remaining symptoms. Standard anti-epileptic drugs are usually ineffective in controlling seizures, and it may be necessary to surgically remove or disconnect the affected cerebral hemisphere, in an operation called hemispherectomy. This usually results in further weakness, hemianopsia and cognitive problems, but the other side of the brain may be able to take over some of the function, particularly in young children. The operation may not be advisable if the left hemisphere is affected, since this hemisphere contains most of the parts of the brain that control language. However, hemispherectomy is often very effective in reducing seizures.

To minimise the risk of this condition developing from its most common cause, overly rapid reversal of hyponatremia, the hyponatremia should be corrected at a rate not exceeding 10 mmol/L/24 h or 0.5 mEq/L/h; or 18 m/Eq/L/48hrs; thus avoiding demyelination. No large clinical trials have been performed to examine the efficacy of therapeutic re-lowering of serum sodium, or other interventions sometimes advocated such as steroids or plasma exchange.

Alcoholic patients should receive vitamin supplementation and a formal evaluation of their nutritional status.

Once osmotic demyelination has begun, there is no cure or specific treatment. Care is mainly supportive. Alcoholics are usually given vitamins to correct for other deficiencies. The favourable factors contributing to the good outcome in CPM without hyponatremia were: concurrent treatment of all electrolyte disturbances, early Intensive Care Unit involvement at the advent of respiratory complications, early introduction of feeding including thiamine supplements with close monitoring of the electrolyte changes and input.

Research has led to improved outcomes. Animal studies suggest that inositol reduces the severity of osmotic demyelination syndrome if given before attempting to correct chronic hyponatraemia. Further study is required before using inositol in humans for this purpose.

Exercise is a promising mechanism of prevention and treatment for various diseases characterized by neuroinflammation. Aerobic exercise is used widely to reduce inflammation in the periphery. Exercise has been shown to decreases proliferation of microglia in the brain, decrease hippocampal expression of immune-related genes, and reduce expression of inflammatory cytokines such as TNF-α.

Currently no treatment for vegetative state exists that would satisfy the efficacy criteria of evidence-based medicine. Several methods have been proposed which can roughly be subdivided into four categories: pharmacological methods, surgery, physical therapy, and various stimulation techniques. Pharmacological therapy mainly uses activating substances such as tricyclic antidepressants or methylphenidate. Mixed results have been reported using dopaminergic drugs such as amantadine and bromocriptine and stimulants such as dextroamphetamine. Surgical methods such as deep brain stimulation are used less frequently due to the invasiveness of the procedures. Stimulation techniques include sensory stimulation, sensory regulation, music and musicokinetic therapy, social-tactile interaction, and cortical stimulation.

Treatment is variable depending on individuals. Some treatments work extremely well with some patients and not at all with others. Some treatments include Therapy with thiamine and vitamin B complex. Alcohol consumption should be stopped. Some patients survive, but with residual brain damage and dementia. Others remain in comas that eventually lead to death. Nutritional counseling is also recommended. Treatment is often similar to those administered for Wenicke-Korsakoff syndrome or for alcoholism.

Type A has 21% mortality rate and an 81% long-term disability rate. Type B has a 0% mortality rate and a 19% long-term disability rate.

Currently no effective treatment exists for kernicterus. Future therapies may include neuroregeneration. A handful of patients have undergone deep brain stimulation, and experienced some benefit. Drugs such as baclofen, clonazepam, and artane are often used to manage movement disorders associated with kernicterus. Proton pump inhibitors are also used to help with reflux. Cochlear implants and hearing aids have also been known to improve the hearing loss that can come with kernicterus (auditory neuropathy - ANSD).

There is limited evidence that the hypnotic drug zolpidem has an effect. The results of the few scientific studies that have been published so far on the effectiveness of zolpidem have been contradictory.

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.

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.

Binswanger's disease has no cure and has been shown to be the most severe impairment of all of the vascular dementias. The best way to manage the vascular risk factors that contribute to poor perfusion in the brain is to treat the cause, such as chronic hypertension or diabetes. It has been shown that current Alzheimer’s medication, donepezil (trade name Aricept), may help Binswanger’s Disease patients as well . Donepezil increases the acetylcholine in the brain through a choline esterase inhibitor which deactivates the enzyme that breaks down acetylcholine. Alzheimer as well as Binswanger patients have low levels of acetylcholine and this helps to restore the normal levels of neurotransmitters in the brain. This drug may improve memory, awareness, and the ability to function. If no medical interception of the disease is performed then the disease will continue to worsen as the patient ages due to the continuing atrophy of the white matter from whatever was its original cause.

Certain facilities are equipped to handle TBI better than others; initial measures include transporting patients to an appropriate treatment center. Both during transport and in hospital the primary concerns are ensuring proper oxygen supply, maintaining adequate blood flow to the brain, and controlling raised intracranial pressure (ICP), since high ICP deprives the brain of badly needed blood flow and can cause deadly brain herniation. Other methods to prevent damage include management of other injuries and prevention of seizures. Some data supports the use of hyperbaric oxygen therapy to improve outcomes.

Neuroimaging is helpful but not flawless in detecting raised ICP. A more accurate way to measure ICP is to place a catheter into a ventricle of the brain, which has the added benefit of allowing cerebrospinal fluid to drain, releasing pressure in the skull. Treatment of raised ICP may be as simple as tilting the patient's bed and straightening the head to promote blood flow through the veins of the neck. Sedatives, analgesics and paralytic agents are often used. Hypertonic saline can improve ICP by reducing the amount of cerebral water (swelling), though it is used with caution to avoid electrolyte imbalances or heart failure. Mannitol, an osmotic diuretic, appears to be equally effective at reducing ICP. Some concerns; however, have been raised regarding some of the studies performed. Diuretics, drugs that increase urine output to reduce excessive fluid in the system, may be used to treat high intracranial pressures, but may cause hypovolemia (insufficient blood volume). Hyperventilation (larger and/or faster breaths) reduces carbon dioxide levels and causes blood vessels to constrict; this decreases blood flow to the brain and reduces ICP, but it potentially causes ischemia and is, therefore, used only in the short term. Administration of corticosteroids is associated with an increased risk of death, and so it is recommended that they not be given routinely.

Endotracheal intubation and mechanical ventilation may be used to ensure proper oxygen supply and provide a secure airway. Hypotension (low blood pressure), which has a devastating outcome in TBI, can be prevented by giving intravenous fluids to maintain a normal blood pressure. Failing to maintain blood pressure can result in inadequate blood flow to the brain. Blood pressure may be kept at an artificially high level under controlled conditions by infusion of norepinephrine or similar drugs; this helps maintain cerebral perfusion. Body temperature is carefully regulated because increased temperature raises the brain's metabolic needs, potentially depriving it of nutrients. Seizures are common. While they can be treated with benzodiazepines, these drugs are used carefully because they can depress breathing and lower blood pressure. TBI patients are more susceptible to side effects and may react adversely or be inordinately sensitive to some pharmacological agents. During treatment monitoring continues for signs of deterioration such as a decreasing level of consciousness.

Traumatic brain injury may cause a range of serious coincidental complications that include cardiac arrhythmias and neurogenic pulmonary edema. These conditions must be adequately treated and stabilised as part of the core care for these patients.

Surgery can be performed on mass lesions or to eliminate objects that have penetrated the brain. Mass lesions such as contusions or hematomas causing a significant mass effect (shift of intracranial structures) are considered emergencies and are removed surgically. For intracranial hematomas, the collected blood may be removed using suction or forceps or it may be floated off with water. Surgeons look for hemorrhaging blood vessels and seek to control bleeding. In penetrating brain injury, damaged tissue is surgically debrided, and craniotomy may be needed. Craniotomy, in which part of the skull is removed, may be needed to remove pieces of fractured skull or objects embedded in the brain. Decompressive craniectomy (DC) is performed routinely in the very short period following TBI during operations to treat hematomas; part of the skull is removed temporarily (primary DC). DC performed hours or days after TBI in order to control high intracranial pressures (secondary DC) has not been shown to improve outcome in some trials and may be associated with severe side-effects.

Like diagnosis, treating CSE is difficult due to how vaguely defined it is, as well as lack of data on the mechanism of CSE effects on neural tissue. There is no existing treatment that is effective at completely recovering any neurological or physical function lost due to CSE. This is believed to be because of the limited regeneration capabilities in the central nervous system. Furthermore, existing symptoms of CSE can potentially worsen with age. Some symptoms of CSE, such as depression and sleep issues, can be treated separately, and therapy is available to help patients adjust to any disabilities. Current treatment for CSE involves treating accompanying psychopathology, symptoms, and preventing further deterioration.

It is important to begin emergency treatment within the so-called "golden hour" following the injury. People with moderate to severe injuries are likely to receive treatment in an intensive care unit followed by a neurosurgical ward. Treatment depends on the recovery stage of the patient. In the acute stage the primary aim of the medical personnel is to stabilize the patient and focus on preventing further injury because little can be done to reverse the initial damage caused by trauma. Rehabilitation is the main treatment for the subacute and chronic stages of recovery. International clinical guidelines have been proposed with the aim of guiding decisions in TBI treatment, as defined by an authoritative examination of current evidence.

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.

The onset of Wernicke's encephalopathy is considered a medical emergency, and thus thiamine administration should be initiated immediately when the disease is suspected. Prompt administration of thiamine to patients with Wernicke's encephalopathy can prevent the disorder from developing into Wernicke–Korsakoff syndrome, or reduce its severity. Treatment can also reduce the progression of the deficits caused by WKS, but will not completely reverse existing deficits. WKS will continue to be present, at least partially, in 80% of patients. Patients suffering from WE should be given a minimum dose of 500 mg of thiamine hydrochloride, delivered by infusion over a 30-minute period for two to three days. If no response is seen then treatment should be discontinued but for those patients that do respond, treatment should be continued with a 250 mg dose delivered intravenously or intramuscularly for three to five days unless the patient stops improving. Such prompt administration of thiamine may be a life-saving measure. Banana bags, a bag of intravenous fluids containing vitamins and minerals, is one means of treatment.

As described, Korsakoff 's syndrome usually follows or accompanies Wernicke's encephalopathy. If treated quickly, it may be possible to prevent the development of Korsakoff's syndrome with thiamine treatments. This treatment is not guaranteed to be effective and the thiamine needs to be administered adequately in both dose and duration. A study on Wernicke-Korsakoff's syndrome showed that with consistent thiamine treatment there were noticeable improvements in mental status after only 2–3 weeks of therapy. Thus, there is hope that with treatment Wernicke's encephalopathy will not necessarily progress to WKS.

In order to reduce the risk of developing WKS it is important to limit the intake of alcohol or drink in order to ensure that proper nutrition needs are met. A healthy diet is imperative for proper nutrition which, in combination with thiamine supplements, may reduce the chance of developing WKS. This prevention method may specifically help heavy drinkers who refuse to or are unable to quit.

The only effective way at preventing kernicterus is to lower the serum bilirubin levels either by phototherapy or exchange transfusion. Visual inspection is never sufficient; therefore, it is best to use a bilimeter or blood test to determine a baby's risk for developing kernicterus. These numbers can then be plotted on the Bhutani nomogram.

There are no effective drugs that inhibit or cure the virus infection without toxicity. Therefore, treatment aims at reversing the immune deficiency to slow or stop the disease progress. In patients on immunosuppression, this means stopping the drugs or using plasma exchange to accelerate the removal of the biologic agent that put the person at risk for PML.

In HIV-infected people, this may mean starting highly active antiretroviral therapy (HAART). AIDS patients starting HAART after being diagnosed with PML tend to have a slightly longer survival time than patients who were already on HAART and then develop PML. Some AIDS patients with PML have been able to survive for several years, with HAART. A rare complication of effective HAART is immune reconstitution inflammatory syndrome (IRIS), in which increased immune system activity actually increases the damage caused by the JCV infection; although IRIS can often be managed with medication, it is extremely dangerous in PML.

Cidofovir was studied as possible treatment for PML and has been used on a case by case basis, working in some, but not others.

Cytarabine (also known as ARA-C), a chemotherapy drug used to treat certain cancers, has been prescribed on an experimental basis for a small number of non-AIDS PML patients and stabilized the neurological condition of a minority of these patients. One patient regained some cognitive function lost as a result of PML.

In June 2010, the first case report appeared of a PML patient being successfully treated with the anti malaria drug mefloquine with activity against the JC virus. The patient cleared the virus and had no further neurological deterioration.

Two case reports of using interleukin-2 successfully have been published. Some success have been reported with mirtazapine, but this has not been demonstrated in clinical trials.

A number of drugs work against JC virus in cell culture, but there is no proven, effective therapy in humans.

For example, 1-O-hexadecyloxypropyl-cidofovir (CMX001), suppresses JCV but has been found to have toxicity at therapeutic dosage. The number of patients treated with other therapies is too low to demonstrate effectiveness.

There is no current cure for superficial siderosis, only treatments to help alleviate the current symptoms and to help prevent the development of further symptoms. If a source of bleeding can be identified (sources are frequently not found), then surgical correction of the bleeding source can be performed; this has proved to be effective in halting the development of further symptoms in some cases and has no effect on symptoms that have already presented.

Patients with superficial siderosis are often treated with deferiprone, a lipid-soluble iron chelator, as this medication has been demonstrated to chelate iron in the central nervous system.

While on this drug you will need a frequent blood test (weekly) to keep an eye on the blood levels as this drug is known to lower certain blood levels such as the neutrophils and WBC (white blood count) and etc. While it is ok if these levels go low in the average person, if they go low while taking Deferiprone Ferriprox it can cause life threatening infections that can result in death.

Alleviation of the most common symptom, hearing loss, has been varyingly successful through the use of cochlear implants. Most people do not notice a large improvement after successful implantation, which is most likely due to damage to the vestibulocochlear nerve (cranial nerve VIII) and not the cochlea itself. Some people fare far better, with a return to near normal hearing, but there is little ability to detect how well a person will respond to this treatment at this time.

Treatment of OBS varies with the causative disorder or disease. It is important to note that it is not a primary diagnosis and a cause needs to be sought out and treated.

It was once assumed that anyone suffering from Korsakoff's syndrome would eventually need full-time care. This is still often the case, but rehabilitation can help regain some, albeit often limited, level of independence. Treatment involves the replacement or supplementation of thiamine by intravenous (IV) or intramuscular (IM) injection, together with proper nutrition and hydration. However, the amnesia and brain damage caused by the disease does not always respond to thiamine replacement therapy. In some cases, drug therapy is recommended. Treatment of the patient typically requires taking thiamine orally for 3 to 12 months, though only about 20 percent of cases are reversible. If treatment is successful, improvement will become apparent within two years, although recovery is slow and often incomplete.

As an immediate form of treatment, a pairing of IV or IM thiamine with a high concentration of B-complex vitamins can be administered three times daily for period of 2–3 days. In most cases, an effective response from patients will be observed. A dose of 1 gram of thiamine can also be administered to achieve a clinical response. In patients who are seriously malnourished, the sudden availability of glucose without proper bodily levels of thiamine to metabolize is thought to cause damage to cells. Thus, the administration of thiamine along with an intravenous form of glucose is often good practice.

Treatment for the memory aspect of Korsakoff's syndrome can also include domain-specific learning, which when used for rehabilitation is called the method of vanishing cues. Such treatments aim to use patients' intact memory processes as the basis for rehabilitation. Patients who used the method of vanishing cues in therapy were found to learn and retain information more easily.

People diagnosed with Korsakoff's are reported to have a normal life expectancy, presuming that they abstain from alcohol and follow a balanced diet. Empirical research has suggested that good health practices have beneficial effects in Korsakoff's syndrome.