http://observer.guardian.co.uk/print/0,3858,5282821-102285,0 0.html
Call for more therapists to end Prozac nation
Anushka Asthana and Ned Temko
Sunday September 11, 2005
Observer
Thousands of people are on prescriptions for anti-depression drugs such as Prozac because of a lack of therapists who could be much more effective in treating the condition.
Richard Layard, the eminent professor and Labour peer, will say tomorrow that people suffering from depression are given little 'except a few minutes with the GP and some pills'.
Layard, who wrote the Downing Street strategy paper, 'Mental Health: Britain's Biggest Social Problem?', will say there is a 'mass of suffering' with half of all those with clinical depression receiving no help. He will call for 10,000 new therapists to be trained over the next five to 10 years.
In his lecture at the Sainsbury Centre for Mental Health, Layard will add: 'We have effective means of treating it, which are enshrined in the [government] guidelines but they can't be implemented with the current resources of people and money.'
He believes that options such as cognitive behavioural therapies (CBT), that are 'in heavy demand but not adequately available', are as effective as drugs and carry a lower risk of relapse.
'Having only drugs as an option is unsatisfactory,' Layard told The Observer. 'Many people do not get treated at all because they don't want drugs. There is a huge demand for therapy because people want to understand what is wrong with them. We have such heavy prescription of drugs, because there is no choice.'
His comments come as the Healthcare Commission reveal significant gaps in the provision for mental health patients in England. A survey of 25,000 patients being released tomorrow, is expected to show that only 40 per cent had been given any access to talking therapies over the past 10 months.
Layard said that he was not against prescribing drugs but wanted to highlight the fact that powerful therapies exist: 'If a person is given Prozac and keeps taking it [continously], their profile of depression and risk of relapse is about the same as 16 weekly sessions of cognitive behavioural therapy,' he said.
Last night, Health Department official said they would be 'reading with attentiveness' Lord Layard's comments and were 'already committed to a series of steps to widen access to mental-health care'. Next month will see a 'focus on child and adolescent mental-health services around the country with a view to ensuring they are providing the maximum possible access and care.'
Dr Andrew McCullock, chief executive of the Mental Health Foundation, said that mental health provisions were a 'postcode lottery' and welcomed Layard's call for more funding. 'Our information is that there are huge gaps in access to CBT.
'It works - there is overwhelming evidence of that. It is patient specific and it is relatively cheap in comparison to medication.'
Meanwhile, a report by mental health charity, MIND has revealed the difficulties for patients coming off psychiatric drugs.
Coping with Coming Off shows that four out of 10 patients found their GP unhelpful when they were coming off drugs. More than nine out of 10 turned instead to internet and email groups for support.
curus38639.1215277778when my brother was coming off effexor, he suffered from severe anxiety, headaches, depression and suicidal thoughts..
Is he OK now? Some people get affected long term, it seems more often when being taken off Effexor and similar without being tapered off.
Then they often end up in the system on a 'drug roundabout', drugged then withdrawal, back and forth. Some of them never even having been depressed to begin with - the drugs being given for other reasons (hormones, pain, diet, etc).
I hope he's recovered, Brooklea.
curus38639.1293287037Suicidality (and homicidality) is often caused by severe drug-induced akathisia. It says in this that its Junior Doctors that fail to recognise it. I think general experience of people is that almost ALL doctors (especially psychiatrists protecting the 'good name' of the drugs) fail to recognise (or in some cases, acknowledge) it.
http://www.smj.org.uk/1001/aka1001.htm
"Scottish Medical Journal
Editorials/Comments
October 2001
AKATHISIA - A BRIEF REVIEW
D E Nelson
The Orchard Clinic
Royal Edinburgh Hospital
Morningside Terrace
Edinburgh
SMJ 2001;46: 133-134
Akathisia is a common and unpleasant side effect of many psychotropic medications. Junior doctors are often slow to recognise it with consequences for the patient which include reduced compliance, exacerbation of psychotic symptoms and an increased risk of suicide and violence. The word akathisia comes from the Greek meaning literally “not to sit’ and was initially used by Haskovec in 19021 to refer to restless patients with hysteria and neurasthenia. Akathisia is a relatively common side effect of antipsychotic medication, although other drugs including antidepressants, metoclopramide, some calcium channel blockers, dopamine agonists, amphetamine and buspirone have all been shown to cause it. The symptoms consist of objective and subjective components. Subjectively there are symptoms of dysphoria including tension, panic, irritability and impatience2 and objectively there are movements usually taking the form of shuffling of feet while sitting and pacing or rocking while standing. Fidgety leg movements may occur while lying down.3 The differential diagnosis includes agitation secondary to psychotic symptoms, the restless legs syndrome, anxiety, drug withdrawal states and a number of neurological disorders.
Clinical implications
Non-compliance is likely to be increased in patients suffering from the unpleasant symptoms of akathisia. Associated severe anxiety may exacerbate psychosis and there is an increased risk of suicide and violence.4,5 Patients may not be able to distinguish akathisia from the ongoing symptoms of illness leading to despair.6 Patients are also at increased risk of developing tardive dyskinesia.7 It is important that akathisia is recognised and treated appropriately as misdiagnosis and a further increase in antipsychotic medication dosage may further exacerbate the condition.
Epidemiology
Studies have reported incidences ranging between 20 and 75%.1,3 Varying diagnostic approaches and differences in study populations account for much of the difference in incidence quoted. Gender does not seem to influence occurrence8 however it appears that acute akathisia and pseudoakathisia are more common in men and chronic akathisia is more common in women.2 There is no evidence any one race is particularly vulnerable.8 The risk is increased with higher potency drugs, higher dose, increased rate of dose escalation, the presence of extrapyramidal side effects (EPSEs), and parenteral administration.8,9 Age does not have a significant influence on the occurrence of acute akathisia.10
Pathophysiology
The underlying cause of akathisia is still far from clear.4 There appears to be dopamine receptor blockade in the mesocortical dopamine system. PET studies show D2 receptor occupancy in the striatum plays a role12 and noradrenergic and serotonergic systems also appear to he involved.13 Antipsychotics with potent 5HT receptor antagonism show a lower incidence of akathisia and some 5HT2 antagonists eg cyproheptadine, have therapeutic efficacy. There is a possible association between low iron status and akathisia which was initially described by Ekbom in his investigation of patients with restless legs syndrome.4,11
Classification
There have been a number of subtypes of akathisia proposed, although a lack of consensus in the use of the terms is evident. Most authors refer to acute, tardive, chronic, withdrawal and pseudoakathisia. Acute akathisia has an onset within hours or days, however some authors suggest the onset may be up to six months after an increase in dosage.7 Tardive akathisia is generally taken to mean akathisia of delayed onset (usually three months), not related to a recent change in drug or dose.10,11 It has been found to be significantly associated with tardive dyskinesia3 and some have proposed it to be a variant where the trunk and limbs are most affected. Activation procedures may help distiniguish between the two, for example finger tapping may increase symptoms in tardive dyskinesia but decrease the compulsion to move in akathisia. Chronic akathisia usually refers to a persistence of symptoms for three months irrespective of the type of onset. 10,11 Withdrawal akathisia starts within six weeks of discontinuation or a significant dose decrease10 and pseudoakathisia refers to a variant where there are objective symptoms but no subjective awareness or distress. These individuals tend to display more negative symptoms of psychotic illness.
Assessment
There are a number of rating scales available. The most commonly used is the Barnes Akathisia Scale.15 This has objective, subjective and global clinical assessment components. It has good reliability and inter-rater reliability and takes less than five minutes to complete.4
Newer antipsychotics
The newer or 'atypical’ antipsychotics have a much lower propensity to cause movement disorders. They have however been shown to cause akathisia and some studies have shown the incidence may be as high as that for chlorpromazine.13,16 Sandoz pharmaceuticals have criticised the methodology in these trials and quote an incidence of akathisia with clozapine of 3% in their large trial.17 Some other studies have suggested clozapine may permit recovery from chronic akathisia.18 In a study looking at risperidone, a point prevalence of akathisia of 13% was calculated19 and in an open study of amisulpiride, 3 of 14 patients developed akathisia.8
Treatment
Optimal management is to prevent akathisia in the first instance. Patients should be forewarned of possible side effects and educated and reassured regarding these. Drugs which have been found to have some efficacy in the treatment of akathisia are outlined below.
Anticholinergics
These are probably most useful when akathisia is accompanied by parkinsonian side effects and are usually only partially efficacious.4,10 Studies have shown response rates between 39 and 73%.3
Beta blockers.
(B2 blockers). These are the most useful group of drugs in the treatment of akathisia.10 The mechanism is thought to be antagonism of the adrenergic system which is overactive due to neuroleptic blockade of presynaptic dopamine receptors. The initial use of propranalol is suggested, starting at 10mg three times a day and increasing every few days to a maximum of 90-120 mg. The onset of action is usually fairly rapid (4-40 hours) and it is well tolerated.4
Benzodiazepines
These may be effective in acute and chronic akathisia. Clonazepam is preferable due to its long half life. Tolerance and dependence are issues which limit their use and withdrawal should be slow and begin after 2-4 weeks.20
Cyproheptadine
This is an anti 5HT agent which has been shown to be efficacious in some studies.4,21 Continuing its administration for more than a few months is not recommended due to potential adverse effects.20
Clonidine
This is a centrally acting alpha 2 agonist which decreases central noradrenergic neurotransmission. Studies have shown some improvement but adverse effects such as sedation and hypotension can limit its use.10 If tolerated it may be continued although its withdrawal should be gradual.
Mianserin
This is a 5HT2A antagonist. One trial showed a response to treatment of 40% compared with 9.1 % in a placebo group.22
A number of other treatments have been proposed. Iron has been discussed above although the rationale for its use remains weak and there is the possibility of adverse effects. Some efficacy has been described for both nicotine patches4,23 and amantadine10 although the studies were small and not methodologically sound. Piracetam is structurally similar to GABA, induces neuronal metabolism and possibly alters membrane permeability in the central nervous system. One study showed a beneficial effect compared with placebo although more research into its use is required.10
A proposed plan of treatment
Initially reduce the dose or the potency of the drug, perhaps considering a newer (atypical) antipsychotic. If this is of no benefit consider an anticholinergic drug and if this fails to help, a beta blocker. Next a trial of a benzodiazepine (diazepam up to 15mg or clonazepam, 0.5-3mg) should be considered. Where there is still no improvement a trial of cyproheptadine, 16mg, followed by clonidine 0.2 to 0.8 mg is suggested.20 The other treatments listed above may be considered in treatment resistant cases however the evidence for their efficacy is as yet weak."
curus38639.1380787037
Brooklea, if you mean that there's STILL no change - then I'll post more stuff on a thread title AKATHISIA so you know its there, some of which might help you to help him.
If his situation is still the same, and doctors are unaware of the dangers of cold turkey (or changing from a drug like Effexor to a different class of drugs, which amounts to cold turkey) then maybe you could go here:
http://www.benzo.org.uk/healy.htm
Dependence on Antidepressants & Halting SSRIs
PROTOCOL FOR THE WITHDRAWAL
OF SSRI ANTIDEPRESSANTS
by Dr David Healy MD, FRCPsych
North Wales Department of Psychological Medicine,
Bangor, Gwynedd LL57 2PW, Wales, UK
and print out the article for his doctors?
First bit is the history of antidepressants, then it goes on to symptoms of withdrawal and how to determine between that an 'original symptoms' (if he was depressed when he was first given them) and then about half way down or more is how to taper off SSRIs (effexor is an SSRI under 150 mgs then becomes and SNRI, affecting serotonin AND another neurotransmitter).
curus, thanks for the info, it really is informative...
Brooklea - I've come back for a sec because I remembered I hadn't checked for an answer.
(((Brooklea))) I'm so very sorry to read about your cousin. Its happened to far too many people on these drugs, depressed or not depressed when starting, and each time its heartbreaking.
As far as your brother is concerned (lovan is the Australian term for Prozac isn't it?) I'll start a thread with a title of Akathisia (easiest to remember than one of the titles of articles) and put some info on there for you - anything which might be useful, not all of it on akathisia. But I probably won't be able to do it today because I've got to clear a room today, ready for a carpet to be laid tomorrow - maybe not over the weekend either cos of putting everything back, but I will get around to it soon and in the meantime you've got a bit on Akasthisia and how to withdraw if its needed.
Take care.
thanks curus...