Step I : Decide the dominant type of movement disorder

Step II : Make differential diagnosis of the particular disorder

Step II: Confirm the diagnosis by lab tests

- Metabolic screening

- Microbiology

- Immunology

- CSF examination

- Genetics

- Imaging

- Neurophysiological tests

- Pharmacological tests

Treatment depends upon the underlying disorder. Movement disorders have been known to be associated with a variety of autoimmune diseases.

Therapeutic interventions are best individualized to particular patients.

Basic principles of treatment for hypertonia are to avoid noxious stimuli and provide frequent range of motion exercise.

Recent research indicates that the biomolecule taurine may be effective for hypertonia, perhaps through its benzodiazepine-like modulation of the inhibitory neurotransmitter GABA or the neuromuscular effects of increasing intracellular calcium levels.

Paratonia is the inability to relax muscles during muscle tone assessment. There are two types of paratonia: oppositional and facilitatory. Oppositional paratonia ("gegenhalten") occurs when subjects involuntary resist to passive movements, while facilitatory paratonia ("mitgehen") occurs when subjects involuntary assist passive movements.

Both types of paratonia have been associated with cognitive impairment or mental disorders, particularly in relation to frontal lobe dysfunction. Paratonia is frequently encountered in clinical practice.

Paratonia can be assessed with rating scales during clinical examination. Paratonia scale is a semi-quantitative score to rate the amount of oppositional and facilitatory paratonia separately. Kral modified procedure is a more objective semi-quantitative rating of upper limb facilitatory paratonia easily applicable while patients are seated. The Paratonia Assessment Instrument (PAI) was also used in a physiotherapic setting for the assessment of oppositional paratonia.

In 2017 facilitatory and oppositional paratonia have been assessed with surface electromyography, allowing a quantitative measure and better characterization of paratonia. Recording paratonia with electromyography on elbow flexor and extensors during repetitive continuous or discontinuous elbow movements may help distinguish paratonia from other forms of altered muscle tone. Both facilitatory and oppositional paratonia increase during continuous flexion and extension movements, moreover, oppositional paratonia increases with movement velocity. Spasticity also is velocity-dependent, but, differently from oppositional paratonia, if repeatedly elicited decreases instead of increasing. Conversely, parkinsonian rigidity is independent from movement velocity and probably also from movement repetition.

SPS is diagnosed by evaluating clinical findings and excluding other conditions. There is no specific laboratory test that confirms its presence. Underdiagnosis and misdiagnosis are common.

The presence of antibodies against GAD is the best indication of the condition that can be detected by blood and cerebrospinal fluid (CSF) testing. Anti-GAD65 is found in about 80 percent of SPS patients. Anti-thyroid, anti-intrinsic factor, anti-nuclear, anti-RNP, and anti-gliadin are also often present in blood tests. Electromyography (EMG) demonstrates involuntary motor unit firing in SPS patients. EMG can confirm the diagnosis by noting spasms in distant muscles as a result of subnoxious stimulation of cutaneous or mixed nerves. Responsiveness to diazepam helps confirm that the patient is suffering from SPS, as this decreases stiffness and motor unit potential firing.

The same general criteria are used to diagnose paraneoplastic SPS as the normal form of the condition. Once SPS is diagnosed, poor response to conventional therapies and the presence of cancer indicate that it may be paraneoplastic. CT scans are indicated for SPS patients who respond poorly to therapy to determine if this is the case.

A variety of conditions have similar symptoms to SPS, including myelopathies, dystonias, spinocerebellar degenerations, primary lateral sclerosis, neuromyotonia, and some psychogenic disorders. Tetanus, neuroleptic malignant syndrome, malignant hyperpyrexia, chronic spinal interneuronitis, serotonin syndrome, Multiple sclerosis, Parkinson's disease, and Isaacs syndrome should also be excluded.

Patients' fears and phobias often incorrectly lead doctors to think their symptoms are psychogenic, and they are sometimes suspected of malingering. It takes an average of six years after the onset of symptoms before the disease is diagnosed.

The progression of SPS depends on whether it is a typical or abnormal form of the condition and the presence of comorbidities. Early recognition and neurological treatment can limit its progression. SPS is generally responsive to treatment, but the condition usually progresses and stabilizes periodically. Even with treatment, quality of life generally declines as stiffness precludes many activities. Some patients require mobility aids due to the risk of falls. About 65 percent of SPS patients are unable to function independently. About ten percent of SPS patients require intensive care at some point; sudden death occurs in about the same number of patients. These deaths are usually caused by metabolic acidosis or an autonomic crisis.

Opisthotonus or opisthotonos, from Greek roots, ὄπισθεν, "opisthen" meaning "behind" and τόνος "tonos" meaning "tension", is a state of severe hyperextension and spasticity in which an individual's head, neck and spinal column enter into a complete "bridging" or "arching" position. This abnormal posturing is an extrapyramidal effect and is caused by spasm of the axial muscles along the spinal column.

Two other types, primary ciliary dyskinesia and biliary dyskinesia, are caused by specific kinds of ineffective movement of the body, and are not movement disorders.

Spastic thrusting of hip area can occur in Sodemytopic Parkinson's.

Methylphenidate, commonly used to treat ADHD, has been used in conjunction with levodopa to treat hypokinesia in the short term. The two work together to increase dopamine levels in the striatum and prefrontal cortex. Methylphenidate mainly inhibits dopamine and noradrenaline reuptake by blocking presynaptic transporters, and levodopa increases the amount of dopamine, generally improving hypokinesic gait. Some patients, however, have adverse reactions of nausea and headache to the treatment and the long-term effects of the drug treatment still need to be assessed.

It is seen in some cases of severe cerebral palsy and traumatic brain injury or as a result of the severe muscular spasms associated with tetanus. It can be a feature of severe acute hydrocephalus.

Opisthotonus can be produced experimentally in animals by transection of the midbrain (between the superior colliculus and the inferior colliculus), which results in severing all the corticoreticular fibers. Hyperextension occurs due to facilitation of the anterior reticulospinal tract caused by the inactivation of inhibitory corticoreticular fibers, which normally act upon the pons reticular formation. It has been shown to occur naturally only in birds and placental mammals.

Opisthotonus is more pronounced in infants. Opisthotonus in the neonate may be a symptom of meningitis, tetanus, severe kernicterus, or the rare Maple syrup urine disease. This marked extensor tone can cause infants to "rear backwards" and stiffen out as the mother or nurse attempts to hold or feed them. Opisthotonus can be induced by any attempt at movement such as smiling, feeding, vocalization, or by seizure activity. A similar tonic posturing may be seen in Sandifer syndrome. Individuals with opisthotonus are quite challenging to position, especially in wheelchairs and car seats.

Opisthotonus can sometimes be seen in lithium intoxication. It is a rare extrapyramidal side effect of phenothiazines, haloperidol, and metoclopramide.

Opisthotonus with the presence of the risus sardonicus is also a symptom of strychnine poisoning.

Opisthotonus is also described as a potential CNS symptom of heat stroke along with bizarre behavior, hallucinations, decerebrate rigidity, oculogyric crisis and cerebellar dysfunction.

Opisthotonus is seen with drowning victims – called the "Opisthotonic Death Pose". This pose is also common in complete dinosaur skeletal fossils and it has been suggested that this is due to the animal drowning or being immersed in water soon after death.

Once the reaction to dopaminergic drugs begins to fluctuate in Parkinson’s patients, deep brain stimulation (DBS) of the subthalamic nucleus and medial globus pallidus is often used to treat hypokinesia. DBS, like dopaminergic drugs, initially provides relief, but chronic use causes worse hypokinesia and freezing of gait. Lower-frequency DBS in irregular patterns has been shown to be more effective and less detrimental in treatment.

Posteroventral pallidotomy (PVP) is a specific kind of DBS that destroys a small part of the globus pallidus by scarring the neural tissue, reducing brain activity and therefore tremors and rigidity. PVP is suspected to recalibrate basal ganglia activity in the thalamocortical pathway. PVP in the dominant hemisphere has been reported to disrupt executive function verbal processing abilities, and bilateral PVP may disturb processes of focused attention.

Many akinesia patients also form a linguistic akinesia in which their ability to produce verbal movements mirrors their physical akinesia symptoms, especially after unsuccessful PVP. Patients are usually able to maintain normal levels of fluency, but often stop midsentence, unable to remember or produce a desired word. According to a study of Parkinson's patients with articulatory hypokinesia, subjects with faster rates of speech experienced more problems trying to produce conversational language than those who normally spoke at slower rates.

Diagnosis of MSA can be challenging because there is no test that can definitively make or confirm the diagnosis in a living patient. Clinical diagnostic criteria were defined in 1998 and updated in 2007. Certain signs and symptoms of MSA also occur with other disorders, such as Parkinson's disease, making the diagnosis more difficult.

Both MRI and CT scanning frequently show a decrease in the size of the cerebellum and pons in those with cerebellar features. The putamen is hypodense on T2-weighted MRI and may show an increased deposition of iron in Parkinsonian form. In cerebellar form, a "hot cross" sign has been emphasized; it reflects atrophy of the pontocereballar fibers that manifest in T2 signal intensity in atrophic pons.

A definitive diagnosis can only be made pathologically on finding abundant glial cytoplasmic inclusions in the central nervous system.

Due to the condition's rarity, it is frequently misdiagnosed, often as cerebral palsy. This results in patients often living their entire childhood with the condition untreated.

The diagnosis of SS can be made from a typical history, a trial of dopamine medications, and genetic testing. Not all patients show mutations in the GCH1 gene (GTP cyclohydrolase I), which makes genetic testing imperfect.

Sometimes a lumbar puncture is performed to measure concentrations of biopterin and neopterin, which can help determine the exact form of dopamine-responsive movement disorder: early onset parkinsonism (reduced biopterin and normal neopterin), GTP cyclohydrolase I deficiency (both decreased) and tyrosine hydroxylase deficiency (both normal).

In approximately half of cases, a phenylalanine loading test can be used to show decreased conversion from the amino acid phenylalanine to tyrosine. This process uses BH4 as a cofactor.

During a sleep study (polysomnography), decreased twitching may be noticed during REM sleep.

An MRI scan of the brain can be used to look for conditions that can mimic SS (for example, metal deposition in the basal ganglia can indicate Wilson's disease or pantothenate kinase-associated neurodegeneration). Nuclear imaging of the brain using positron emission tomography (PET scan) shows a normal radiolabelled dopamine uptake in SS, contrary to the decreased uptake in Parkinson's disease.

Other differential diagnoses include metabolic disorders (such as GM2 gangliosidosis, phenylketonuria, hypothyroidism, Leigh disease) primarily dystonic juvenile parkinsonism, autosomal recessive early onset parkinsonism with diurnal fluctuation, early onset idiopathic parkinsonism, focal dystonias, dystonia musculorum deformans and dyspeptic dystonia with hiatal hernia.

- Diagnosis - main

- typically referral by GP to specialist Neurological Hospital e.g. National Hospital in London.

- very hard to diagnose as condition is dynamic w.r.t. time-of-day AND dynamic w.r.t. age of patient.

- correct diagnosis only made by a consultant neurologist with a complete 24-hour day-cycle observation(with video/film) at a Hospital i.e. morning(day1)->noon->afternoon->evening->late-night->sleep->morning(day2).

- patient with suspected SS required to walk in around hospital in front of Neuro'-consultant at selected daytime intervals to observe worsening walking pattern coincident with increased muscle tension in limbs.

- throughout the day, reducing leg-gait, thus shoe heels catching one another.

- diurnal affect of condition: morning(fresh/energetic), lunch(stiff limbs), afternoon(very stiff limbs), evening(limbs worsening), bedtime(limbs near frozen).

- muscle tension in thighs/arms: morning(normal), lunch(abnormal), afternoon(very abnormal), evening(bad), bedtime(frozen solid).

- Diagnosis - additional

- lack of self-esteem at school/college/University -> eating disorders in youth thus weight gains.

- lack of energy during late-daytime (teens/adult) -> compensate by over-eating.

Acute dystonia is a sustained muscle contraction that sometimes appears soon after administration of antipsychotic medications. Any muscle in the body may be affected, including the jaw, tongue, throat, arms, or legs. When the throat muscles are involved, this type of dystonia is called an acute laryngospasm and is a medical emergency because it can impair breathing. Older antipsychotics such as Haloperidol or Fluphenazine are more likely to cause acute dystonia than newer agents. Giving high doses of antipsychotics by injection also increases the risk of developing acute dystonia.

Methamphetamine, other amphetamines and dopaminergic stimulants including cocaine and pemoline can produce choreoathetoid dyskinesias; the prevalence, time-frame and prognosis are not well established. Amphetamines also cause a dramatic increase in choreoathetoid symptoms in patients with underlying chorea such as Sydenham’s, Huntington’s, and Lupus. Long-term use of amphetamines may increase the risk of Parkinson's disease (PD): in one retrospective study with over 40,000 participants it was concluded that amphetamine abusers generally had a 200% higher chance of developing PD versus those with no history of abuse; the risk was much higher in women, almost 400%. There remains some controversy as of 2017.

Levodopa-induced dyskinesia (LID) is evident in patients with Parkinson's disease who have been on levodopa () for prolonged periods of time. LID commonly first appears in the foot, on the most affected side of the body. There are three main types that can be classified on the basis of their course and clinical presentation following an oral dose of :

- Off-period dystonia – correlated to the akinesia that occurs before the full effect of sets in, when the plasma levels of are low. In general, it occurs as painful spasms in the foot. Patients respond to therapy.

- Diphasic dyskinesia – occurs when plasma L-DOPA levels are rising or falling. This form occurs primarily in the lower limbs (though they can happen elsewhere) and is usually dystonic (characterized by apparent rigidity within muscles or groups thereof) or (characterized by involuntary movement of muscles) and will not respond to dosage reductions.

- Peak-dose dyskinesia – the most common form of levodopa-induced dyskinesia; it correlates with the plateau plasma level. This type usually involves the upper limbs more (but could also affect the head, trunk and respiratory muscles), is choreic (of chorea), and less disabling. Patients will respond to reduction but may be accompanied by deterioration of parkinsonism. Peak-dose L-DOPA-induced dyskinesia has been suggested to be associated with cortical dysregulation of dopamine signaling.

The types of imaging techniques that are most prominently utilized when studying and/or diagnosing CBD are:

- magnetic resonance imaging (MRI)

- single-photon emission computed tomography (SPECT)

- fluorodopa positron emission tomography (FDOPA PET)

Developments or improvements in imaging techniques provide the future possibility for definitive clinical diagnosis prior to death. However, despite their benefits, information learned from MRI and SPECT during the beginning of CBD progression tend to show no irregularities that would indicate the presence of such a neurodegenerative disease. FDOPA PET is used to study the efficacy of the dopamine pathway.

Despite the undoubted presence of cortical atrophy (as determined through MRI and SPECT) in individuals experiencing the symptoms of CBD, this is not an exclusive indicator for the disease. Thus, the utilization of this factor in the diagnosis of CBD should be used only in combination with other clinically present dysfunctions.

One of the most significant problems associated with CBD is the inability to perform a definitive diagnosis while an individual exhibiting the symptoms associated with CBD is still alive. A clinical diagnosis of CBD is performed based upon the specified diagnostic criteria, which focus mainly on the symptoms correlated with the disease. However, this often results in complications as these symptoms often overlap with numerous other neurodegenerative diseases. Frequently, a differential diagnosis for CBD is performed, in which other diseases are eliminated based on specific symptoms that do not overlap. However, some of the symptoms of CBD used in this process are rare to the disease, and thus the differential diagnosis cannot always be used.

Postmortem diagnosis provides the only true indication of the presence of CBD. Most of these diagnoses utilize the Gallyas-Braak staining method, which is effective in identifying the presence of astroglial inclusions and coincidental tauopathy.

Anticholinergic drugs are used to control neuroleptic-induced EPS, although akathisia may require beta blockers or even benzodiazepines. If the EPS are induced by an antipsychotic, EPS may be reduced by dose titration or by switching to an atypical antipsychotic, such as aripiprazole, ziprasidone, quetiapine, olanzapine, risperidone, or clozapine. These medications possess an additional mode of action that is believed to negate their effect on the nigrostriatal pathway, which means they are associated with fewer extrapyramidal side-effects than "conventional" antipsychotics (chlorpromazine, haloperidol, etc.), although some research has shown that second generation neuroleptics cause EPS at the same rate as the first generation drugs.

Commonly used medications for EPS are anticholinergic agents such as benztropine (Cogentin), diphenhydramine (Benadryl), and trihexyphenidyl (Artane). Another common course of treatment includes dopamine agonist agents such as pramipexole. These medications reverse the symptoms of extrapyramidal side effects caused by antipsychotics or other drugs that either directly or indirectly inhibit dopaminergic neurotransmission.

Studies are yet to be undertaken on the optimum dosage of the causative drugs to reduce their side effects (extrapyramidal symptoms (EPS)).

MSA usually progresses more quickly than Parkinson's disease. There is no remission from the disease. The average remaining lifespan after the onset of symptoms in patients with MSA is 7.9 years. Almost 80% of patients are disabled within five years of onset of the motor symptoms, and only 20% survive past 12 years. Rate of progression differs in every case and speed of decline may vary widely in individual patients.

O’Sullivan and colleagues (2008) identified early autonomic dysfunction to be the most important early clinical prognostic feature regarding survival in MSA. Patients with concomitant motor and autonomic dysfunction within three years of symptom onset had a shorter survival duration, in addition to becoming wheelchair dependent and bed-ridden at an earlier stage than those who developed these symptoms after three years from symptom onset. Their study also showed that when patients with early autonomic dysfunction develop frequent falling, or wheelchair dependence, or severe dysphagia, or require residential care, there is a shorter interval from this point to death.

Treatment consists of high-dose lorazepam or in some cases ECT. The response to the treatment is usually good, especially if detected early

The prognosis is best when identified early and treated aggressively. In these cases NMS is not usually fatal. In previous studies the mortality rates from NMS have ranged from 20%–38%; however, in the last two decades, mortality rates have fallen below 10% due to early recognition and improved management. Re-introduction to the drug that originally caused NMS to develop may also trigger a recurrence, although in most cases it does not.

Memory impairment is a consistent feature of recovery from NMS, and usually temporary, though in some cases, may become persistent.

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.

When diagnosing any neurological condition, history and examination are fundamental. History is obtained by family, friends or EMS. The Glasgow Coma Scale is a helpful system used to examine and determine the depth of coma, track patients progress and predict outcome as best as possible. In general a correct diagnosis can be achieved by combining findings from physical exam, imaging, and history components and directs the appropriate therapy.

A coma can be classified as (1) supratentorial (above Tentorium cerebelli), (2) infratentorial (below Tentorium cerebelli), (3) metabolic or (4) diffused. This classification is merely dependent on the position of the original damage that caused the coma, and does not correlate with severity or the prognosis.

The severity of coma impairment however is categorized into several levels. Patients may or may not progress through these levels. In the first level, the brain responsiveness lessens, normal reflexes are lost, the patient no longer responds to pain and cannot hear.

The Rancho Los Amigos Scale is a complex scale that has eight separate levels, and is often used in the first few weeks or months of coma while the patient is under closer observation, and when shifts between levels are more frequent.

This condition is very rare, only affecting one in two million people. It is more common in females than in males. There are several hundred cases in the United States, 25 known cases in the United Kingdom, and less than that in Australia and New Zealand.