This is a share from a Facebook friend that I thought applicable for the KIP Central site because, of course, knowledge is power and it is when we get sucked into the idea that “doctors” or “therapists” (or any “helper” in fact) is the one with the knowledge and therefore we are conditioned to be dependent on them that this often this plays out, as I experienced, in a new form of the dance of drama and dysfunction, where the “professionals” chides (or some other form of coercion) the “laymen” for seeking their own knowledge.
Thus – another reminder of why the KIP site exists.
Read on – and learn more about the extended withdrawals that can occur in particularly with Benzos and anti depressants.
Protracted Withdrawal Syndrome from Benzodiazepines and Anti Depressants
Dr David Healy’s explanation of protracted withdrawl
I asked Dr Healy to explain why after 4 + years off Seroxat I was still unwell, he very kindly offered this explanation:
It is now generally accepted that antidepressants can cause physical dependence and a withdrawal syndrome, so that stopping antidepressants can commonly lead to withdrawal problems, that these problems may be severe in some instances but are generally less severe, and that these problems may last for months but are more often over within weeks. This piece outlines what is known about states of persisting difficulty and what can be done to remedy them.
First, it has been known since the 1960s when dependence on and withdrawal from antipsychotics was first outlined that in addition to classic states such as tardive dyskinesia that might be revealed by withdrawal, a variety of stress syndromes and persisting affective disturbances that have been termed tardive dysthymia, tardive akathisia and other tardive syndromes might also emerge.
Second, by the time enduring problems emerge after antidepressant discontinuation, the character of the initial problem has commonly changed. The initial problems often centre on phenomena that have been termed electric zaps, and electric head, but later these recede into the background and are replaced by a restless or dysphoric state consistent with a tardive dysthymia or tardive akathisia.
It should be noted that in addition to the abnormalities of sensation common in the initial phases, many of those affected complain of anxiety and depressive symptoms also. It may not be clear to patients or their doctors that these later onset depressive states are new developments, as they may often appear continuous with early onset withdrawal states and may even harder to distinguish from an original depression than the initial withdrawal state was.
Enduring states of this type can follow discontinuation from almost all antidepressants active on the serotonin system. The problem has not been as apparent on other antidepressants but this may reflect frequency of usage of SSRIs rather than anything else.
The problems appear more common in women than in men but this again may reflect frequency of usage.
The characteristic symptoms include “depression”, depersonalisation, agitation/akathisia, a generally labile state and stress intolerance.
Enduring problems can follow either abrupt or tapered discontinuation of treatment. One difficulty lies in knowing how common such states are.
A great number of individuals presenting to their doctors with these disorders are in all likelihood being told they have a recurrent affective disorder and are probably commonly being put back on an antidepressant.
This will happen for three reasons. First the problems will often look “depressive”. Second, most physicians simply do not think that higher order neurological problems of this sort could persist this long. Third, the problems at this point may seem to physicians to be different to the original problems on withdrawal and those affected may be persuaded of this. This interpretation is made more likely by the fact that most people will have had slightly better periods before a bad period leads them to seek help. But even tardive dyskinesia goes through good and bad phases.
Finally, this scenario overlaps with problems that can appear after stopping benzodiazepines, where the acute phases of withdrawal, which overlap with acute SSRI withdrawal, differed in profile from more chronic syndromes. The profile of chronic post-benzodiazepine difficulties is similar to that of chronic post-SSRI problems, with the chronic syndromes being more apparent in women.
Treating Severe Discontinuation Difficulties
In terms of the initial treatment of severe discontinuation difficulties, there are serotonergic and non-serotonergic options.
The serotonergic options as outlined in a number of withdrawal protocols involve going on a serotonin reuptake inhibitor such as fluoxetine or imipramine, often in liquid form and tapering extremely gradually.
A second option involves moving to a tricyclic antidepressant or an antihistamine or St John’s Wort on the basis that these share antihistaminic and serotonin reuptake inhibiting properties in common but are less potent (“gentler”) than SSRIs.
A third option involves treating with agents acting on different systems. Apparent success has been reported with choline-esterase inhibitors or lamotrigine. These have appeared in some instances to ease withdrawal problems in individuals who have found it very difficult to get off treatment.
Managing Tardive Dysthymia
The management of tardive dysthymia is a different problem to managing severe withdrawal. At present it is not clear what if anything might help the difficulties some people seem faced with 6 months or more into the discontinuation period.
Faced with ongoing problems, people commonly ask whether it might be worth going back on the original antidepressant and starting a new and even more gradual taper.
This seems problematic for two reasons. First going back on something that has caused such difficulties, perhaps through some vulnerability of the taker’s serotonergic or a related system, seems risky.
Second at least some of those who have gone back on treatment have needed to go back on a higher dose than previously in order to alleviate problems and in some instances a return to the original medication has not alleviated the problem.
Generally the longer the interval off the drug, the less likely it has been that reinstituting the treatment will lead to a resolution of the symptoms.
If an individual does return successfully to treatment, the question is what next.
Based on experience with the management of withdrawal from antipsychotics, one option might be to remain on treatment indefinitely. There are several drawbacks to this.
In the case of the antidepressants it is not at present known if ongoing treatment increases the risk of premature mortality or other disorder. The risks of fractures or haemorrhages seem slightly increased, and perhaps more substantially increased if combined with other treatments like aspirin.
If the taker has found the SSRI helpful but also emotionally blunting, this would be a significant impairment to quality of life to have to live with.
A second option is to turn to an antihistamine, such as chlorpheniramine, or to a tricyclic antidepressant, such as dosulepin or imipramine, or to St John’s Wort. The rationale here that a small amount of serotonin reuptake inhibition is all that is needed to produce a helpful anxiolytic effect in those suited to drugs of this type. SSRIs are in fact almost grotesquely overpowered for the purpose – using one is rather like having a sports car in a 30 mph zone.
Third turn to a completely different therapeutic principle. Among the options are drugs active on the cholinergic system, calcium channel blockers or dopamine agonists.
Choline-esterase inhibitors may help tardive dysthymic states, in that they have been reported to offer a benefit in tardive dyskinesia, and have been helpful in some cases of SSRI withdrawal.
Calcium channel blockers have been reported to benefit some individuals with enduring problems after antipsychotic withdrawal.
Dopamine agonists or stimulants are used in restless legs and related syndromes, and restlessness is often a component of the problems facing individuals after stopping antidepressants.
The final point concerns the likely duration of a tardive dysthymic episode. Based on the precedent of tardive dyskinesia, and of the difficulties some patients faced on discontinuation from benzodiazepines such states may last for 1-4 years. In older individuals there is a possibility they may last indefinitely. In younger individuals, they are more likely to clear up in a 12-36 month timeframe.
The resolution of difficulties may require something like a synthesis of new receptors to replace receptors that have been jettisoned in the face of physiological stressor of the SSRI. Whatever the mechanism recovery does happen but may take years and seems likely to be facilitated by activity of various sorts and most probably an avoidance of psychotropic medication – including antihistamines and other compounds.
Pregnancy – a Special Consideration
The issues above are particularly complex for women considering pregnancy, given evidence that serotonin reuptake inhibitors increase the risk of birth defects, spontaneous abortions, primary pulmonary hypertension and neonatal withdrawal syndromes.
Although more women on antidepressants have perfectly normal babies than have babies with one of the above problems, there is also the issue of the toll that 9 months of worrying might take on a mother and the effect of this on the relationship between mother and child.
Women contemplating pregnancy or suspecting or finding themselves pregnant and anxious to withdraw may have very real problems in the event of a significant withdrawal. A cross taper to fluoxetine liquid is problematic in that fluoxetine is also linked to an excess of birth defects and the other problems found with Seroxat.
Managing New Affective Episodes
Another issue that needs to be addressed is the emergence of what is in fact a new affective episode rather than a flare-up of tardive dysthymia.
In this case, it seems likely that if someone got well on a serotonergic agent in the first instance, they are more likely to show a better initial response to another such agent than they are to respond to an agent from a different class.
This raises the question of whether the short term benefit is worth taking given the likely longer term problems. To some extent this issue depends on what the alternatives are.
First if this is a depressive disorder that has responded to a serotonergic agent in the first instance, it is less likely to be severe and as such the risks of attempting to bring about a quick response with drugs – such as the risk of suicide – are not high.
It would seem best however to take a drug that has less potent serotonin reuptake inhibiting properties – such as imipramine.
Second, not intervening pharmacologically is a reasonable option for two reasons. One is that the natural history of such disorders is that they will resolve on average within 12-16 weeks. Another is that there is considerable evidence to suggest that those who respond without pharmacological or other interventions are less likely to relapse in future.
Third, related to not-intervening there are a number of things affected individuals can do for themselves. Exercising, particularly in a routine, is likely to be helpful, as is physical work generally. Diet, especially avoiding alcohol, is likely to be of some importance.
There are other more esoteric steps a person can take. One is sleep deprivation, which is undertaken regularly as an antidepressant treatment in many European countries.
Finally, CBT or other psychotherapeutic procedures may be of benefit, where they would seem to be less likely to be helpful in tardive dysthymic states.
A large number of doctors still halt antidepressants abruptly, possibly for 2 reasons. One, they are not aware they should taper the treatment. Second, it is not possible to taper the treatment as only a few drugs come in liquid form – fluoxetine, paroxetine and imipramine. Given that a transfer to fluoxetine liquid can cause its own problems, making liquid forms of all SSRIs available or disseminating information on how such formulations may be prepared is important.
Patients undergoing a marked withdrawal from antidepressants need an account of what is known about what is happening to them. Something on these lines:
Your brain has adjusted to the presence of an antidepressant and the removal of this stimulus now requires the brain to readjust. In some cases, some people readjust in the way a spring does when a weight is removed – it springs back into shape. For others the spring will get back to normal provided the weight is removed gradually. For some others, the spring will not readjust.
Some antidepressants appear to cause more problems than others but we do not know why this is. Fluoxetine may be helpful for some people as it makes the readjustment process more gradual but it is not helpful for all and comes with its own problems.
There are a number other possibilities, one of which is that problems are more likely with potent serotonin reuptake inhibitors such as paroxetine and venlafaxine, in which case the best strategy is to move to low potency serotonin reuptake inhibitor.
Managing Tardive Dysthymia
It is particularly important for patients suffering from this condition to have a name for the state and an explanation for what is happening.
For this reason it is proposed to name the enduring condition that can happen after discontinuation of an antidepressant tardive dysthymia. It is not clear how great the overlap might be between the tardive dysthymia linked to antidepressant, antipsychotic or benzodiazepine withdrawals.
That a number of people exposed to antipsychotics, benzodiazepines or antidepressants may have an enduring problem has been recognized for some decades. The risks of having an enduring problem appear slightly greater for women, and may increase with age.
There is no clear understanding of what happens in the brain to trigger such problems but it may be that with extended exposure to an antidepressant, some sensitive individuals lose receptors from the ends of their nerve terminals as part of an adaptive mechanism and when the drug is removed these receptors do not simply return to normal.
If the explanation offered above is even partly correct, it implies that with time the condition should resolve but this resolution may take months or years. It would seem intuitively sensible to suggest that activity, which helps to refashion nerve endings, would help and those affected should therefore be encouraged to be physically active and in general to live life as fully as possible and avoid shutting down or withdrawing from activities.
Activities such as walking or swimming may be helpful especially if undertaken in a graded programme that ensures there is daily activity and over time builds the activity levels up.