Akathisia is a movement disorder characterized by feelings of inner anxiety and inability to remain silent. Usually the most prominent legs affected. People may be nervous, sway back and forth, or pacing. Others may feel uncomfortable. Complications include suicide.
Antipsychotics, especially first-generation antipsychotics, are a major cause. Other causes may include selective serotonin reuptake inhibitors, metoclopramide, reserpine, Parkinson's disease, and untreated schizophrenia. Can also occur after stopping antipsychotics. The underlying mechanism is believed to involve dopamine. Diagnosis is based on symptoms. This is different from restless leg syndrome in akatisia that is not associated with sleep.
Treatment may include switching to antipsychotics with a lower risk of the condition. Drugs with evidence of temporary benefits include diphenhydramine, trazodone, benztropine, mirtazapine, and beta blockers. Vitamin B6 or iron deficiency can also be beneficial. About half of people taking antipsychotics experience this condition. This term was first used by Ladislav Ha? Kovec, which describes the phenomenon in 1901. It comes from the Greek a - which means "no" and ????? ??? kathÃÆ'zein meaning "sitting" or in other words "inability to sit".
Video Akathisia
Signs and symptoms
The symptoms of akathisia may vary from a little anxiety or anxiety to a sense of terror. People usually race for hours because the pressure on the knee reduces discomfort; once their knees and feet become tired and they can not continue pacing, they sit or lie down, although this does not eliminate akathisia. When misdiagnosis occurs in neuroleptic-induced antipsychotic acematism, more antipsychotics may be prescribed, potentially exacerbating symptoms. Neuro-psychologist Dennis Staker had drug-induced akathisia for two days. His explanation of his experience is this: "It was the worst feeling I have ever had in my entire life I would not wish on my worst enemy." Many patients describe symptoms of neuropathic pain similar to fibromyalgia and restless leg syndrome. In Han et al. (2013), the authors describe the anxious foot syndrome relationship for akathisia, "Some researchers regard RLS as a 'focal akathisia' [at the foot]." Although these side effects disappear rapidly and overwhelmingly when the drug is stopped, late or persisted akathisia may persist long after the offending drug is stopped, sometimes for a period of several years.
Healy, et al. (2006), described the following about akathisia: tension, insomnia, discomfort, motor unrest, and marked anxiety and panic. Increased lability may result, such as irritability.
Jack Henry Abbott (1981) describes the sensation:
... [It comes] from within you, you can not find the source of pain... The muscles of your jaw bone rage, so you bite the inside of your mouth and your jaw is locked and the pain throbs.... Your spine column tightens so you can barely move your head or neck and sometimes your back is bent like a bow and you can not stand.... You are sick with anxiety, so you feel you have to walk, keep pace. And as soon as you start to move, the opposite happens to you; You have to sit down and rest. Back and forth, up and down you go... you can not be relieved...
Moreover, not all the restless movements observed are akathisia. For example, mania, restless depression, and Attention Deficit Hyperactivity Disorder may look like akathisia, but the movement feels voluntary and not out of anxiety.
Maps Akathisia
Cause
Drug-induced
Akathisia is often associated with the use of dopamine receptor antipsychotic antagonists. Understanding is still limited to the pathophysiology of akathisia, but it appears to be related to drugs that block dopaminergic transmission in the brain. In addition, drugs with a successful therapeutic effect in drug-induced drug treatment may have additional insight into the involvement of other transmitting systems. This includes benzodiazepines ,? -adrenergic blockers, and serotonin antagonists. Another major cause of this syndrome is the withdrawal observed in drug-dependent individuals. Because dopamine deficiency (or disturbance in dopamine signals) appears to play an important role in RLS development, a form of limb-focused akathisia, sudden withdrawal or a rapidly decreasing dose of drugs that enhances dopamine signaling can create the same deficit of chemicals mimicking antagonism dopamine and thus may trigger RLS. This is why the cessation of opioids, cocaine, serotonergics, and other euphoric substances that suddenly produce RLS as a side effect.
This has been correlated with Parkinson's disease and related syndromes. It is unclear whether this is more of Parkinson's or drugs used to treat it, such as carbidopa/levodopa (levocarb).
Antidepressants can also induce the appearance of akatisia, because of increased serotonin signals in the central nervous system. It also explains why serotonin antagonists are often a very effective treatment. Research UK 2006 by Healy et al. observed that akathisia is often wrong in antidepressant clinical trials as "agitation, emotional lability, and hyperkinesis (overactive)". This study further indicates that misdiagnosis of akathisia as a simple motor anxiety occurs, but it is more aptly categorized as dyskinesia.
It was found that akathisia involves increased levels of norepinephrine neurotransmitters, which are associated with mechanisms governing aggression, alertness, and arousal.
The table below summarizes the factors that can induce akathisia, grouped by type, by example or brief explanation for each:
Diagnosis
The presence and severity of akathisia can be measured using the Barnes Akathisia Scale, which assesses objective and subjective criteria. Proper assessment of akathisia is a problem, as it is difficult to distinguish from many disorders with similar symptoms. In a study of motion disorders caused by neuroleptics, akathisia was found in only 26% of patients initially diagnosed with akathisia. The main feature that distinguishes akathisia compared to other syndromes is particularly subjective characteristics, such as feelings of inner anxiety. Akathisia can generally be misinterpreted as secondary agitation due to psychotic symptoms or mood disorders, antipsychotic dysphoria, restless legs syndrome (RLS), anxiety, insomnia, drug withdrawal state, tardive dyskinesia, or other neurological and medical conditions.
In addition, the controversial diagnosis of "pseudoacathisia" is given, as noted by Mark J. Garcia. In his article discussing akathisia among adults with severe and profound intellectual disabilities, he described pseudoacathisia as "composed of all symptoms of abnormal movement seen with akathisia, but without anxiety."
Classification
Treatment
Case reports and small randomized studies suggest benzodiazepines, propranolol, and anticholinergics can help treat acute acute, but are much less effective in treating chronic acute dysfunction. Taylor et al. found success in lowering doses of antipsychotic drugs as a preliminary response to drug-induced akathisia, which should be done gradually, if possible. To minimize the risk of akathisia from antipsychotics, doctors are advised to be conservative when increasing the dose.
One study showed vitamin B 6 was effective for the treatment of neuroleptic induced akatisia.
Additional pharmacologic interventions have been found to have antiacathisia effects (especially for neuroleptic induced akatisia) including? -adrenergic antagonists (eg, propranolol), benzodiazepines (eg, lorazepam), anticholinergics (eg, benztropin), and serotonin antagonists (eg, cyproheptadine) as an alternative.
Epidemiology
The published epidemiological data for akathisia is largely limited in the treatment period prior to the arrival of second-generation antipsychotics. Sachdev (1995) reported an acute case of acute incidence 31% for 100 patients treated for 2 weeks with antipsychotic drugs. Sachdev (1995) reported a prevalence range from 0.1% to 41%. In all likelihood, a lower prevalence rate for current treatment as second generation antipsychotics carries a lower risk of akathisia.
References
External links
Source of the article : Wikipedia
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