I NEVER HEARD THIS TERM BEFORE. gOOGLE SEARCH RESULT ATTACHED. NEXT TIME ASK DOCTOR TO EXPLAIN WORDS YOU DON'T UNDERTAND.BEST5 REGARDS ALEX






Akathisia


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Akathisia


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Common symptom-expression of akathisia


Classification and external resources


Specialty
Neurology

ICD-10
G21.1

ICD-9-CM
781.0, 333.99

DiseasesDB
32479

eMedicine
neuro/362 emerg/338

MeSH
D011595

Akathisia, or acathisia (from Greek kathzein "to sit", a- indicating negation or absence, lit. "inability to sit") is a movement disorder characterized by a feeling of inner restlessness and a compelling need to be in constant motion, as well as by actions such as rocking while standing or sitting, lifting the feet as if marching on the spot, and crossing and uncrossing the legs while sitting. People with akathisia are unable to sit or keep still, complain of restlessness, fidget, rock from foot to foot, and pace.[1]

The term was coined by the Czech neuropsychiatrist Ladislav Haskovec (18661944), who described the phenomenon in 1901.[2][3]

Antipsychotics (also known as neuroleptics), particularly the first generation antipsychotics, may cause akathisia. Other known causes include side effects of certain medications, and nearly any physical dependence-inducing drug during drug withdrawal.[4] It is also associated with Parkinson's disease and related syndromes.[5]



Contents [hide]
1 Signs and symptoms
2 Causes 2.1 Pathophysiological
2.2 Drug-induced

3 Diagnosis 3.1 Classification

4 Treatment
5 Epidemiology
6 References


Signs and symptoms[edit]

Akathisia may range in intensity from a sense of disquiet or anxiety, to excruciating discomfort, particularly in the knees. Patients typically pace for hours because the pressure on the knees reduces the discomfort somewhat; once their knees and legs become fatigued and they are unable to continue pacing, they sit or lie down, although this does not relieve the akathisia. At high doses or with potent drugs such as haloperidol (Haldol) or chlorpromazine (Thorazine/Largactil), the feeling can last all day from awakening to sleep. When misdiagnosis occurs in antipsychotic neuroleptic-induced akathisia, more antipsychotic neuroleptics may be prescribed, potentially worsening the symptoms.[5] High-functioning patients have described the feeling as a sense of inner tension and torment or chemical torture. Many patients describe symptoms of neuropathic pain akin to fibromyalgia and restless legs syndrome.[6] In Han et al. (2013), the authors describe restless legs syndrome's relation to akathisia, "Some researchers regard RLS as a 'focal akathisia' [in the legs]."[7] Although these side effects disappear quickly and remarkably when the medication is stopped, tardive, or late-persisting akathisia may go on long after the offending drug is discontinued, sometimes for a period of years. Healy, et al. (2006), described the following regarding akathisia: tension, insomnia, a sense of discomfort, motor restlessness, and marked anxiety and panic. Increased labile affect can result, such as weepiness. [8]

Severe akathisia can become a very harrowing experience. Jack Henry Abbot (1981) describes the sensation:[9]


...[It comes] from so deep inside you, you cannot locate the source of the pain The muscles of your jawbone go berserk, so that you bite the inside of your mouth and your jaw locks and the pain throbs. Your spinal column stiffens so that you can hardly move your head or your neck and sometimes your back bends like a bow and you cannot stand up. You ache with restlessness, so you feel you have to walk, to pace. And then as soon as you start pacing, the opposite occurs to you; you must sit and rest. Back and forth, up and down you go you cannot get relief

In a psychiatric setting, patients who suffer from neuroleptic-induced akathisia often react by refusing treatment.[10]

Causes[edit]

Pathophysiological[edit]

Han et al. (2013)[7] reported that upon examination of three patients who experienced abrupt onset of restlessness characteristic of akathisia and RLS, magnetic resonance imaging of the brain revealed pontine infarction (lack of blood to the pons area of the brain). Han et al. wrote, "The features of our three patients suggest that RLS and akathisia may have a common pathophysiological mechanism related to the pontine region of the brain."[7]

Drug-induced[edit]

Akathisia is frequently associated with the use of dopamine receptor antagonist antipsychotic drugs.[11] Understanding is still limited on the pathophysiology of akathisia, but it is seen to be associated with medications which block dopaminergic transmission in the brain. Additionally, drugs with successful therapeutic effects in the treatment of medication-induced akathisia have provided additional insight into the involvement of other transmitter systems. These include benzodiazepines, -adrenergic blockers, and serotonin antagonists.[11] Another major cause of the syndrome is the withdrawal observed in dependent individuals.[4]

It has been correlated with Parkinson's disease and related syndromes.[5] It is unclear, however, whether this is due more to Parkinson's or the drugs used to treat it, such as carbidopa/levodopa (levocarb).[12]

Antidepressants can also induce the appearance of akathisia.[13][14][15][16] The 2006 UK study by Healy et al. observed that akathisia is often miscoded in antidepressant clinical trials as "agitation, emotional lability, and hyperkinesis (overactivity)".[17] The study further points out that misdiagnosis of akathisia as simple motor restlessness occurs, but that this is more properly classed as dyskinesia.

It was discovered that akathisia involves increased levels of the neurotransmitter norepinephrine, which is associated with mechanisms that regulate aggression, alertness, and arousal.[18]

The table below summarizes factors that can induce akathisia, grouped by type, with examples or brief explanations for each:


Category

Examples

Antipsychotics[19] Haloperidol (Haldol), droperidol, pimozide, trifluoperazine, amisulpride, risperidone, aripiprazole (Abilify), lurasidone (Latuda), ziprasidone (Geodon), and asenapine (Saphris)
SSRIs[20] Fluoxetine (Prozac),[20] paroxetine (Paxil),[17] citalopram (Celexa)
Antidepressants Venlafaxine (Effexor), tricyclics, and trazodone (Desyrel)
Antiemetics Metoclopramide (Reglan), prochlorperazine (Compazine), and promethazine
Antihistamines Cyproheptadine (Periactin) or diphenhydramine (Benadryl) this is more commonly seen at very high doses
Drug withdrawal Opioid withdrawal, barbiturates withdrawal, cocaine withdrawal, and benzodiazepine withdrawal
Serotonin syndrome Harmful combinations of psychotropic drugs

Diagnosis[edit]

The presence and severity of akathisia can be measured using the Barnes Akathisia Scale,[21][22] which assesses both objective and subjective criteria.[21] Precise assessment of akathisia is problematic, as it is difficult to differentiate from a multitude of disorders with similar symptoms. In a study of movement disorders induced by neuroleptics, akathisia was found in only 26% of patients originally diagnosed with akathisia.[10] The primary distinguishing features of akathisia in comparison with other syndromes are primarily subjective characteristics, such as the feeling of inner restlessness.[23] Akathisia can commonly be mistaken for agitation secondary to psychotic symptoms or mood disorder, antipsychotic dysphoria, restless legs syndrome (RLS), anxiety, insomnia, drug withdrawal states, tardive dyskinesia, or other neurological and medical conditions.[11]

Additionally, the controversial diagnosis of "pseudoakathisia" is given, as noted by Mark J. Garcia. In his article discussing akathisia among adults with severe and profound intellectual disability, he describes pseudoakathisia as "comprising all the symptoms of abnormal movements seen with akathisia, but without a sense of restlessness".[24]

Classification[edit]

Acute akathisia[11]Duration of less than 6 months
Develops soon after: starting antipsychotic medication or following dose increase
switching to a high-potency antipsychotic
withdrawal of an anticholinergic medication

Intense dysphoria
Awareness of restlessness
Complex and semipurposeful motor fidgetiness
Chronic akathisia[11]Persists for over 6 months after last dosage increment
Subjective sense of restlessness may be less marked
Mild dysphoria
Awareness of restlessness
Motor fidgetiness with stereotyped movement
Limb and orofacial dyskinesia often present
Pseudoakathisia[11]Motor manifestations without subjective component
Predominantly in men
Possibly late stage of chronic akathisia
No dysphoria
No awareness of restlessness
Motor fidgetiness with stereotyped movement
Great overlap with limb and orofacial dyskinesia
Tardive akathisia[11]Delayed onset (usually 3 months)
Not related to a recent change in drugs or dose
Significantly associated with tardive dyskinesia
Withdrawal or "rebound" akathisia[11]Associated with switching antipsychotic medications
Onset usually within 6 weeks of discontinuation or dose decrease
Anticholinergic discontinuation reaction


Treatment[edit]

Akathisia is sometimes reversible once the causative agent has been identified and discontinued, but in some cases may become permanent.[25] Case reports and small randomized studies suggest benzodiazepines, propranolol, and anticholinergics may help treat acute akathisia, but are much less effective in treating chronic akathisia.[26] Taylor et al. found success in lowering the dose of antipsychotic medication as an initial response to drug-induced akathisia,[24] which should be done gradually, if possible.[26] To minimize the risk of akathisia from antipsychotics, the clinician is advised to be conservative when increasing dosages.[24]

If the patient is experiencing akathisia due to opioid withdrawal, and continuing use of opioids is not viable, drugs typically prescribed for acute idiopathic akathisia can be effective. GABA analogues pregabalin and gabapentin, as well as drugs approved for treating RLS, may also be effective in certain cases.[citation needed]

One study showed vitamin B6 to be effective for the treatment of neuroleptic-induced akathisia.[27]

N-acetylcysteine also showed a positive effect on akathisia in a randomized control trial.[28]

Additional pharmacologic interventions found to have antiakathisia effects (especially for neuroleptic-induced akathisia) include -adrenergic antagonists (e.g., propranolol), benzodiazepines (e.g., lorazepam), anticholinergics (e.g., benztropine), and serotonin antagonists (e.g., cyproheptadine) as an alternative.[11]

Trihexyphenidyl has also been prescribed to treat akathisia.

Epidemiology[edit]

Published epidemiological data for akathisia are mostly limited to treatment periods preceding the arrival of second-generation antipsychotics.[26] Sachdev (1995)[29] reported an incidence rate of acute akathisia of 31% for 100 patients treated for 2 weeks with antipsychotic medications. Sachdev (1995) reported a prevalence range from 0.1% to 41%.[29] In all likelihood, rates of prevalence are lower for current treatment as second-generation antipsychotics carry a lower risk of akathisia.[26]

References[edit]

1.Jump up ^ "Definition of Akathisia". MedicineNet.
2.Jump up ^ Brune, M. (2002). "Ladislav Haskovec and 100 Years of Akathisia". American Journal of Psychiatry 159 (5): 727. doi:10.1176/appi.ajp.159.5.727.
3.Jump up ^ Mohr, P. (2002). "Ladislav Haskovec and akathisia: 100th anniversary". The British Journal of Psychiatry 181 (6): 537a. doi:10.1192/bjp.181.6.537-a.
4.^ Jump up to: a b Kaye, Neil S. (2003). "Psychic akathisia". Journal of Clinical Psychopharmacology 23 (2): 206; discussion 2067. doi:10.1097/00004714-200304000-00015. PMID 12640224.
5.^ Jump up to: a b c Szabadi, E (1986). "Akathisiaor not sitting". BMJ 292 (6527): 10345. doi:10.1136/bmj.292.6527.1034. PMC 1340104. PMID 2870759.
6.Jump up ^ Sachdev, Perminder (2006). Akathisia and Restless Legs. Cambridge University Press. p. 299. ISBN 978-0-521-03148-6.
7.^ Jump up to: a b c Han, Su-Hyun; Park, Kwang-Yeol; Youn, Young Chul; Shin, Hae-Won (2013). "Restless legs syndrome and akathisia as manifestations of acute pontine infarction". Journal of Clinical Neuroscience 21 (2): 3545. doi:10.1016/j.jocn.2013.03.021. PMID 23953640.
8.Jump up ^ Healy, David; Herxheimer, Andrew; Menkes, David B. (2006). "Antidepressants and Violence: Problems at the Interface of Medicine and Law". PLoS Medicine 3 (9): e372. doi:10.1371/journal.pmed.0030372. PMC 1564177. PMID 16968128.
9.Jump up ^ Jack Henry Abbot In the Belly of the Beast (1981/1991). Vintage Books, 3536. Quoted in Robert Whitaker, Mad in America (2002, ISBN 0-7382-0799-3), 187.
10.^ Jump up to: a b Akagi, H.; Kumar, TM (2002). "Lesson of the week: Akathisia: Overlooked at a cost". BMJ 324 (7352): 15067. doi:10.1136/bmj.324.7352.1506. PMC 1123446. PMID 12077042.
11.^ Jump up to: a b c d e f g h i Kane, John M.; Fleischhacker, Wolfgang W.; Hansen, Lars; Perlis, Roy; Pikalov a, Andrei; Assuno-Talbott, Sheila (2009). "Akathisia: An Updated Review Focusing on Second-Generation Antipsychotics". The Journal of Clinical Psychiatry 70 (5): 62743. doi:10.4088/JCP.08r04210. PMID 19389331.
12.Jump up ^ Tack, E.; De Cuypere, G.; Jannes, C.; Remouchamps, A. (1988). "Levodopa addiction". Acta Psychiatrica Scandinavica 78 (3): 35660. doi:10.1111/j.1600-0447.1988.tb06347.x. PMID 2973725.
13.Jump up ^ Stahl, SM; Lonnen, AJ (2011). "The Mechanism of Drug-induced Akathsia". CNS spectrums. PMID 21406165.
14.Jump up ^ Lane, RM (1998). "SSRI-induced extrapyramidal side-effects and akathisia: Implications for treatment". Journal of psychopharmacology 12 (2): 192214. doi:10.1177/026988119801200212. PMID 9694033.
15.Jump up ^ Makela, Eugene H.; Makela, EH (2009). "Selective serotonin reuptake inhibitor-induced akathisia". Journal of the American Pharmacists Association 49 (2): e2836; quiz e378. doi:10.1331/JAPhA.2009.08083. PMID 19289334.
16.Jump up ^ Leo, RJ (1996). "Movement disorders associated with the serotonin selective reuptake inhibitors". The Journal of clinical psychiatry 57 (10): 44954. doi:10.4088/JCP.v57n1002. PMID 8909330.
17.^ Jump up to: a b Healy, David; Herxheimer, Andrew; Menkes, David B. (2006). "Antidepressants and Violence: Problems at the Interface of Medicine and Law". PLoS Medicine 3 (9): e372. doi:10.1371/journal.pmed.0030372. PMC 1564177. PMID 16968128.
18.Jump up ^ Marc E. Agronin, Gabe J. Maletta (2006). "Chapter 14: Pharmacotherapy in the Elderly". Principles and Practice of Geriatric Psychiatry (illustrated ed.). Lippincott Williams & Wilkins. p. 215. ISBN 978-0-7817-4810-0. Retrieved 2013-11-23.
19.Jump up ^ Diaz, Jaime (1996). How Drugs Influence Behavior. Englewood Cliffs: Prentice Hall.[page needed]
20.^ Jump up to: a b Hansen, Lars (2003). "Fluoxetine Dose-Increment Related Akathisia in Depression: Implications for Clinical Care, Recognition and Management of Selective Serotonin Reuptake Inhibitor-Induced Akathisia". Journal of Psychopharmacology 17 (4): 4512. doi:10.1177/0269881103174003. PMID 14870959.
21.^ Jump up to: a b Barnes, T. R. (1989). "A rating scale for drug-induced akathisia". The British Journal of Psychiatry 154 (5): 6726. doi:10.1192/bjp.154.5.672. PMID 2574607.
22.Jump up ^ Barnes, Thomas R. E. (2003). "The Barnes Akathisia Rating ScaleRevisited". Journal of Psychopharmacology 17 (4): 36570. doi:10.1177/0269881103174013. PMID 14870947.
23.Jump up ^ Kim, JH; Byun, HJ (2003). "Prevalence and characteristics of subjective akathisia, objective akathisia, and mixed akathisia in chronic schizophrenic subjects". Clinical neuropharmacology 26 (6): 3126. doi:10.1097/00002826-200311000-00010. PMID 14646611.
24.^ Jump up to: a b c Garcia, Mark J.; Matson, Johnny L. (2008). "Akathisia in adults with severe and profound intellectual disability: A psychometric study of the MEDS and ARMS". Journal of Intellectual and Developmental Disability 33 (2): 1716. doi:10.1080/13668250802065190. PMID 18569404.
25.Jump up ^ Munetz, MR; Cornes, CL (December 1983). "Distinguishing akathisia and tardive dyskinesia: a review of the literature.". Journal of Clinical Psychopharmacology 3 (6): 34350. doi:10.1097/00004714-198312000-00003. PMID 6139392.
26.^ Jump up to: a b c d Bratti, I. M.; Kane, J. M.; Marder, S. R. (2007). "Chronic Restlessness with Antipsychotics". American Journal of Psychiatry 164 (11): 164854. doi:10.1176/appi.ajp.2007.07071150. PMID 17974927.
27.Jump up ^ Lerner, Vladimir; Bergman, Joseph; Statsenko, Nikolay; Miodownik, Chanoch (2004). "Vitamin B6 Treatment in Acute Neuroleptic-Induced Akathisia". The Journal of Clinical Psychiatry 65 (11): 15504. doi:10.4088/JCP.v65n1118. PMID 15554771.
28.Jump up ^ Berk, Michael; Copolov, David; Dean, Olivia; Lu, Kristy; Jeavons, Sue; Schapkaitz, Ian; Anderson-Hunt, Murray; Judd, Fiona; Katz, Fiona; Katz, Paul; Ording-Jespersen, Sean; Little, John; Conus, Philippe; Cuenod, Michel; Do, Kim Q.; Bush, Ashley I. (2008). "N-Acetyl Cysteine as a Glutathione Precursor for SchizophreniaA Double-Blind, Randomized, Placebo-Controlled Trial". Biological Psychiatry 64 (5): 3618. doi:10.1016/j.biopsych.2008.03.004. PMID 18436195.
29.^ Jump up to: a b Sachdev P (1995). Akathisia and Restless Legs. New York: Cambridge University Press.[page needed]



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t
e


Pathology of the nervous system, primarily CNS (G04G47, 323349)



Inflammation



Brain

Encephalitis (Viral encephalitis
Herpesviral encephalitis
Limbic encephalitis
Encephalitis lethargica)

Cavernous sinus thrombosis
Brain abscess (Amoebic)




Spinal cord

Myelitis: Poliomyelitis
Demyelinating disease (Transverse myelitis)

Tropical spastic paraparesis
Epidural abscess



Both/either

Encephalomyelitis (Acute disseminated
Myalgic)

Meningoencephalitis




Brain/
encephalopathy



Degenerative



Extrapyramidal and
movement disorders

Basal ganglia disease (Parkinsonism (PD
Postencephalitic
NMS)

PKAN
Tauopathy (PSP)

Striatonigral degeneration
Hemiballismus
HD
OA)

Dyskinesia (Dystonia (Status dystonicus
Spasmodic torticollis
Meige's
Blepharospasm)

Athetosis
Chorea (Choreoathetosis)

Myoclonus (Myoclonic epilepsy)

Akathisia)

Tremor (Essential tremor
Intention tremor)

Restless legs
Stiff person



Dementia

Tauopathy (Alzheimer's (Early-onset)

Primary progressive aphasia)

Frontotemporal dementia/Frontotemporal lobar degeneration (Pick's
Dementia with Lewy bodies)

Posterior cortical atrophy
Vascular dementia



Mitochondrial disease

Leigh's disease




Demyelinating

autoimmune (Multiple sclerosis
Neuromyelitis optica
Schilder's disease)

hereditary (Adrenoleukodystrophy
Alexander
Canavan
Krabbe
ML
PMD
VWM
MFC
CAMFAK syndrome)

Central pontine myelinolysis
Marchiafava-Bignami disease
Alpers' disease



Episodic/
paroxysmal



Seizure/epilepsy

Focal
Generalised
Status epilepticus
Myoclonic epilepsy



Headache

Migraine (Familial hemiplegic)

Cluster
Tension



Cerebrovascular

TIA (Amaurosis fugax
Transient global amnesia
Acute aphasia)

Stroke (MCA
ACA
PCA
Foville's
Millard-Gubler
Lateral medullary
Weber's
Lacunar stroke)




Sleep disorders

Insomnia
Hypersomnia
Sleep apnea (Obstructive
Ondine's curse)

Narcolepsy
Cataplexy
Kleine-Levin
Circadian rhythm sleep disorder (Advanced sleep phase disorder
Delayed sleep phase disorder
Non-24-hour sleepwake disorder
Jet lag)





CSF

Intracranial hypertension (Hydrocephalus/NPH
Choroid plexus papilloma
Idiopathic intracranial hypertension)

Cerebral edema
Intracranial hypotension



Other

Brain herniation
Reye's
Hepatic encephalopathy
Toxic encephalopathy
Hashimoto's encephalopathy




Spinal cord/
myelopathy

Syringomyelia
Syringobulbia
Morvan's syndrome
Vascular myelopathy (Foix-Alajouanine syndrome)

Spinal cord compression



Both/either



Degenerative



SA

Friedreich's ataxia
Ataxia telangiectasia



MND

UMN only: (Primary lateral sclerosis
Pseudobulbar palsy
Hereditary spastic paraplegia)

LMN only: (Distal hereditary motor neuropathies
Spinal muscular atrophies (SMA
SMAX1
SMAX2
DSMA1
Congenital DSMA
SMA-PCH
SMA-LED
SMA-PME)

Progressive muscular atrophy
Progressive bulbar palsy (FazioLonde
Infantile progressive bulbar palsy)
)

both: (Amyotrophic lateral sclerosis)








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t
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Index of the central nervous system



Description

Anatomy (meninges
cortex (association fibers
commissural fibers)

lateral ventricles
basal ganglia
diencephalon
mesencephalon
pons
cerebellum
medulla
spinal cord (tracts)
)

Physiology (neutrotransmission (enzymes
intermediates)
)

Development



Disease

Cerebral palsy
Meningitis
Demyelinating diseases
Seizures and epilepsy
Headache
Stroke
Sleep
Congenital
Injury
Neoplasms and cancer
Other (paralytic syndromes
ALS)

Symptoms and signs (head and neck
eponymous
lesions)

Tests (CSF)




Treatment

Procedures
Drugs (general anesthetics
analgesics
addiction
epilepsy
cholinergics
migraine
Parkinson's
vertigo
other)








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In simple terms according to my medical dictionary.

AKATHISIA

Motor restlessness; intolerance of inactivity. Side effect of antipsychotic drug therapy.

Symptoms: Affected persons cannot sit still, are jumpy, and may appear distracted.

Thanks to you both. As recently diagnosed with PD I am still very new to this and I forget to ask the questions that I should. Thank you again Alex and Rosanne.