What is akathisia? How does restlessness manifest itself? Akathisia Why does akathisia occur?

The clinical significance of this syndrome is associated not only with the discomfort experienced by the patient, but also with the frequent prognostically unfavorable combination with dysphoria, depression, suicidal risk, aggression and agitation, exacerbation of psychopathological symptoms, and reduced compliance with antipsychotic therapy. Despite its obvious importance, akathisia is often underestimated or overlooked in everyday practice.

Akathisia (from the Greek kathisis - sitting down [“a” - a particle of denial = “not”]) is included in the group of extrapyramidal hyperkinetic syndromes and literally means “restlessness”, i.e. a condition characterized by an irresistible need to move in order to lessen an unbearable feeling of inner restlessness.

Haley (Healy) et al in 2006 described akathisia as follows: internal tension, insomnia, a feeling of internal discomfort, restlessness or agitation, marked anxiety or panic. As a consequence, increased lability of affect may develop, for example, increased tearfulness, or irritability, irascibility, increased excitability, impulsiveness or aggressiveness.

Drug akathisia is usually associated with the prescription of typical antipsychotics (neuroleptics), but sometimes occurs with the use of atypical drugs (atypical antipsychotics) and some antidepressants (fluoxetine, paroxetine, less often venlafaxine, duloxetine, tricyclic antidepressants and trazodone). The neurochemical nature of this phenomenon is caused by an increase in the activity of the dopaminergic system and / or a violation of the activity of the GABAergic and cholinergic systems.

Jack Henry Abbott in 1981 gave the following artistic description of akathisia caused by antipsychotic drugs: “... These drugs, drugs in this group, do not calm or relieve nervous tension. They suppress and attack. They attack you from the inside, so deep from the inside that you are unable to find the source of your mental pain and discomfort ... Your jaw muscles go crazy and refuse to obey you, they convulse convulsively so that you bite the inside of your cheeks, lips or tongue , your jaws click, your teeth chatter, and the pain shoots right through you. And every day this goes on for hours. Your back becomes stiff, tense, and terribly straight, so that you can hardly move your head or neck sideways, bend or straighten, and sometimes your back bends against your will and you cannot stand straight. Inner pain permeates you and swims along your nerve fibers. You suffer from morbid anxiety, and you feel that you need to move, walk, take a walk, and this will relieve your anxiety. But as soon as you start moving or walking, you get tired and feel anxious again, you feel like you are doing something wrong and you need to sit down and rest. And so it is repeated again and again, again and again, you walk, sit down, jump up and walk again, and sit down again. Feeling the pain, the source of which you cannot find, you go crazy with anxiety, it eats you from the inside, and you cannot find relief even in breathing. .

Read about the clinical phenomenology of akathisia in the post: Akathisia(to the website)

If akathisia occurs within a few days after the appointment or increase in the dose of an antipsychotic, then this is "acute akathisia" (OA), and if - against the background of long-term treatment (several months or years after its start), then this is late akathisia (PA). There is also withdrawal akathisia (withdrawal akathisia), which occurs in the process of reducing doses or canceling antipsychotics.

OA occurs in 3-50% of patients taking neuroleptics, usually within a week after starting the drug or increasing its dose. But in some cases, the symptoms of akathisia appear within a few hours after the first dose of the drug, and sometimes even a few minutes after the intravenous administration of an antipsychotic. Cases of development of OA are also described after several weeks of treatment. With the abolition of the neuroleptic or a decrease in its dose, OA gradually regresses. But if the manifestations of akathisia are mistakenly regarded as an increase in the symptoms of a mental illness for which an antipsychotic was prescribed, and the dose of the drug is increased, then the symptoms of OA increase. If the patient continues to take the neuroleptic at the same dose, then over time the severity of akathisia may decrease, but more often it persists and is often a reason for unauthorized termination of treatment.

OA is more commonly caused by potent antipsychotics (eg, haloperidol), but this complication can occur with any antipsychotic, including droperidol, clozapine, and other atypical antipsychotics. The likelihood of developing OA and the intensity of its symptoms depend on the dose of the drug. In addition, the risk of OA is higher with the introduction of long-acting drugs. OA is somewhat more common in middle-aged women.

Late akathisia (PA) develops in 25-30% of patients taking antipsychotics, usually not earlier than 3 months of treatment with the drug at a stable dose (on average, one year after the start of treatment). PA persists for a long time after the withdrawal of neuroleptics. In addition, unlike acute akathisia, PA often manifests itself against the background of a decrease in the dose of an antipsychotic or its withdrawal (rather than an increase in the dose) and decreases (rather than increases) immediately after the resumption of antipsychotic therapy or an increase in the dose of the drug.

Drug-Induced Akathisia Scale (Burns)

Patients should be examined in a sitting position, then standing in a free position (minimum 2 minutes in each position). Symptoms detected in another situation (for example, during activity in the ward) should also be evaluated. Subsequently, with the help of a clinical interview, the subjective feelings of the patient should be revealed.

objectively:	0 - normal joint movements; 1 - motor anxiety i.e. shuffling of feet, stepping from foot to foot, trampling on the spot (provided that these movements were observed in less than half the time of the examination); 2 - the identified signs described above (in paragraph 1) were observed approximately at half the time of the examination; 3 - the severity of movements is such that the patient cannot remain in one place throughout the examination.
subjective awareness of motor restlessness:	0 - no anxiety; 1 - indefinite anxiety; 2 - awareness of the impossibility to keep the legs at rest and / or an increase in anxiety at rest; 3 - Feeling compelled to move most of the time and/or a strong desire to walk, shift from foot to foot during the examination.
experiencing restlessness:	0 - no; 1 - weak; 2 - average; 3 - expressed.
global assessment of akathisia:	1 - doubtful (only subjective complaints, i.e. pseudo-akathisia); 2 - mild (non-specific complaints + fussiness); 3 - medium (non-specific complaints + akathisia); 4 - distinct (complaints of internal restlessness + akathisia); 5 - severe (complaints of anxiety + insomnia + akathisia).

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Akathisia should be distinguished from restless leg syndrome (RLS). The fundamental difference between these conditions is that patients with akathisia are forced to move to relieve a sense of internal tension, while with RLS, leg movements can reduce paresthesia in them. In addition, akathisia is usually present throughout the day, while in RLS symptoms increase in the evening and at night. These patients do not have a family history, but often there is information about taking antipsychotics.

read also the post: restless leg syndrome(to the website)

If OA occurs, the drug that caused it should be discontinued. Under this condition, the symptoms usually regress within a few days or weeks, but sometimes linger for several months. If the patient needs to continue antipsychotic therapy, then you need to reduce the dose of the drug or replace it with another agent, such as a milder antipsychotic (eg, sulpiride, tiapride, thioridazine) or an atypical antipsychotic (clozapine, quetiapine, etc.). Small doses of beta-blockers are also used to reduce OA. Most often prescribed propranolol at a dose of 20 - 60 mg / day, but some patients are helped by higher doses of propranolol (80 - 100 mg / day). Benzodiazepines also contribute to the reduction of akathisia (clonazepam 0.5–4 mg/day, diazepam 5–15 mg/day, lorazepam 1–4 mg/day). They are primarily indicated in the presence of severe anxiety. Cholinolytics (biperiden 4-6 mg/day) are especially effective in cases where akathisia is combined with parkinsonism, but they are less effective in isolated OA. However, it is still unclear whether prophylactic administration of an anticholinergic prevents akathisia. In resistant cases, to reduce akathisia, they resort to amantadine (200-400 mg / day), which often has a good, but transient effect, clonidine (clonidine, 0.15-0.6 mg / day), piracetam (800-1600 mg / day). days), amitriptyline (25–100 mg/day), as well as codeine and other opioids. In recent years, a favorable effect has been shown in OA of serotonin 5-HT2 receptor blockers (ritanserin, mianserin, cyproheptadine), as well as nicotine (in the form of skin patches).

In PA, if possible, the drug should be discontinued, replacing it with an atypical antipsychotic (clozapine, olanzapine), or at least its dose should be reduced. After discontinuation of the drug, the symptoms regress within a few months or years. Beta-blockers and anticholinergics are ineffective. The drugs of choice are sympatholytics (reserpine, tetrabenazine), which have a positive effect in more than 80% of patients. Opiategics are as effective in PA as they are in OA. In case of iron deficiency, its compensation is necessary. In resistant cases of PA, electroconvulsive therapy sometimes has a positive effect.

In addition, when correcting OA and PA, one should not underestimate the importance of psychological and psychotherapeutic factors associated with treatment, intensive contact between the doctor and the patient, as well as the environment, and the patient's personality.

Treatment of akathisia according to George Arana, Jerrold Rosenbaum ("Handbook of Psychiatric Drug Therapy", 4th ed., 2001):

A. If the patient is treated with a highly potent typical antipsychotic and has no other extrapyramidal symptoms (EPS). 1. Drug 1st choice: β-blocker, such as propranolol at a dose of 10-30 mg 3 times a day (nadolol can also be used) (see chapter 6). 2. 2nd choice drug: anticholinergics such as benztropine 2 mg twice daily. 3. 3rd choice drug: benzodiazepine, eg lorazepam 1 mg 3 times a day or clonazepam 0.5 mg 2 times a day.

B. If the patient is taking low-potency typical antipsychotics (eg, thioridazine) or an antipsychotic in combination with a tricyclic antidepressant and no other EPS. 1. The drug of the 1st choice: propranolol - 10 - 30 mg 3 times a day. 2. Drug of the 2nd choice: lorazepam - 1 mg 3 times a day or clonazepam - 0.5 mg 2 times a day. 3. Drug of the 3rd choice: benztropine - 1 mg 2 times a day (possibly increased anticholinergic toxicity).

C. If a patient taking antipsychotics has other EPS (dystonia or parkinsonism). 1. Drug of the 1st choice: benztropine - 2 mg 2 times a day. 2. Second choice drug: benztropine in combination with propranolol at a dose of 10-30 mg 3 times a day. 3. Drug of 3rd choice: benztropine with lorazepam at a dose of 1 mg 3 times a day or clonazepam at a dose of 0.5 mg 2 times a day.

D. If the patient has other EPS; however, akathisia does not respond to anticholinergic monotherapy. 1. Preparations of the 1st choice: benztropine - 2 mg 2 times a day with propranolol - 10 - 30 mg 3 times a day. 2. Drugs of the 2nd choice: benztropine - 2 mg 2 times a day with lorazepam - 1 mg 3 times a day or clonazepam - 0.5 mg 2 times a day.

E. If a patient has EPS or akathisia, the clinician should consider switching the patient to an atypical antipsychotic, given that the new drug is not always as effective as the previous one.

Additional Information:

article "Diagnosis and treatment of neuroleptic extrapyramidal syndromes" Fedorova N.V., Vetokhina T.N., RMAPE "Neurology and neurosurgery in Belarus" No. 1 (01), 2009) [read];

article “Intravenous administration of biperidene for the treatment of akathisia: an open pilot study” by Sh. Hirose (Psychiatric Hospital of Fukui Prefecture, Japan), K.R. Ashby (St. John's University); journal "Social and Clinical Psychiatry" 2014, vol. 24, no. 1) [read];

article "Medicated dyskinesias" by O.S. Levin, Department of Neurology, RMAPO Center for Extrapyramidal Diseases (Journal "Modern Therapy in Psychiatry and Neurology" No. 3, 2014) [read];

article (review) "Akathisia: clinical analysis of pathology with recommendations and literature review" R.A. Becker, Yu.V. Bykov; University. David Ben-Gurion in the Negev, Israel, Beer Sheva; State Budgetary Educational Institution of Higher Professional Education Stavropol State Medical University of the Ministry of Health of Russia (

Akathisia(from other Greek ἀ- / a- / - “not” and καθίζειν / kathízein / - “sit”) - a clinical syndrome characterized by a constant or periodically occurring unpleasant feeling of internal motor restlessness, an internal need to move or change posture, and manifested in the inability of the patient to sit still for a long time in one position or to remain motionless for a long time. In common parlance, as a synonym for the term "akathisia", patients also use the word "restlessness".

The most common cause of akathisia is the side effects of drugs, primarily traditional antipsychotics ("typical antipsychotics") and, to a lesser extent, atypical ones. Less commonly, akathisia occurs with the use of antidepressants (primarily SSRIs and SNRIs) and psychostimulants. Sometimes it can be caused by Parkinson's disease or be part of the clinical picture of parkinsonism and other similar syndromes. In addition, akathisia is a common, almost constant symptom in opiate, less commonly alcohol, benzodiazepine, or barbiturate withdrawal syndrome; it can occur in cocaine addicts against the background of cocaine intoxication and even during post-anesthetic awakening in healthy individuals. Akathisia may also occur with abrupt withdrawal of neuroleptics or antidepressants (the so-called “withdrawal akathisia”, withdrawal akathisia).

The term was introduced by the Czech psychiatrist Ladislav Gaskovec (Czech. Ladislav Haskovec, 1866-1944) in 1901, long before the advent of neuroleptics. After the introduction of neuroleptics into clinical practice, the incidence of akathisia increased significantly. As of 1992, akathisia occurred in 30% of cases of taking antipsychotics. Often it is combined with depression.

Although akathisia may be associated with other extrapyramidal side effects of antipsychotics, in many cases it occurs in isolation.

The reasons

Most often, akathisia is a side effect of antipsychotic medications (the risk of akathisia exists with the use of almost any antipsychotic), but it can have other causes. Akathisia can be caused by:

• Non-sedating typical antipsychotics such as haloperidol, droperidol, pimozide, trifluoperazine.
• The so-called "atypical" antipsychotics (much less often): the tendency to cause extrapyramidal side effects, and in particular akathisia, is lower than that of typical antipsychotics, due to a pronounced blockade of serotonin 5-HT 2 receptors (as in risperidone, olanzapine, quetiapine), which enhances dopaminergic transmission in the nigrostriatal system and counterbalances the blockade of dopamine D 2 receptors, or due to the presence of a built-in dopaminergic agonist activity in the drug (as in aripiprazole).
• Sedating typical antipsychotics (also less common than non-sedating ones), such as zuclopenthixol or chlorpromazine, in which the tendency to cause akathisia is reduced due to the drug's anticholinergic (anticholinergic) and antihistamine activity.
• Selective serotonin reuptake inhibitors (SSRIs), especially fluoxetine, paroxetine. Akathisia (along with the initial exacerbation of anxiety, insomnia, and along with the fact that the well-being and energy levels in patients receiving antidepressants usually return to normal before sadness, depressed mood and suicidal thoughts disappear) is one of the possible mechanisms leading to an increase in suicidal risk, risk of manifestations of aggressiveness or dangerous impulsive acts in patients receiving SSRIs.
• Rarely - other antidepressants. Akathisia can be associated with the prescription of almost any antidepressant; in particular, akathisia has been described with the appointment of TCAs, SSRIs, MAOIs, mirtazapine, mianserin, trazodone, agomelatine.
• Antiemetics, especially D2-blockers such as metoclopramide, promethazine, thiethylperazine, domperidone.
• Reserpine, tetrabenazine, methyldopa.
• Levodopa and dopamine receptor agonists (bromocriptine, pergolide, pramipexole), which have a "prodopaminergic" effect, glucocorticoids, thyroid hormones, psychostimulants, opioids (in particular, pethidine).
• lithium preparations.
• Occasionally - anticonvulsants (valproate, carbamazepine).
• Benzodiazepines (alprazolam, lorazepam).
• Calcium antagonists, in particular cinnarizine, flunarizine, less often - diltiazem, verapamil, dihydropyridines.
• Antiserotonin agents (methisergide, ondansetron).
• Antihistamines, eg diphenhydramine, clemastine, chloropyramine, doxylamine, hydroxyzine, chlorpheniramine maleate and cold mixtures containing it.
• Non-psychotropic drugs: interferons, macrolide antibiotics (particularly azithromycin, clarithromycin), fluoroquinolone antibiotics, anti-tuberculosis drugs cycloserine and isoniazid, antiviral drug foscarnet, antimalarials (eg, mefloquine), proton pump inhibitors, sibutramine, some antiarrhythmics (amiodarone, novocaine inovocainamide, aprindine, etafenone, papaverine, propiverine, pentoxyverine, oxobutynine), sumatriptan.

In addition, the reasons may be:

• taking drugs, in particular GHB, amphetamine, methamphetamine, cocaine, "bath salts" (methylenedioxypyrovalerone and its analogues), "ecstasy" (MDMA), "spice" (synthetic cannabinoids), etc .;
• opiate, alcohol, benzodiazepine, barbiturate or nicotine withdrawal;
• sudden discontinuation of benzodiazepines.

Akathisia Binga - Sekara called akathisia, spontaneously occurring in the absence of any medicinal effect in neurological diseases manifested by parkinsonism and other extrapyramidal disorders (Parkinson's disease, postencephalitic, post-traumatic or post-stroke parkinsonism, etc.).

Akathisia can also occur spontaneously, in the absence of any drug effect, in other neurological diseases not associated with parkinsonism or extrapyramidal disorders - for example, in traumatic brain injuries, strokes. Such akathisia is not classified as Bing-Sekar akathisia.

Akathisia has also been described on awakening after general anesthesia in mentally and neurologically healthy individuals who did not receive drugs capable of causing it, including akathisia after ECT.

Spontaneous akathisia called akathisia, which occurs in the absence of drug exposure in mental (and not neurological) diseases. For example, the development of spontaneous akathisia in schizophrenia, in affective disorders, has been described, and Ladislav Gaskovets, who originally described akathisia, indicated that it can occur as a component of severe anxiety in anxiety, hysterical and conversion disorders.

Severe akathisia has also been described in patients with hypoxic lesions of the basal ganglia resulting from carbon monoxide poisoning.

Risk factors in antipsychotic therapy

• Genetic predisposition to akathisia
• Treatment with an antipsychotic or antidepressant that has a high potential for this complication
• Combined psychopharmacotherapy (for example, a combination of two or more antipsychotics, an antipsychotic with an antidepressant with a high potential for developing akathisia, an antipsychotic and lithium, etc.)
• High dose of the drug or its rapid increase
• History of traumatic brain injury or other organic lesions of the central nervous system, especially if the prefrontal cortex is damaged
• The presence of cancer
• Iron or magnesium deficiency
• Dementia
• Pregnancy (probably as one of the causes of iron deficiency)
• Elderly and senile or, conversely, childhood and adolescence
• Mood or anxiety disorders, and among people with schizophrenia, patients who initially have a high proportion of negative and / or affective, as well as cognitive symptoms are more predisposed
• Neurological and extrapyramidal disorders before antipsychotic therapy

Low-potent typical antipsychotics with a pronounced sedative effect, strong antiserotonin, M-anticholinergic, α-adrenergic blocking, H 1 -histamine blocking properties, such as chlorprothixene or thioridazine, are less likely to cause akathisia than high-potency typical antipsychotics, non-sedative or with a mild sedative effect, blocking mainly D 2 dopamine receptors such as haloperidol.

Among atypical antipsychotics, the most common cause of akathisia is risperidone (7% to 50%) and aripiprazole (23% to 42%). Significantly lower than that of risperidone and aripiprazole, the incidence of akathisia in the treatment of such atypical antipsychotics as ziprasidone, olanzapine (from 3% to 16%), asenapine, lurasidone, amisulpride, sulpiride. The lowest incidence of akathisia among all atypical antipsychotics seems to be characteristic of quetiapine (2% to 13%) and iloperidone. Data on the incidence of akathisia when taking clozapine are contradictory: some sources note that clozapine has the lowest risk of developing akathisia, others that akathisia occurs when taking it with a frequency of 15% to 31%, and in the third - that it occurs with a frequency , comparable to the incidence of akathisia during therapy with typical antipsychotics (39% with clozapine therapy, 45% with typical antipsychotics).

Pathogenesis

The pathogenesis of akathisia is unknown, but presumably it is associated with impaired functioning of the dopaminergic mesocortical pathways innervating the frontal and cingulate cortex, mesolimbic and/or nigrostriatal. Perhaps for this reason, akathisia, unlike other extrapyramidal side effects, often occurs when taking the atypical antipsychotic clozapine, which mainly acts on D 4 receptors in the cortex and limbic system.

However, recent studies indicate that the pathogenesis of akathisia seems to be more complex and not limited to disturbances in the dopaminergic system, and that disturbances in other monoaminergic systems (serotonin, noradrenergic), opioid, NMDA- and GABA systems, in neurokinin systems, as well as oxidative stress in neurons.

Another explanation for the mechanism of akathisia has been proposed, according to which a generalized decrease in dopaminergic activity in the CNS, caused, in particular, by the use of antipsychotics or antidepressants of the SSRI group or observed in Parkinson's disease, can lead to the activation of compensatory mechanisms, one of which is also a generalized increase in noradrenergic activity in the CNS emanating from the bluish spot. Since noradrenergic axons emanating from the bluish spot innervate the shell of the nucleus accumbens to a greater extent than his body, this imbalance of noradrenergic innervation in the nucleus accumbens, in fact, causes the development of dysphoric sensations, anxiety and motor restlessness characteristic of akathisia, movement needs. And then descending noradrenergic impulses from the central nervous system lead to an increase in the secretion of adrenaline by the adrenal medulla and to the development of akathisia, agitation and anxiety. This theory well explains both the effectiveness of direct or indirect antiadrenergic drugs such as beta-blockers, clonidine, benzodiazepines or opioids in the treatment of akathisia, and the fact that not all patients taking typical antipsychotics occur in akathisia, even if many of them have There are clear symptoms of nigrostriatal D 2 blockade (drug-induced parkinsonism): apparently, these patients simply do not develop a compensatory increase in noradrenergic activity in response to D 2 blockade.

In addition, it has been found that akathisia, as well as restless legs syndrome, can be aggravated by the administration of a peripheral D 2 -blocker domperidone (motilium), which does not penetrate the blood-brain barrier. This presumably indicates the participation in the pathogenesis of akathisia, in addition to central, also peripheral dopaminergic mechanisms.

Differences in the response to antipsychotic drugs make it possible to understand that acute akathisia and tardive akathisia, with external similarities, may have a different pathophysiological basis - tardive akathisia may be based, in particular, on hypersensitivity of dopamine receptors.

general description

The severity and severity of akathisia can vary from a slight feeling of internal tension, anxiety or restlessness (which may not even be realized by the patient himself and easily go unnoticed by the doctor even with a careful examination and detailed questioning of the patient) to a complete inability to sit still, accompanied by severe debilitating anxiety, as if "Eating" or gnawing the patient from the inside, a constant feeling of fatigue, fatigue and weakness, severe depression and dysphoria (manifested by irritability, nervousness, impulsiveness and aggressiveness, and sometimes - a feeling of fear, horror or panic that is difficult to describe).

Akathisia is often difficult to describe by the patient and in many cases remains undiagnosed or misdiagnosed (interpreted by doctors as an exacerbation of psychosis, an increase in agitation or anxiety, or the condition can be mistaken for mania, for agitated depression or anxiety). Difficulties in diagnosing akathisia are further aggravated by the fact that akathisia and the associated severe anxiety, fear, and dysphoria actually exacerbate the mental state of patients and can lead to an increase in arousal, an exacerbation of psychosis, an increase in hallucinations and delusions, worsening of depression, or to the development of true or apparent resistance to neuroleptics and/or antidepressants. In cases where such an error in diagnosis occurs against the background of the use of antipsychotic drugs (neuroleptics), that is, in the context of akathisia caused by antipsychotics, it very often leads to an erroneous increase in the doses of antipsychotics used, to an unreasonable transfer of the patient to a more powerful antipsychotic, or to the unreasonable addition of additional neuroleptics (for example, low-potency sedative NL). This, in turn, may exacerbate akathisia and other extrapyramidal side effects of antipsychotics. Responsible patients often describe what happens to them at the same time as an increasing feeling of internal tension and discomfort, or as "chemical torture".

Clinical picture and typical history

Akathisia is not a single symptom, but a complex clinical syndrome or phenomenon consisting of subjective and objective components. The subjective component of akathisia includes the patient's complaints of subjective internal discomfort, internal tension, restlessness, anxiety, irritability, insomnia, the need to move, change posture, and the inability to sit or lie still. The objective component (“motor component”, motor akathisia) is the objectively observed external, motor manifestations of the akathisia syndrome.

The most characteristic motor manifestations of severe akathisia are stereotypical senseless leg movements, usually involving both lower limbs as a whole, from the hips to the ankles (the patient marks time, shuffles, often changes position when standing; walks a lot, often along the same route, for example, from from one corner of the room to another; when sitting, often crosses and uncrosses his legs, shakes them, fidgets in a chair, spins; lying in bed, often moves his legs, fidgets, turns and rolls over in bed, bends and unbends his legs). The tendency to predominantly involve the lower extremities is useful in the differential diagnosis of akathisia from other extrapyramidal disorders (eg, acute dystonia, tardive dyskinesias, tics, and hyperkinesias). With mild akathisia, stereotyped, monotonous movements may be outwardly subtle or absent, movements may seem meaningful.

According to Russian authors, the motor activity that accompanies akathisia can be different, but often, especially with a significant severity of this syndrome, it acquires a stereotypical character (tapping fingers, crossing fingers, “striking the rosary”, swaying the legs, aimlessly walking from corner to corner and etc.).

With severe akathisia, the tendency to predominantly involve the lower extremities becomes less noticeable, and severe akathisia can affect almost the entire body - as a rule, it spreads as the severity of the "bottom up" increases (starting from the legs, to the pelvis, lower back and lower trunk , then to the upper torso, upper limbs, face, and even the eyes, which the akathisic patient can often switch from one subject to another). As a result, a patient with severe akathisia can continuously “twist” and “wriggle”, “writhe”, “sway”, or sway back and forth or from side to side with the whole torso and even the whole body, sometimes taking strange postures, sometimes even resorting to antics, jumping, running, or suddenly jumping up from a bed or chair, "getting out" of the mating in an attempt to achieve relief (this can be mistakenly perceived as "foolish hebephrenic or catatonic excitement").

Sometimes there are unusual, atypical manifestations of akathisia, which may not involve the lower limbs and generally the lower half of the trunk. For example, a case of akathisia of the occipital muscles and oculomotor muscles is described, in which the patient constantly extended and flexed his neck, looked from one object to another (this symptom was even mistakenly considered nystagmus) without involving the muscles of the legs. Unilateral (left-sided) akathisia induced by antipsychotic therapy has also been described in a patient with schizoaffective disorder, and in the same patient, on the contrary, periodic movements of the limbs on the opposite, right side were noted during sleep. Although no organic cause of akathisia could be found in this patient, the authors who described this case note that in all such cases, the unusual clinical presentation of akathisia should raise the doctor's suspicion of an organic cause, such as a brain tumor, brain abscess, or cerebral infarction. , stroke, and lead to the appointment of appropriate examinations. Other authors described four more cases in which patients developed unilateral akathisia and concurrent unilateral manifestations of other extrapyramidal disorders (drug-induced parkinsonism and/or dystonia) without any observable organic cause.

The subjective component of akathisia can also be observed separately from objective motor manifestations (in their absence), especially with mild akathisia. In many cases, especially with mild akathisia, the patient is able to completely or partially suppress, by an effort of will, its external motor manifestations, hide them or actively dissimulate (for example, fearing that this condition will be misinterpreted by the psychiatrist as "excitation" or as "aggravation of psychosis" and as a result, the patient will have to increase the dose of the antipsychotic).

The subjective component of akathisia can be subdivided into a sensory component, or sensory akathisia (which is subjectively described by patients as "tingling in the legs", "twisting" or "twisting" of the joints or muscles, vague "burning" or "itching" in the legs, and in depth , in the muscles or joints, and not on the skin; as a vague need to move, move the legs and the temporary relief of these sensations experienced during movement), and a mental component, or mental akathisia (subjectively described by patients as "anxiety", "fear", " inner tension", "restlessness", "inability to relax", "inability to sit or lie still", "insomnia, inability to sleep, tossing in bed; nighttime awakenings due to desire to walk", "wanting to jump out of your skin").

It is very significant that the sensations characteristic of the subjective component of akathisia are often very difficult to formalize and adequately describe, convey in words (much more difficult than, for example, anxiety or depression), and for this reason, patient complaints are often vague, non-specific and incomprehensible. doctor. One possible explanation for this phenomenon (the extreme difficulty of describing the subjective discomfort of akathisia) is that akathisia, unlike, for example, anxiety or depression, lies far outside our "normal" sensory experience. Herman Berrios, an eminent researcher of both akathisia and the phenomenon of depersonalization and derealization, points out that the sensations experienced by patients during depersonalization and derealization are just as difficult to formalize and vague as in akathisia, and cause an equally pronounced discomfort that cannot be expressed in words. ; as a result, they are just as often misinterpreted by doctors, which can be explained by the "beyond" and unusual sensory experience in depersonalization-derealization and in akathisia.

As a consequence of akathisia, increased lability of affect may develop, such as increased tearfulness or irritability, irascibility, increased excitability, impulsiveness, or aggressiveness. Interestingly, in some patients, the opposite clinical response to SSRIs or antipsychotics is observed - in the form of a decrease in affect fluctuations, a decrease in spontaneity and impulsivity, the development of apathy and adynamia (a decrease in spontaneous motor activity) up to the occurrence of emotional flattening, which is called SSRI apathy syndrome and Neuroleptic-induced deficiency syndrome (NIDS) respectively in the case of SSRIs and antipsychotics. The reasons for this difference in the reactions of different patients to the same drugs are unknown, since research in this area is still not enough. However, it is known that SSRI apathy syndrome and NIDS are usually delayed, late effects of long-term treatment with SSRIs or antipsychotics. At the same time, akathisia is more characteristic of the acute phase of treatment. In addition, there is neither antagonism nor a direct correlation between akathisia and these two clinical syndromes: the presence or absence of akathisia in a patient does not mean that he will not develop later NIDS or SSRI apathy, but does not mean the opposite.

Jack Henry Abbott, a convicted murderer, described in 1981 his feelings after being forced to take antipsychotic drugs:

These medicines, the medicines of this group, do not calm or relieve nervous tension. They suppress and attack. They attack you from the inside, so deep from the inside that you are unable to find the source of your mental pain and discomfort ... Your jaw muscles go crazy and refuse to obey you, they convulse convulsively so that you bite the inside of your cheeks, lips or tongue , your jaws click, your teeth chatter, and the pain shoots right through you. And every day this goes on for hours. Your back becomes stiff, tense, and terribly straight, so that you can hardly move your head or neck sideways, bend or straighten, and sometimes your back bends against your will and you cannot stand straight. Inner pain permeates you and swims along your nerve fibers. You suffer from morbid anxiety and you feel that you need to move, walk, take a walk and this will ease your anxiety. But as soon as you start moving or walking, you get tired and feel anxious again, you feel like you are doing something wrong and you need to sit down and rest. And so it is repeated again and again, again and again, you walk, sit down, jump up and walk again and sit down again. Feeling the pain, the source of which you cannot find, you go crazy with anxiety, it eats you from the inside, and you cannot even breathe relief.

Classification

Akathisia is subdivided depending on its dominant or main manifestations into: Classification

• predominantly motor akathisia(mainly motor restlessness, restlessness, restlessness), which in the limit (in the presence of only motor manifestations) turns into the so-called pseudoakathisia, or "pseudo-akathisia type I";
• predominantly psychic akathisia(anxiety, internal tension, restlessness, irritability, not necessarily manifested in the motor sphere);
• predominantly sensory akathisia(peculiar sensations of "twisting", "twisting", "itching", or "itching", or "pulling" in the muscles or joints, which are not always realized in specific motor acts and are often interpreted by the attending physicians as senestopathies); in the limit, as well as predominantly mental akathisia, with relatively mild forms of akathisia, it may not have visible motor manifestations at all, which in both cases was called “type II pseudo-akathisia”;
• classic akathisia, which is characterized by a more or less uniform representation in the clinical picture of both the subjective (mental and sensory) and objective components of akathisia.

Often the term " pseudoakathisia» without specifying its type - this term refers to motor restlessness in the absence of mental symptoms of akathisia. A similar term is also used tasykinesia"- according to A. Timkov, K. Kirov (1976), with tasikinesia, there are no painful sensations characteristic of akathisia, the need for movement is the primary tendency, defined as an irresistible internal pressure.

The existence of type I pseudo-akathisia is questioned by a number of experts: for example, it is argued that the patient can simply hush up or actively hide, dissimulate akathisic complaints and the presence of subjective discomfort, or simply not understand what is happening to him, or underestimate the importance of these complaints due to cognitive impairment , low level of intelligence and education, or due to a general mental state, disorganization of mental activity, the presence of severe psychosis or an affective syndrome, whether it be depression or mania.

Depending on the time of occurrence in the course of treatment, akathisia is divided into:

• sharp akathisia ( acute akathisia), arising in the first days and weeks, and sometimes even in the first hours or tens of minutes from the start of treatment with antipsychotics or antidepressants;
• subacute and chronic akathisia ( chronic akathisia), which occurs in the first weeks or months of therapy, but, unlike late akathisia, gradually decreases or disappears after discontinuation of the drug or a decrease in its dose;
• akathisia withdrawal (withdrawal akathisia), usually occurring up to two weeks after dose reduction or drug withdrawal; gradually it decreases and usually disappears by a period of about 6 weeks; if the “withdrawal akathisia” persists longer, then in all likelihood it is in fact a late akathisia, described below);
• late, or tardive akazitiya ( tardive akathisia), usually occurring after many months and sometimes years of treatment with antipsychotics or antidepressants; tardive akathisia may temporarily increase with dose reduction or withdrawal of the drug, may temporarily mask or disappear with increasing dose and then reappear in an enhanced form, persist for a long time - months or years, and sometimes for life - even after the drug that caused it is discontinued, and if and decreases over time after withdrawal, then usually slowly.

It is sometimes argued that tardive and chronic akathisia can occur solely as a result of the use of antipsychotics, in contrast to acute akathisia, the occurrence of which is associated not only with the use of antipsychotics, but also with the use of certain other drugs.

Complications

A frequent consequence of akathisia caused by neuroleptics or antidepressants is refusal of treatment (lack of compliance with treatment), distrust or hostility towards doctors and medical staff, fear of treatment and drugs. In the most extreme cases of treatment withdrawal due to akathisia, patients treated with antipsychotics for psychotic disorders or nausea may attempt to escape from the hospital due to drug-induced distress. Taking into account the ability of patients to dissimulate and conceal both subjective complaints and external motor manifestations of akathisia, it sometimes erroneously seems that its only manifestation is the patient's "inexplicable" negativism in relation to treatment or a sudden refusal of it.

Akathisia can also lead to the impossibility of the patient's full participation in psychotherapy or in labor and socio-rehabilitation activities, to the patient's inability to perceive and assimilate psychotherapy, to perform tasks.

Akathisia, especially in the case of its significant severity, can cause the patient to exhibit aggressive or impulsive behavior, self-harm or harm to other people, animals, objects of the environment, even cause the emergence or actualization of suicidal thoughts and tendencies, lead to suicidal attempts and completed suicides.

Timely not stopped or inadequately treated akathisia sometimes leads to the development of the phenomenon of complete intolerance (intolerance, negative resistance) of antipsychotics, antidepressants and other psychopharmacological drugs that can cause it; with repeated attempts to prescribe these or even other drugs of a similar class, akathisia sometimes quickly reappears even at low doses (probably due to a mechanism similar to the mechanism for the development of idiosyncratic reactions of individual intolerance, or it arises on the basis of psychological factors, according to the mechanism by which "waiting vomiting" in cancer patients with repeated exposure to chemotherapy and radiation).

The presence of akathisia can worsen the course of any mental illness, increase the manifestations of any psychopathology present in the patient, and even lead to the development of resistance to psychopharmacotherapy (to antidepressants, antipsychotics and other psychopharmacological agents). In particular, akathisia can enhance the manifestations of psychosis, especially agitation, anxiety, disorganization of thinking and behavior, hallucinatory and delusional phenomena, affective symptoms (depressive or manic). Successful treatment (stopping) of akathisia with central anticholinergics and / or β-blockers leads to a rapid overall clinical improvement, to a decrease in both the total scores of the BPRS and PANSS scales, and such specific indicators as hallucinations, delusions, disorganized thinking, behavioral disorders, aggression, mania and depression.

Akathisia and its characteristic excessive motor activity can exacerbate in patients suffering from comorbid social anxiety their characteristic feeling of their own “inadequacy”, “inappropriateness in society”, shyness, shyness, and avoidance of social contacts. Anxiety caused by akathisia can contribute to the occurrence of panic attacks and interfere with the manifestation of the anti-panic and anti-anxiety activity of antidepressants and antipsychotics, and cause resistance to them. Meanwhile, the relief of akathisia increases the effectiveness of the treatment of anxiety disorders and anxiety symptoms in other diseases. Akathisia can also intensify obsessive-compulsive manifestations (obsessive thoughts, fears, rituals), interfere with psychotherapy for obsessive-compulsive disorder.

One of the most undesirable complications of untreated akathisia is the development in patients of the iatrogenic depersonalization-derealization syndrome (DP / DR) as a protective reaction of the psyche to akathisia and to the severe, sometimes unbearable anxiety and dysphoria it causes. The DP/DR syndrome, which has arisen against the background of akathisia, is difficult (like any other DP/DR syndrome) to treat and often shows a high degree of resistance to various treatment options; this is associated with an increase in suicidal risk and a deterioration in the quality of life of patients and the possible development of secondary psychopathological phenomena (for example, depersonalization itself can cause secondary anxiety, depression or social anxiety, "obsession with one's condition", etc.).

Due to the strong negative impact of akathisia on any psychopathology present in the patient (for example, anxiety disorder, depression, or psychosis), the tendency of this existing psychopathology to "come to the fore" in the clinical picture, the difficulty in formulating and verbalizing the patient's feelings with akathisia, the well-known tendency of faces with mental disorders to hide and dissimulate their feelings and experiences, their ability to suppress by an effort of will the external motor manifestations of akathisia, and sometimes due to the masking effect of depersonalization on akathisia, akathisia is often not recognized, underestimated in severity or misdiagnosed by doctors and regarded, for example, as "increased anxiety", "exacerbation of psychosis", "psychomotor agitation", "insufficient effectiveness of therapy". This leads to the wrong choice of therapeutic tactics, often - an increase in the dose of an antipsychotic or antidepressant, or even the addition of a second antipsychotic or antidepressant, as a result of which the patient often becomes even worse.

In patients with psychosis, akathisia and the sensations associated with it may receive delusional coloring and interpretation; in addition, the unusualness of sensory sensations in akathisia leads to the fact that the attending physician may mistake these sensations for senestopathies, and this also complicates the problem of correctly diagnosing the condition and choosing the right treatment tactics.

Long-existing akathisia can lead to the development of specific pathological changes in personality, changes in character. According to V. M. Banshchikov and T. A. Nevzorova, patients with akathisia “become obsessive, even importunate, sugary, fawning, anxious and suspicious, hypochondriacal, constantly asking for correctors, sleeping pills and tranquilizers, irritable, especially when they are denied this ".

Trying to achieve relief of the symptoms of akathisia, some of the patients smoke heavily, abuse alcohol, tranquilizers, central anticholinergics, pregabalin, various psychoactive substances (eg, cannabinoids, psychostimulants). That said, while alcohol and cannabinoids can alleviate akathisia in the here and now, their abuse itself can cause or exacerbate akathisia, especially in the setting of alcohol or cannabinoid withdrawal. The severity of akathisia during treatment with antipsychotics or antidepressants correlates with the frequency and severity of substance abuse, especially alcohol and cannabinoids. Even a single recent use of cocaine or another "street" psychostimulant, such as amphetamine, contributes to an increase in the severity of extrapyramidal disorders, and in particular akathisia. The frequency and intensity of tobacco smoking also correlate with the severity of akathisia in individuals with schizophrenia; while tobacco abuse itself can cause or exacerbate akathisia, psychomotor agitation, nervousness.

Diagnostics

Diagnosis of akathisia is based on the observed clinical symptoms (motor manifestations of akathisia, as well as the frequent presence of external manifestations of other extrapyramidal disorders, such as drug-induced parkinsonism, tremor, acute dystonia), on asking patients about the presence of subjective complaints about mental and / or sensory manifestations of akathisia ( anxiety, restlessness, internal tension, irritability, insomnia, depression, suicidal thoughts, restlessness, need to move, change body position, sensations such as "crawling on the legs", "twisting muscles or joints"; complaints of stiffness, motor inhibition, unusual movements in the presence of comorbid extrapyramidal disorders) and on careful history taking (taking, increasing or reducing the dose of drugs that can cause akathisia; recent substance abuse, withdrawal syndrome; traumatic brain injury, stroke, neuroinfections, Parkinson's disease, postencephalitic severe parkinsonism and other organic lesions of the central nervous system, which can also cause akathisia; recent blood loss, antitumor chemotherapy, anorexia, which can cause iron deficiency, which increases the manifestations of akathisia; the presence of mental disorders that may be the cause of spontaneous akathisia or the reason for prescribing drugs that can cause it, even if the patient denies taking them; recent vomiting, cancer, general anaesthesia, or gastrointestinal disturbances that may warrant antiemetics or prokinetics, etc.).

Currently, there are no objective neurophysiological, neuroimaging, or laboratory methods that can confirm or refute the presence of akathisia in a patient or help in its diagnosis, so the clinician should rely only on his own judgment and experience.

Timely and correct diagnosis of akathisia and a more objective assessment of its severity is facilitated by the use of formalized scales, such as the Burns akathisia scale.

Diagnosis and differential diagnosis of akathisia is sometimes difficult due to its similarity with some other pathological conditions; the tendency of patients to dissimulate and conceal symptoms; the ability of akathisia to enhance the manifestations of any existing psychopathology, which is why this psychopathological symptomatology comes to the fore, obscuring or masking akathisia; objective difficulty for the patient to express their feelings associated with akathisia; etc. Due to the tendency of patients to completely or partially suppress the external motor manifestations of the akathisic syndrome by an effort of will, a tendency to dissimulate, and sometimes difficulties in being aware of the presence of akathisia, it is very useful to express your feelings in words. situations where he does not know that he is being observed by the attending psychiatrist (for example, while waiting for an appointment, outside the office door, and not directly at the reception, or in the department, according to staff and relatives).

Considering the insufficient detection of akathisia in clinical practice, its ability to complicate any psychopathology, the extreme importance of its timely detection and treatment (which helps to ensure patient compliance, prevent suicide and aggressive behavior, prevent the development of resistance to antidepressants and antipsychotics or their intolerance), it is much it is better to err on the side of overdiagnosing akathisia and overestimating its severity and prescribing a more active, multicomponent treatment for akathisia than underestimating its severity or skipping it.

The main differential diagnostic issue is the distinction between akathisia and states of psychomotor agitation. A study published in 2006 by D. Healy, A. Herxheimer and D. Menkes in the UK indicates that akathisia is very often misdiagnosed and described in reports of the incidence of side effects of antidepressants in clinical studies as "arousal", "insomnia" , "anxiety", "hyperkinetic syndrome" or "motor hyperactivity". Thus, the actual incidence of akathisia in antidepressant treatment is systematically underestimated in RCTs, leading to misleading publications in drug formularies and labels and misjudgment of the risk of akathisia by practitioners.

This study also shows that akathisia is often misunderstood and too narrowly defined as motor akathisia- simple motor restlessness, which can be more accurately described as dyskinesia. This does not take into account the likelihood that the patient may experience mental(non-motor) akathisia, not manifested by a pronounced increase in motor activity, but internally felt as anxiety, discomfort, restlessness or tension, or experience sensory akathisia - sensations of "itching", "tingling" or "pulling" in the muscles and joints, not necessarily leading to visible frequent changes in postures. In addition, Healy et al showed that there is a strong association between antidepressant or antipsychotic-induced akathisia and dangerous behavior, aggressiveness, and impulsivity, including sudden suicides and hospital escapes, and that akathisia can worsen the mental state of patients and lead to an exacerbation of the patient's pre-existing psychopathology (particularly psychoses, depressions, manias or anxiety states). The study also states that there is a large clinical evidence base linking akathisia to SSRIs, and that patients receiving SSRIs are approximately 10 times more likely to drop out of treatment due to severe akathisia than patients receiving placebo (5% versus 0.5% ).

Treatment

General events

The treatment of akathisia depends on its etiology, therefore, first of all, it is necessary to accurately determine the cause that caused akathisia. Since in clinical practice the vast majority of patients with akathisia are patients with drug-induced akathisia, among which, in turn, the majority are patients receiving antipsychotics and / or antidepressants, the first step in the algorithm for treating this syndrome should be the analysis of the patient's current drug regimen. and the determination in its composition of drugs that may be potential culprits in the development of akathisia.

The next step, if possible, should be to reduce the dose or discontinue drugs that can cause akathisia, or replace them with other drugs with less extrapyramidal potential (for example, replacing a typical antipsychotic with an atypical one, and among atypical ones, replacing, for example, risperidone with quetiapine or olanzapine, olanzapine - quetiapine), if the mental state of the patient and the characteristics of the course of his disease allow. This step is not always possible due to objective reasons, in particular due to the mental state of the patient and the risk of its deterioration when the drug is discontinued, its dose is reduced or replaced with another psychotropic drug, and often for financial, organizational reasons (lack of necessary drugs, their unacceptable high cost), in some cases - due to poor tolerance of alternative drugs due to other side effects.

When evaluating the effectiveness of such an event as lowering the dose, canceling or replacing the drug, one should take into account the possibility of “overlapping” the so-called “withdrawal akathisia” on the patient’s already existing akathisia and, as a result, a temporary deterioration in his condition. It is necessary to assess the mental state and the degree of reduction of akathisia several weeks (from 2 to 6 weeks) after reducing the dose, discontinuation or replacement of the drug and not jump to conclusions about the ineffectiveness of this measure in terms of stopping akathisia or about "deterioration of mental state", "exacerbation of psychosis ”, “increasing arousal” with dose reduction or drug change, since this apparent worsening may actually be due to withdrawal akathisia.

In addition, as an important component of the treatment of akathisia, the possibility of prescribing drugs that can potentiate (enhance) the desired effects of antipsychotics or antidepressants without potentiating their extrapyramidal side effects should be considered: this may allow reducing the doses of drugs that induced akathisia. For example, lithium carbonate is ineffective against akathisia as such, but it potentiates the anti-manic effect of antipsychotics and can help to quickly reduce psychotic arousal, aggressiveness, and impulsivity. Lithium may also potentiate the action of antidepressants; in the case of its effectiveness in a patient, this allows to reduce the doses of antipsychotics and antidepressants required to normalize his mental state - which, in turn, can reduce akathisia or reduce the risk of its occurrence. However, when prescribing additional drugs, their own toxicity and side effects should be taken into account and the benefit / harm ratio for the patient should be weighed in each case individually.

It is also important to correct iron and zinc deficiencies, if present. The appointment of magnesium preparations is indicated regardless of the presence or absence of magnesium deficiency, since magnesium has a positive effect on the symptoms of extrapyramidal disorders, has a sedative, anti-anxiety, antidepressant and muscle relaxant effect. With severe akathisia, an intramuscular or intravenous administration of magnesium sulfate is justified by the course.

Antiparkinsonian drugs

Most often, for the treatment of akathisia caused by antipsychotics, antiparkinsonian drugs from the group of central anticholinergics, such as trihexyphenidyl (cyclodol), biperiden (akineton), benztropine, are prescribed. These drugs are so often prescribed concomitantly with antipsychotics to prevent or eliminate their extrapyramidal side effects that they are even often called "correctors" of the side effects of antipsychotics. However, these drugs are much more effective in the prevention and treatment of true extrapyramidal side effects of antipsychotics, such as acute dyskinesias (muscle spasms), muscle tension and rigidity, tremor, drug-induced parkinsonism (stiffness in movements, weakness, brady - or akinesia / hypokinesia). They are not sufficiently effective or ineffective (at least as monotherapy) in akathisia, since akathisia is not a true extrapyramidal side effect, but a complex psychosomatic phenomenon, the causes and mechanisms of which have not yet been fully studied.

Other anticholinergics and antihistamines

Other drugs with a strong central anticholinergic and/or antihistamine effect that do not formally belong to the group of antiparkinsonian drugs can also be used in the treatment of akathisia. For example, diphenhydramine (diphenhydramine), hydroxyzine (atarax) or small doses of tricyclic antidepressants with pronounced anticholinergic and antihistamine activity (for example, amitriptyline), small doses of sedative neuroleptics with concomitant anticholinergic and antihistamine activity (in particular, chlorpromazine or levomepromazine, chlorprothixene). An additional advantage of using these drugs may be their pronounced sedative and hypnotic activity, which allows you to remove or reduce anxiety, fear, internal tension, agitation or insomnia, both associated and not associated with akathisia. Often, these drugs (especially sedative antipsychotics) are prescribed in cases where the doctor has difficulty in differential diagnosis of the condition - whether it is due to akathisia or exacerbation of psychosis, an increase in arousal and anxiety (according to the principle "it will help from both").

Benzodiazepines

Benzodiazepine tranquilizers, such as clonazepam, diazepam, lorazepam, phenazepam, also contribute to the reduction of akathisia. These drugs also contribute to the elimination or reduction of anxiety, agitation and insomnia, not associated with akathisia, and potentiate the sedative (but not antipsychotic) effect of neuroleptics, helping to quickly stop arousal, manic state or exacerbation of psychosis. Therefore, they are also often prescribed in cases where it is difficult to conduct an accurate differential diagnosis of the condition.

Benzodiazepines eliminate the motor component of akathisia to a much lesser extent than the subjective discomfort, anxiety, agitation, and insomnia caused by it, so it is advisable to combine them with beta-blockers and / or central anticholinergic correctors. It has been shown that patients with akathisia who are reasonably prescribed benzodiazepines are not inclined to abuse them and can take a stable dose for years.

Beta blockers

In addition, lipophilic (central nervous system penetrating) beta-blockers such as propranolol, betaxolol, nadolol, or metoprolol are effective for akathisia. Some doctors consider them the most effective treatment for akathisia. For resistant akathisia or akathisia with parkinsonian symptoms, beta-blockers can be used in combination with anticholinergic drugs.

Beta-blockers also help to reduce the tachycardia, tremors associated with the use of neuroleptics or antidepressants, reduce anxiety (mainly by reducing external autonomic manifestations of anxiety and interrupting the positive feedback anxiety - autonomic manifestations - anxiety). Beta-blockers may also slightly enhance the antipsychotic and antimanic effects of antipsychotics. Pindolol (Whisken) has an advantage when used with SSRIs and SNRIs, as it seems to potentiate the effect of serotonergic antidepressants, and not just reduce the akathisia they cause.

Alpha blockers

The observation that iloperidone's low propensity to cause akathisia and other extrapyramidal disorders is based on its strong α 1 -adrenergic blocking activity and that blockade of α 1 -adrenergic receptors in the prefrontal cortex leads to an increase in the release of dopamine in the nigrostriatal pathway led to the conclusion that it can be used to treat akathisia caused by other drugs (not iloperidone), such selective α 1 -blockers as prazosin, doxazosin. This treatment was effective not only in reducing akathisia, but also in reducing nightmares, for which these drugs are also effective.

The theory of the noradrenergic origin of akathisia served as a theoretical basis for the successful use of antiadrenergic drugs in akathisia, such as the central α2-agonists clonidine and guanfacine, the imidazoline I1-agonists moxonidine (physiotens) and rilmenidine, and even the sympatholytics reserpine and tetrabenazine, sometimes themselves capable of causing akathisia.

Drugs with antiserotonin activity

With akathisia, 5-HT 2 receptor blockers are also effective, in particular the antihistamine drug cyproheptadine (peritol), the specific serotonin antagonist ritanserin, the antidepressants mianserin, trazodone, mirtazapine.

This treatment option also includes the use in the treatment of akathisia of low doses of some atypical antipsychotics (quetiapine, clozapine) or low-potency typical antipsychotics (levomepromazine, chlorprothixen, alimemazine, chlorpromazine, etc.) with a strong 5-HT 2 -blocking and weak D 2 - blocking action in addition to the main high-potency antipsychotic. However, it is possible that the effectiveness of this tactic is also associated with the M-anticholinergic, α 1 -adrenergic blocking and / or H 1 -antihistamine action of these drugs. In general, the use of this tactic is not recommended, since the degree of D 2 -blockade and the severity of extrapyramidal disorders can increase even with low doses of a second, sedative antipsychotic, for example, due to undesirable pharmacokinetic interactions with the main antipsychotic, and choose the right ratio of 5-HT 2 - and D 2 blockade with this tactic is more difficult than when adding a “pure” 5-HT 2 blocker without D 2 blocking activity such as mirtazapine, mianserin or trazodone to an antipsychotic.

Anticonvulsants

Often with akathisia, GABAergic drugs are highly effective: valproates, gabapentin, pregabalin, baclofen, carbamazepine, piracetam. Some of these drugs, taking into account their side effect profile and the presence of other positive psychotropic effects, in particular, normothymic, nootropic or anti-anxiety, can be considered as one of the components of first-line therapy for akathisia, either alone or in combination with others. drugs.

Valproate is able to potentiate the anti-manic effect of antipsychotics, reduce arousal, aggressiveness and impulsivity, which may allow to reduce doses of antipsychotics. The literature describes cases where the administration of valproic acid, gabapentin, or pregabalin made it possible to avoid the use of several drugs and be limited to monotherapy in the complete absence of visible akathisia in the patient.

Weak opioids

Weak opioids such as codeine, hydrocodone, propoxyphene are also effective in akathisia. At the same time, studies emphasize that patients suffering from akathisia, like patients with severe chronic pain, are generally not prone to unauthorized excess of opioid doses and to the development of true drug addiction. It has also been shown that in patients with akathisia caused by antipsychotics, the endogenous opioid system is not sufficiently active.

Dopaminergic drugs

In particularly treatment-resistant cases of akathisia, amantadine or D 2 -agonists (bromocriptine, pramipexole, piribedil) can be carefully used, but it should be borne in mind that these drugs can exacerbate psychosis and reduce the antipsychotic effect of antipsychotics. Nevertheless, the risk of exacerbation of psychotic symptoms when using these drugs is small, since they mainly affect the D 2 receptors of the nigrostriatal system, relatively little effect on the D 2 receptors of the mesolimbic system, the blockade of which is due to the antipsychotic effect of neuroleptics. An additional advantage of this approach is the possible correction of concomitant hyperprolactinemia, negative symptoms and depressive disorders. There are even cases when patients with resistant psychoses went into remission precisely after the addition of dopaminergic agents, despite fears that these drugs can weaken the antipsychotic effect of neuroleptics, and this is due to a large extent to the elimination of the adverse effect of akathisia and hyperprolactinemia on concomitant psychopathology.

Other drugs

In case of insufficient effectiveness of first-line drugs (which include central anticholinergic correctors, beta-blockers, 5-HT 2 blockers, benzodiazepines and other GABAergic drugs, antiadrenergic and dopaminergic drugs), further selection of treatment for akathisia should largely be based on empirical observations and individual case reports, as there are very few RCTs on the treatment of akathisia "beyond the first line". Thus, the effectiveness of vitamin B6, antioxidants (vitamins E and C) and omega-3 fatty acids, tizanidine, with the abolition of which extrapyramidal disorders reappeared, N-acetylcysteine, memantine, testosterone in men and a low-dose testosterone patch in women, pregnenolone, dehydroepiandrosterone (DHEA) in both sexes, estrogen replacement therapy in post-menopausal women, buspirone, melatonin, upon withdrawal of which akathisia and withdrawal dyskinesias were observed.

According to some reports, nootropic drugs - piracetam, pantogam, picamilon can be effective.

Polytherapy

Most patients with akathisia (especially those with severe, severe) are not helped by monotherapy and require the combined use of 2-3 or more drugs, for example, an antiparkinsonian agent (cyclodol) + a benzodiazepine tranquilizer (diazepam) + a beta-blocker (propranolol).

Treatment of tardive akathisia

In late akathisia, the drug should be discontinued if possible, replaced with an atypical antipsychotic (clozapine, olanzapine), or at least a dose reduction. After discontinuation of the drug, regression of symptoms is observed within several months or years. Beta-blockers and anticholinergics are ineffective in tardive akathisia. The drugs of choice are sympatholytics (reserpine, tetrabenazine), which have a positive effect in more than 80% of patients. Opiates are as effective in tardive akathisia as they are in acute akathisia. With iron deficiency (according to some reports, it may be one of the factors in the development of akathisia), its compensation is necessary. In resistant cases, electroconvulsive therapy sometimes has a positive effect.

Prevention

Like any other complication of treatment, akathisia is much easier to prevent than to treat if it occurs. Measures to prevent drug akathisia include:

• preferential use of atypical rather than typical antipsychotics, and, if possible, atypical ones with the least potential for developing extrapyramidal disorders, and akathisia in particular (for example, quetiapine, iloperidone, and not risperidone, aripiprazole), and among typical drugs, drugs with less potential for extrapyramidal disorders are also preferred disorders (eg, zuclopenthixol or flupenthixol rather than haloperidol) if the patient's condition permits;
• the use of the minimum required doses of antipsychotics and antidepressants, the rejection of unreasonable overestimation of doses, especially in such categories of patients sensitive to extrapyramidal disorders, such as children and adolescents, the elderly and senile, pregnant women, patients with organic lesions of the central nervous system, with a history of traumatic brain injury and etc.;
• if possible, refusal to use antipsychotics or increase their doses in order to achieve non-specific sedation or relief of psychomotor agitation (in psychosis, if the standard antipsychotic doses of one or another antipsychotic do not adequately provide sedation, it is better to add a high-potency benzodiazepine, rather than increase dose of antipsychotic)
• refusal of unreasonable polyneurolepsy (a combination of two or more antipsychotics), which significantly increases the risk of developing extrapyramidal disorders, including akathisia;
• taking into account possible drug interactions when prescribing combination therapy (for example, a number of SSRIs can increase the blood concentration of antipsychotics, and for this reason the risk of extrapyramidal disorders, and akathisia in particular, increases; ketoconazole, clarithromycin, in particular, have the same properties);
• if it is necessary to prescribe a drug with a high potential for the development of akathisia (a typical antipsychotic and a number of atypical ones, such as risperidone, aripiprazole in antipsychotic doses, SSRIs, etc.), it is desirable to simultaneously prophylactically prescribe anticholinergic correctors and / or benzodiazepine tranquilizers, beta-blockers, at least at the initial stage of treatment, before adaptation to the drug;
• if possible, smoothly increase the doses of antipsychotics and antidepressants at the beginning of treatment, as well as smoothly reduce them (to prevent the development of withdrawal akathisia) at the end of treatment, if the patient's condition allows it;
• as antiemetics in preoperative sedation, in oncology, etc., it is desirable to use setrons, dexamethasone, domperidone, rather than metoclopramide or antipsychotics, due to the higher potential for the development of extrapyramidal disorders, including akathisia, when using them.

Akathisia is a very uncomfortable clinical syndrome for patients. It is often called restlessness, which very accurately conveys the essence of emerging psychomotor disorders. With akathisia, a person has an almost irresistible physical need to change position of the body and move, because of which he cannot even sit still. It becomes difficult to fall asleep, but in a dream, akathisia subsides, which distinguishes it from.

What causes akathisia

Akathisia is usually one of the complications of ongoing drug therapy. It develops shortly after the appointment of a new drug or an increase in the dose of an already received drug. Restlessness can also be provoked by the abolition of auxiliary drugs (for example, tranquilizers) or the addition of a substance that potentiates the action of the main drug to the therapy regimen.

The main drugs, the intake of which can lead to the development of acute akathisia:

• neuroleptics (groups of butyrophenones, phenothiazines, piperazines and thioxanthenes) - the most common cause, the use of these drugs causes the most pronounced akathisia;
• , predominantly belonging to the SSRI and SNRI groups, less often akathisia occurs when taking TCAs;
• lithium preparations;
• MAO inhibitors (infrequently);
• antiemetics of the metoclopramide, promethazine and prochlorperazine groups;
• some first-generation antihistamines (rarely and at high doses);
• reserpine, which can be used in psychiatry and for the correction of arterial hypertension;
• levodopa preparations;
• calcium antagonists.

Akathisia can develop not only while taking drugs, but also when they are abruptly canceled after prolonged treatment, even in small doses. This occurs at the completion of antipsychotic and antidepressant therapy. In some cases, restlessness is included in the withdrawal symptoms in the presence of dependence on opiates, barbiturates, benzodiazepines and alcohol.

The medical literature also describes cases of the development of akathisia against the background of iron deficiency states, carbon monoxide poisoning. With (or a pronounced syndrome of parkinsonism of non-drug etiology), this syndrome may appear without any apparent connection with the intake of any drugs.

Why does akathisia occur?

Most often, the development of akathisia is associated with Parkinson-like manifestations due to the effect of drugs taken on dopamine transmission in the brain. Some of them directly block dopamine receptors in the nigrostiar subcortical complex and the pathways leading from here. Others (for example, antidepressants) act indirectly, due to the competitive action of the serotonergic and dopaminergic systems.

It is also assumed that disturbances in the opioid and noradrenergic transmission of nerve impulses in the central nervous system play a certain role in the pathogenesis of akathisia. But these changes are likely to be complementary or secondary. But disturbances in the peripheral link of the nervous system are of no importance for the development of the restlessness syndrome.

Clinical picture

Akathisia is characterized by a feeling of internal tension and restlessness, which a person can describe as a feeling of anxiety. Mental and physical discomfort is often accompanied by irritability, instability of emotions with a tendency to a depressive mood background. In the absence of pronounced motor manifestations, an insufficiently experienced or not very attentive doctor may mistake this condition for other mental disorders. For example, agitated depression, inversion of affect in bipolar affective disorder (manic-depressive psychosis in the old classification), or even signs of the development of psychosis are diagnosed. Such an erroneous interpretation of the mental component of akathisia leads to inadequate therapy, which can aggravate the existing restlessness syndrome.

Internal discomfort leads to the need to constantly change the position of the body, to do something. Moreover, the actions performed are conscious, a person can suppress them for a short time by an effort of will, while maintaining immobility. But diverting attention, entering into a conversation, or exhausting the possibility of internal control leads to a rapid resumption of stereotyped movements.

Motor restlessness in akathisia can have varying degrees of severity. The load on the feet and knee joints somewhat alleviates the condition. Therefore, most often people with restlessness shift in a standing position (trample), walk from corner to corner, try to march. In the sitting position, they shuffle their feet, change the position of their limbs, fidget, get up, tap their feet on the floor. Even in bed, the akathisia sufferer may move the legs over and over. A severe degree of the syndrome with severe motor restlessness and strong psycho-emotional stress leads to insomnia.

Forms of akathisia

Restlessness syndrome can be acute (with development during the first week after the start of therapy or increasing the dose of the drug), chronic (lasting more than 6 months). With long-term antipsychotic therapy, akathisia may be late, in which case it develops several months after the appointment of an antipsychotic and may persist even after its withdrawal. Separately, the so-called withdrawal akathisia is distinguished, which appears after a sharp cessation of the use of various psychotropic drugs.

Depending on the clinical picture, motor, mental and sensory akathisia are distinguished. In the latter case, unpleasant sensations appear in the lower extremities, often misdiagnosed as senestopathies.

Diagnostics

To confirm the diagnosis of akathisia, no instrumental studies are required. The doctor evaluates the history, existing mental and motor disorders, and necessarily determines the form and severity of restlessness. To standardize the clinical examination, a specially developed Barnes scale is used. And to exclude extrapyramidal disorders, other scales are used.

Akathisia should be differentiated from various mental deteriorations, extrapyramidal complications of drug therapy, and restless legs syndrome. It is important to identify the cause of restlessness, this will help the doctor choose the necessary therapy and make the right decision regarding the drugs received.

Treatment

To eliminate akathisia, it is necessary to stop using the drug that caused the development of this syndrome. If this is not possible, the doctor may decide to temporarily stop antipsychotic or antidepressant therapy with subsequent replacement of the drug. For example, such a tactic is used in the treatment of an acute psychotic state or depressive disorder, during maintenance antipsychotic therapy. Sometimes it is effective to reduce the dose of the main agent with the addition of auxiliary medications to the treatment regimen.

To reduce the severity of symptoms, benzodiazepines, anticholinergic and antiparkinsonian drugs of various groups, beta-blockers, amantadines, and some are used. Vitamins of group B and nootropics enhance the effectiveness of therapy. The selection of the drug and its dosage is carried out only by a doctor, often a combination of medicines from different groups is used. With a severe degree of akathisia, it is necessary to accelerate the elimination of the main drug from the body, for which infusion therapy is prescribed.

The prognosis depends on the form, severity and cause of akathisia. Even with the early initiation of adequate therapy and the withdrawal of the main drug, the symptoms can persist for quite a long time. It depends on the sensitivity of various receptors, the persistence of metabolic disorders that have developed in the brain, and comorbidities. At the first signs of the appearance of akathisia, it is necessary to inform the attending physician about this, which will allow developing the correct tactics for further therapy.

Imagine that you are overcome by an unbearable desire to move, your legs seem to be carrying somewhere, and by an effort of will you are not able to stop them. This condition may be a manifestation of akathisia, which is often associated with the use of potent drugs.

Akathisia is not just a symptom, but rather a complex phenomenon that includes, on the one hand, internal painful sensations of discomfort, the desire to move, anxious feelings, insomnia, and, on the other hand, external motor manifestations. In ICD-10, this syndrome belongs to the group of parkinsonisms.

Symptoms and development of the syndrome

The course of akathisia can be quite mild, with a mild sense of internal anxiety, moderate anxiety and tension. Such symptoms are difficult to recognize even for an experienced doctor. In a severe course, a person experiences a deep depression, panic, becomes nervous and aggressive, feels severe fatigue, excruciating anxiety. He is simply unable to sit quietly or stand still. The motor symptoms of akathisia most often affect the legs. These are not just paroxysmal twitches, but complex motor acts. The patient shakes his legs, stomps in one place, walks back and forth, fidgets, shuffles, crosses his legs, and makes other senseless stereotyped movements. He cannot stay in one position for long. The more pronounced akathisia, the more motor excitation spreads from the legs to the whole body.

What do such people feel? Internal sensory sensations may resemble itching in the legs, tingling, twisting in the muscles and joints, and an inexplicable desire to move. The mental component of the syndrome includes anxiety, fear, inability to relax, tension and restlessness. Patients sometimes cannot describe their feelings at all. Therefore, doctors are not always able to understand the patient's complaints. Sometimes akathisia is accompanied by atypical symptoms, for example, the patient may feel as if his fingers are cold, his chest begins to feel cold. Unusual clinical manifestations include restless eye movements and akathisia in one leg, arm, or side of the entire body.

Why does akathisia occur?

The most common cause of internal motor restlessness is the use of psychotropic drugs, more often traditional antipsychotics. Risk factors for the development of akathisia when taking antipsychotics are anxiety, affective, neurological disorders in history, young and old age, pregnancy, dementia, oncology, brain injury, magnesium and iron deficiency, genetic predisposition, as well as a combination of several psychostimulants and high doses of drugs. Other reasons can provoke the syndrome:

• some mental illnesses, for example, schizophrenia, anxiety, conversion, affective, hysterical disorders;
• rarely, but there are manifestations of akathisia when a person moves away from general anesthesia or electroconvulsive therapy;
• various parkinsonisms and other extrapyramidal disorders, strokes, neurological disorders, as well as craniocerebral injuries;
• drugs, withdrawal syndrome after intoxication with nicotine, opiates, barbiturates, benzodiazepines, alcohol;
• sedative and non-sedative antipsychotics, SSRIs and other antidepressants, lithium preparations, anticonvulsants, psychostimulants, benzodiazepines, antihistamines and antiemetics;
• some non-psychotropic drugs, such as antibiotics, antiviral and anti-tuberculosis drugs, interferons, antiarrhythmic drugs.

Classification

Akathisia can develop in an acute form in the first days or even hours of taking medications, or it can begin after several weeks or months of therapy, while the symptoms decrease after the end of the medication or the appointment of a lower dosage. There is also akathisia of withdrawal, when the syndrome develops in the first weeks after a dose reduction or discontinuation of antipsychotics. Late akathisia in the treatment of psychotropic drugs can develop after six months and even after several years of therapy, persists for a long time, sometimes for life. This motor syndrome can manifest itself in different ways, with the dominance of certain symptoms. Depending on this, the following forms of akathisia are distinguished:

• classical, in which psycho-sensory sensations and external objective symptoms are fairly evenly manifested;
• predominantly sensory when unpleasant sensations in the arms, legs and other muscles come to the fore, and motor disorders are implicitly expressed;
• predominantly mental, with a high level of internal restlessness, tension, anxiety;
• predominantly motor this is the very example of a person who does not sit still, manifests itself to a greater extent in motor restlessness and restlessness.

Separately, it is necessary to highlight such a form as tasikinesia. Tasikinesia differs from akathisia in the absence of internal painful sensations. First of all, the patient shows a desire to constantly move, his legs are drawn somewhere.

Tasikinesia often occurs as a transient increase in motor activity, however, sometimes tasikinesia can become chronic.

Why is akathisia dangerous?

Motor anxiety in drug akathisia is fraught with a violation of the treatment process. It is simply impossible to experience painful feelings, not to be able to sit still and at the same time feel comfortable. Therefore, patients often experience hostile feelings towards health workers, fear of medications, and even completely refuse treatment. Akathisia interferes not only with full-fledged work and study, but also with attending psychotherapy sessions and labor rehabilitation activities.

The presence of this syndrome, especially in severe form, leads to an exacerbation of paroxysmal schizophrenia, neurosis, depression and any other mental disorder. The patient may show aggression, impulsiveness, the desire to harm themselves and others. Suicidal tendencies may also be exacerbated. Some people try to drown out the painful sensations with alcohol, drugs, antidepressants, smoking, which only exacerbates nervousness. If akathisia is not recognized and treated in time, the patient may develop deeper psychopathology, such as derealization, severe anxiety, dysphoria, depersonalization, and pathological personality changes.

Treatment and prevention

The method of treatment of akathisia directly depends on the cause. This is what needs to be determined first. It is worth starting with an analysis of the drugs taken, since it is the drugs that are the most common cause of the syndrome. The dosage regimen should be reviewed, possibly reducing the dosage, replacing certain drugs, or adding new ones that can enhance the effects of antipsychotics and antidepressants without the risk of extrapyramidal side effects. The diagnosis and treatment of akathisia in children should be approached more carefully. If a child in a healthy state could not sit in one place for a long time due to character traits, then motor anxiety during drug treatment should not always be treated with caution. However, this is an occasion to conduct more careful monitoring of the child and additional examinations. In most cases, polytherapy helps to eliminate the manifestation of akathisia, it is better to prescribe not only one antipsychotic drug, but to supplement it with several other drugs, such as a tranquilizer and a beta-blocker.

anonymous , Woman, 39

Hello, Igor Evgenievich! In one of your answers you mentioned akathisia and that's why I want to turn to you. Until October 2015, I took venlaxor (85 mg) for 3 years and while taking it, my condition suddenly worsened: severe irritable bowel syndrome, shaking limbs, nausea, terrible anxiety. After consulting with my doctor, I canceled venlaxor for 3 weeks. But after a few weeks, nausea remained, I could hardly eat and lost a lot of weight, and most importantly - a terrible, all-consuming anxiety. I was prescribed gidazepam, and once, when I was especially ill, "eglonil", I took it at 50 mg per day for 17 days in late November-early. December 2015 Against its background, my chest hurt and the cycle shifted. But anxiety, nausea did not go away, and in mid-December, on the advice of a doctor, I went to the hospital, where I was prescribed Mirazep 15 mg per day. He helped with sleep and appetite, reduced anxiety, but I had a huge feeling of weakness - physical and mental, which persisted after discharge. At first I attributed it to general fatigue from what had happened over the past months, but it did not go away, headaches began to increase. From the beginning of February, I began to gradually reduce the dosage of mirazep (from 15 mg) and by the end of February I brought the dosage to a quarter (3.75 mg). And from March 1, I began to have a strange phenomenon: I felt a strong need to move and began to walk aimlessly around the room. In the following days, this phenomenon began to grow and for several weeks now I have been tormented by a kind of swelling from the inside, a burning or tickling sensation in the muscles, very painful, and to alleviate it, I spend most of the day moving around the apartment - I walk back and forth, bend, I take different positions. When I sit down - I want to get up, when I stand - to walk, when I walk - to sit down, etc. At the same time, I have terrible insomnia, I can’t sleep at all without sleeping pills. Trying to find out what was happening to me, I began to read the instructions for the drugs and found akathisia, the symptoms of which correspond to my current condition. Therefore, I have a question: could that 2-week intake of an antipsychotic 3 months ago, which just now had an effect, cause this akathisia? Or taking mirazep (does it have side effects of akathisia?) Have you experienced this and is it going away? I must say that I have never had anything like this before - I have always been a rather slow person, there were no tics or other movement disorders either. The psychiatrist says that this is a manifestation of anxiety, but it has never manifested itself in me like this, and this is a completely unnatural, terrible state of internal excitement, leading to terrible restlessness. I really look forward to your answer, such a state is inexpressible torture!

Indeed, according to the description, it is very similar to akathisia. But this side effect of taking neuroleptics occurs only during their administration, and even if it were so, only 50 mg of eglonil are practically unable to cause it. Akathisia from antidepressants is an extremely rare phenomenon, as doctors say, casuistry. Moreover, the dosage of 3.75 mg cannot even be called symbolic, it is 10 times less than the therapeutic one. Therefore, the situation is not clear. Your references to "terrible anxiety" still do not allow us to completely abandon the idea that anxiety, and not akathisia, is the cause of motor restlessness. In such cases, it is customary to focus on the criterion of pharmacological effectiveness: akathisia is eliminated by antiparkinsonian drugs (, akineton, pk-Merz) and non-selective beta-blockers (anaprilin), and anxiety is eliminated by benzodiazepine tranquilizers (clonazepam, diazepam, alprazolam, phenazepam). Those. "whatever helps, that's what it is." Obviously, you need to cancel everything that you are taking now and try these options separately. Of course - all under the guidance of your doctor.

anonymously

Igor Evgenievich, thanks for the answer! Thank you for your answer and that you acknowledged that it looks like akathisia. I am terribly worried about the vagueness of the situation. I read about many cases when people with akathisia were helped by the abolition of an antipsychotic or antidepressant, but I don’t take an antipsychotic, and I canceled the antidepressant more than 4 weeks ago, but there is no improvement, my health is simply terrifying! I have been taking anaprilin for 3 weeks at a dosage of 80-90 mg, but it does not help. As for anxiety, it's not "mental" anxiety, I know it well, but physical anxiety - it seems to come from the body itself, as if every cell is tense, as if weak electricity is running through the muscles all the time. As far as anti-parkinsonian drugs are concerned, as far as I understand, they are prescribed for people suffering from parkinson's disease (and related disorders) and schizophrenia who are taking neuroleptics. And what will happen if a person who does not have these disorders takes them, will it not make me feel even worse? Have you had such cases in practice?

Trihexyphenidyl (cyclodol) or biperiden (akineton) are widely used as correctors for the side effects of neuroleptic drugs. Extrapyramidal disorders that develop when taking antipsychotics are, in fact, artificially induced parkinsonism. "Correction of the side effects of antipsychotics" is one of the indications for the use of cyclodol or akineton, indicated in their annotations. Akathisia, as a rule, is also eliminated with the help of these drugs. A positive effect is possible, although less pronounced when using amantadine (PK-Merz). Cyclodol requires a special accounting form of prescription forms, akineton - a regular prescription, PK-Merz - can be sold without a prescription. Also, akathisia can be relieved by benzodiazepine tranquilizers (eg, phenazepam), diphenhydramine, caffeine. But the main question remains the same - where does akathisia come from if there is no antipsychotic? Have you by chance been injected with long-acting antipsychotics - fluanxol-depot, clopixol-depot, moditen-depot, haloperidol-decanoate, rispolept-consta, xeplion?

anonymously

Igor Evgenievich, I definitely didn’t have injections of antipsychotics, I had only 2 weeks of eglonil in capsules in early December, 50 mg each. Perhaps I have akathisia due to hypersensitivity to mirtazapine, because he has it in the side effects? By the way, I found information from Western sources that, in fact, akathisia from antidepressants is a much more common occurrence than is commonly believed. The fact is that manufacturers in the results of studies often recorded it as "agitation, emotional lability, anxiety" and etc., and doctors also often interpret it in this way. In addition, it is difficult to describe it, and to the interlocutor - to understand how unnatural this state is. It is so unbearable that you often want to do something with yourself, if only it would pass - at least bang your head against the wall so that everything inside falls into place! I'm going to have an MRI of the brain and I just dream that they find a tumor there and I can do an operation, if only this is over! As for tranquilizers - as far as I understand, they do not cure this condition, but only slightly muffle it (I tried gidazepam, it softens the severity of the condition a little, but in some ways it even becomes more unpleasant - the tension sits inside and cannot break out in movements). As for the drugs you write about, if I take them, then only in a hospital, although I am now afraid to go there, given the result of the past treatment. Who knows what side effects will come out this time - some kind of tardive dyskinesia or dystonia, and cyclodol is generally a heavy narcotic drug with hallucinations (!!!), What would happen to me from taking it ?? I feel driven into a corner, it’s impossible to live like this, and there is practically no way out ... Julia

Akathisia is not excluded when taking antidepressants, but this is an extremely rare occurrence. Personally, I have not met him in my 18-year practice and I know of only one confirmed case from a colleague. You also have mirtazapine in such a tiny amount. Obviously, it is worth conducting a diazepam test: if, with a sufficient dosage of a tranquilizer, the "akathisia" completely disappears, then this is still not akathisia, but neurotic anxiety and agitation. Cyclodol provokes psychosis only in the case of a severe 5-10-fold overdose or in very old people. Severe poisoning with hallucinations can be caused by a huge amount of pharmacological agents, taking them in a toxic dose.

anonymously

Igor Evgenievich, what was the treatment for akathisia from an antidepressant in the case you are writing about? And did you manage to get rid of it?