Akathisa ( the deadliest of paxils side effects)

[mouse]

http://www.yourlawyer.com/topics/overview/akathisia

Akathisia

One side effect of SSRIs is a sensation called Akathisia. Akathisia is a restless agitation ranging from jitteriness to a sensation described by "jumping out of one’s skin." Some researchers and physicians believe that akathisia is the principal trigger for impulsive violence in some people taking SSRIs. Patients become anxious, agitated, terrified, unable to sleep at night and restless. There have long been signs that SSRIs sometimes cause these reactions, which drug manufacturers have tried to keep out of the public eye and off the labels.

The akathisia issue first arose a couple years after Prozac went on the market, amidst media reports about grisly acts of murder and suicide. One event took place in 1989, when Joseph Wesbecker went on a shooting frenzy, killing nine fellow workers of a Louisville, Ky., printing plant before turning his gun on himself. Wesbecker, who had a history of mental problems, was taking Prozac. No one could prove Prozac caused his rampage, but by early 1991, some 350 suicides of Prozac patients had been reported to the FDA, according to one former FDA official. Those reports, which occurred outside the context of scientific clinical trials, were dismissed as anecdotal and sensational by company officials.

Martin Teicher, a Harvard researcher published a study in the American Journal of Psychiatry in 1990 about six patients who developed "violent suicidal preoccupation" after taking Prozac for two to seven weeks. "It was also remarkable how violent these thoughts were," the authors reported. "Two patients fantasized, for the first time, about killing themselves with a gun," they wrote, while one placed a loaded gun to her head, another had to be restrained to prevent self- mutilation, and another fantasized about killing himself in a gas explosion.

None of the patients was suicidal when they started taking Prozac, the researchers reported, and their fixation with violence and death abated when they stopped. Similar symptoms were noted the next year in a paper in the American Journal of Child and Adolescent Psychiatry about six children ages 10 to 17 who developed "intense self-injurious ideation or behavior" while taking Prozac. While the Yale University authors noted the complexity of reaching any conclusion about the cause of these events, they also noted that many children taking Prozac become agitated, restless, and dis-inhibited and developed insomnia to boot.

In 1998, Roger Lane, a scientist at Pfizer, the maker of Zoloft, stated in a paper that "all SSRIs have the rare potential to cause akathisia." In its most extreme form, Lane wrote, patients may feel that "death is a welcome result."

[Samalabear]

I didn't know this is what I was starting to suffer from two months ago, but this is what it felt like and it really scared me. That's when I came back to PaxilProgress after not posting for a couple of months. I also went back to taking all of my nutrients three times a day with meals. I'm watching what I eat and I'm now adding reflexology back into the mix. I think it's working.

[Buxy`s Back]

mmm interesting...i was given seroxat after suffering badly from akasthesia for 3 drugs i was told i was in a severe anxious state...sounds about right

[Scott]

i had it horribly the last time i went off lexapro 15 months ago... it was so bad i remember standing in front of the mirror gripping my hair.. other times i had the urge to scratch the skin off my arms. Terrible urge to get out of my body. These people are nothing short of criminal for hiding this.

[zappelina]

Wonder why it is that you can get this either while on or coming off the drugs.. or both if unlucky. Does anyone know why people who never got it on the drugs get it in withdrawal?

[Samalabear]

My brother is on Lexapro and in spite of what I've told him and what I'm going through, he's going to be okay, his doctor is knowledgeable, and he's only on it every other day and, of course, he said it's only for anxiety, not depression.

He has major blinders on and, in fact, on Christmas Day blew up at me and told me he was tired of hearing my problems with Paxil. This was during a dinner out that I really didn't want to go to and, in fact, I had dinner out with him on Friday at restaurant in Stony Brook.

Both times my entire dinner had to be packed up as I got sicker and sicker with anxiety. This also happened on Thanksgiving. I told my brother that he may not believe totally what I'm going through or how sick I am, but I can no longer go out to dinner until my body indicates that it's going to be okay.

I fear for my brother as he has always suffered from anxiety and has never been half as stable as I am. He's also never taken my suggestion for therapy.
I really love my brother and I get this sinking feeling when I realize that I can't save him from potential harm.

[Scott]

i was never on it for depression

[Scott]

from wikipedia

Akathisia (or "acathisia") is an often extremely unpleasant subjective sensation of "inner" restlessness that manifests itself with an inability to sit still or remain motionless, hence the origin of its name: Greek a (without) + kathesis (sitting). Its most common cause is as a side effect of medications, mainly neuroleptics, and rarely, antidepressants.

Akathisia may range in intensity from a mild sense of disquiet or anxiety (which may be easily overlooked) to a total inability to sit still with overwhelming anxiety and severe dysphoria (manifesting as an almost indescribable sense of terror and doom). In the most severe cases, dysphoria can be so severe that the patient is literally compelled to take action, leading, possibly, to suicide attempts.

It is not unknown to have patients (who have been treated most often with neuroleptics for psychotic episodes or prochlorperazine for nausea) to bolt out of hospitals or emergency rooms due to this odd and disconcerting emotion.

Partially due to the fact that the condition (and its attendant feeling) is difficult for the patient to describe, it is often misdiagnosed and can lead the patient to commit suicide in or outside the hospital. Furthermore, many clinical definitions of akathisia, as studied by psychiatrists and psychologists, may downplay the true psychological gravity of this symptom and simply refer to its psychological effects as "a subjective inner restlessness".

The presence and severity of akathisia can be measured using the Barnes Akathisia Scale.

[Samalabear]

Well, with that definition I now know that this is what I have been suffering the last two months in varying degrees. This is, in my opinion, one of the worst effects of withdrawal. No, I never felt like this until six months off of Paxil.

[Buxy`s Back]

I went to my gp for nausea,tiredness and gyne problems,but mentally i was fine just a little run down from losing a lot of bloood and being anemic.
I was then given 3 drugs...one to stop my monthly cycle,an anti histamine and an anti depressant(didnt know this at the time)..i took them for 4 days and boy i was pacing up and down ,inner agitaion,feelings of despair,crying,agraphobia,throwing up,unable to eat,hyperventilating and just couldnt calm myself down.
Went back to my gp who said i was ion an anxious state no mention of drug reaction(surely he should of known),i was then given Stelazine which calmed me down to a degree but i had become agraphobic over night.I was then given a beta blocker,which caused bad panic attacks so was then given seroxat and boy ...no looking back since then,been 8 years of hell the worst of my entire life...oh yes i had a life before prescribed drugs i didnt know what anxiety was.
Still had anxiety and crap on seroxat,went through a cold turkey attempt in 2002 off seroxat and im lucky to be alive as the suicide urges were so strong,ended up on a phsyc ward where i put myself to stop me hanging myself,and to the present day still badly affected by the effects from seroxat..........great eh? from having a life to this hell and for what??? for seeing my doc for gyne probs which led to akasthesia...when will docs accept the diagnosis of akasthesia????and look at the problems with thier so called legal drugs b4 palming peeps off with mental illnesses they havnt got???

[altostrata]

This is from the drug company AstraZeneca which, of course, wants to sell their drug Seroquel. (Scotty, could you correct the spelling of the title of this topic so it comes up in searches? Also, maybe it belongs in Health Challenges? Thanks.)

http://www.seroquel.com/prof_asp/res...08.asp?flash=1

Akathisia

AstraZeneca Newsletter

Note: SEROQUEL is indicated for the treatment of acute manic episodes associated with bipolar I disorder and the treatment of schizophrenia.

Vol. 4, Ed. 4, December 2004

Akathisia
by Dr. Idan Sharon

Akathisia (from the Greek "not to sit") was first described by Haskovec in 1901.1 It has both subjective and objective symptoms. Subjective symptoms are dysphoric and include irritability, impatience, tension, and panic.2 Objective symptoms range from a need to move to foot tapping, rocking, or running. Akathisia is a common neuroleptic-induced movement disorder; some examples are neuroleptic-induced Parkinsonism, neuroleptic-induced tardive dyskinesia, and dystonia.3 The reports of the prevalence of akathisia in patients taking neuroleptics range from 9% to 35%.4 The differential diagnosis of akathisia includes restless leg syndrome, drug withdrawal, increased psychotic symptoms, and other neurologic disorders.5 Akathisia may result in nonadherence to medication regimen6, violence including suicide7,8, and an increased risk of developing tardive dyskinesia.9,10

The pathophysiology of akathisia is unknown. Dopamine receptor blockade in the mesocortical dopamine tracts appears to be involved. PET studies have shown D2 receptor occupancy in the striatum is associated with the development of akathisia.2 The noradrenergic and serotonergic systems also are involved.2

Five subtypes of akathisia have been described: acute, chronic, tardive, withdrawal, and pseudoakathisia.5 Acute has an onset within hours or days of taking a neuroleptic, although some clinicians think that the onset may take up to six months after an increase in dosage. Tardive akathisia is akathisia that has a delayed onset, usually about three months, and is not related to a change in dosage or medication. This type of akathisia has been found to be strongly associated with the development of tardive dyskinesia. Akathisia is considered chronic when symptoms persist for more than three months. Withdrawal akathisia occurs within six weeks of discontinuation of medication or a decrease in dosage. Pseudoakathisia is an akathisia variant in which the patient has objective symptoms but not subjective symptoms.2

There are a number of rating scales for akathisia. They include the Barnes Akathisia Scale, the Abnormal Involuntary Movement Scale, and the Simpson and Angus Scale for Extrapyramidal Side Effects.2,5

Akathisia is best managed by prevention. The dosage of the neuroleptic can be decreased or the medication changed to alleviate symptoms.11 There are several medications that can be used to help alleviate symptoms. Beta blockers are the most effective and well tolerated agents for akathisia. Anticholinergics have produced equivocal results in akathisia, and their use is limited by side effects such as blurred vision, constipation, and urinary retention.12 Benzodiazepines have some efficacy in acute and chronic akathisia. Other medications that have been used to treat akathisia with some success are cyproheptadine, clonidine, and mianserin.2

Akathisia is a relatively common, disturbing side effect of neuroleptic agents.2 Fortunately, atypical antipsychotic medications have been shown to have a greatly reduced rate of occurrence of akathisia.13 In fact, the American Psychiatric Association recommends considering atypical antipsychotics for first-line treatment of schizophrenia because of the decreased risk of extrapyramidal side effects, including akathisia.14

Note: SEROQUEL is indicated for the treatment of acute manic episodes associated with bipolar I disorder and the treatment of schizophrenia.

The content within this article is the opinion of the physician and does not constitute a recommendation by AstraZeneca.

Dr. Idan Sharon is dedicated to serving the neurological and psychiatric needs of Brooklyn, and Staten Island, New York, and the surrounding communities. Dr. Sharon has extensive experience in the diagnosis and treatment of neurological and psychiatric disorders and conditions. He combines clinical services and expertise with state-of-the-art therapies. Dr. Sharon specializes in ADD/ADHD, anxiety, Alzheimer's disease, dementia, depression, headache/migraine, and sleep disorders. He also diagnoses and treats general neurological disorders.
REFERENCES

Brune M. Ladislav Haskovec and 100 years of Akathisia. Am J Psychiatry. 2002;159:727.
Nelson DE. Akathisia — A Brief Review. SMJ. 2001;46:133-134.
Lohr JB, Browning JA. Movement disorders in neuropsychiatry. Current Opin Psychiatr 1996;9:85-88.
Janno S, Holi M, Tuiski K, et al. Prevalence of neuroleptic-induced movement disorders in chronic schizophrenia inpatients. Am J Psychiatry. 2004;161:160-163.
Sachdev P, Kruk JB. Clinical characteristics and predisposing factors in acute drug-induced akathisia. Arch Gen Psychiatry. 1994;51(12):963-97.
Perkins DO. Predictors of noncompliance in patients with schizophrenia. J Clin Psychiatry. 2002;63(12):1121-1128.
Blaisdell GD. Akathisia: A comprehensive review and treatment summary. Psychopsychiatry. 1994;27(4):139-146.
Leong GB, Silva JA. Neuroleptic induced violence and akathisia: a review. J Forensic Sci. 2003;48(1):187-189.
Sachev P. Early extrapyramidal side-effect as a risk factor for later tardive dyskinesia: a prospective study. Aust N Z J Psychiatry. 2004;38(6):445-449.
Muscettola G, Barbato G, Pampallona, S, et al. Extrapyramidal syndromes in neuroleptic-treated patients: prevalence, risk factors, and association with tardive dyskinesia. J Clin Psychopharmacol. 1999;19(3):203-208.
Sethi K. Movement disorders induced by dopamine blocking agents. Seminars in Neurology. 2001;21(1):59-68.
Poyurovsky M, Weizman A. Serotonin-based pharmacotherapy for acute neuroleptic-induced akathisia: a new approach to an old problem. Br J Psychiatry. 2001;179:4-8.
Holloman LC, Marder SR. Management of acute extrapyramidal effects induced by antipsychotic drugs. Am J Health Syst Pharm. 1997;54(21):2461-2477.
Lehman AF, Lieberman JA, Dixon LB, and the Work Group on Schizophrenia. Practice Guideline for the Treatment of Patients with Schizophrenia, Second Edition. Am J Psychiatry. 2004:161(2 Suppl):1-56.

[LCrawford67]

That is the absolute WORST feeling ever!

[altostrata]

This is from NAMI Santa Cruz County, just south of San Francisco. The folks at NAMISCC seem to have gone off the usual NAMI reservation.

http://www.namiscc.org/newsletters/July01/tardive.htm

Drug Induced & Tardive Movement Disorders

Gwyn M. Vernon

This work that is presented for education and research.
Lynn Schmidt-Speed. Section Editor

Since knowledge of pharmacology is important to neuroscience
nurses. Pharmacology Update is presented as a regular feature.
Drug-induced movement disorders are discussed in this issue.

Drug-induced and Tardive Movement Disorders

Questions or comments about this article may be directed to Gwyn
M. Vernon, RN. MS at The Graduate Hospital Parkinson's Disease
and Movement Disorder Center 1500 Lombard Street, Suite 900
Philadelphia, Pennsylvania 19146. She is the coordinator.
Copyright American Association of Neuroscience Nurses
J Neuroscience Nursing 1991; 23(3):183-187.

Introduction

Drug-induced movement disorders and tardive syndromes present a
unique challenge for neuroscience practitioners. Our
understanding of the pathophysiology of these iatrogenic
problems has developed mainly through clinical observations,
while treatment and prognosis in most cases are complex and less
than optimal. This article discusses drug-induced and tardive
movement disorders, risk factors, management and nursing
implications.

Causative Agents

Movement disorders secondary to pharmacological agents
represent a large number of extrapyramidal disorders seen by
neurologists and psychiatrists in the outpatient setting.
Involuntary movements, including tremor, chorea, athetosis,
dyskinesias, dystonia, myoclonus, tics, ballismus and akathisia,
may be symptoms of primary neurologic disease or occur secondary
to pharmacotherapy (Table 1). Drug-induced abnormal movement
syndromes have been recognized since the 1950s, following the
introduction of chlorpromazine (Thorazine) to treat
schizophrenia.

The risk of developing a drug-induced movement disorder begins
at the onset of treatment with an offending agent. Drug-induced
syndromes may develop acutely, within hours or a few days, or
subacutely, over several weeks. Yet others may develop after
prolonged exposure to an offending agent. When a movement
disorder develops six months or longer after exposure, the term
"tardive" is used, implying a late or delayed onset.

Most of our understanding of the pathophysiology of movement
disorders has developed from clinical observations of response
to pharmacotherapy.[5] Tardive syndromes appear to originate
from drug effects on the striatal dopaminergic system. Five
classes of drugs are known to affect central dopaminergic
systems:[5,15]

-------------------------------------------------------------------
Table 1
Movement Characteristics
Tremor Rhythmic. oscillatory movement categorized
according to its relationship to activity or
posture
Chorea Irregular, unpredictable brief jerky movements
Athetosis Slow, writhing movements of distal parts of
limbs
Dyskinesias Recessive abnormal involuntary movements
Dystonia Slow sustained, posturing or contractions of a
muscle or group of muscles
Myoclonus Rapid, brief shocklike muscle jerks
Tic Repetitive. irregular stereotype movements or
vocalizations
Bellismus Wild flinging or throwing movements
Akathisia Subjective sensation of restlessness often
associated with inability to keep still. Easily
confused with psychiatric symptoms such as
agitation, hyperactivity and anxiety
-----------------------------------------------------------
* Central stimulants that act as indirect dopainine
agonists such as amphetamine
* Levodopa, a precursor of dopamine
* Direct dopamine agonists such as bromocriptine
* Presynaptic dopamine antagonists (dopamine depleting
agents) such as reserpine
* Neuroleptics such as haloperidol (Haldol) or
chlorpromazine (Thorazine), and other medications such as
metoclopramide (Reglan) which antagonize or block central
dopamine receptors

By far, the most common cause of drug-induced and tardive
syndromes are those that block or antagonize dopamine receptors,
usually the neuroleptics.

Prognosis for the patient with a drug-induced movement disorder
ranges from complete recovery to chronic, persistent movements,
often resistant to therapy. Tragically, many patients develop
these syndromes after insufficient consideration of the
ever present danger of this adverse effect. Neuroleptics and
other drugs known to commonly cause movement disorders (Table 2)
should be used cautiously and reserved for situations where the
benefits outweigh the risks. Even then, short-term therapy of
minimal therapeutic dosages should he the strategy employed.
While drug-induced and tardive syndromes can present with any of
the involuntary movements, parkinsonism, dyskinesias and
dystonia tend to be the most common.

Parkinsonian

Drug-induced and tardive parkinsonism resemble idiopathic
parkinsonism, and are therefore characterized by tremor,
rigidity and most commonly an extreme paucity of movement called
akinesia. Ironically, tardive parkinsonism was recognized as a
reserpine induced akinesia prior to our understanding of the
importance of dopamine deficiency to the manifestations of
idiopathic parkinsonism. Today, neuroleptic induced parkinsonism
is the second leading cause of parkinsonism symptomatology
following idiopathic Parkinson's disease.[9]

The mechanism of tardive parkinsonism appears to be the
drug-induced opposition or blockade of striatal dopamine
receptors. This results in a subsequent imbalance in the normal
acetylcholine-dopamine relationship.[5]

While parkinsonism may begin within several days of treatment,
it usually follows a more delayed or subacute onset with 90% of
cases evidenced within three months.[1] Women appear to have a
higher incidence than men. Overall the incidence of developing a
drug-induced parkinsonism ranges from 5-60% depending on the
type of neuroleptic employed.[7] Drug-induced parkinsonism
appears dependent on two variables, drug type and dosage. The
relative dopamine receptor blocking activity varies between
offending agents, however all patients have the potential for
developing tardive parkinsonism if dosages are continually
escalated.[15] Additionally, research supports the hypothesis
there may be subclinical deficits in the dopaminergic system
related to normal aging or even preclinical Parkinson's disease
which may contribute a significant risk for developing tardive
parkinsonism.[1,8]

When drug-induced parkinsonism occurs, the offending medication
should be reduced, withdrawn or changed to an agent with a lower
propensity for causing this adverse effect. However, this plan
is not always feasible because of the underlying psychiatric or
medical illness. Anticholinergics, or more commonly, amantadine
(Symmetrel) are used to treat symptoms in cases where drug
reduction, withdrawal or alternative therapy fail. Routine use
of anticholinergics in patients receiving neuroleptics is not
suggested as prophylaxis as there is evidence anticholinergics
may reduce therapeutic efficscy of neuroleptics.[11] Moreover,
adverse effects of anticholinergics such as hallucinations and
confusion may exacerbate underlying psychiatric symptoms.

Tardive Dyskinesia

Following the introduction of chlorpromazine (Thorazine) in
1952, several researchers began to describe a complicated
movement disorder following exposure to this drug. Lipsmacking,
facial and lingual masticatory movements, trunk rocking and
restless foot movements were some of the movements described.
Faurbye and his colleagues coined the term tardive dyskinesia
and described it as a syndrome of abnormal movements following
at least six months and often many years of neuroleptic therapy,
hence, tardive or late onset.[4] Today, tardive dyskinesia is
characterized by choreiform movements of the mouth, tongue,
face, arms, legs and body, in order of decreasing frequency.[15]

Risk factors for developing tardive dyskinesia include:
* chronic neuroleptic therapy especially polypharmacy
* age greater than 40 years
* chronic schizophrenia
* institutionalization

Females are more commonly affected than males.

Institutionalization is included as a risk factor becausc of
long-term, high dose neuroleptic therapy frequently employed in
chronic care facilities. Indiscriminate use of anticholinergics
may also increase a patient's risk for developing tardive
dyskinesia by blocking the cholinergic system and thereby
enhancing dopamine hence creating a neurotransmitter imbalance.

Onset of tardive dyskinesia may be insidious or emerge as
neuroleptics are being reduced or discontinued. This pattern
theoretically is related to denervation-hypersensitivity
phenomenon. It appears with prolonged receptor blockade by a
neuroleptic, the receptors rebound, becoming supersensitized.

Medication noncompliance such as running out of a prescription
or undergoing sudden drug withdrawals and resumptions are a
common cause of this denervation-hypersensitivity rebound
phenomenon.

The best treatment for tardive dyskinesia is prevention. The
indication for long-term neuroleptics must be well established
and continually re-evaluated, with alternatives considered. Once
tardive dyskinesia presents, a gradual reduction of the
neuroleptic should be attempted in hopes of a spontaneous
remission. Overall 60% of persons may improve, however it may
take two or more years for a remission to occur.[6] Drug
interventions for persistent dyskinesias include low doses of
benzodiazepines, dopamine antagonists and other dopamine
depleting agents such as reserpine and tetrabenazine.

Frequently, patients prefer the neuroleptic be resumed as the
effectiveness of other agents is often insufficient to bring a
satisfactory level of relief from the abnormal involuntary
movements. At best, the prognosis for patients with tardive
dyskinesia is poor. Emphasis must be placed on prevention,
appropriate use of antipsychotics and early recognition of this
phenomenon.
------------------------------------------------------------
Table 2
Syndrome Drugs responsible
-----------------------------------------------------------
Postural tremor Sympathomimetica ++
Levodopa ++
Amphetamines ++
Bronchodilators ++
Tricyclic antidepressants ++
Lithium carbonate ++
Caffeine ++
Thyroid hormone ++
Sodium valproate ++
APDs (1) ++
Hypoglycemic agent ++
Anrenocorticosteroids ++
Alcohol withdrawal ++
Amiodarone +
Cyclosporin A +
Others
Acute dystonic APDs ++
reactions Metoclopramid ++
Antimalarials +
Tetrabenazin +/-
Diphenhydramine +/-
Mefenamic acid +/-
Oxatomide +/-
Flunarizine and cinnarizine +/-
Akathisia APDs ++
Metoclopramid ++
Reserpine ++
Tetrabenazine +
Levodopa & DA agonists (3,4) +
Flunarizine and cinnarizine +/-
Ethosuximide +/-
Methysergide +/-
Parkinsonism APDs ++
Metoclopramide ++
Reserpine ++
Tetrabenazine +
Alphamethyldopa +
Flunarizine and cinnarizine +/-
Lithium +/-
Phenytonin +/-
Captopril +/-
Alcohol withdrawal +
MPTP (2) +
Other toxins (Mn, Carbon disulfide
cyanide) +
Cytosine arabinoside +/-
Chorea,including APDs ++
tardive Metoclopramide ++
dyskinesis and Levodopa ++
orofacial Direct DA agonists (3) ++
dyskinesia Indirect DA Agoniets and other
Catecholaminergic Drugs (4) ++
Anticholinergics +
Antihistaminics +
Oral Contraceptives +
Phenytonin (T) +
Carbamazepine (T) +/-
Ethosuximide +/-
Phenobarbital (T) +/-
Lithium (T) +/-
Benzodiazepines +/-
MAO Inhibitors +/-
Tricyclic antidepressants +/-
Methyldopa +/-
Methadone +/-
Digoxin +/-
Alcohol withdrawal +/-
Toluene (glue) snifling +/-
Flunarizine and cinnarizine +/-
Dystonia, APDs ++
including Metoclopramide ++
tardive Levodopa ++
dystonia Direct DA agonists (3) +
(excluding acute Phenytoin (T) +
dystonic Carbamazepine (T) +/-
reactions) Flunarizine and cinnarizine +/-
Neuroleptic APDs +
malignant Tetrabenazine + AMPT +/-
syndrome Withdrawal of antiparkinsonian
drugs in Parkinson's disease +/-
Tics (simple and Levodopa +
complex), Direct PA agonists +
including Indirect PA agonists ++
aggravation of APDs +
pre-existing tic Carbamazepine +/-
disorders
Myoclonus Levodopa (T) ++
Anticonvulsants (5) (T) ++
Tricyclic antidepressants ++
APDs +/-
Others (6)
Asterixis Anticonvulsants (5) (T) ++
Levodopa +/-
Hepatotoxins (T) ++
Respiratory Depressants (T) ++
Others (6) (T) ++
++=Well documented common or not infrequent
+=Relatively we11 documented; uncommon
+/-=Not well documented or only sma11 number of cases in
literature
T=Usually other evidence of drug toxicity present
(including serum drug levels)
1. APDs=antipsychotic drugs
2. MPTP=1-lMNethyl-4-Phenyl-1,2,3,6-Tetrahydropyridine
3. Includes: Apomorphine, Bromocriptine, Lisuride,
Pergolide, Others
4. Includes: Amphetamines, Methylphenidate, Amantadine,
Pemoline, Fenfluramine, Nomifensine
5. Includes most categories of anticonvulsant drugs
6. Includes wide variety of other drugs capable of causing
toxic encephalopathy
From Weiner WJ, Lang AE. Pages 600-602 in: Movement Disorders:
A Comprehensive Survey. Futura Publishing Co., 1989. Reprinted
with permission.
Editors note: The abbreviation DA in this table is used to
denote dopamine.
------------------------------------------------------------------------

Tardive Dystonia

Tardive dystonia, resembling idiopathic torsion dystonia, is
characterized by contorting posture(s) of a muscle or muscle
groups. Tardive dystonia commonly affects the face or neck, but
may also involve the leg or trunk. Other drug-induced movement
disorders including tardive dyskinesia, akathisia (a subjective
sensation of restlessness) or myoclonus may accompany tardive
dystonia, and have led many researchers to classify tardive
dystonia as a variant of tardive dyskinesia, Unlike tardive
dyskinesia, tardive dystonia is seen in children as well as
adults. As many as 2% of psychiatric inpatients have been noted
to have features of tardive dystonia.[16]

There are no known biochemical changes in idiopathic dystonia,
however, it has been postulated through pharmacologic
observation an alteration may exist in the cholinergic system.
Clinically, patients with tardive dystonia often respond to
dopamine-depleting drugs or antagonists. However, if
ineffective, patients should be offered trials of the
pharmacological therapy used in patients with primary idiopathic
dystonia.

Infrequent Drug-Induced Syndromes

Two other syndromes, although infrequently seen, warrant
consideration because of their potential morbidity and
mortality: acute dystonic reactions and neuroleptic malignant
syndrome.

Acute dystonic reactions have been associated with all
neuroleptics. Swett found an incidence of acute dystonic
reactions in 10.1% of patients studied on a variety of
antipsychotic drugs; males under the age of 30 were most
commonly affected.[12] Acute dystonic reactions are frequently
seen in the psychiatric setting, or bring patients in the
community to the emergency room within hours or a few days after
the initiation of therapy with a neuroleptic, metoclopramide
(Reglan) or other potential drugs. Like idiopathic and tardive
dystonia, the pathophysiology of acute dystonic reactions
remains obscure.

Treatment for acute dystonic reactions includes withdrawal of
the offending agent and parenteral infusion of an
anticholinergic or antihistamine such as benztropine (Cogentin)
or diphenhydramine (Benadryl) followed by oral anticholinergic
therapy every 4-6 hours for the next 24-48 hours.

Neuroleptic malignant syndrome is the least common of the
extrapyramidal adverse effects of neuroleptic drugs, but the
most dangerous.[2] Idiosyncratic reactions including fever,
severe rigidity, tremor, autonomic instability and obtundation
lead to pulmonary embolism, myocardial infarction and
disseminated intravascular coagulation. Death occurs in 20-80%
of the cases while gradual spontaneous resolution over 2 weeks
occurs in the remainder.[15] Infrequently, patients continue to
exhibit involuntary movements including dyskinesia or
parkinsonism upon recovery from the acute phase.

The pathological mechanism of neuroleptic malignant syndrome is
uncertain, however, it is thought the neuroleptic blocking
effects on striatal dopamine receptors result in severe rigidity
and excessive heat production from severe muscle contraction.
Additionally, thermoregulatory function maybe altered by central
effects of the neuroleptics.

Life supporting care including provision of fluids and
electrolytes, cooling and artificial ventilation may be
required. Dopamine agonists and direct acting skeletal muscle
relaxants such as dantrolene sodium have been used with fair to
good results.[2]

Nursing Implications

Nurses in many settings are exposed to patients at risk for, or
who suffer from drug-induced and tardive syndromes. Prevention
of these complications is the best treatment. Careful assessment
of the need for antipsychotic treatment must be considered along
with knowledge of the risk of a persistent, irreversible
involuntary movement disorder evolving as a complication of
neuroleptic therapy. Nurses are in a position to carefully
discuss these risks and benefits with the medical team, patient
and family. Constant weekly monitoring for early detection of
abnormal involuntary movements is an important role of the
nurse. Education of the patient and family is of utmost
importance, with emphasis placed on the goals of treatment,
medication effects and potential adverse effects. Compliance
should be monitored and patients must be discouraged from sudden
drug discontinuance, Additionally, comprehensive care including
options such as day programs and counseling should be considered
to assist in resolving or optimally managing psychiatric
problems. Once a movement disorder develops, nurses must
carefully monitor the patient, assess therapeutic alternatives
and provide reassurance and counseling for the patient and
family.

Summary

Drug-induced and tardive movement disorders represent a large
number of extrapyramidal disorders seen in neurologic practice.
Iatrogenically induced, most commonly by neuroleptics, these
disorders can be characterized by any abnormal body movement
including tremor, chorea, athetosis, dyskinesias, dystonia,
myoclonus, tics, ballismus or akathisia. Parkinsonism,
dyskinesias and dystonia tend to be the most common. Management
of patients with drug-induced or tardive syndromes is complex.

Prognosis is frequently poor as patients usually need the
offending agent to manage their underlying psychiatric or
medical problem. Neuroleptics and other drugs known commonly to
cause movement disorders should be used cautiously and
significant consideration of all risks and benefits measured
before initiating therapy.

Acknowledgment

The author wishes to thank Matthew B. Stern, MD, for useful
comments in support of this article, and Rita Verrilli for her
assistance in the preparation of the manuscript.

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[elisa]

Akathisia can occur with other AD's as well.

My previous psychiatrist prescribed Effexor a very long time ago. Some hours after the first dose, I developed severe restlessness, pacing around like a caged lion, vomiting, diarrhea and unable to eat. The good pdoc instructed to titrate the dose rapidly. The weirdest thing was that I had no brainfog on this drug, unlike all the others I had tried before. In 3 days I lost 5 lbs and called this doc. He told me to keep on taking it as prescribed and hang on to it. I told him I couldn't hold out for longer and that I wouldn't take the Effexor any more. So I was switched again to another AD.

Fast forward.... The next pdoc and I had run out of options (brands) and I suggested to try once again the Effexor, but XR this time because I remembered that I had no brain fog on it. I asked her to titrate me very, very slowly and she did. This time my reaction was completely different, none of the above symptoms happened but the brain fog did not disappear at this time. I was on this drug since Feb 2001 and in 2004 decided to wean off it due to some real nasty side-effects and wanted to be drug free.

Fast forward.... April 15, 2006. I was desperate to get out of withdrawal hell and was desperate for relief. I tried 37.5 mg of Effexor XR again and my reaction to it was the same as the very first time, on the regular Effexor, in addition to withdrawal. The akathisa didn't go away. This time I decided to stick with it until August when a pdoc doubled the dose and another pdoc and I decided that it had no use, so I was tapered of this drug rapidly.

So took Effexor at 3 different times and the first and third attempts produced akathisia.

Lesson learned.... one never knows how the same drug will affect one the 2nd or 3rd time around.....

[cmeffa]

I had this manifest it so many ways. Hell it caused me to make so many destructive descions. Thanks for posting this.

[sheacarney]

Made me want to pull my head apart; just between my eyebrows, so as to escape from my body.

[mouse]

Yup me too...
Was like wanting to actually rip my own skin off...
Absolute torture...
How are you Shea?...

[sheacarney]

Today, I'm okay. The pregnancy has been a bit rough (all day sickness; not just morning and hypertension), plus I've had some pretty nasty external stressors (Ed's surgery/infection/vicodin withdrawal & my mother's health scare). Finances are not so good at present, as Ed was out of work for quite some time. I am absolutely hating Final Cut Pro. I am constantly running into "unknown errors" as I try to log footage for the documentary. I'd love to be able to speed things up, but we are learning as we go. Ugh. Pardon me, but I had to vent.

-Shea

[mouse]

Fianl cut pro eh?...
Are you using a Mac or a PC ?..

[Squidgy]

I couldn't pass up adding this...

I still have signs of akathisia. After I got it, I spent days researching it. Turns out there is a book written about it, called Akathisia and Restless Legs. I was pretty desperate, and almost ordered it. That was until I found out the author, a Perminder Sachdev, holds two unrestricted grants from Eli Lilly makers of Zyprexa and Prozac, both of which can cause it. See:

http://web.med.unsw.edu.au/npi/Contact/Sachdev


This guy also researches "neurosurgery" (read lobotomies.) It makes me sick to think of the esteem and respect someone like him is granted for ruining peoples' lives.

Okay, done ranting.

Squidgy

[sheacarney]

Are you using a Mac or a PC ?..

Mac.

[angels]

Originally Posted by Squidgy

I couldn't pass up adding this...

I still have signs of akathisia. After I got it, I spent days researching it. Turns out there is a book written about it, called Akathisia and Restless Legs. I was pretty desperate, and almost ordered it. That was until I found out the author, a Perminder Sachdev, holds two unrestricted grants from Eli Lilly makers of Zyprexa and Prozac, both of which can cause it. See:

http://web.med.unsw.edu.au/npi/Contact/Sachdev


This guy also researches "neurosurgery" (read lobotomies.) It makes me sick to think of the esteem and respect someone like him is granted for ruining peoples' lives.

Okay, done ranting.

Squidgy

I'm so in agreement with you. This is what caused me to ditch the Paxil after 4 days. I knew this was very bad stuff. When someone is in distress, akathesis could send them over the edge. I think it could have done that to me. That akethesis is where the extra energy of desperation comes from -- not a "brightening" of mood.

[sheacarney]

Turns out there is a book written about it, called Akathisia and Restless Legs.

"Restless Legs." I've always suspected that restless legs was a mild version of akathisia, most likely mitigated by the sedative effects of the drug that created the neurological damage that caused the problem in the first place. Anyone ever listen to the advertisements for "restless legs syndrome?" Apparently, we "don't know what causes restless legs" and it "may run in families." It appears to effects about 12% of the population. Hmmmmm. What percentage of the population is currently taking the most widely prescribed class of drugs (hint: SSRIs are estimated to be used by approximately 10-12% of the general populous of the US)? Do you know what Requip, the drug used to treat restless legs also treats? Parkinson's Disease. Gee, isn't that one of those long term side effects, along with akathisia (tics and dystonia as well) that is LINKED TO AND CAUSED BY SSRI USE?

HELLO WORLD.

[angels]

Originally Posted by sheacarney

"Restless Legs." I've always suspected that restless legs was a mild version of akathisia, most likely mitigated by the sedative effects of the drug that created the neurological damage that caused the problem in the first place. Anyone ever listen to the advertisements for "restless legs syndrome?" Apparently, we "don't know what causes restless legs" and it "may run in families." It appears to effects about 12% of the population. Hmmmmm. What percentage of the population is currently taking the most widely prescribed class of drugs (hint: SSRIs are estimated to be used by approximately 10-12% of the general populous of the US)? Do you know what Requip, the drug used to treat restless legs also treats? Parkinson's Disease. Gee, isn't that one of those long term side effects, along with akathisia (tics and dystonia as well) that is LINKED TO AND CAUSED BY SSRI USE?

HELLO WORLD.

yes, I've listened to them. No one talked about this problem until the onslaught of SSRIs. The author of Freakanomics could paint a devastating picture of SSRIs and many other drugs.

[Messedup]

I took Zoloft for only 4 days and exactly 14 days after I stopped I developed severe Akathisia. I thought I was going to kill myself cause the pain was so bad. My doc said it was the depression coming back (total B.S.!) and told me to take Lexapro. I did but only for 5 days and then quit that cause the burning in my face and arms was just too much. Since quitting the burning has gone away but I fear it will come back during my withdrawal from only a few days of SSRI use. I have a few questions about it. Has anyone taken anything to relieve the pain of akithisia? Since this happened during withdrawal, is it permanent or should it subside over a day or two? Does it get better with time off the drug? It's by far the most painful frightening thing I think a person can experience.