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.

Currently there is no curative treatment for KSS. Because it is a rare condition, there are only case reports of treatments with very little data to support their effectiveness. Several promising discoveries have been reported which may support the discovery of new treatments with further research. Satellite cells are responsible for muscle fiber regeneration. It has been noted that mutant mtDNA is rare or undetectable in satellite cells cultured from patients with KSS. Shoubridge et al. (1997) asked the question whether wildtype mtDNA could be restored to muscle tissue by encouraging muscle regeneration. In the forementioned study, regenerating muscle fibers were sampled at the original biopsy site, and it was found that they were essentially homoplasmic for wildtype mtDNA. Perhaps with future techniques of promoting muscle cell regeneration and satellite cell proliferation, functional status in KSS patients could be greatly improved.

One study described a patient with KSS who had reduced serum levels of coenzyme Q10. Administration of 60–120 mg of Coenzyme Q10 for 3 months resulted in normalization of lactate and pyruvate levels, improvement of previously diagnosed first degree AV block, and improvement of ocular movements.

A screening ECG is recommended in all patients presenting with CPEO. In KSS, implantation of pacemaker is advised following the development of significant conduction disease, even in asymptomatic patients.

Screening for endocrinologic disorders should be performed, including measuring serum glucose levels, thyroid function tests, calcium and magnesium levels, and serum electrolyte levels. Hyperaldosteronism is seen in 3% of KSS patients.

The importance of correctly recognizing progressive muscular atrophy as opposed to ALS is important for several reasons.

- 1) the prognosis is a little better. A recent study found the 5-year survival rate in PMA to be 33% (vs 20% in ALS) and the 10-year survival rate to be 12% (vs 6% in ALS).

- 2) Patients with PMA do not suffer from the cognitive change identified in certain groups of patients with MND.

- 3) Because PMA patients do not have UMN signs, they usually do not meet the "World Federation of Neurology El Escorial Research Criteria" for “Definite” or “Probable” ALS and so are ineligible to participate in the majority of clinical research trials such as drugs trials or brain scans.

- 4) Because of its rarity (even compared to ALS) and confusion about the condition, some insurance policies or local healthcare policies may not recognize PMA as being the life-changing illness that it is. In cases where being classified as being PMA rather than ALS is likely to restrict access to services, it may be preferable to be diagnosed as "slowly progressive ALS" or "lower motor neuron predominant" ALS.

An initial diagnosis of PMA could turn out to be slowly progressive ALS many years later, sometimes even decades after the initial diagnosis. The occurrence of upper motor neurone symptoms such as brisk reflexes, spasticity, or a Babinski sign would indicate a progression to ALS; the correct diagnosis is also occasionally made on autopsy.

Physiotherapy

To increase strength of muscle

To improve muscle functions

Electrical modalities =Electric stimulation.etc.

Occupational Therapy

Positioning, ROM, Sensory, Splinting

As with other neuroleptic-induced tardive syndromes, there is no definite treatment for tardive dysphrenia. The continuing to take the drug or changing the dosage of the atypical antipsychotic drug in use, or augmenting it with a typical antipsychotic, can alleviate symptoms temporarily. However, these solutions carry the risk of worsening or perpetuating the iatrogenesis in the long term.

Some patients could gradually benefit from changing to a dopamine D2 receptor partial agonist agent like clozapine. These drugs do not induce up-regulation, instead acting as a prophylactic.

Muscle atrophy can be opposed by the signaling pathways which induce muscle hypertrophy, or an increase in muscle size. Therefore, one way in which not exercise induces an increase in muscle mass is to down regulate the pathways which have the opposite effect.

β-hydroxy β-methylbutyrate (HMB), a metabolite of leucine which is sold as a dietary supplement, has demonstrated efficacy in preventing the loss of muscle mass in several muscle wasting conditions in humans, particularly sarcopenia. A growing body of evidence supports the efficacy of HMB as a treatment for reducing, or even reversing, the loss of muscle mass, muscle function, and muscle strength in hypercatabolic disease states such as cancer cachexia; consequently, it is recommended that both the prevention and treatment of sarcopenia and muscle wasting in general include supplementation with HMB, regular resistance exercise, and consumption of a high-protein diet. Based upon a meta-analysis of seven randomized controlled trials that was published in 2015, HMB supplementation has efficacy as a treatment for preserving lean muscle mass in older adults. More research is needed to determine the precise effects of HMB on muscle strength and function in this age group.

Since the absence of muscle-building amino acids can contribute to muscle wasting (that which is torn down must be rebuilt with like material), amino acid therapy may be helpful for regenerating damaged or atrophied muscle tissue. The branched-chain amino acids or BCAAs (leucine, isoleucine, and valine) are critical to this process, in addition to lysine and other amino acids.

In severe cases of muscular atrophy, the use of an anabolic steroid such as methandrostenolone may be administered to patients as a potential treatment. A novel class of drugs, called SARM (selective androgen receptor modulators) are being investigated with promising results. They would have fewer side-effects, while still promoting muscle and bone tissue growth and regeneration. These claims are, however, yet to be confirmed in larger clinical trials.

One important rehabilitation tool for muscle atrophy includes the use of functional electrical stimulation to stimulate the muscles. This has seen a large amount of success in the rehabilitation of paraplegic patients.

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.

Treatment of Sydenham's Chorea is based on the following principles:

1. The first tenet of treatment is to eliminate the streptococcus at a primary, secondary and tertiary level. Strategies involve the adequate treatment of throat and skin infections, with a course of penicillin when Sydenham's Chorea is newly diagnosed, followed by long-term penicillin prophylaxis. Behavioural and emotional changes may precede the movement disorders in a previously well child.

2. Treatment of movement disorders. Therapeutic efforts are limited to palliation of the movement disorders. Haloperidol is frequently used because of its anti-dopaminergic effect. It has serious potential side-effects, e.g., tardive dyskinesia. In a study conducted at the RFC, 25 out of 39 patients on haloperidol reported side-effects severe enough to cause the physician or parent to discontinue treatment or reduce the dose. Other medications which have been used to control the movements include pimozide, clonidine, valproic acid, carbamazepine and phenobarbitone.

3. Immunomodulatory interventions include steroids, intravenous immunoglobulins, and plasma exchange. Patients may benefit from treatment with steroids; controlled clinical trials are indicated to explore this further.

4. There are several historical case series reporting successful treatment of Sydenham's Chorea by inducing fever.

Olivopontocerebellar atrophy (OPCA) is the degeneration of neurons in specific areas of the brain – the cerebellum, pons, and inferior olives. OPCA is present in several neurodegenerative syndromes, including inherited and non-inherited forms of ataxia (such as the hereditary spinocerebellar ataxia known as Machado–Joseph disease) and multiple system atrophy (MSA), with which it is primarily associated.

OPCA may also be found in the brains of individuals with prion disorders and inherited metabolic diseases. The characteristic areas of brain damage that indicate OPCA can be seen by imaging the brain using CT scans or MRI studies.

The term was originally coined by Joseph Jules Dejerine and André Thomas.

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.

Progressive muscular atrophy (PMA), also known as Duchenne-Aran muscular atrophy and by various other names, is a rare subtype of motor neuron disease (MND) that affects only the lower motor neurons. PMA is thought to account for around 4% of all MND cases. This is in contrast to amyotrophic lateral sclerosis (ALS), the most common form of MND, which affects both the upper and lower motor neurones, or primary lateral sclerosis, another rare MND variant, which affects only the upper motor neurons. The distinction is important because PMA is associated with a better prognosis than classic ALS.

Treatment requires a firm and transparent diagnosis based on positive features which both health professionals and patients can feel confident about. It is essential that the health professional confirms that this is a common problem which is genuine, not imagined and not a diagnosis of exclusion.

Confidence in the diagnosis does not improve symptoms, but appears to improve the efficacy of treatments such as physiotherapy which require altering established abnormal patterns of movement.

A multi-disciplinary approach to treating functional neurological disorder is recommended.

Treatment options can include:

- Physiotherapy and occupational therapy

- Medication such as sleeping tablets, painkillers, anti-epileptic medications and anti-depressants (for patients suffering with depresssion co-morbid or for pain relief)

Physiotherapy with someone who understands functional disorders may be the initial treatment of choice for patients with motor symptoms such as weakness, gait (walking) disorder and movement disorders. Nielsen et al. have reviewed the medical literature on physiotherapy for functional motor disorders up to 2012 and concluded that the available studies, although limited, mainly report positive results. Since then several studies have shown positive outcomes. In one study, up to 65% of patients were very much or much improved after five days of intensive physiotherapy even though 55% of patients were thought to have poor prognosis. In a randomised controlled trial of physiotherapy there was significant improvement in mobility which was sustained on one year follow up. In multidisciplinary settings 69% of patients markedly improved even with short rehabilitation programmes. Benefit from treatment continued even when patients were contacted up 25months after treatment.

For patients with severe and chronic FND a combination of physiotherapy, occupational therapy and cognitive behavioural therapy may be the best combination with positive studies being published in patients who have had symptoms for up to three years before treatment.

Cognitive behavioural therapy (CBT) alone may be beneficial in treating patients with dissociative (non-epileptic) seizures. A randomised controlled trial of patients who undertook 12 sessions of CBT which taught patients how to interrupt warning signs before seizure onset, challenged unhelpful thoughts and helped patients start activities they had been avoiding found a reduction in the seizure frequency with positive outcomes sustained at six month follow up. A large multicentre trial of CBT for dissociative (non-epileptic) seizures started in 2015 in the UK.

For many patients with FND, accessing treatment can be difficult. Availability of expertise is limited and they may feel that they are being dismissed or told 'it's all in your head' especially if psychological input is part of the treatment plan. Some medical professionals are uncomfortable explaining and treating patients with functional symptoms. Changes in the diagnostic criteria, increasing evidence, literature about how to make the diagnosis and how to explain it and changes in medical training is slowly changing this

After a diagnosis of functional neurological disorder has been made, it is important that the neurologist explains the illness fully to the patient to ensure the patient understands the diagnosis.

Some, but not all patients with FND may experience low moods or anxiety due to their condition. However, they will often not seek treatment due being worried that a doctor will blame their symptoms on their anxiety or depression.

It is recommended that the treatment of functional neurological disorder should be balanced and involve a whole-person approach. This means that it should include professionals from multiple departments, including neurologists, general practitioners (or primary health care providers), physiotherapists, occupational therapists. At the same time, ruling out secondary gain, malingering, conversion disorder and other factors, including the time and financial resources involved in assessing and treating patients who demand hospital resources but would be better served in psychological settings, must all be balanced.

Dejerine–Sottas disease, also known as Dejerine–Sottas syndrome, Dejerine–Sottas neuropathy, progressive hypertrophic interstitial polyneuropathy of childhood and onion bulb neuropathy (and, "hereditary motor and sensory polyneuropathy type III" and "Charcot–Marie–Tooth disease type 3"), is a hereditary neurological disorder characterised by damage to the peripheral nerves and resulting progressive muscle wasting. The condition is caused by mutations in a various genes and currently has no known cure.

The disorder is named for Joseph Jules Dejerine and Jules Sottas, French neurologists who first described it.

Onset occurs in infancy or early childhood, usually before 3 years of age. Progression is slow until the teenage years at which point it may accelerate, resulting in severe disability.

Symptoms are usually more severe and rapidly progressive than in the other more common Charcot–Marie–Tooth diseases. Some patients may never walk and solely use wheelchairs by the end of their first decade, while others may need only a cane (walking stick) or similar support through life.

Dejerine–Sottas disease is characterized by moderate to severe lower and upper extremity weakness and loss of sensation, which occur mainly in the lower legs, forearms, feet and hands. Loss of muscle mass and reduced muscle tone can occur as the disease progresses. Other symptoms may include pain in the extremities, curvature of the spine, clawed hands, foot deformities, ataxia, peripheral areflexia, and slow acquisition of motor skills in childhood. Symptoms that are less common can include limitation of eye movements, other eye problems such as nystagmus or anisocoria, or mild hearing loss.

Facioscapulohumeral muscular dystrophy (FSHMD, FSHD or FSH)—originally named Landouzy-Dejerine—is a usually autosomal dominant inherited form of muscular dystrophy (MD) that initially affects the skeletal muscles of the face (facio), scapula (scapulo) and upper arms (humeral). FSHD is the third most common genetic disease of skeletal muscle. Orpha.net lists the prevalence as 4/100,000 while a 2014 population-based study in the Netherlands reported a significantly higher prevalence of 12 in 100,000.

Symptoms may develop in early childhood and are usually noticeable in the teenage years, with 95% of affected individuals manifesting disease by age 20 years. A progressive skeletal muscle weakness usually develops in other areas of the body as well; often the weakness is asymmetrical. Life expectancy can be threatened by respiratory insufficiency, and up to 20% of affected individuals become severely disabled, requiring use of a wheel chair or mobility scooter. In a Dutch study, approximately 1% of patients required (nocturnal or diurnal) ventilatory support. Non-muscular symptoms frequently associated with FSHD include subclinical sensorineural hearing loss and retinal telangiectasia.

In more than 95% of known cases, the disease is associated with contraction of the D4Z4 repeat in the 4q35 subtelomeric region of Chromosome 4. Seminal research published in August 2010 now shows the disease requires a second mechanism, which for the first time provides a unifying theory for its underlying genetics. The second mechanism is a "toxic gain of function" of the DUX4 gene, which is the first time in genetic research that a "dead gene" has been found to "wake up" and cause disease.

Building on the 2010 unified theory of FSHD, researchers in 2014 published the first proposed pathophysiology definition of the disease and four viable therapeutic targets for possible intervention points.

In 2007 the FSHD Global Research Foundation was established to increase the amount of funding available to research bodies. The Foundation has identified 13 priority areas of interest for FSHD research.

Fifty percent of patients with acute Sydenham's chorea spontaneously recover after two to six months whilst mild or moderate chorea or other motor symptoms can persist for up to and over two years in some cases. Sydenham's is also associated with psychiatric symptoms with obsessive compulsive disorder being the most frequent manifestation.

EMG &NCV can help to treatment with the diagnosis of the location and severity of the lesion.

Inactivity and starvation in mammals lead to atrophy of skeletal muscle, accompanied by a smaller number and size of the muscle cells as well as lower protein content. In humans, prolonged periods of immobilization, as in the cases of bed rest or astronauts flying in space, are known to result in muscle weakening and atrophy. Such consequences are also noted in small hibernating mammals like the golden-mantled ground squirrels and brown bats.

Bears are an exception to this rule; species in the family Ursidae are famous for their ability to survive unfavorable environmental conditions of low temperatures and limited nutrition availability during winter by means of hibernation. During that time, bears go through a series of physiological, morphological and behavioral changes. Their ability to maintain skeletal muscle number and size at time of disuse is of significant importance.

During hibernation, bears spend four to seven months of inactivity and anorexia without undergoing muscle atrophy and protein loss. There are a few known factors that contribute to the sustaining of muscle tissue. During the summer period, bears take advantage of the nutrition availability and accumulate muscle protein. The protein balance at time of dormancy is also maintained by lower levels of protein breakdown during the winter time. At times of immobility, muscle wasting in bears is also suppressed by a proteolytic inhibitor that is released in circulation. Another factor that contributes to the sustaining of muscle strength in hibernating bears is the occurrence of periodic voluntary contractions and involuntary contractions from shivering during torpor. The three to four daily episodes of muscle activity are responsible for the maintenance of muscle strength and responsiveness in bears during hibernation.

Kearns–Sayre syndrome (KSS) is a mitochondrial myopathy with a typical onset before 20 years of age. KSS is a more severe syndromic variant of chronic progressive external ophthalmoplegia (abbreviated CPEO), a syndrome that is characterized by isolated involvement of the muscles controlling movement of the eyelid (levator palpebrae, orbicularis oculi) and eye (extra-ocular muscles). This results in ptosis and ophthalmoplegia respectively. KSS involves a combination of the already described CPEO as well as pigmentary retinopathy in both eyes and cardiac conduction abnormalities. Other symptoms may include cerebellar ataxia, proximal muscle weakness, deafness, diabetes mellitus, growth hormone deficiency, hypoparathyroidism, and other endocrinopathies. In both of these diseases, muscle involvement may begin unilaterally but always develops into a bilateral deficit, and the course is progressive. This discussion is limited specifically to the more severe and systemically involved variant.

The surgery takes place under general anaesthesia and lasts less than 1 hour. The surgeon prepares the locus to the size of the implant after performing a 8-cm axillary incision and inserts the implant beneath the skin. The closure is made in 2 planes.

The implant will replace the pectoralis major muscle, thus enabling the thorax to be symmetrical and, in women, the breast as well. If necessary, especially in the case of women, a second operation will complement the result by the implantation of a breast implant and / or lipofilling.

Lipomodelling is progressively used in the correction of breast and chest wall deformities. In Poland syndrome, this technique appears to be a major advance that will probably revolutionize the treatment of severe cases. This is mainly due to its ability to achieve previously unachievable quality of reconstruction with minimal scaring.

The complete or partial absence of the pectoralis muscle is the malformation that defines Poland Syndrome. It can be treated by inserting a custom implant designed by CAD (computer aided design). A 3D reconstruction of the patient's chest is performed from a medical scanner to design a virtual implant perfectly adapted to the anatomy of each one. The implant is made of medical silicone unbreakable rubber. This treatment is purely cosmetic and does not make up for the patient's imbalanced upper body strength.

The Poland syndrome malformations being morphological, correction by custom implant is a first-line treatment. This technique allows a wide variety of patients to be treated with good outcomes. Poland Syndrome can be associated with bones, subcutaneous and mammary atrophy: if the first, as for pectus excavatum, is successfully corrected by a custom implant, the others can require surgical intervention such as lipofilling or silicone breast implant, in a second operation.

A functional neurological disorder (FND) is a condition in which patients experience neurological symptoms such as weakness, movement disorders, sensory symptoms and blackouts. The brain of a patient with functional neurological symptom disorder is structurally normal, but functions incorrectly. According to consensus from the literature and from physicians and psychologists practicing in the field, "functional symptoms, also called 'medically unexplained,' 'psychogenic,' or [in outdated terminology] 'hysterical,' are symptoms that are clinically recognisable as not being caused by a definable organic disease". The intended contrast is with an organic brain syndrome, although the terms imply a level of certainty about causation that is often clinically unconfirmed. Subsets of functional neurological disorders include functional neurological symptom disorder (FNsD), conversion disorder, and psychogenic movement disorder/non-epileptic seizures. Functional neurological disorders are common in neurological services, accounting for up to one third of outpatient neurology clinic attendances, and associated with as much physical disability and distress as other neurological disorders.

The diagnosis is made based on positive signs and symptoms in the history and examination during consultation of a neurologist (see below). Physiotherapy is particularly helpful for patients with motor symptoms (weakness, gait disorders, movement disorders) and tailored cognitive behavioural therapy has the best evidence in patients with dissociative (non-epileptic) attacks.

Post-traumatic wrist osteoarthritis can be treated conservatively or with a surgical intervention. In many patients, a conservative (non-surgical) approach is sufficient. Because osteoarthritis is progressive and symptoms may get worse, surgical treatment is advised in any stage.

Medial medullary syndrome, also known as inferior alternating syndrome, hypoglossal alternating hemiplegia, lower alternating hemiplegia, or Dejerine syndrome, is a type of alternating hemiplegia characterized by a set of clinical features resulting from occlusion of the anterior spinal artery. This results in the infarction of medial part of the medulla oblongata.