![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 17 to 41 of 45. Go back in thread:
Posted by Chairman_MAO on November 25, 2005, at 13:02:06
In reply to Re: Experiences on Risperdal... Im afraid of TD » Tepiaca, posted by alexandra_k on November 23, 2005, at 15:31:56
The notion that TD is somehow a result of schizophrenia is madness in my opinion; in the 1950s or early 60s (I forget which) some investigators announced they'd found the biological basis of schizoprenia. There was a lot to do about this announcement. There was a "spot" found on a specific area of the brain post-mortem in schizophrenics that was not there in controls. Excitement faded when it was found that this abberation--the "spot"--" was caused by the administration of chlorpromazine and had nothing to do with schizophrenia.
How can this person say such things in light of what I have just described? I would like to see references to these cases of TD in people who've never taken an antipsychotic. I am open to new ideas, but am very--and understandably--extremely skeptical here, considering that we do not understand the biological basis for any mental illness. Sure, there are tons of potentially meaningful correlates (that is, Tom Cruise is not Tom Szasz!), but we have no concept of what an actual "biological model" of mental illness would even look like.
Posted by med_empowered on November 25, 2005, at 17:36:04
In reply to Re: Experiences on Risperdal... Im afraid of TD » alexandra_k, posted by Chairman_MAO on November 25, 2005, at 13:02:06
I'm really skeptical about this, too. There were apparently mentions of it here and there in the past, but there are problems with that..first of all, TD-like movements are common after a bout of encephalitis lethargica (which, interestingly enough, causes a brain pathology quite similar to the effects of full-dose conventional antipsychotics). Also, lots of people with advanced syphillis and nutritional problems were diagnosed with "schizophrenia" In addition, the people I read pushing this theory the most tend to be the most adamantly pro-neuroletpics...people like E. Fuller Torrey, who advocates allowing more involuntary drugging and outpatient commitment laws. These people have a vested interest in making neuroleptics seem more benign--after all, what psychiatrist wants to go on record saying in public "I 100% support forcing people to take neurotoxic compounds that can cause intellectual impairment, weight gain, akathisia, emotional blunting, EPS, and tardive dyskinesia." The more palatable they make medication seem, the easier it is for them to sell their "shoot 'em up with haldol" argument. The worst part about Torrey at least is when he argues that the ill-effects of the old school neuroleptics are, in fact, being confused with schizophrenia itself. Come on. I've taken the *new* neuroleptics, and I felt like a zombie. I'd really appreciate it if Torrey and other like-minded "mental health professionals" would avoid p*ssing on my leg and telling me its raining. I'd also like if they'd stop abusing and misusing data and statistics to back up their pre-formed conceptions and beliefs. Such behavior is dogmatic, not scientific.
Posted by alexandra_k on November 25, 2005, at 19:20:45
In reply to TD in untreated schizophrenics, posted by med_empowered on November 25, 2005, at 17:36:04
i will check the book (i have it - so i'll find the bit and quote it later today or tomorrow).
I'm not sure about whether to believe him or not, but I'm fairly sure he will have referenced that thought so we can have a little look at his sources.
A bit about Frith...
He is a psychologist, not a psychiatrist.
The book is (as I was saying...)
"The Cognitive Neuro-Psychology of Schizophrenia"
What that means... He does consider the abnormalities in structure / neurotransmission that have been found upon autopsy.
He does consider how much the abnormality may be due to medication vs the degenerative nature of the illness.
He does acknowledge that the brain abnormalities are a matter of 'tendancies' across population samples rather than being a litmus test for whether individuals have been appropriately diagnosed or not.
He does acknowledge that the brain abnormalities tend to be a matter of 'degree' rather than a huge difference in kind.
He is most interested to develop cognitive models of positive and negative symptoms.
Cognitive models of what cognitive-neurological factors might be responsible for delusions of alien control, thought withdrawal, passivity phenomena, negative symptoms, speech / communication problems etc.He doesn't have a drug line to push either way...
(In fact you would expect him to be sceptical being a psychologist rather than a psychiatrist)I'll chase those up...
Thanks for the interest...
:-)
Posted by alexandra_k on November 25, 2005, at 20:57:00
In reply to Re: thanks for the thoughts., posted by alexandra_k on November 25, 2005, at 19:20:45
Okay. So some of my thoughts were a little off (in the above post).
Here is what Frith has to say:
'My purpose in this chapter is to outline the evidence for believing that schizophrenia results from a brain disorder. A recent and detailed account of some of this evidence may be found in Kerwin (1992)...
Nevertheless, it was believed that brain abnormalities would soon be found. This has proved to be more difficult than expected. Neuropathologists searched diligently and abnormalities were frequently reported, but they were never replicated. Indeed, schizophrenia eventually came to be known as "the graveyard of neuropathology" (Plum, 1972). I have known neuropathologists to remark facetiously that it is easy to recognise the brains from schizophrenic patients because they are the ones which look normal... (p.15)
It is not suprising, in such a climate, many people came to believe that there was no brain abnormality associated with schizophrenia...
There were two major reasons for the dramatic switch of opinion in recent years towards the belief that schizophrenia is essentially a disease of the brain. The first was the chance discovery of antipsychotic drugs and the subsequent demonstration of their association with the neurotransmitter, dopamine. The second was the development of quantitative rather than qualitative studies of brain structure... (p. 16)
There are two distinct types of effects of treatment with antipsychotics on the movement system. Many patients treated with these drugs show signs similar to those observed in patients with Parkinson's disease: tremor, stiffness, and an abnormal gait. These "Parkinsonian" side-effects appear soon after drug treatment commences and disappear when treatment is discontinued. They are a direct consequence of the effects of the drugs on the dopamine system (Marsden, Tarsy, & Baldessarini, 1975). We know that Parkinson's disease is a consequence of the loss of dopamine-containing nerve terminals in the striatum (Ehringer & Hornykiewicz, 1960). A similar, but temporary, lack of dopamine is produced by antipsychotic drugs. The Parkinsonian side-effects of these drugs are very common and many schizophrenic patients are given additional drugs (usually anticholinergics such as procylindine) in the belief that these drugs will combat these side effects.
In addition to these Parkinsonian side-effects there is another kind of movement disorder associated with anti-psychotic drug treatment known as "tardive dyskinesia" (Jeste & Wyall, 1982). The most striking signs of the syndrome are strange involountary movements of the mouth, tongue, and jaw (orofacial dyskinesia, buccal dyskinesia). These signs are widely believed to be the irreversible consequence of long-term treatment with antipsychotics. They are believed to continue and, perhaps, even to get worse when treatment with antipsychotics is discontinued. There is evidence, however, that these movement disorders were observed in chronic schizophrenic patients before antipsychotic treatment was available, and they can also be observed in patients today who have never been treated with antipsychotics (Owens, Johnstone, & Frith, 1982) (p.20).
Regarding structural changes (brain abnormalities). He does not talk about it being 'degenerative' in fact he argues that it is not, so sorry for misrepresenting him there. He says
'In the 1970's there was a technological breakthrough, which is continuing to revolutionise the study of the brain in man. Computerised axial tomography (CAT) permitted a detailed image of the brain to be obtained from a living subject. In particular it was possible to measure the size of the ventricles (the fluid-filled spaces in the middle of the brain).
Simple measurement of the cross-sectional area of the lateral ventricles revealed them to be significantly enlarged in schizophrenic patients (Johnstone et al., 1956). Furthermore, for the first time in neuropathological studies of schizophrenia, this result has been replicated repeatedly (Gattaz, Kohlmeyer, & Gasser, 1991). Of course, the difference is quantitative, not qualitative. It is not the case that all schizophrenic patients have abnormally large ventricles. Rather it is the case that the mean ventricle size of a group of schizophrenic patients is larger than that of a control group matched for age, sex, and socioeconomic status. At the most, perhaps 25% of chronic schizophrenics have abnormally large ventricles. Inevitably this quantitative difference was missed by the classical neuropathologists, who were seeking qualitative differences. From their point of view the discovery of enlarged ventricles in schizophrenia is not very satisfactory. The enlargement is certainly not unique to schizophrenia, it is also observed in a more exaggerated form in all kinds of organic dementia. Furthermore, the enlargement is not found in all schizophrenics. What, then, does it tell us about schizophrenia?
We might first consider whether enlarged ventricles are associated with a particular kind of schizophrenia in terms of signs and symptoms. (p.20)
We would expect them to be associated with a more "organic" picture. To some extent this is true. Enlarged ventricles are associated with involvountary movement disorders (Owens et al., 1985), a lack of response to drug treatment (Weinberger et al., 1980), and negative signs, rather than positive symptoms (Andreasen et al., 1982)...
There is evidence that the enlargement is more marked in the part of the ventricular system that lies within the temporal lobe (the temporal horn) particularly on the left side of the brain (Crow et al., 1989). Consistent with these observations, some studies have found that the hippocampus and the adjacent area of cortex, the parahippo-campal gyrus, are reduced in size in schizophrenia (Bogerts et al., 1985; Brown et al., 1986). Both of these structures are part of the temporal lobe. Here again the differences are quantitative rather than qualitative. The differences may well represent a general reduction in the size of temporal lobe structures of all patients relative to the distribution in the normal population. The overlap between patients and normal subjects is such, however, that the size of the brain structures cannot qualify as "markers" for schizophrenia. (p.23)
... Repeated scans or scans of schizophrenic patients who have been ill for different lengths of time have not provided any evidence that the ventricles become progressively larger (Gattaz et al., 1991). There are a few instances where patients happened to have received scans well before the onset of schizophrenia. These cases have been found to have had large ventricles even at that early time, well before the onset of symptoms (O'Callaghan et al., 1998; Weinberger, 1998). These results suggest that schizophrenia is not a neurodegenerative disease and that brain abnormalities, including enlarged ventricles, precede the onset of the illness' (p.24).
Hmm.Nature / Nurture...
Some people have more of a biological componant than others...
And by the sounds of it...
Those are the people who are more likely to develop TD regardless of whether they take AP's or not...Still...
Maybe thats not quite right?
The full reference is:
Owens, D.G.C., Johnstone, E.C., & Frith, C.D (1982) Spontaneous involountary disorders of movement. *Archives of General Psychiatry, 39* 452-461.
Posted by alexandra_k on November 25, 2005, at 22:11:46
In reply to Experiences on Risperdal... Im afraid of TD, posted by Tepiaca on November 22, 2005, at 21:04:17
> I still have muscles twitches.I wonder if they might have something to do with your anxiety?
Or if they might be caused by some other reason.
I don't know.
Could you check with a GP about some of the causes of muscle twitches?
How often do you have them?
I'm just thinking...
That if you are very worried about them then that might make them worse too...I don't know.
Posted by ed_uk on November 26, 2005, at 14:02:10
In reply to TD in untreated schizophrenics, posted by med_empowered on November 25, 2005, at 17:36:04
>I'd really appreciate it if Torrey and other like-minded "mental health professionals" would avoid p*ssing on my leg and telling me its raining.
LOL, that really made me laugh :D
Ed
Posted by Tepiaca on November 26, 2005, at 15:20:11
In reply to Re: Experiences on Risperdal... Im afraid of TD » Tepiaca, posted by alexandra_k on November 25, 2005, at 22:11:46
> I wonder if they might have something to do with your anxiety?
Maybe , but they started when I begin taking APs
>>
> How often do you have them?
>Sometimes they just last 1 or 2 minutes but other times like in these days they last 2 or 3 hours.
In this moment my rigth eye is twitching , I also have some very little moves in my tongue. They dont bother me, but I am worried that these are the first signs of TD.> I'm just thinking...
> That if you are very worried about them then that might make them worse too...
>
> I don't know.Yes maybe If y try to stop thinking in them ,I would be better
Thank you alexandra
Posted by zeugma on November 26, 2005, at 15:39:49
In reply to Re: Experiences on Risperdal... Im afraid of TD » alexandra_k, posted by Tepiaca on November 26, 2005, at 15:20:11
I have read that TD is actually more prevalent in people with affective disorders who take AP's.
Clozapine is the only AP definitely not associated with TD risk.
While movement disorders of all kinds occur without AP use, including syndromes that resemble TD, this merely means that your chances of getting TD are greatly heightened by AP use (excluding clozapine and possibly a few others, most likely Seroquel and Abilify).
The reason AP's are in vogue so much these days is because a lot of them are still on patent. And by the time their true long term safety profiles are known, they will be off patent, which is convenient for the makers of such drugs.
-z
Posted by ed_uk on November 26, 2005, at 16:07:18
In reply to Re: Experiences on Risperdal... Im afraid of TD, posted by zeugma on November 26, 2005, at 15:39:49
Hi Tepi
>The reason AP's are in vogue so much these days is because a lot of them are still on patent. And by the time their true long term safety profiles are known, they will be off patent, which is convenient for the makers of such drugs.
So true, especially in the US. Things are a bit different here, doctors are strongly encouraged to prescribe the cheapest generic drugs unless there is no alternative, it's all about avoiding wastage of National Health Service resources. Lexapro, for example, is much less popular in the UK than generic fluoxetine (Prozac), which is cheaper by a factor of TEN - and generally similarly effective. The side effects are also broadly comparable.
Kind regards
Ed
Posted by ed_uk on November 26, 2005, at 16:08:11
In reply to Re: Experiences on Risperdal... Im afraid of TD » zeugma, posted by ed_uk on November 26, 2005, at 16:07:18
Posted by ed_uk on November 26, 2005, at 16:32:28
In reply to Re: Experiences on Risperdal... Im afraid of TD, posted by zeugma on November 26, 2005, at 15:39:49
Prescribing escitalopram (Cipralex, Lexapro) instead of fluoxetine (as a first line treatment for depressive illness) would be a massive waste of UK taxpayers money! In the UK, fluoxetine 20mg costs the NHS about £1.50 ($2.57) for a box of 30 caps (one month supply), escitalopram 10mg costs about £15.00 ($25.74) for a box of 28 tabs (one month supply).
Ed
Posted by zeugma on November 26, 2005, at 17:40:08
In reply to Re: Experiences on Risperdal... Im afraid of TD » zeugma, posted by ed_uk on November 26, 2005, at 16:07:18
Lexapro, for example, is much less popular in the UK than generic fluoxetine (Prozac), which is cheaper by a factor of TEN - and generally similarly effective. The side effects are also broadly comparable.>>
Hi Ed
In the U.S., the way it would work for the typical patient with symptoms of depression is that they would be given Lexapro samples for free. Then if the decision was made that the pills were needed a prescription would be written for Lexapro. Insidious, isn't it?By the way, most studies that show that SSRI's have fewer side effects than TCA's use studies that compare them against imipramine or amitriptyline. If the studies were made against the secondary amine TCA's, the results would be about equal. Lofepramine invalidates the argument that even a well-tolerated TCA is cardiotoxic, but for that reason will never be an option here. Instead we can pay through the nose for Strattera which IMO is not in the same league as any of the major TCA's as an AD, but has as its great selling point the fact that it is not 'cardiotoxic.' It may not be, but it's certainly on patent, and doctors' offices are crammed with samples.
-z
-z
Posted by zeugma on November 26, 2005, at 17:51:23
In reply to Re: Experiences on Risperdal... Im afraid of TD » ed_uk, posted by zeugma on November 26, 2005, at 17:40:08
I do need to add in fairness that Strattera is more effective for ADD than nortriptyline, though maybe not desipramine or lofepramine. I would be interested in a study that compared Strattera to either of these drugs, but Lilly probably has little incentive to do so. And the pharmaceutical industry is tied to the patent laws, not to optimizing treatment either financially or medically. This also slows the acquisition of knowledge about these disorders, but industry is not science.
-z
Posted by alexandra_k on November 26, 2005, at 20:23:17
In reply to Re: Experiences on Risperdal... Im afraid of TD, posted by zeugma on November 26, 2005, at 17:51:23
I have been reading...
Interesting...
How much are scientists morally responsible for the likely consequences of their inventions?
(working on atomic weapons, chemical warfare, etc etc)
one might worry a bit about working for a drug company too...
(for example)
grr
Posted by Dr. Bob on November 26, 2005, at 22:16:16
In reply to Re: Experiences on Risperdal... Im afraid of TD, posted by alexandra_k on November 26, 2005, at 20:23:17
> How much are scientists morally responsible for the likely consequences of their inventions?
Sorry to interrupt, but I'd like to redirect follow-ups regarding moral responsibility to Psycho-Babble Social. Here's a link:
http://www.dr-bob.org/babble/social/20051120/msgs/582547.html
Thanks,
Bob
Posted by alexandra_k on November 27, 2005, at 0:52:38
In reply to Redirect: moral responsibility, posted by Dr. Bob on November 26, 2005, at 22:16:16
no moral responsibility on the meds board...
;-)
Posted by ed_uk on November 27, 2005, at 11:32:17
In reply to Re: Experiences on Risperdal... Im afraid of TD » ed_uk, posted by zeugma on November 26, 2005, at 17:40:08
Hi Zeugie :-)
>In the U.S., the way it would work for the typical patient with symptoms of depression is that they would be given Lexapro samples for free. Then if the decision was made that the pills were needed a prescription would be written for Lexapro. Insidious, isn't it?
LOL, they get free Lexapro to start with then have to pay LOTS of money to continue it! Free samples are certainly a very effective way of getting doctors to prescribe new drugs. Would be cheaper for the patient if they started on generic fluoxetine and received NO 'free' samples :-)
>By the way, most studies that show that SSRI's have fewer side effects than TCA's use studies that compare them against imipramine or amitriptyline.
IMO, TCA side effects tend to be more obvious eg. urinary retention. SSRI side effects like apathy and loss of libido tend to be more insidious.
>lofepramine
At 'standard' doses, Gamanil works out as being about 10 times cheaper than Strattera!
RE antidepressants, lofepramine and nortriptyline are currently a lot more expensive than generic fluoxetine, which is now the cheapest AD in the UK!
Kind regards
Ed
Posted by ace on November 28, 2005, at 8:25:46
In reply to Experiences on Risperdal... Im afraid of TD, posted by Tepiaca on November 22, 2005, at 21:04:17
>
> Hello, I called today to my first doctor in my life. He is the one that knows my problem better
> One thing I dont like about him is that he prescribes APs like candies. I understand that
> I had my first push with Zyprexa, but I dont want to take AP forever. They are dangerous.
> I still have muscles twitches. Im 25 . If I continue taking this drugs , I will develope for sure TD in my mid thirties. Im afraid !
>
> I dont know If I should take Risperdal 1mg. I only want this fear to dissapear. It seems nothing works on me. 10 years taking meds!!!
> I am sinking again. Why Should I live more?
> Im only suffering
>
>
I have known peopleon OLD antipsychotics for 30 years with no TD!!!!!!Don't worry!!!.....remember,and this is factual, TD is usually reversible.
Maybe this excess worry is a manifestation of OCD or a Generalized anxiety disorder???
Stay Cool and trust this universe!!!
Ace
Posted by Larry Hoover on November 29, 2005, at 12:00:18
In reply to Re: Experiences on Risperdal... Im afraid of TD » alexandra_k, posted by Chairman_MAO on November 25, 2005, at 13:02:06
> The notion that TD is somehow a result of schizophrenia is madness in my opinion;
> I would like to see references to these cases of TD in people who've never taken an antipsychotic.
I'm sorry to simply leap into this discussion, but I'd like to provide you with some links that show dyskinesia and parkinsonism associated with increasing age in untreated schizophrenia.
The main researcher in this realm to look at is McCreadie. Some of his work is free full-text, if you follow the Pubmed links I've included. He's published a lot more than I reference here. Many many Pubmed references.
By no means am I intending to suggest that dyskinesia is not attributable to neuroleptic medication. Those meds bring about abrupt and severe dyskinetic syndromes. My thinking is that perhaps those with the pre-existing diathesis are rapidly induced. I really don't know.
Maybe we can treat the disease, and by so doing, reduce dyskinetic morbidity? I think that's possible, and maybe the atypicals are capable of accomplishing it, a little bit? Surely not by design, but that's still a good thing.
Lar
Here are the Pubmed links/abstracts:
J Psychiatr Res. 2005 May;39(3):261-6.
Extrapyramidal symptoms in unmedicated schizophrenia.McCreadie RG, Srinivasan TN, Padmavati R, Thara R.
Crichton Royal Hospital, Dumfries, DG1 4XB, Scotland, UK.
Studies of spontaneous extrapyramidal symptoms, dyskinesia and parkinsonism, in unmedicated schizophrenia are of importance in understanding their underlying pathology and relation to the psychosis. This is a study of extrapyramidal symptoms using Abnormal Involuntary Movements Scale for dyskinesia and Simpson-Angus Scale for parkinsonism in 143 schizophrenia patients who never received antipsychotic medication. Psychopathology was measured using the Positive and Negative Syndrome Scale. Dyskinesia was present in 35% of patients and parkinsonism in 15%. The two disorders coexisted in 11 subjects. Orofacial dyskinesia, rigidity and tremor were common symptoms noted. There was no significant change in the rates and total scores of dyskinesia and parkinsonism with gender, age, duration of illness or age at onset of psychosis. Dyskinesia was unrelated to psychopathology. Parkinsonism score correlated positively with the motor symptom cluster of psychopathology. Dyskinesia and parkinsonism scores correlated positively with each other and parkinsonism score discriminated presence of dyskinesia. The associations between the spontaneous abnormal movements and other aspects of schizophrenia differed from those described in treated patients. Dyskinesia and parkinsonism are an integral part of the schizophrenia disease process whose relationship with other factors could be influenced by antipsychotic drug treatment.
Br J Psychiatry. 2002 Aug;181:135-7.
Spontaneous dyskinesia and parkinsonism in never-medicated, chronically ill patients with schizophrenia: 18-month follow-up.McCreadie RG, Padmavati R, Thara R, Srinivasan TN.
Crichton Royal Hospital, Dumfries, UK. rgmccreadie_crh@compuserve.com
BACKGROUND: Spontaneous dyskinesia and parkinsonism have been reported in never-medicated patients with schizophrenia but there has been no previous study of the natural history of these conditions. AIMS: To determine the prevalence of spontaneous dyskinesia and parkinsonism in a group of never-medicated, chronically ill patients with schizophrenia on two occasions separated by an 18-month interval. METHOD: Dyskinesia was assessed by the Abnormal Involuntary Movements Scale using Schooler and Kane criteria for its presence; parkinsonism by the Simpson and Angus scale; and mental state by the Positive and Negative Syndrome Scale for schizophrenia. RESULTS: Thirty-seven patients were examined on two occasions. Nine (24%) had dyskinesia on both occasions, 12 (33%) on one occasion and 16 (43%) on neither occasion. Twenty-one (57%) had dyskinesia on at least one occasion. Thirteen patients (35%) had parkinsonism on at least one occasion. CONCLUSIONS: Spontaneous dyskinesia and parkinsonism fluctuate over time. The former was found on at least one occasion in the majority of patients. It is an integral part of the schizophrenic disease process.
J Clin Psychiatry. 2000;61 Suppl 4:10-4.
Prevalence of spontaneous dyskinesia in schizophrenia.
Fenton WS.
Chestnut Lodge Hospital, Rockville, MD 20850, USA. WSFMD@AOL.COM
Spontaneous abnormal involuntary movements phenomenologically identical to neuroleptic-induced tardive dyskinesia have been described in schizophrenia for over a century. Because at present nearly all patients with schizophrenia are exposed to neuroleptic medications, information about the prevalence of spontaneous dyskinesia is obtained from accounts from the preneuroleptic era, evaluations of first-episode patients before neuroleptic treatment, and the identification and assessment of drug-naive patients in developing countries. In this report, data from 14 studies of neuroleptic-naive patients with schizophrenia are used to generate age-adjusted estimates of the prevalence of spontaneous dyskinesia. While the precision of this estimate is limited by the difficulty of obtaining large, untreated samples, available data suggest a spontaneous dyskinesia rate of approximately 4% in first-episode schizophrenic patients, 12% for patients ill several years but below age 30 years, 25% for those aged between 30 and 50 years, and 40% for those aged 60 years or older. Relative to the incidence and accrued prevalence of spontaneous dyskinesia expected during the natural history of untreated schizophrenia, the cumulative impact of treatment with new neuroleptic agents has yet to be determined.
Br J Psychiatry. 1996 Feb;168(2):221-6.
Abnormal movements in never-medicated Indian patients with schizophrenia.
McCreadie RG, Thara R, Kamath S, Padmavathy R, Latha S, Mathrubootham N, Menon MS.
Clinical Research, Crichton Royal Hospital, Dumfries.
BACKGROUND: Historical records suggest dyskinesia was observed in severely ill institutionalised patients with schizophrenia in the pre-neuroleptic era. More recent work has not found dyskinesia in never-medicated younger and middle aged patients. The present study complements this recent work and avoids the confounders of severity of illness and institutionalism by examining elderly patients in a wide variety of community settings. METHOD: Movement disorders were examined in 308 elderly individuals in Madras, India, using the Abnormal Involuntary Movements Scale, the Simpson and Angus Parkinsonism Scale and the Barnes Akathisia Scale. Patients' mental state was assessed by the Positive and Negative Syndrome Scale. RESULTS: Dyskinesia was found in 15% of normal subjects (n = 101, mean age 63 years), 15% of first degree blood relatives of younger schizophrenic patients (n = 103, mean age 63 years), 38% of never medicated patients (n = 21, mean age 65 years) and 41% of medicated patients (n = 83, mean age 57 years). The respective prevalences for Parkinsonism were 6%, 11%, 24% and 36%; and for akathisia 9%, 5%, 21% and 23%. Dyskinesia was associated with negative schizophrenic symptoms. CONCLUSIONS: Dyskinesia in elderly schizophrenic patients is an integral part of the illness and not associated with antipsychotic medication.
Posted by Larry Hoover on November 30, 2005, at 17:01:24
In reply to TD in untreated schizophrenia » Chairman_MAO, posted by Larry Hoover on November 29, 2005, at 12:00:18
Don'tcha hate it when you post and it just stops? I have three threads like that. :-/
Posted by gardenergirl on November 30, 2005, at 19:17:18
In reply to Re: TD T(he post of) Death, posted by Larry Hoover on November 30, 2005, at 17:01:24
Somebody's got to be the last...
But I know what you mean.
gg
Posted by jamestheyonger on November 30, 2005, at 21:16:57
In reply to Re: Experiences on Risperdal... Im afraid of TD » Tepiaca, posted by ace on November 28, 2005, at 8:25:46
> Don't worry!!!.....remember,and this is factual, TD is usually reversible.
>
AP supress TD so it often does not appear till a dosage reduction.
Posted by alexandra_k on December 2, 2005, at 0:30:10
In reply to Re: Experiences on Risperdal... Im afraid of TD, posted by jamestheyonger on November 30, 2005, at 21:16:57
> > Don't worry!!!.....remember,and this is factual, TD is usually reversible.
?
Er...
I thought it was irreversible...
By definition...The symptoms that are reversible...
I didn't think they counted as TD symptoms.
Movement disorder symptoms to be sure.
But I thought the TD label was reserved for chronic symptoms that don't go away...
Posted by ed_uk on December 3, 2005, at 12:53:31
In reply to Re: Experiences on Risperdal... Im afraid of TD, posted by alexandra_k on December 2, 2005, at 0:30:10
Hi Alex
Tardive = a syndrome which appears after long term use of a medication
Dyskinesia = a movement disorder
Antipsychotic-induced TD is not necessarily permanent - although it certainly can be.
Ed
Posted by alexandra_k on December 3, 2005, at 16:18:43
In reply to Re: Experiences on Risperdal... Im afraid of TD » alexandra_k, posted by ed_uk on December 3, 2005, at 12:53:31
> Tardive = a syndrome which appears after long term use of a medication
> Dyskinesia = a movement disorder
> Antipsychotic-induced TD is not necessarily permanent - although it certainly can be.Hmm. I guess I was going with Frith:
There are two distinct types of effects of treatment with antipsychotics on the movement system. Many patients treated with these drugs show signs similar to those observed in patients with Parkinson's disease: tremor, stiffness, and an abnormal gait. These "Parkinsonian" side-effects appear soon after drug treatment commences and disappear when treatment is discontinued. They are a direct consequence of the effects of the drugs on the dopamine system (Marsden, Tarsy, & Baldessarini, 1975). We know that Parkinson's disease is a consequence of the loss of dopamine-containing nerve terminals in the striatum (Ehringer & Hornykiewicz, 1960). A similar, but temporary, lack of dopamine is produced by antipsychotic drugs. The Parkinsonian side-effects of these drugs are very common and many schizophrenic patients are given additional drugs (usually anticholinergics such as procylindine) in the belief that these drugs will combat these side effects.
In addition to these Parkinsonian side-effects there is another kind of movement disorder associated with anti-psychotic drug treatment known as "tardive dyskinesia" (Jeste & Wyall, 1982). The most striking signs of the syndrome are strange involountary movements of the mouth, tongue, and jaw (orofacial dyskinesia, buccal dyskinesia). These signs are widely believed to be the irreversible consequence of long-term treatment with antipsychotics. They are believed to continue and, perhaps, even to get worse when treatment with antipsychotics is discontinued. There is evidence, however, that these movement disorders were observed in chronic schizophrenic patients before antipsychotic treatment was available, and they can also be observed in patients today who have never been treated with antipsychotics (Owens, Johnstone, & Frith, 1982) (p.20).
But you think that they do allow that some people recover from TD symptoms?
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