There is no known cure for PSP and management is primarily supportive. PSP cases are often split into two subgroups, PSP-Richardson, the classic type, and PSP-Parkinsonism, where a short-term response to levodopa can be obtained. Dyskinesia is an occasional but rare complication of treatment. Amantadine is also sometimes helpful. After a few years the Parkinsonian variant tends to take on Richardson features. Other variants have been described. Botox can be used to treat neck dystonia and blephrospasm, but this can aggravate dysphagia.

Two studies have suggested that rivastigmine may help with cognitive aspects, but the authors of both studies have suggested a larger sampling be used. There is some evidence that the hypnotic zolpidem may improve motor function and eye movements, but only from small-scale studies.

Nicotinamide administration on patients was associated with a sustained improvement in frataxin concentrations towards those seen in asymptomatic carriers during 8 weeks of daily dosing. The daily oral administration of 3.8 g nicotinamide resulted in a 1.5-times increase, whereas 7.5 g resulted in a doubling of frataxin protein concentration.

Idebenone, an antioxidant, was recently removed from the Canadian market in 2013 due to lack of effectiveness. A Cochrane review on antioxidants and other pharmacological treatment of patients with Friedreich ataxia concluded that there is limited but not persuasive evidence of efficacy.

Currently, there is no cure for porencephaly because of the limited resources and knowledge about the neurological disorder. However, several treatment options are available. Treatment may include physical therapy, rehabilitation, medication for seizures or epilepsy, shunt (medical), or neurosurgery (removal of the cyst). According to the location, extent of the lesion, size of cavities, and severity of the disorder, combinations of treatment methods are imposed. In porencephaly patients, patients achieved good seizure control with appropriate drug therapy including valproate, carbamazepine, and clobazam. Also, anti-epileptic drugs served as another positive method of treatment.

Currently, there are no treatments prescribed for PVL. All treatments administered are in response to secondary pathologies that develop as a consequence of the PVL. Because white matter injury in the periventricular region can result in a variety of deficits, neurologists must closely monitor infants diagnosed with PVL in order to determine the severity and extent of their conditions.

Patients are typically treated with an individualized treatment. It is crucial for doctors to observe and maintain organ function: visceral organ failure can potentially occur in untreated patients. Additionally, motor deficits and increased muscle tone are often treated with individualized physical and occupational therapy treatments.

Patients with PSP usually seek or are referred to occupational therapy, speech-language pathology for motor speech changes typically a spastic-ataxic dysarthria, and physical therapy for balance and gait problems with reports of frequent falls. Evidence-based approaches to rehabilitation in PSP are lacking, and currently the majority of research on the subject consists of case reports involving only a small number of patients.

Case reports of rehabilitation programs for patients with PSP generally include limb-coordination activities, tilt-board balancing, gait training, strength training with progressive resistive exercises and isokinetic exercises and stretching of the neck muscles. While some case reports suggest that physiotherapy can offer improvements in balance and gait of patients with PSP, the results cannot be generalized across all patients with PSP as each case report only followed one or two patients. The observations made from these case studies can be useful, however, in helping to guide future research concerning the effectiveness of balance and gait training programs in the management of PSP.

Individuals with PSP are often referred to occupational therapists to help manage their condition and to help enhance their independence. This may include being taught to use mobility aids. Due to their tendency to fall backwards, the use of a walker, particularly one that can be weighted in the front, is recommended over a cane. The use of an appropriate mobility aid will help to decrease the individual’s risk of falls and make them safer to ambulate independently in the community.

Due to their balance problems and irregular movements individuals will need to spend time learning how to safely transfer in their homes as well as in the community. This may include rising from and sitting in chairs safely.

Due to the progressive nature of this disease, all individuals eventually lose their ability to walk and will need to progress to using a wheelchair. Severe dysphagia often follows, and at this point death is often a matter of months.

As of 2017, data on optimal treatment was limited. Therapies with hormones is the standard of care, namely adrenocorticotrophic hormone (ACTH), or oral

corticosteroids such as prednisone. Vigabatrin is also a common consideration, though there is a risk of visual field loss with long term use. The high cost of ACTH leads doctors to avoid it in the US; higher dose prednisone appears to generate equivalent outcomes.

As of 2017 data from clinical trials of the ketogenic diet for treating infantile spams was inconsistent; most trials were as a second-line therapy after failure of drug treatment, and as of 2017 it had not been explored as a first line treatment in an adequately designed clinical trial.

Many chemical medications have been used for a broad range of neuropathic pain including Dejerine–Roussy syndrome. Symptoms are generally not treatable with ordinary analgesics. Traditional chemicals include opiates and anti-depressants. Newer pharmaceuticals include anti-convulsants and Kampo medicine. Pain treatments are most commonly administered via oral medication or periodic injections. Topical In addition, physical therapy has traditionally been used alongside a medication regimen. More recently, electrical stimulation of the brain and spinal cord and caloric stimulation have been explored as treatments.

The most common treatment plans involve a schedule of physical therapy with a medication regimen. Because the pain is mostly unchanging after development, many patients test different medications and eventually choose the regimen that best adapts to their lifestyle, the most common of which are orally and intravenously administered.

Expensive and invasive, the above treatments are not guaranteed to work, and are not meeting the needs of patients. There is a need for a new, less expensive, less invasive form of treatment, two of which are postulated below.

- Spinal cord stimulation has been studied in the last couple of years. In a long case study, 8 patients were given spinal cord stimulation via insertion of a percutaneous lead at the appropriate level of the cervical or thoracic spine. Between 36 and 149 months after the stimulations, the patients were interviewed. 6 of the 8 had received initial pain relief, and three experienced long-term pain relief. Spinal cord stimulation is cheaper than brain stimulation and less invasive, and is thus a more promising option for pain treatment.

- In 2007, Dr. V. S. Ramachandran and his lab proposed that caloric stimulation might be effective in treating Dejerine–Roussy syndrome. They hypothesized that if cold water was streamed into the ear down the auditory canal, the symptoms associated with Dejerine–Roussy syndrome would be alleviated. Ramachandran stated that he had carried out provisional experiments on two patients and believed that their reactions supported his theory.

There are several different treatment approaches to dealing with athetosis. The most common methods are the use of drugs, surgical intervention, and retraining movements of the afflicted person. It is suggested that training a person to relearn movements can be helpful in select situations. Though, generally, this type of treatment will not work, in certain cases it can be found to be very helpful in treating the symptom of athetosis.

Drugs can also be used in the treatment of athetosis, however their collective effectiveness is not very convincing. There is not a single drug that is a standard among treatment. Many different medicines can be used, including:

- Artane

- Cogentin

- Curare, though not practical due to respiratory paralysis

- Tetrabenazine

- Haloperidol

- Thiopropazate

- Diazepam

Most instances of drug use where the symptoms seem to be lessened tend to be in more mild cases of athetosis.

Treatment by surgical intervention can obviously have the most immediate impact, again however, it is not a cure-all. In patients that have cerebral palsy as the cause of their athetosis, it has been demonstrated that a subthalamotomy tends to help relieve the extent of athetosis in approximately half of patients. Additionally, late 19th and early 20th century surgical accounts state that athetosis can be relieved by the removal of a part of the cerebral motor cortex or by cutting a part of the posterior spinal roots. Patients who undergo surgical treatment to relieve the athetosis often see significant improvement in the control of their limbs and digits. While surgery is often very beneficial in the short term and can produce near immediate results, in the long term it has been seen that its effects are not incredibly long lasting.

The severity of the symptoms associated with porencephaly varies significantly across the population of those affected, depending on the location of the cyst and damage of the brain. For some patients with porencephaly, only minor neurological problems may develop, and those patients can live normal lives. Therefore, based on the level of severity, self-care is possible, but for the more serious cases lifelong care will be necessary. For those that have severe disability, early diagnosis, medication, participation in rehabilitation related to fine-motor control skills, and communication therapies can significantly improve the symptoms and ability of the patient with porencephaly to live a normal life. Infants with porencephaly that survive, with proper treatment, can display proper communication skills, movement, and live a normal life.

With many different types of leukodystrophies and causes, treatment therapies vary for each type. Many studies and clinical trials are in progress to find treatment and therapies for each of the different leukodystrophies. Stem cell transplants and gene therapy appear to be the most promising in treating all leukodystrophies providing it is done as early as possible.

For hypomyelinating leukodystrophies, therapeutic research into cell-based therapies appears promising. Oligodendrocyte precursor cells and neural stem cells have been transplanted successfully and have shown to be healthy a year later. Fractional anisotropy and radial diffusivity maps showed possible myelination in the region of the transplant. Induced pluripotent stem cells, oligodendrocyte precursor cells, gene correction, and transplantation to promote the maturation, survival, and myelination of oligodendrocytes seem to be the primary routes for possible treatments.

For three types of leukodystrophies (X-linked adrenoleukodystrophy (X-ALD), metachromatic leukodystrophy (MLD) and Krabbe Disease (globoid cell leukodystrophy - GLD), gene therapy using autologous hematopoietic stem cells to transfer the disease gene with lentiviral vectors have shown to be successful and are currently being used in clinical trials for X-ALD and MLD. The progression of X-ALD has shown to be disrupted with hematopoietic stem cell gene therapy but the exact reason why demyelination stops and the amount of stem cells needed is unclear. While there is an accumulation of very long chain fatty acids in the brain, it does not seem to be the reason behind the disease as gene therapy does not correct it.

Adeno-associated vectors have also been used in intracerebral injections to treat MLD. In some patients with MLD, their IQ increased, nerve conduction improved, their MRIs appeared stable, and had normal enzyme levels. Although the greater majority of patients seem to improve after the transplant, some do not respond well to treatment, which may cause devastating outcomes. For those leukodystrophies that result from a deficiency of lysozyme enzymes, such as Krabbes disease, enzyme replacement therapy seems hopeful, however, this proves difficult as the blood-brain barrier severely limits what can pass through into the central nervous system. Due to this obstacle, most research and clinical trials are turning to allogeneic hematopoietic stem cell transplantation.

There are no treatments, only precautions which can be taken, mainly to reduce trauma to the head and avoiding physiological stress. Melatonin has been shown to provide cytoprotective traits to glial cells exposed to stressors such as excitotoxicity and oxidative stress. These stressors would be detrimental to cells with a genetically reduced activity of protein eIF2B. However, research connecting these ideas have not been conducted yet.

Lesionsing is the intentional destruction of neuronal cells in a particular area used for therapeutic purposes. Though this seems dangerous, vast improvements have been achieved in patients with movement disorders. The exact process generally involves unilateral lesioning in the sensorimotor territory of the GPi. This process is called pallidotomy. It is believed that the success of pallidotomies in reducing the effects of movement disorders may result from the interruption of abnormal neuronal activity in the GPi. This ablation technique can be viewed as simply removing a faulty piece of a circuit. With the damaged piece of the circuit removed, the healthy area of the circuit can continue normal function.

The fetal and neonatal brain is a rapidly changing, developing structure. Because neural structures are still developing and connections are still being formed at birth, many medications that are successful for treatment and protection in the adult central nervous system (CNS) are ineffective in infants. Moreover, some adult treatments have actually been shown to be toxic to developing brains.

Parkinson-plus syndromes are usually more rapidly progressive and less likely to respond to antiparkinsonian medication than PD. However, the additional features of the diseases may respond to medications not used in PD.

Current therapy for Parkinson-plus syndromes is centered around a multidisciplinary treatment of symptoms.

These disorders have been linked to pesticide exposure.

Research has focused on finding a pharmacological treatment that is specific for intention tremor. Limited success has been seen in treating intention tremor with drugs effective at treating essential tremor. Clinical trials of levetiracetam, typically used to treat epilepsy, and pramipexole, used to treat resting tremor, were completed in 2009-2010 to establish their effectiveness in treating kinetic tremor. A clinical trial for riluzole, typically used to treat amyotrophic lateral sclerosis, was completed at the Sapienza University of Rome to evaluate its effectiveness of treating cerebellar ataxia and kinetic tremor.

The eye findings of Parinaud's Syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3–6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported.

Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well.

It is very difficult to treat an intention tremor. The tremor may disappear for a while after a treatment has been administered and then return. This situation is addressed with a different treatment. First, individuals will be asked if they use any of the drugs known to cause tremors. If so, they are asked to stop taking the medication and then evaluated after some time to determine if the medication was related to the onset of the tremor. If the tremor persists, treatment that follows may include drug therapy, lifestyle changes, and more invasive forms of treatment, such as surgery and thalamic deep brain stimulation.

Intention tremors are known to be very difficult to treat with pharmacotherapy and drugs. Although there is no established pharmacological treatment for an intention tremor, several drugs have been found to have positive effects on intention tremors and are used as treatment by many health professionals. Isoniazid, buspirone hydrochloride, glutethimide, carbamazepine, clonazepam, topiramate, zofran, propranolol and primidone have all seen moderate results in treating intention tremor and can be prescribed treatments. Isoniazid inhibits γ-aminobutyric acid-aminotransferase, which the first step in enzymatic breakdown of GABA, thus increasing GABA, the major inhibitory neurotransmitter in the central nervous system. This causes a reduction in cerebellar ataxias. Another neurotransmitter targeted by drugs that has been found to alleviate intention tremors is serotonin. The agonist buspirone hydrochloride, which decreases serotonin's function in the central nervous system, has been viewed as an effective treatment of intention tremors.

Physical therapy has had great results in reducing tremors but usually does not cure them. Relaxation techniques, such as meditation, yoga, hypnosis, and biofeedback, have seen some results with tremors. Wearing wrist weights which weigh down one's hands as they make movements, masking much of the tremor, is a proven home remedy. This is not a treatment, since wearing the weights does not have any lasting effects when they are not on. However, they do help the individual cope with the tremor immediately.

A more radical treatment that is used in individuals who do not respond to drug therapy, physical therapy, or any other treatment listed above, with moderate to severe intention tremors, is surgical intervention. Deep brain stimulation and surgical lesioning of the thalamic nuclei has been found to be an effective long-term treatment with intention tremors.

Deep brain stimulation treats intention tremors but does not help related diseases or disorders such as dyssynergia and dysmetria. Deep brain stimulation involves the implantation of a device called a neurostimulator, sometimes called a 'brain pacemaker'. It sends electrical impulses to specific parts of the brain, changing brain activity in a controlled manner. In the case of an intention tremor, the thalamic nuclei is the region targeted for treatment. This form of treatment causes reversible changes and does not cause any permanent lesions. Since it is reversible, deep brain stimulation is considered fairly safe: Reduction in tremor amplitude is almost guaranteed and sometimes resolved. Some individuals with multiple sclerosis have seen sustained benefits in MS progress.

Thalamotomy is another surgical treatment where lesions of the thalamus nucleus are created to disrupt the tremor circuit. Thalamotomy has been used to treat many forms of tremors, including those that arise from trauma, multiple sclerosis, stroke, and those whose cause it unknown. This is a very invasive, high-risk treatment with many negative effects, such as multiple sclerosis worsening, cognitive dysfunction, worsening of dysarthria, and dysphagia. Immediate positive effects are seen in individuals treated with a thalamotomy procedure. However, the tremor often comes back; it is not a complete treatment. Thalamotomy is in clinical trials to determine the validity of the treatment of intention tremors with all its high risks.

As athetosis is relatively difficult to treat, efforts are being made to help those with the condition live and perform tasks more effectively and more efficiently. One such example of work that has been recently undertaken is a project to help those affected with athetosis to use a computer with more ease. Software for the control of the computer uses joysticks that perform linear filtering to aid in control.

An additional possible treatment option for those afflicted with the symptom is neurostimulation. Studies have begun, and in cerebral palsy patients affected with dystonia-choreoathetosis, it has been demonstrated that neurostimulation has been an effective treatment in lessening symptoms in patients. There has not been a tremendous amount of experimentation, though, in this as a possible treatment option.

There are several different modes of treatment for people with paralysis in their upper limbs. For example, behavioral and environmental treatments may include physiotherapy, occupational therapy, motor learning, strength training, and neurodevelopment treatment. Another treatment may be through the use of splints and casts. Electrophysical agents may be used such as neuromuscular electrical stimulation (NMES). Sometimes pharmacological treatments are necessary such as Botulinum toxin type A. On more severe cases surgery of the upper limbs may be required.

Immediate treatment of drug induced OGC can be achieved with intravenous antimuscarinic benzatropine or procyclidine; which usually are effective within 5 minutes, although may take as long as 30 minutes for full effect. Further doses of procyclidine may be needed after 20 minutes. Any causative new medication should be discontinued. Also can be treated with 25 mg diphenhydramine.

Many disorders of the basal ganglia are due to the dysfunction of a localized area. For this reason gene therapy seems viable for neurodegenerative disorders. Gene therapy is performed by replacing diseased phenotypes with new genetic material. This process is still in the early stages but early results are promising. An example of this therapy might involve implanting cells genetically modified to express tyrosine hydroxylase which, in the body, could be converted to dopamine. Increasing dopamine levels in the basal ganglia could possibly offset the effects of the Parkinson’s Disease.

Although there is no known cure for Krabbe disease, bone marrow transplantation has been shown to benefit cases early in the course of the disease. Generally, treatment for the disorder is symptomatic and supportive. Physical therapy may help maintain or increase muscle tone and circulation. Cord blood transplants have been successful in stopping the disease as long as they are given before overt symptoms appear.

Treatment of any kind of complex visual hallucination requires an understanding of the different pathologies in order to correctly diagnose and treat. If a person is taking a pro-hallucinogenic medication, the first step is to stop taking it. Sometimes improvement will occur spontaneously and pharmacotherapy is not necessary. While there is not a lot of evidence of effective pharmacological treatment, antipsychotics and anticonvulsants have been used in some cases to control hallucinations. Since peduncular hallucinosis occurs due to an excess of serotonin, modern antipsychotics are used to block both dopamine and serotonin receptors, preventing the overstimulation of the lateral geniculate nucleus. The drug generically called carbamazepine increases GABA, which prevents the LGN from firing, thereby increasing the inhibition of the LGN. Regular antipsychotics as well as antidepressants can also be helpful in reducing or eliminating peduncular hallucinosis.

More invasive treatments include corrective surgery such as cataract surgery, laser photocoagulation of the retina, and use of optical correcting devices. Tumor removal can also help to relieve compression in the brain, which can decrease or eliminate peduncular hallucinosis. Some hallucinations may be due to underlying cardiovascular disease, so in these cases the appropriate treatment includes control of hypertension and diabetes. As described, the type of treatment varies widely depending on the causation behind the complex visual hallucinations.