Dyskinesias are abnormal involuntary movements. Linked to abnormal muscle activity, dyskinesia thus leads to involuntary movements of the head, face and even the tongue. It can also affect the limbs or the trunk. There are drugs that can cause this symptom of dyskinesia, such as neuroleptics, which mainly cause tardive dyskinesia. This most commonly affects the face and mouth.

There is also a form called ciliary dyskinesia, with very different manifestations: linked to the immobility of the body’s cilia, it causes frequent respiratory consequences. This ciliary dyskinesia can be primary, that is to say present from birth and linked to a genetic cause, or secondary, therefore acquired in connection with another pathology.

Different treatments exist, including Lepticur, which corrects tardive dyskinesia associated with taking neuroleptics. Daily respiratory physiotherapy makes it possible to limit the risk of respiratory infection linked to ciliary dyskinesia.

What is dyskinesia

The term dyskinesia comes from the Greek, “dys”, a prefix which means “defect of”, and from “kine” which means movement. Dyskinesia therefore means a lack of movement, mobility. This is, according to the medical dictionary of the Academy of Medicine, “A difficulty or an anomaly in the exercise of a movement”.

The term hyperkinesia, which means exaggeration of movement, should in fact be preferred to that of dyskinesia, etymologically understood as difficulty, or even reduction or abolition of the latter. Dyskinesia represents “A set of abnormal involuntary movements, of variable amplitude, irregular, sometimes rhythmic, extended or localized, in particular on the bucco-linguo-facial sphere (ie that of the mouth, tongue and face)”, details this dictionary of the Academy of Medicine.

• La dyskinésie is therefore abnormal muscle activity that causes involuntary movements. These movements can affect the face, head, and even the tongue. They can also affect the limbs, the trunk, sometimes also the wall of the heart. Dyskinesia is thus a sign present in Parkinson’s disease, in particular in connection with antiparkinsonian treatments.
• There exists a late dyskinésie, which is a side effect of taking neuroleptic drugs (also called antipsychotics), which are drugs prescribed to treat people with psychosis (mainly schizophrenics and people with bipolar disorder). This side effect is said to be of the extrapyramidal type.
• In addition, there is also a dyskinésie ciliaire primitive (DCP), a very rare genetic disease transmitted by parents at the time of conception and present from birth, which affects both girls and boys. It can be detected more or less late, and its course varies from one patient to another. This general disease affects all organs with hair cells: respiratory system, sinuses, ear, sperm. In about 50% of cases of PCD, we find in parallel the Kartagener syndrome, which associates a dilation of the bronchi, a chronic sinusitis and a reverse rotation of all the thoraco-abdominal viscera (the heart is on the right, the liver left, etc.) In addition, there is also a secondary ciliary dyskinesia, which appears secondarily to another pathology.

How to recognize dyskinesia?

• The clinical examination can make it possible to observe tremors, chorea, hemiballism, myoclonus, tics or dystonia, etc., all these types of involuntary muscular movements being able to represent a dyskinesia. Besides, electromyogram is a technique commonly used to determine the nature and pathophysiology of these abnormal muscle movements.
• Regarding ciliary dyskinesias, the diagnosis can be made at any age. The presence of respiratory distress, as well as the rotation of the viscera, are factors that strongly guide the diagnosis of ciliary dyskinesia. Specific examinations can confirm the diagnosis, because they study the beating of the eyelashes: this is the saccharin test, as well as the sample under local anesthesia followed byhair cell analysis, the only way to certify the diagnosis of ciliary dyskinesia. 

Risk factors

• There is a risk factor genetic, with regard to primary ciliary dyskinesia (which is very rare: barely 50 births per year in France, one in 16).
• La dopathotherapy, for parkinsonian syndrome, can also be complicated by dyskinesias.
• Taking neuroleptic drugs is the major risk factor for tardive dyskinesia. 

In the latter two cases, hypersensitivity of receptors to endogenous dopamine (produced by the body) is noted.

Drug-induced dyskinesias

Drug-induced dyskinesias are side effects; they are mainly caused by neuroleptics.

• They are either waters, which can then appear within 36 hours, mainly in predisposed subjects. They then include hypertonic attacks, that is to say an increase in muscle tone, which is often accompanied by hypersalivation, as well as swallowing disorders, and there are sometimes also attacks of akathisia ( impatience and inability to remain in a sitting position, the need to stomp or swing while standing) or also hyperkinesia (a state of hyperactivity associated with impaired concentration and attention).
• These dyskinesias linked to neuroleptics can also be late, and they are especially oral-facial: they present a rabbit syndrome, with protraction and retraction of the lips, for example. This is the major problem with neuroleptics after three months of continuous administration. It is caused by an extrapyramidal reaction, which is a subcortical system comprising all of the basal ganglia (i.e., islets of gray matter embedded in white matter) from which motor nerve fibers and afferent and efferent fibers originate. (arriving in the nuclei or leaving).

The tardive dyskinesias are, in fact, due to a phenomenon of hypersensitization by an increase in dopaminergic receptors in the locus niger (an area of ​​the central nervous system) and the striated bodies (bundles of fibers at the level of the central nervous system).

Dyskinesias due to immobility of the cilia

Primary ciliary dyskinesia is due to the immobility of the body’s vibratile cilia, present in particular in the respiratory system (nose, sinuses, bronchi), in the ears, and there are also in the spermatozoa (it s then acts of their tail, called flagellum). This dyskinesia can be primary, when it is present from birth. There are also secondary ciliary dyskinesias: these are then triggered by another pathology during life.

Eyelash movement may be insufficient or absent in ciliary dyskinesia. In the nose, this then causes stagnation of the mucus which contains the external particles, thus causing nasal and bronchial congestion. These secretions can then become infected.

• The complication of tardive dyskinesia would be more frequent duringdiagnostic errors : thus, bipolar diseases treated by classic neuroleptic would cause more tardive dyskinesia.
• Patients with ciliary dyskinesia may have complications such as the risk of developing lung infections. Infection of the secretions, following nasal and bronchial congestion, can lead to irreversible lesions in the lungs such as dilation of the bronchi, or bronchiectasis, obstructive bronchopulmonary pathologies.

Tardive dyskinesia

• Atypical neuroleptics. To prevent the onset of tardive dyskinesia, a side effect occurring at any time during treatment with a neuroleptic, there have been so-called atypical neuroleptics since the 1990s, which present fewer undesirable effects: these side effects such as dyskinesia are thus less frequent with these atypical neuroleptics than with conventional neuroleptics. Despite this, however, an atypical antipsychotic such as risperidone can also cause tardive dyskinesias.
• Lepticur. The treatment of this type of side effect, such as tardive dyskinesia linked to neuroleptics, is treated fairly quickly with Lepticur (or Tropatépine).
• Changing doses. A temporary improvement in dyskinesia is observed by increasing the dose of neuroleptics: however, it is not advisable to do so. Prophylaxis by minimum doses is preferred.
• Discontinuation of treatment. Once the tardive dyskinesias have set in, stopping the neuroleptic treatment may stop the dyskinesia, but this is not guaranteed, and there are even cases where it gets worse when the treatment is stopped. .

Currently, research protocols for the treatment of the most disabling forms of tardive dyskinesia are underway. It could be improved by implanting an intracerebral stimulation electrode in certain basal ganglia. In addition, vitamin E intake may help improve the symptom.

Treatment of ciliary dyskinesia

The aim of the treatment is to limit the appearance of lesions as much as possible, more particularly in the bronchi.

• It is therefore necessary to evacuate the secretions regularly, which can be done via a daily care, sometimes even several daily, in respiratory physiotherapy, in order to empty the nose and the bronchi of the secretions.
• It also implies compliance with several hygiene rules, including hand washing.
• In addition, it is necessary to treat as early as possible, and effectively, any type of infectious episode. In the event of an infectious episode detected in the sinus, ear or bronchi, antibiotic treatment may be prescribed by the general practitioner.
• It is necessary to well hydrate, because of the losses in the bronchi, it is also necessary to drink well before any physiotherapy session in order to thin the secretions. This is because the mucus secreted along the respiratory system is essentially made up of water. However, the quantity of secreted mucus will increase during a bronchial congestion. And the secretions can be sticky, which will not help their evacuation during the physiotherapy session.