There have been no major breakthroughs in the treatment of PKAN, with most pharmacologic treatments focusing on the easing or temporary relieving of PKAN’s symptoms. Iron chelating agents have been used somewhat successfully in retarding the disorder, but they have not been a significant success.

Current research focuses on the future use of high dose pantothenate, the PANK2 enzyme substrate, in possibly alleviating symptoms as well as the further development of iron chelating agents that may be better aimed at reaching the central nervous system and working to better remove excess iron from the individual’s system.

Complications may result from the medication used to treat symptoms. Immobility from the disease can also lead to skin breakdown, respiratory infections, and blood clots, among others.

There is no cure for spinocerebellar ataxia, which is currently considered to be a progressive and irreversible disease, although not all types cause equally severe disability.

In general, treatments are directed towards alleviating symptoms, not the disease itself. Many patients with hereditary or idiopathic forms of ataxia have other symptoms in addition to ataxia. Medications or other therapies might be appropriate for some of these symptoms, which could include tremor, stiffness, depression, spasticity, and sleep disorders, among others. Both onset of initial symptoms and duration of disease are variable. If the disease is caused by a polyglutamine trinucleotide repeat CAG expansion, a longer expansion may lead to an earlier onset and a more radical progression of clinical symptoms. Typically, a person afflicted with this disease will eventually be unable to perform daily tasks (ADLs). However, rehabilitation therapists can help patients to maximize their ability of self-care and delay deterioration to certain extent. Researchers are exploring multiple avenues for a cure including RNAi and the use of Stem Cells and several other avenues.

On January 18, 2017 BioBlast Pharma announced completion of Phase 2a clinical trials of their medication, Trehalose, in the treatment of SCA3. BioBlast has received FDA Fast Track status and Orphan Drug status for their treatment. The information provided by BioBlast in their research indicates that they hope this treatment may prove efficacious in other SCA treatments that have similar pathology related to PolyA and PolyQ diseases.

In addition, Dr. Beverly Davidson has been working on a methodology using RNAi technology to find a potential cure for over 2 decades. Her research began in the mid-1990s and progressed to work with mouse models about a decade later and most recently has moved to a study with non-human primates. The results from her most recent research "are supportive of clinical application of this gene therapy". Dr. Davidson along with Dr. Pedro Gonzalez-Alegre are currently working to move this technique into a Phase 1 clinical trial.

Finally, another gene transfer technology discovered in 2011 has also been shown by Dr. Davidson to hold great promise and offers yet another avenue to a potential future cure.

Physical therapists can assist patients in maintaining their level of independence through therapeutic exercise programmes. One recent research report demonstrated a gain of 2 SARA points (Scale for the Assessment and Rating of Ataxia) from physical therapy. In general, physical therapy emphasises postural balance and gait training for ataxia patients. General conditioning such as range-of-motion exercises and muscle strengthening would also be included in therapeutic exercise programmes. Research showed that spinocerebellar ataxia 2 (SCA2) patients with a mild stage of the disease gained significant improvement in static balance and neurological indices after six months of a physical therapy exercise training program. Occupational therapists may assist patients with incoordination or ataxia issues through the use of adaptive devices. Such devices may include a cane, crutches, walker, or wheelchair for those with impaired gait. Other devices are available to assist with writing, feeding, and self care if hand and arm coordination are impaired. A randomised clinical trial revealed that an intensive rehabilitation program with physical and occupational therapies for patients with degenerative cerebellar diseases can significantly improve functional gains in ataxia, gait, and activities of daily living. Some level of improvement was shown to be maintained 24 weeks post-treatment. Speech language pathologists may use both behavioral intervention strategies as well as augmentative and alternative communication devices to help patients with impaired speech.

In terms of a cure there is currently none available, however for the disease to manifest itself, it requires mutant gene expression. Manipulating the use of protein homoestasis regulators can be therapuetic agents, or a treatment to try and correct an altered function that makes up the pathology is one current idea put forth by Bushart, et al. There is some evidence that for SCA1 and two other polyQ disorders that the pathology can be reversed after the disease is underway. There is no effective treatments that could alter the progression of this disease, therefore care is given, like occupational and physical therapy for gait dysfunction and speech therapy.

Survival rates for those diagnosed with typical PKAN is 11.18 years with a standard deviation of 7.8 years.

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.

There is a wide range of treatments for central nervous system diseases. These can range from surgery to neural rehabilitation or prescribed medications.

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 typically involves improving the patient's quality of life. This is accomplished through the management of symptoms or slowing the rate of demyelination. Treatment can include medication, lifestyle changes (i.e. quit smoking, adjusting daily schedules to include rest periods and dietary changes), counselling, relaxation, physical exercise, patient education and, in some cases, deep brain thalamic stimulation (in the case of tremors). The progressive phase of MS appears driven by the innate immune system, which will directly contribute to the neurodegenerative changes that occur in progressive MS. Until now, there are no therapies that specifically target innate immune cells in MS. As the role of innate immunity in MS becomes better defined, it may be possible to better treat MS by targeting the innate immune system.

Treatments are patient-specific and depend on the symptoms that present with the disorder, as well as the progression of the condition.

Because neuroinflammation has been associated with a variety of neurodegenerative diseases, there is increasing interest to determine whether reducing inflammation will reverse neurodegeneration. Inhibiting inflammatory cytokines, such as IL-1β, decreases neuronal loss seen in neurodegenerative diseases. Current treatments for multiple sclerosis include interferon-B, Glatiramer actetate, and Mitoxantrone, which function by reducing or inhibiting T Cell activation, but have the side effect of systemic immunosuppression In Alzheimer's disease, the use of non-steroidal anti-inflammatory drugs decreases the risk of developing the disease. Current treatments for Alzheimer's disease include NSAIDs and glucocorticoids. NSAIDs function by blocking conversion of prostaglandin H2 into other prostaglandins (PGs) and thromboxane (TX). Prostoglandins and thromboxane act as inflammatory mediators and increase microvascular permeability.

There is no cure for Canavan disease, nor is there a standard course of treatment. Treatment is symptomatic and supportive. There is also an experimental treatment using lithium citrate. When a person has Canavan disease, his or her levels of N-acetyl aspartate are chronically elevated. The lithium citrate has proven in a rat genetic model of Canavan disease to be able to significantly decrease levels of N-acetyl aspartate. When tested on a human, the subject's condition reversed during a two-week wash-out period after withdrawal of lithium.

The investigation revealed both decreased N-acetyl aspartate levels in regions of the brain tested and magnetic resonance spectroscopic values that are more characteristic of normal development and myelination. This evidence suggests that a larger controlled trial of lithium may be warranted as supportive therapy for children with Canavan disease.

Experimental gene therapy trial results, published in 2002, used a healthy gene to take over for the defective one that causes Canavan disease.

In human trials, the results of which were published in 2012, this method appeared to improve the life of the patient without long-term adverse effects during a 5-year follow-up.

Ataxia usually goes away without any treatment. In cases where an underlying cause is identified, your doctor will treat the underlying cause. In extremely rare cases, you may have continuing and disabling symptoms. Treatment includes corticosteroids, Intravenous immunoglobulin, or plasma exchange therapy. Drug treatment to improve muscle coordination has a low success rate. However, the following drugs may be prescribed: clonazepam, amantadine, gabapentin, or buspirone. Occupational or physical therapy may also alleviate lack of coordination. Changes to diet and nutritional supplements may also help. Treatment will depend on the cause. If the acute cerebellar ataxia is due to bleeding, surgery may be needed. For a stroke, medication to thin the blood can be given. Infections may need to be treated with antibiotics. Steroids may be needed for swelling (inflammation) of the cerebellum (such as from multiple sclerosis). Cerebellar ataxia caused by a recent viral infection may not need treatment.

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.

Experimentation has shown that manipulating the levels of thyroid hormone can be considered as a strategy to promote remyelination and prevent irreversible damage in Multiple sclerosis patients. N-cadherin agonists have been identified and observed to stimulate neurite growth and cell migration, key aspects of promoting axon growth and remyelination after injury or disease. It has been shown that intranasal administration of aTf (apotransferrin) can protect myelin and induce remyelination.

Much of the research referenced in this section has been conducted in 2012 and represents very new information about demyelinating diseases and potential therapies for them.

Every disease has different signs and symptoms. Some of them are persistent headache; pain in the face, back, arms, or legs; an inability to concentrate; loss of feeling; memory loss; loss of muscle strength; tremors; seizures; increased reflexes, spasticity, tics; paralysis; and slurred speech. One should seek medical attention if affected by these.

Treatment also involves central nervous system penetrating chemotherapy. Options include intrathecal, intraventricular, and systemic chemotherapy. These must penetrate the blood-brain barrier in order to be effective. Sometimes mixing multiple forms of treatment with chemotherapy seems to be the best route. For example, some significant improvement has been shown as a result of cranial radiation treatment preceding a brief course of intrathecal chemotherapy. Although this is an effective treatment to do, penetrating the blood-brain barrier can cause side effects due to the toxicity in the nervous system. These would include dizziness, confusion, and changes in mental status. Another form could be the use of pharmaceuticals, which have all shown positive results for treatment but should always be consulted with a physician to asses risks.

Autologous stem-cell transplants are shown to be an effective treatment. However, this should be only considered for certain people due to toxicity concerns. It is possible that the transplant may cause problems like septic shock.

Research involving triacetin supplementation has shown promise in a rat model. Triacetin, which can be enzymatically cleaved to form acetate, enters the brain more readily than the negatively charged acetate. The defective enzyme in Canavan disease, aspartoacylase, converts N-acetylaspartate into aspartate and acetate. Mutations in the gene for aspartoacylase prevent the breakdown of N-acetylaspartate, and reduce brain acetate availability during brain development. Acetate supplementation using Triacetin is meant to provide the missing acetate so that brain development can continue normally.

A team of researchers headed by Paola Leone at the University of Medicine and Dentistry of New Jersey, has trialed a procedure involving the insertion of six (6) catheters into the brain that deliver a solution containing 600 billion to 900 billion engineered virus particles. The virus, a modified version of AAV, is designed to replace the aspartoacylase enzyme. Children treated with this procedure to date have shown marked improvements, including the growth of myelin, with decreased levels of the n-acetyl-aspartate toxin.

People whose condition was caused by a recent viral infection should make a full recovery without treatment in a few months. Fine motor skills, such as handwriting, typically have to be practised in order to restore them to their former ability. In more serious cases, strokes, bleeding or infections may sometimes cause permanent symptoms.

Transneuronal degeneration is the death of neurons resulting from the disruption of input from or output to other nearby neurons. It is an active excitotoxic process when a neuron is overstimulated by a neurotransmitter (most commonly glutamate) causing the dysfunction of that neuron (either damaging it or killing it) which drives neighboring neurons into metabolic deficit, resulting in rapid, widespread loss of neurons. This can be either anterograde or retrograde, indicating the direction of the degeneration relative to the original site of damage (see types). There are varying causes for transneuronal degeneration such as brain lesions, disconnection syndromes, respiratory chain deficient neuron interaction, and lobectomies. Although there are different causes, transneuronal degeneration generally results in the same effects (whether they be cellular, dendritic, or axonal) to varying degrees. Transneuronal degeneration is thought to be linked to a number of diseases, most notably Huntington's disease and Alzheimer's disease, and researchers recently have been performing experiments with monkeys and rats, monitoring lesions in different parts of the body to study more closely how exactly the process works.

Autosomal dominant cerebellar ataxia (ADCA) is a form of spinocerebellar ataxia inherited in an autosomal dominant manner. ADCA is a genetically inherited condition that causes deterioration of the nervous system leading to disorder and a decrease or loss of function to regions of the body.

Degeneration occurs at the cellular level and in certain subtypes results in cellular death. Cellular death or dysfunction causes a break or faulty signal in the line of communication from the central nervous system to target muscles in the body. When there is impaired communication or a lack of communication entirely, the muscles in the body do not function correctly. Muscle control complications can be observed in multiple balance, speech, and motor or movement impairment symptoms. ADCA is divided into three types and further subdivided into subtypes known as SCAs (spinocerebellar ataxias).

Transneuronal degeneration can be grouped into two general categories: anterograde and retrograde.

The treatment of dysautonomia can be difficult; since it is made up of many different symptoms, a combination of drug therapies is often required to manage individual symptomatic complaints. Therefore, if an autoimmune neuropathy is the case, then treatment with immunomodulatory therapies is done, or if diabetes mellitus is the cause, control of blood glucose is important. Treatment can include proton-pump inhibitors and H2 receptor antagonists used for digestive symptoms such as acid reflux.

For the treatment of genitourinary autonomic neuropathy medications may include sildenafil (a guanine monophosphate type-5 phosphodiesterase inhibitor). For the treatment of hyperhidrosis, anticholinergic agents such as trihexyphenidyl or scopolamine can be used, also intracutaneous injection of botulinum toxin type A can be used for management in some cases.

Balloon angioplasty, a procedure referred to as transvascular autonomic modulation, is specifically not approved for the treatment of autonomic dysfunction.

It should be noticed that describing the causation of reversible dementia is extremely difficult due to the complicated biopsychological systems and the hard-to-define collection of factors associated with cognitive decline.

Roughly, the etiological factors that contribute to cognitive decline could be assigned into four categories: chemical, environmental, physical, and psychiatric. Chemical intoxication might be attributed to anesthesia, alcohol, heavy metal and commonly used medications. Jenike (1988) has recorded a certain amount of medications which may induce cognitive change in elder people.

The list is provided below.

Environmental sources include overstimulation, radical changes in lifestyle, and sensory impairment. Physical disorders which are mostly induced by the aging process, consist of thyroid and other endocrine-system deprivation; metabolic disturbance, and vitamin deficiency. Psychiatric disorders, such as chronic schizophrenia and depression could also produce cognitive decline.

In summary, the etiological factors of reversible dementia are various, subtle and frequently interactive. Therefore, in-depth medical and psychosocial evaluations are vital for accurate diagnosis and treatment design. It is important for families and patients to understand the difficulties in determining an correct diagnosis and be prepared for probable frustration and confusion during evaluation and assessment process.

Articulation problems resulting from dysarthria are treated by speech language pathologists, using a variety of techniques. Techniques used depend on the effect the dysarthria has on control of the articulators. Traditional treatments target the correction of deficits in rate (of articulation), prosody (appropriate emphasis and inflection, affected e.g. by apraxia of speech, right hemisphere brain damage, etc.), intensity (loudness of the voice, affected e.g. in hypokinetic dysarthrias such as in Parkinson's), resonance (ability to alter the vocal tract and resonating spaces for correct speech sounds) and phonation (control of the vocal folds for appropriate voice quality and valving of the airway). These treatments have usually involved exercises to increase strength and control over articulator muscles (which may be flaccid and weak, or overly tight and difficult to move), and using alternate speaking techniques to increase speaker intelligibility (how well someone's speech is understood by peers). With the speech language pathologist, there are several skills that are important to learn; safe chewing and swallowing techniques, avoiding conversations when feeling tired, repeat words and syllables over and over in order to learn the proper mouth movements, and techniques to deal with the frustration while speaking. Depending on the severity of the dysarthria, another possibility includes learning how to use a computer or flip cards in order to communicate more effectively.

More recent techniques based on the principles of motor learning (PML), such as LSVT (Lee Silverman voice treatment) speech therapy and specifically LSVT may improve voice and speech function in PD. For Parkinson's, aim to retrain speech skills through building new generalised motor programs, and attach great importance to regular practice, through peer/partner support and self-management. Regularity of practice, and when to practice, are the main issues in PML treatments, as they may determine the likelihood of generalization of new motor skills, and therefore how effective a treatment is.

Augmentative and alternative communication (AAC) devices that make coping with a dysarthria easier include speech synthesis and text-based telephones. These allow people who are unintelligible, or may be in the later stages of a progressive illness, to continue to be able to communicate without the need for fully intelligible speech.