![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 5 to 29 of 36. Go back in thread:
Posted by jay on February 17, 2002, at 23:24:03
In reply to Anti-depressants and dystonia/dyskenesia, posted by borderliner21 on February 16, 2002, at 11:25:51
> I was on paxil a while back and it was a life saver for me but it gave me terrible dystonia especially when I stopped it. Why do ssri's cause dystonia in some people?(I was predisposed to it). Is it the weak blocking of dopamine in the basal ganglia? I am terrified to go near any more antidepressants.
> I am about to try serzone. Does it have any action on dopamine?Just a question. The tricyclics seem to offer many differences in these areas. Maybe it is because of their broader action. Comments?
Jay
Posted by borderliner21 on February 18, 2002, at 20:29:17
In reply to tricyclics= no dystonia/dyskenesia???, posted by jay on February 17, 2002, at 23:24:03
Paxil gave me nerve damage. My jaw was out of place and my back was arched a little bit. My voice was affected for a few days after I stopped paxil too. There is a history of dystonia in my family. If the 5ht-2 theory its true about the dopamine being depleted then serzone wouldn't cause any EPS like dystonia and restlessnes?
Posted by Ritch on February 18, 2002, at 21:25:44
In reply to Re: tricyclics= no dystonia/dyskenesia???, posted by borderliner21 on February 18, 2002, at 20:29:17
> Paxil gave me nerve damage. My jaw was out of place and my back was arched a little bit. My voice was affected for a few days after I stopped paxil too. There is a history of dystonia in my family. If the 5ht-2 theory its true about the dopamine being depleted then serzone wouldn't cause any EPS like dystonia and restlessnes?
Bd21,
Interesting, I had the *worst* dystonia from trying Paxil (of all the SSRI's). I only tried 4mg/day for about three days (liquid) and had to stop it. My tongue was *zapping* and making it hard to talk-like way back when I tried Stelazine in the '80's. I for sure didn't get any restlessness or dystonia on the Serzone. It would be worth a try (the Serzone). The question is whether it does as much good as *standard* SSRI's, or whether its unique side-effect profile is OK.
Mitch
Posted by Mr. Scott on February 18, 2002, at 23:03:45
In reply to Anti-depressants and dystonia/dyskenesia, posted by borderliner21 on February 16, 2002, at 11:25:51
In addition to to comments John, Mitch, and Jay have spoken about Serzone, Trazodone can be added to other ADs to accomplish similar results in theory at a lower cost.
Scott
Posted by borderliner21 on February 18, 2002, at 23:53:52
In reply to Re: Anti-depressants and dystonia/dyskenesia » borderliner21, posted by Mr. Scott on February 18, 2002, at 23:03:45
I am sort of glad to have gotten dystonia from paxil because it wasn't permanent like it is from anti-psychotics (it did take a while for my brain to rewire so my dystonia could go away). My psychiatrist started me on zyprexa a few weeks ago(I have schizoaffective disorder) but I am discontinuing because it already aggrivated my dysotnia and tardive dyskenesia. The only AP I will take it clozaril (NO EPS) but he won't prescribe that to me. I hope they make a new anti-psychotic that has no EPS or fatal side effects liek clozaril. Also, would the new anti-depressants in development carry any eps risks?
Posted by OldSchool on February 20, 2002, at 18:33:14
In reply to Anti-depressants and dystonia/dyskenesia, posted by borderliner21 on February 16, 2002, at 11:25:51
SSRIs like Paxil should not generally cause movement disorders like dystonia. HOWEVER, it is becoming known more and more that the SSRIs have a dampening effect on dopamine which in susceptible individuals could lead to development or exacerbation of problems like you are talking about. Dystonia is more of a problem with anti-psychotics, but serotonergic antidepressants do rarely cause movement problems.
Here is an article about SSRIs and induction of movement disorders:
http://www.mhsource.com/pt/p010533.html
Movement Disturbances Associated With SSRIs
by Raphael J. Leo, M.D.
Psychiatric Times May 2001 Vol. XVIII Issue 5
--------------------------------------------------------------------------------
The selective serotonin reuptake inhibitors are employed to treat an array of disorders, including depression, social phobia, panic disorder, posttraumatic stress disorder and obsessive-compulsive disorder. With generally fewer side effects and better tolerability than tricyclic antidepressants and monoamine oxidase inhibitors, the SSRIs have become the most widely prescribed antidepressants in the United States.
Owing to this popularity, adverse drug events previously unappreciated in premarketing clinical trials have gained increasing attention. The most notable of these has been the effect on sexual functioning. Less well-known, yet clinically significant, are movement disturbances that can occur with SSRI use. This should be of concern to clinicians, as movement disorders are uncomfortable, can adversely impact compliance, and can undermine the alliance between clinician and patient.In a review of the literature, 71 cases of SSRI-associated extrapyramidal symptoms (EPS) were found (Leo, 1996) (Table). Akathisia was most common, followed by dystonia, parkinsonism and tardive dyskinesia-like states. In addition, 16 cases of worsening parkinsonism were found in patients with pre-existing Parkinson's disease.
Any review of case reports is subject to inherent limitations. First, some case reports are limited by ambiguous descriptions that make movement disorders difficult to distinguish from other psychiatric disorders or other potential SSRI side effects. This is most notable in case reports of akathisia attributed to SSRI use. At times, it becomes difficult to differentiate akathisia from anxiety or jitteriness (Amsterdam et al., 1994; Maany and Dhopesh, 1990). Mistaking comorbid anxiety for SSRI-associated akathisia may delay or interfere with the appropriate treatment of the patient's anxiety disorder.
Second, in only limited numbers of case reports was the SSRI the sole agent administered. Often, the coadministered medications were also capable of producing EPS. Since the movement disturbances did not appear to occur until after addition of the SSRI, it is possible that pharmacokinetic interactions may have occurred -- leading to increased bioavailability of the SSRI, the concurrently administered drug or both -- thus leading to the emergence of the dyskinesia (Leo, 1996). For example, when coadministered with paroxetine (Paxil), serum perphenazine (Trilafon) levels were significantly increased and accompanied by increased rates of akathisia and parkinsonism (Ozdemir et al., 1997). In addition, medications that normally do not produce EPS may, when combined with an SSRI, predispose patients to dyskinesia (Leo et al., 1995).
Third, in several reports, the presence of pre-existing neurologic disease was evident. Conditions such as head trauma (Coulter and Pillans, 1995) or Parkinson's disease (Jimenez-Jimenez et al., 1994; Steur, 1993) can account for the development or emergence of movement disorders. It is also unclear how many of the patients reported in the literature had undiagnosed or overlooked neurologic conditions coincidentally manifesting around the time of SSRI exposure.
Fourth, reports of SSRI rechallenges are rare (Coulter and Pillans, 1995; Reccoppa et al., 1990). Despite the presence of confounding variables, re-exposure to the SSRI would establish a stronger causal relationship between SSRI treatment and the emergence of movement disorders. These factors limit the ability to draw firm conclusions about a causal relationship between SSRI use and the emergence and/or exacerbation of movement disorders.
Pathophysiology
A simple schematic model of movement disorders is provided in the Figure. Normally, voluntary movements arise when corticospinal tracts generate impulses to anterior horn cells in the spinal cord, modulated by basal ganglia output. Gamma-aminobutyric acid (GABA) from the basal ganglia is inhibitory, refining the corticospinal tract activation. Deficiency of GABA outflow, e.g., Huntington's disease, is characterized by herky-jerky and extraneous movements.
The GABA outflow from the basal ganglia is, in turn, controlled by the balance between two neurotransmitter systems, i.e., dopamine (DA) arising from the substantia nigra and acetylcholine (ACh). The latter have opposing influences on the activity and, therefore, the outflow from the basal ganglia. Disturbance in the balance between ACh and DA alters the net outflow from the basal ganglia, producing movement disturbances (Figure). Thus, idiopathic parkinsonism arises from cell loss in the substantia nigra, reducing the amount of inhibitory DA input to the basal ganglia. The ACh, now relatively less opposed, stimulates the basal ganglia, increasing the inhibitory output to the corticospinal tracts, producing the bradykinesia, rigidity, mask-like facies, shuffling gait and other symptoms characteristic of Parkinson's disease.
The (Figure) also depicts, therefore, the effect of conventional high-potency antipsychotics in producing dyskinesia. These agents, such as haloperidol (Haldol), bind DA receptors in the basal ganglia, thereby preventing access to DA arising from the substantia nigra. The net effect, like that in Parkinson's disease, is unopposed excitatory input from ACh-containing neurons. Consequently, treatment consists of the addition of an anticholinergic agent like benztropine (Cogentin) restoring balance between DA and ACh and re-establishing the normal inhibitory outflow from the basal ganglia.
Serotonin (5-HT)-containing raphe nuclei extend diffuse interconnections to the DA-rich substantia nigra (Dray, 1981). Neurophysiologic and electric stimulation studies demonstrated that the 5-HT released by the raphe nuclei inhibit striatal neurons, an effect which is reversed by 5-HT antagonists (Davies and Tongroach, 1978). Thus, it is plausible that inhibitors of neuronal 5-HT reuptake, by increasing the availability of 5-HT, might be expected to produce an effect similar to that of DA-blocking agents (Figure). In fact, high doses of fluoxetine (Prozac) have been shown to inhibit DA synthesis in the forebrain, hippocampus and portions of the basal ganglia, specifically the caudate-putamen (Baldessarini and Marsh, 1990). Hence, it can be expected that movement disturbances might arise from SSRI use.
The physiologic processes underlying the development of akathisia may involve the interaction of serotonergic and DA pathways innervating mesolimbic systems. While not depicted here, it is suggested that the inhibitory input to these DA pathways produces the overt and covert restlessness characteristic of akathisia. Noradrenergic mechanisms may also be involved.
The mechanisms underlying SSRI-induced movement disorders are likely to be more complex than has been suggested above. A few case reports suggest improvement of parkinsonism and dystonia with the addition of SSRIs (Durif et al., 1995; Keppel Hesselink, 1993; Meerwaldt, 1986). It is possible that other interconnections between 5-HT containing innervations with those of GABA and ACh may contribute to the development of movement disturbances (Fibiger and Lloyd, 1984; Schreiber and Pick, 1995). However, these interconnections have yet to be clarified.
Just how SSRIs induce EPS and other movement disorders in some patients, but potentially improve parkinsonism and dystonia in others, remains unclear. Furthermore, were the mechanisms underlying SSRI-induced movement disorders as simple as illustrated here, the expectation would be that SSRI-induced movement disorders would be common. In fact, the rates of such movement disturbances remain quite low.
Who Is at Risk?
It is possible that some patients are more vulnerable to SSRI-induced movement disorders than are others. Included in the higher-risk category are a) the elderly; b) those exposed to high levels of SSRIs (due to high doses or altered metabolism due to drug interactions); c) patients with concurrent neuroleptic exposure; and d) patients with compromised nigro-striatal functioning. Elder patients may be susceptible to neuronal loss, rendering them vulnerable to the effects of enhanced 5-HT input to nigro-striatal pathways. In addition, due to decreased hepatic functioning, they may be vulnerable by virtue of increased levels of exposure to administered SSRIs. Clearly, neuroleptic exposure increases one's risk of movement disorders, and such exposure may increase the vulnerability of patients who are simultaneously administered SSRIs.
One can only speculate on the influence of gender. While reports featuring female patients who developed dyskinesia associated with SSRI use outnumber those featuring males (Table), one cannot assume that females are more vulnerable. On the one hand, the gender differences observed may merely reflect another trend, i.e., the prevalence of depression is greater among females and more females than males seek treatment for depression (Weissman and Klerman, 1977). In fact, it may be possible that males may be more susceptible than females to dyskinesia associated with SSRI use. Among SSRI-treated patients in a New Zealand medication monitoring program, females (n=3,539) exceeded males (n=1,917) (Coulter and Pillans, 1995). Nevertheless, the proportion of males developing movement disorders (n=8, 0.42%) exceeded the proportion of females (n=7, 0.2%) who did so.
While a majority of cases of SSRI-induced movement disorders involved fluoxetine, at the time of my initial review, fluoxetine had exceeded the other SSRIs in sales and had been available longer than the others. Consequently, the numbers of reports involving fluoxetine may simply have been an artifact of these trends.
On the other hand, there are differences among the effects of SSRIs on DA-reuptake inhibition. For example, sertraline (Zoloft) exhibits a direct augmenting effect on DA-reuptake inhibition (Koe et al., 1983); inhibitory serotonergic input to dopaminergic systems would be mitigated by such direct augmentation. Paroxetine and fluoxetine have lower potencies than sertraline for DA-reuptake inhibition in vitro (Richelson, 1994). Paroxetine also has anticholinergic properties in vitro, which may contribute to reducing the likelihood of EPS as compared to some of the other SSRIs.
Treatment Options, Conclusion
The most prudent treatment measures might be dose reduction or discontinuation of the SSRI, switching to an alternate antidepressant, and/or reducing the coadministered medications that may have led to drug interactions and potentiation of the movement disturbances after SSRI administration. Other interventions employed to mitigate dyskinesia associated with SSRI use are summarized in the Table.
Given that patient exposure to the aforementioned SSRIs is currently estimated to exceed 85 million, movement disorders associated with SSRI use are rare. Certain patients may be more vulnerable to the emergence of dyskinesia after SSRI treatment, e.g., the elderly or those with neurological insults. Clinicians may need to pay particular attention to patients treated with SSRIs who require multiple medications for co-existing medical conditions or complicating psychiatric symptoms. Because pharmacokinetic interactions may occur that render patients susceptible to dyskinesia, patients should be examined frequently for signs of an emerging movement disorder.
Dr. Leo is assistant professor of psychiatry and director of the consultation-liaison service of the residency training program in psychiatry at Erie County Medical Center, State University of New York. He is also a Fellow of the Academy of Psychosomatic Medicine.
Old School
Posted by borderliner21 on February 20, 2002, at 23:13:41
In reply to Re: Anti-depressants and dystonia/dyskenesia, posted by OldSchool on February 20, 2002, at 18:33:14
thanks for the information. I found it useful.
My dystonia from paxil has gotten a lot better and when taking zyprexa i noticed an improvement also...weird huh
Posted by Ritch on February 20, 2002, at 23:51:53
In reply to Re: Anti-depressants and dystonia/dyskenesia, posted by OldSchool on February 20, 2002, at 18:33:14
> SSRIs like Paxil should not generally cause movement disorders like dystonia. HOWEVER, it is becoming known more and more that the SSRIs have a dampening effect on dopamine which in susceptible individuals could lead to development or exacerbation of problems like you are talking about. Dystonia is more of a problem with anti-psychotics, but serotonergic antidepressants do rarely cause movement problems.
>
> Here is an article about SSRIs and induction of movement disorders:<snip>
Serotonin (5-HT)-containing raphe nuclei extend diffuse interconnections to the DA-rich substantia nigra (Dray, 1981). Neurophysiologic and electric stimulation studies demonstrated that the 5-HT released by the raphe nuclei inhibit striatal neurons, an effect which is reversed by 5-HT antagonists (Davies and Tongroach, 1978). Thus, it is plausible that inhibitors of neuronal 5-HT reuptake, by increasing the availability of 5-HT, might be expected to produce an effect similar to that of DA-blocking agents (Figure). In fact, high doses of fluoxetine (Prozac) have been shown to inhibit DA synthesis in the forebrain, hippocampus and portions of the basal ganglia, specifically the caudate-putamen (Baldessarini and Marsh, 1990). Hence, it can be expected that movement disturbances might arise from SSRI use.
Thanks a whole bunch for that article! It is truly a nightmare that SSri's help my anxiety so well, but give me ever-increasing problems with dystonia and akathisia. I can't take any AP's anyore.I find the terms "neurological insult" and "compromised nigrostriatal functioning" to be a lot closer to home than I would like. It makes me feel very concerned about the possiblity of getting old and what it would be like if I ever get there. Obviously, the question arises-should I also need to stop SSRi use for long-term health in addition to already stopping DA-antagonists as well? If I *need* SSRi's for anxiety/impulsivity problems, will I need to switch-and if I switch-what will I switch to in replacement(that has the efficacy)??
Mitch
Posted by skills on February 21, 2002, at 7:29:48
In reply to Re: Anti-depressants and dystonia/dyskenesia » borderliner21, posted by Mr. Scott on February 18, 2002, at 23:03:45
Mr.Scott is right Trazodone worked for me with SSRI's. Another thing which helped was a 5-10mg dose of procyclidine three times a day.
skills.
Posted by OldSchool on February 21, 2002, at 9:50:27
In reply to Re: Anti-depressants and dystonia/dyskenesia, posted by borderliner21 on February 20, 2002, at 23:13:41
> thanks for the information. I found it useful.
> My dystonia from paxil has gotten a lot better and when taking zyprexa i noticed an improvement also...weird huh
Not really its not weird at all if youve read about this stuff. Its well known that taking anti-psychotics can "mask over" drug induced movement disorders. In fact back in the old days, one of the main ways psychiatrists dealt with neuroleptic induced TD was to increase the dosage of the anti-psychotic. This creates a masking over effect of the TD, the patient physically feels better and stops complaining and everyone is happy. However when the neuroleptic is reduced or removed the movement disorder returns with a vengeance.In fact this is sort of what happened to me this past fall when I developed a bad case of EPS while on low dose Seroquel. I first noticed on the Seroquel that my throat began getting very tight and sore, particularly later in the day when the Seroquel began to wear off. I found that after I took my nightly dose of Seroquel, I loosened up a lot, throat pain and tightness dissipated. Then, as soon as I stopped taking the Seroquel the EPS hit full force. Muscle twitches, muscle tightness and a contraction feeling, tongue numbing, weakness on my right side. It was actually worse OFF the Seroquel than on. I hope you see my point.
Please do not believe these various people who will tell you that atypical anti-psychotics can improve movement disorders. Some on this message board will tell you atypicals can "fix" movement disorders...thats BS and is anything but the truth. There is no anti-psychotic anywhere that will do you any good if you have drug induced movement disorders. You might feel better while on the atypical anti-psychotics, but in the long run you are just doing more damage to yourself.
Drugs useful to combat neuroleptic induced dystonia includes anti-cholinergics (OTC benadryl, Cogentin), Klonopin...it has muscle relaxant properties, dopaminergic drugs...and also, ahem...ECT. ECT is very effective for neuroleptic induced movement disorders. ECT has strong "off label" uses for parkinsons and neuroleptic induced movement disorders. I was reading recently that schizophrenics who have ECT have much lower rates of TD than schizophrenics who dont have ECT.
Old School
Posted by borderliner21 on February 21, 2002, at 17:00:59
In reply to Re: Anti-depressants and dystonia/dyskenesia, posted by OldSchool on February 21, 2002, at 9:50:27
I have a question... Does lithium cause any movement disorders or will it exabberate my dystonia or dyskenesia?
Posted by OldSchool on February 21, 2002, at 18:05:51
In reply to Re: Anti-depressants and dystonia/dyskenesia, posted by borderliner21 on February 21, 2002, at 17:00:59
> I have a question... Does lithium cause any movement disorders or will it exabberate my dystonia or dyskenesia?
I know lithium can cause tremor in some people. However, Ive never read or heard anything about lithium causing EPS like symptoms similar to neuroleptics. That would be a question for your doctor. I know I took lithium to augment my antidepressant once and never noticed any muscle stiffening type side effects like Ive always gotten with atypical anti-psychotics.
I always considered lithium to be a pretty safe drug.
Old School
Posted by Angel-2 on March 6, 2002, at 0:41:30
In reply to Re: Anti-depressants and dystonia/dyskenesia, posted by OldSchool on February 21, 2002, at 18:05:51
Hi. I really don't want to scare you but my mother -who was manic depressive from age 30 to age 60- has been treated on lithium for 1/2 her life. About the movement disorders: besides from the tremor, she did "well" for the first 10-15 years but eventually developed acute akathisia (she HAD to keep on pacing all the time) and diskynesia (mostly strange mouth mov.). Obviously we don't know but I think the EPS can come from ANY meds -it depends on every person and his/her meds storyline.
Good luck,
A-2
Posted by Angel-2 on March 6, 2002, at 0:54:26
In reply to Re: Anti-depressants and dystonia/dyskenesia, posted by borderliner21 on February 18, 2002, at 23:53:52
Hi. IMHO and also judging from my 12 years experience -I tried a LOT of tricyclics and then new meds as SSRI-, they ALL eventually give you EPS. I just came out of my last Prozac episode (3 years at 20 mg/day). I had dystonia 3 years ago (but didn't know it) and it got so much worst in the last year that I had to go off cold turkey (and nope, it's not THAT easy to go off Prozac after years of use and other tryings). I feel like I just came out of a nightmare -it's not really over yet since I have so much sleeping problems- and here it is: as if the dystonia condition was not enough, I now have to deal with an annoying tinnitus. Now THAT might make me go crazy. *** Does anyone know if the ear ringing will ever go away? The dystonia (ocular rest myoclonus, blepharospasm, facial tics, cluster headaches, photophobia) is a misery. But the tinnitus (ear ringing), I think I just can't take it.
Good luck.
A-2
Posted by sue doe on March 6, 2002, at 17:53:59
In reply to Anti-depressants and dystonia/dyskenesia, posted by borderliner21 on February 16, 2002, at 11:25:51
Why do ssri's cause dystonia in some people?(I was predisposed to it).
I am not well informed, but I read a lot. I have seen dystonia mentioned in genetic studies of Tourette's Syndrome. there seem to be genetic connections between many of the mental illnesses, alcoholism, obesity and dystonia. Is the dystonia just another ramification of our proneness to mental illness. In my family three siblings are bi-polar, one is schizophrenic, one committed suicide at age 19, and one has serious problems with dystonia. Our children are beginning to show mental illness symptoms also. My pet theory is that these illnesses are all in the same, they just reveal themselves in different ways.
Does anyone think I may have a good point here?
Sue doe (nym)
Posted by JohnX2 on March 7, 2002, at 3:06:40
In reply to Re: Anti-depressants and dystonia/dyskenesia, posted by sue doe on March 6, 2002, at 17:53:59
Hi Sue,I've looked a bit into a similar phenomina called tardive dyskinesia
and it seems as though the latest concensus is that most of these disorders
occur as a part of a progressive neurodegenerative process. In the case
of schizophernia clearly there is a genetic link. Its my understanding
that people can carry the schizophernia gene but not activate the disease,
I don't know if these people taking SSRIs are predisposed to
dystonia, dyskinesia etc. Down to the nitty gritty it has to do
with glutamate (excitatory) transmission and how serotonin medicines goof with
this.The neurodegenerative process seems to be understood and I even have seen
good strategies to treat it beyond those commerically available (I have dug
up patent disclosures, hints into the future). One curiousity I saw was "trick" published
by a physician to treat dystonia with an anti-alcoholism medication
in Europe called Acamprosate. In just happens to protect the neurons in the
brain pathways that get decomposed from excessive stimulation caused from
these neurodegenerative disorders. Ironically when I saw this medicine I thought it might also be useful
for bipolar disorder as it had neuromodulatory action at multiple sights, and alas
I see clinical trials are popping up for bipolar. There's ?a? connection (grabbing at straws)...
someone like CAM will buzz in and spoil my elaborate hope.Sorry to hear such an ugly story. :(
I loved your poems today by the way.
-John
> Why do ssri's cause dystonia in some people?(I was predisposed to it).
>
> I am not well informed, but I read a lot. I have seen dystonia mentioned in genetic studies of Tourette's Syndrome. there seem to be genetic connections between many of the mental illnesses, alcoholism, obesity and dystonia. Is the dystonia just another ramification of our proneness to mental illness. In my family three siblings are bi-polar, one is schizophrenic, one committed suicide at age 19, and one has serious problems with dystonia. Our children are beginning to show mental illness symptoms also. My pet theory is that these illnesses are all in the same, they just reveal themselves in different ways.
> Does anyone think I may have a good point here?
> Sue doe (nym)
Posted by sue doe on March 7, 2002, at 6:53:53
In reply to Re: Anti-depressants and dystonia/dyskenesia » sue doe, posted by JohnX2 on March 7, 2002, at 3:06:40
Progressive neurodegenerative process??? Maybe I should just sit in my rocking chair and hum. Except I would probably break it with all the weight I have put on.
I have a teen age son who has been using marijuana. Perhaps he's trying to self-medicate. Of course, I don't like it. My husband drives truck. I want to send him off with him. Stress has always been a culprit when my problems have flared up. I've been jailed and hospitalized! What more can THEY do? Maybe if I don't get out from under the stress, that sczisophrenic gene will push forward its ugly face. I'll be hearing voices again! Nonetheless, I am who I am and I have the right to be me. I think I'll go sit in a closet.Please forgive me if I'm too cynical. Sometimes I feel like all is loss. But thanks for complimenting the poetry. Maybe I better write another poem. I think it will be about a dripping faucet, dripping away the last of my brain turned to rain. (That rhymes, you know!)
Thus begins day five. Drug free!! Hee! hee! hee! Crazy me!!! Sue Doe (Nym)
Posted by JohnX2 on March 7, 2002, at 19:00:03
In reply to Re: Progressive neurodegenerative process??? » JohnX2, posted by sue doe on March 7, 2002, at 6:53:53
I like who you are!I was talking to an interesting friend last night about all my
other "boring" friend with "normal" lifes, default marriages, kids,
9-5 jobs, etc. Trying to follow all the trends. Copy what other
people establish. Any i think to my self "when I sit on my death bed,
do I want to look back on my life and feel accomplished that I did my
best to be like everyone else?". NO! Frankly, I've remarked that my
treatment is going better and I'm having fewer of these little
"hypomanic" episodes. But I'm also not having these interesting racing
thoughts were I sometimes "think outside the box" and have something
that makes me a unique person. That's who I AM.Cherish who YOU ARE. I LIKE IT.
MY BEST,
JOHN> Progressive neurodegenerative process??? Maybe I should just sit in my rocking chair and hum. Except I would probably break it with all the weight I have put on.
> I have a teen age son who has been using marijuana. Perhaps he's trying to self-medicate. Of course, I don't like it. My husband drives truck. I want to send him off with him. Stress has always been a culprit when my problems have flared up. I've been jailed and hospitalized! What more can THEY do? Maybe if I don't get out from under the stress, that sczisophrenic gene will push forward its ugly face. I'll be hearing voices again! Nonetheless, I am who I am and I have the right to be me. I think I'll go sit in a closet.
>
> Please forgive me if I'm too cynical. Sometimes I feel like all is loss. But thanks for complimenting the poetry. Maybe I better write another poem. I think it will be about a dripping faucet, dripping away the last of my brain turned to rain. (That rhymes, you know!)
>
> Thus begins day five. Drug free!! Hee! hee! hee! Crazy me!!! Sue Doe (Nym)
Posted by sue doe on March 7, 2002, at 21:37:40
In reply to Re: Progressive neurodegenerative process???, posted by JohnX2 on March 7, 2002, at 19:00:03
Thanks John. That's the idea. I want to learn who I am once I escape this medicated life. It was frightening to consider a degenerative brain disease! I did write a poem about it, by the way. It was pretty morbid. but I'm feeling better this evening.
Brain Drips
Brain drips,
Drips away.
Soggy-bread brain.
Squeeze it, let it leak.Pills to fix it.
Pills to melt it.
Which came first?
Has Dr. dealt it?Try another drug to see if
This one was not right for me.
Just like fashion,
Trying on.
Another drug, a different song.We seek to find a normalcy.
Who is normal? It’s not me.
Normal is a farce, you see.I had a friend once who had recovered from cancer once after horrible sessions of chemo. When she was diagnosed again, she simply decided, no more chemo. She didn't think it was worth it. I guess we need to count the costs. If being dumbed down by medicines is the best way of dealing with my disease, I would rather live less days, only fuller days. Thanks for letting me be me.
Thus ends day five. The worst thing today was that I ate a box of doughnuts, at least most of it. I need to stop this eating. My son has been quite cruel to me. This follows a pattern of always loosing the men in my life. I loose love, then I eat. I understand why my father's leaving hurt me. And I understand why my husband's desertion hurt me (he's back now). but I never believed my son could hurt me too. This always leads to eating, self abuse. I need to rise above it. Day six, I hope to succeed!!
Sue Doe (Nym)
Posted by Zo on March 9, 2002, at 18:43:46
In reply to Re: Progressive neurodegenerative process???, posted by JohnX2 on March 7, 2002, at 19:00:03
Is it just because my TLE is "flowing" today, and everything seems more highly fraught with meaning. . .
. .. or is that one of the best, warmest, most affirming posts anyone ever made?!
. .. and how lucky, sue doe, to have something like that written to you!
Zo
Posted by sue doe on March 10, 2002, at 14:11:45
In reply to Re: Staggered » JohnX2, posted by Zo on March 9, 2002, at 18:43:46
> Is it just because my TLE is "flowing" today, and everything seems more highly fraught with meaning. . .
>
> . .. or is that one of the best, warmest, most affirming posts anyone ever made?!
>
> . .. and how lucky, sue doe, to have something like that written to you!Yes, Zo. I, too, was very touched. And inspired to continue being me. What is TLE? I'm not too well versed on my abbreviations. I finally figured out what an AD was! And thanks, again JohnX2, you are truly wonderful to be so kind and understanding.
Sue Doe (Doing great, mostly, on day eight without any AD's!) I'm so glad for such good people on this site!
Posted by Zo on March 12, 2002, at 2:17:32
In reply to Yes, I'm honored and thanks again johnX2, posted by sue doe on March 10, 2002, at 14:11:45
Temporal Lobe seizures. . And Sue! Thanks for that post about my writing! When my website goes up, end of April, there'll be stuff there to read.
Zo
Posted by sue doe on March 13, 2002, at 11:41:11
In reply to Re: Yes, I'm honored and thanks again johnX2 » sue doe, posted by Zo on March 12, 2002, at 2:17:32
When my website goes up, end of April, there'll be stuff there to read.
>
> Zo
Zo: I am glad to hear about your launching a site. I can't wait to see it. Please announce it on psycho-babble when you open! See you there.
Sue Doe Nym
P.S. I'm on day eleven of med free, still waiting to find the true me!
Posted by groundsquirrel on November 18, 2002, at 19:45:13
In reply to Anti-depressants and dystonia/dyskenesia, posted by borderliner21 on February 16, 2002, at 11:25:51
Do you have continuing dystonia from the paxil, or was it just a one-time thing? If one time, how long did it last?
Thanks!
Posted by oracle on November 19, 2002, at 0:47:51
In reply to Re: Anti-depressants and dystonia/dyskenesia, posted by groundsquirrel on November 18, 2002, at 19:45:13
> Do you have continuing dystonia from the paxil, or was it just a one-time thing? If one time, how long did it last?
>
> Thanks!the last post on this thread was 3/11 so do not expect an answer to your question.
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