Unfortunately, cerebral atrophy is not usually preventable, however there are steps that can be taken to reduce the risks such as controlling your blood pressure, eating a healthy balanced diet including omega-3's and antioxidants, and staying active mentally, physically, and socially.

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During the residual stage of the illness when there is no longer active inflammation, treatment is aimed at improving the remaining symptoms.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.

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.

Although no specific treatment exists, the disease can be managed with anticonvulsants, physiotherapy, etc.

In terms of the management of spinal and bulbar muscular atrophy, no cure is known and treatment is supportive. Rehabilitation to slow muscle weakness can prove positive, though the prognosis indicates some individuals will require the use of a wheelchair in later stages of life.

Surgery may achieve correction of the spine, and early surgical intervention should be done in cases where prolonged survival is expected. Preferred nonsurgical treatment occurs due to the high rate of repeated dislocation of the hip.

There is no known cure for MSA and management is primarily supportive.

Ongoing care from a neurologist specializing in "movement disorders" is recommended as the complex symptoms of MSA are often not familiar to less-specialized health care professionals.

One particularly serious problem, the drop in blood pressure upon standing up (with risk of fainting and thus injury from falling) often responds to fludrocortisone, a synthetic mineralocorticoid. Another common drug treatment is midodrine (an alpha-agonist). Non-drug treatments include "head-up tilt" (elevating the head of the whole bed by about 10 degrees), salt tablets or increasing salt in the diet, generous intake of fluids, and pressure (elastic) stockings. Avoidance of triggers of low blood pressure (such as hot weather, alcohol, and dehydration) are crucial.

Hospice/homecare services can be very useful as disability progresses.

Levodopa (L-Dopa), a drug used in the treatment of Parkinson's disease, improves parkinsonian symptoms in a small percentage of MSA patients. A recent trial reported that only 1.5% of MSA patients experienced a less than 50% improvement when taking levodopa, and even this was a transient effect lasting less than one year. Poor response to L-Dopa has been suggested as a possible element in the differential diagnosis of MSA from Parkinson's disease.

A November, 2008 study conducted in Europe failed to find an effect for the drug riluzole in treating MSA or PSP.

Physiotherapy intervention aims to improve balance and gait of OPCA patients, by stimulating neuroplastic changes in the atrophied neural structure. A challenge-oriented treatment program has previously been shown to be beneficial for individuals with ataxia from OPCA. The treatment program was composed of repetitive training with task challenges (e.g. obstacle course) and/or novel motor skills acquisition over a 12-week period under the supervision of a physiotherapist. Task challenges were progressed only when the patient showed mastery of a task.

Overground harness systems may be used to allow OPCA patients to challenge their balance without chance of falling. Furthermore, home exercise programs and/or aquatic exercises are used to allow more repetitions to facilitate balance learning. Treatment programs should be frequently monitored and adjusted based on a patient's progress. Outcome measures such as the Berg Balance Scale, Dynamic Gait Index and activities-specific balance confidence scales are useful to assess patient’s progress over time.

The treatment for Bonnet–Dechaume–Blanc syndrome is controversial due to a lack of consensus on the different therapeutic procedures for treating arteriovenous malformations. The first successful treatment was performed by Morgan et al. They combined intracranial resection, ligation of ophthalmic artery, and selective arterial ligature of the external carotid artery, but the patient did not have retinal vascular malformations.

If lesions are present, they are watched closely for changes in size. Prognosis is best when lesions are less than 3 cm in length. Most complications occur when the lesions are greater than 6 cm in size. Surgical intervention for intracranial lesions has been done successfully. Nonsurgical treatments include embolization, radiation therapy, and continued observation. Arterial vascular malformations may be treated with the cyberknife treatment. Possible treatment for cerebral arterial vascular malformations include stereotactic radiosurgery, endovascular embolization, and microsurgical resection.

When pursuing treatment, it is important to consider the size of the malformations, their locations, and the neurological involvement. Because it is a congenital disorder, there are not preventative steps to take aside from regular follow ups with a doctor to keep an eye on the symptoms so that future complications are avoided.

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.

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.

Management by rehabilitation professionals (physiatrists, physiotherapists, occupational therapists, speech therapists, and others) for problems with walking/movement, daily tasks, and speech problems is essential.

Physiotherapy can help to maintain the patient’s mobility and will help to prevent contractures. Instructing patients in gait training will help to improve their mobility and decrease their risk of falls. A physiotherapist may also prescribe mobility aids such as a cane or a walker to increase the patient’s safety. Other ways a physiotherapist can help to improve the patient’s safety are to teach them to move and transfer from sitting to standing slowly to decrease risk of falls and limit the effect of postural hypotension. Instruction in ankle pumping helps to return blood in the legs to the systemic circulation. To further control the postural hypotension, raising the head of the bed by 8 in (20.3 cm) while sleeping may be indicated as well as the use of elastic compression garments.

Speech and language therapists may assist in assessing, treating and supporting speech (dysarthria) and swallowing difficulties (dysphagia). Early intervention of swallowing difficulties is particularly useful to allow for discussion around tube feeding further in the disease progression.{doubtful - citation needed} At some point in the progression of the disease, fluid and food modification may be suggested. Speech changes mean that alternative communication may be needed, for example communication aids or word charts.

Social workers and occupational therapists can also help with coping with disability through the provision of equipment and home adaptations, services for caregivers and access to healthcare services, both for the person with MSA as well as family caregivers.

While most cerebral atrophy is said to be irreversible there are some recent studies that show this is not always the case. A child who was treated with ACTH originally showed atrophy, but four months after treatment the brain was seemingly normal again.

Chronic alcoholism is known to be associated with cerebral atrophy in addition to motor dysfunction and impairment in higher brain function. Because some of the behavioral deficits have shown improvement after abstinence from alcohol, a study looked to see if cerebral atrophy could be reversed too. Researchers took CT scans of the 8 study participants in order to measure cortical volume over time. Although decrease in atrophy does not equate clinical improvement, the CT scans of 50% of participants showed partial improvement, giving hope that cerebral atrophy could be a reversible process.

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.

Since pseudobulbar palsy is a syndrome associated with other diseases, treating the underlying disease may eventually reduce the symptoms of pseudobulbar palsy.

Possible pharmacological interventions for pseudobulbar affect include the tricyclic antidepressants, serotonin reuptake inhibitors, and a novel approach utilizing dextromethorphan and quinidine sulfate. Nuedexta is an FDA approved medication for pseudobulbar affect. Dextromethorphan, an N-methyl-D-aspartate receptor antagonist, inhibits glutamatergic transmission in the regions of the brainstem and cerebellum, which are hypothesized to be involved in pseudobulbar symptoms, and acts as a sigma ligand, binding to the sigma-1 receptors that mediate the emotional motor expression.

One drug in test seemed to prevent the type of muscle loss that occurs in immobile, bedridden patients.

Testing on mice showed that it blocked the activity of a protein present in the muscle that is involved in muscle atrophy. However, the drug's long-term effect on the heart precludes its routine use in humans, and other drugs are being sought.

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.

The adrenal glands atrophy during prolonged use of exogenous glucocorticoids like prednisone. Atrophy of the breasts can occur with prolonged estrogen reduction, as with anorexia nervosa or menopause. Testicular atrophy with prolonged use of enough exogenous sex steroid (either androgen or estrogen) to reduce gonadotropin secretion.

Medical management may involve immunosuppressive drugs such as methotrexate, corticosteroids, cyclophosphamide, and azathioprine. No randomized controlled trials have yet been conducted to evaluate such treatments, so the benefits have not been clearly established.

Specific and accepted scientific treatment for PCA has yet to be discovered; this may be due to the rarity and variations of the disease. At times PCA patients are treated with prescriptions originally created for treatment of AD such as, cholinesterase inhibitors, Donepezil, Rivastigmine and Galantamine, and Memantine. Antidepressant drugs have also provided some positive effects.

Patients may find success with non-prescription treatments such as psychological treatments. PCA patients may find assistance in meeting with an occupational therapist or sensory team for aid in adapting to the PCA symptoms, especially for visual changes. People with PCA and their caregivers are likely to have different needs to more typical cases of Alzheimer's disease, and may benefit from specialized support groups such as the PCA Support Group based at University College London, or other groups for young people with dementia. No study to date has been definitive to provide accepted conclusive analysis on treatment options.

Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.

Most ophthalmologists will not advocate any treatment unless visual loss is present and ongoing. Reports of patients with ONSM having no change in their vision for multiple years are not uncommon. If loss of vision occurs, radiation therapy will improve vision in about ⅓ of cases, and preserve vision in about ⅓ of cases. Surgery has traditionally been associated with rapid deteroriation of vision. However, newer surgical techniques may prove better for the treatment of ONSM.

Because the exact cause of CBD is unknown, there exists no formal treatment for the disease. Instead, treatments focus on minimizing the appearance or effect of the symptoms resulting from CBD. The most easily treatable symptom of CBD is parkinsonism, and the most common form of treatment for this symptom is the application of dopaminergic drugs. However, in general only moderate improvement is seen and the relief from the symptom is not long-lasting. In addition, palliative therapies, including the implementation of wheelchairs, speech therapy, and feeding techniques, are often used to alleviate many of the symptoms that show no improvement with drug administration.

Treatment for Sturge–Weber syndrome is symptomatic. Laser treatment may be used to lighten or remove the birthmark. Anticonvulsant medications may be used to control seizures. Doctors recommend early monitoring for glaucoma, and surgery may be performed on more serious cases. When one side of the brain is affected and anticonvulsants prove ineffective, the standard treatment is neurosurgery to remove or disconnect the affected part of the brain (hemispherectomy). Physical therapy should be considered for infants and children with muscle weakness. Educational therapy is often prescribed for those with mental retardation or developmental delays, but there is no complete treatment for the delays.

Brain surgery involving removing the portion of the brain that is affected by the disorder can be successful in controlling the seizures so that the patient has only a few seizures that are much less intense than pre-surgery. Surgeons may also opt to "switch-off" the affected side of the brain.

Latanoprost (Xalatan), a prostaglandin, may significantly reduce IOP (intraocular pressure) in patients with glaucoma associated with Sturge–Weber syndrome. Latanoprost is commercially formulated as an aqueous solution in a concentration of 0.005% preserved with 0.02% benzalkonium chloride (BAC). The recommended dosage of latanoprost is one drop daily in the evening, which permits better diurnal IOP control than does morning instillation. Its effect is independent of race, gender or age, and it has few to no side effects. Contraindications include a history of CME, epiretinal membrane formation, vitreous loss during cataract surgery, history of macular edema associated with branch retinal vein occlusion, history of anterior uveitis, and diabetes mellitus. It is also wise to advise patients that unilateral treatment can result in heterochromia or hypertrichosis that may become cosmetically objectionable.

Direct treatment that stimulates the pyruvate dehydrogenase complex (PDC), provides alternative fuels, and prevents acute worsening of the syndrome. However, some correction of acidosis does not reverse all the symptoms. CNS damage is common and limits a full recovery. Ketogenic diets, with high fat and low carbohydrate intake have been used to control or minimize lactic acidosis and anecdotal evidence shows successful control of the disease, slowing progress and often showing rapid improvement. No study has yet been published demonstrating the effectiveness of the ketogenic diet for treatment of PDCD.

There is some evidence that dichloroacetate reduces the inhibitory phosphorylation of pyruvate dehydrogenase complex and thereby activates any residual functioning complex. Resolution of lactic acidosis is observed in patients with E1 alpha enzyme subunit mutations that reduce enzyme stability. However, treatment with dichloroacetate does not improve neurological damage. Oral citrate is often used to treat acidosis.

In a confirmed medical diagnosis, therapy is used to isolate and begin treating the cause of the disorder. Thereafter, psychiatric medication is used a secondary step in treatment. Medications include antipsychotic, antidepressant, or sedation-inducing, varying on the patients severity.

Treatment of psychorganic syndrome is directed at the main disease. Nootropics like piracetam, have had positive effects on patients. Vitamin therapy, antioxidants, neurotropic, and cerebroprotective have also found to be effective when put on a repeat course.