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Re: Think of it this way Questionmark

Posted by Marilyn on June 4, 2004, at 5:05:42

In reply to Think of it this way Questionmark, posted by linkadge on June 3, 2004, at 9:09:01

>Quite a few people have genes that code for very low MAO-A to begin with. Does this mean that they are born with a
>brain that poisons itself with serotonin ??? Of course not.
>As well, there is a coding for a short allele and long allele (about 40 percent of the population has it) which
>codes for a 2 fold change in the reputake of serotonin. Do these changes imply natural neurotoxicity.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14982105

J Psychosoc Nurs Ment Health Serv. 2004 Feb;42(2):16-20.

Serotonin syndrome and the use of SSRIs.

Finfgeld DL.

Sinclair School of Nursing, University of Missouri, Columbia, Missouri 65211, USA. finfgeldD@health.missouri.edu

Nurses need to become more aware of serotonin
syndrome to avoid its development and to ensure a therapeutic response when early symptoms emerge. While polypharmacy tends to put individuals at greatest risk for the syndrome, use of a single serotonergic agent may also provoke an adverse response. Because the onset and progression of serotonin syndrome are rapid, prompt action may be needed to avoid potentially life-threatening consequences.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12873279

Pain Med. 2003 Mar;4(1):63-74.

Serotonin syndrome and other serotonergic disorders.

Ener RA, Meglathery SB, Van Decker WA, Gallagher RM.

MCP Hahnemann University Hospitals, Philadelphia, Pennsylvania 19102, USA. rae22@drexel.edu

Serotonin syndrome is an iatrogenic disorder induced by pharmacologic treatment with serotonergic agents that increases serotonin activity. In addition, there is a wide variety of clinical disorders associated with serotonin
excess. The frequent concurrent use of serotonergic and neuroleptic drugs and similarities between serotonin
syndrome and neuroleptic malignant syndrome can present the clinician with a diagnostic challenge. In this article, we review the pathophysiology, diagnosis, and treatment of serotonin syndrome as well as other serotonergic
disorders.


>It is well known that SSRI's *prevent* the axonal dammage due to ecstacy use.
>As well paxil prevents the HD neurodenegeration process. Check out www.hdlighthouse.org
>The *only* studies I have seen linking SSRI's to neuonal dammage were the ones that use 50, and 100 times the
>maximum human dose of prozac. And this could have easily been caused by the harsh dirtyness of prozac to begin with.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12717649
Rev Neurol. 2003 Apr 16-30;36(8):724-6. Related Articles, Links

Neonatal convulsions and subarachnoid hemorrhage after in utero exposure to paroxetine

[Article in Spanish]

Salvia-Roiges MD, Garcia L, Gonce-Mellgren A, Esque-Ruiz MT, Figueras-Aloy J, Carbonell-Estrany X.

Servei de Neonatologia, Institut Clinic de Ginecologia, Obstetricia, i Neonatologia, Unitat Integrada de Pediatria,
(ICGON), Barcelona, Espana. dsalvia@clinic.ub.es

INTRODUCTION: Selective serotonin reuptake inhibitors (SSRIs) are often used as antidepressants in pregnant women. SSRIs do not appear to increase the teratogenic risk when used in their recommended doses. However, not enough
information is available at this time about the risk of toxicity and complications in newborns, after mother treatment with SSRI during the third trimester of pregnancy. We are limited to the existing reports that describe newborns with symptoms due to hyperserotoninemia or withdrawal. CASE REPORT: One newborn whose mother had been
treated with paroxetine 20 mg/day during pregnancy, presented convulsions and subarachnoid haemorrhage in the first six hours of life. The newborn did not present symptoms of hypoxic ischaemic encephalopathy, withdrawal syndrome,
infection, metabolic alterations, cerebral malformations or coagulopaties. DISCUSSION: The most probable etiology is that the paroxetine could decrease the seizure threshold, taking place the first seizure during delivery.
The difficult fetal extraction would have provoked the subarachnoid haemorrhage in a patient with an impaired haemostatic function due to a depletion of platelet serotonin and may also contribute the increased vascular fragility due to paroxetine and reported in adults or in animals. CONCLUSION: Neonatal convulsions and subarachnoid haemorrhage may occur after paroxetine treatment in the third trimester of pregnancy. An accurate follow up of
these newborns in the firsts days of life is strongly recommended.

http://www.neurology.org/cgi/content/abstract/58/1/130

Neurology 2002;58:130-133
© 2002 American Academy of Neurology

Cerebral vasoconstriction and stroke after use of serotonergic drugs

A. B. Singhal, MD, V. S. Caviness, MD, A. F. Begleiter, MD, E. J. Mark, MD, G. Rordorf, MD and W. J. Koroshetz, MD

Serotonin (5-hydroxytryptamine) is a potent vasoconstrictor amine. The authors report three patients who developed thunderclap headache, reversible cerebral arterial vasoconstriction, and ischemic strokes (i.e., the Call-Fleming
syndrome). The only cause for vasoconstriction was recent exposure to serotonergic drugs in all patients, and to pseudoephedrine in one patient. These cases, and the literature, suggest that the use of serotonin-enhancing drugs can precipitate a cerebrovascular syndrome due to reversible, multifocal arterial narrowing.

>My rule of thum is this. Take enough that you feel normal, no more. When this happens it is very likely that your
>brain is much heathier than with no meds at all.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12549949

Ann Pharmacother. 2003 Feb;37(2):209-11. Related Articles, Links

Serotonin syndrome induced by low-dose venlafaxine.

Pan JJ, Shen WW.

Department of Psychiatry, Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan.

OBJECTIVE: To report the case of a patient with serotonin syndrome induced by low-dose venlafaxine. CASE SUMMARY:
A 29-year-old Taiwanese woman with major depressive disorder abruptly developed serotonin syndrome during low-dose (37.5 mg/d) venlafaxine monotherapy, with symptoms of restlessness, tremor, shivering, diarrhea, vomiting, ataxia,
tachycardia, and myoclonus. The patient recovered in 2 hours after receiving prochlorperazine and lorazepam in the emergency department. Venlafaxine was discontinued, and she was discharged home. Two weeks later, the patient
started to receive fluoxetine 20 mg/d and reported no adverse adverse effects during follow-up clinic visits. DISCUSSION: The clinical manifestations of this case meet Sternbach's criteria of serotonin syndrome. Its possible
etiologic factors include panic attack, adverse drug reaction, pharmacodynamic interaction, and congenital absence of CYP2D6 enzyme activity. The Naranjo probability scale suggested a probable causality of venlafaxine treatment and serotonin syndrome. CONCLUSIONS: Clinicians should be aware of the risk of serotonin syndrome when the patient receives not only a combination of 2 antidepressants, but also the single potent serotonergic agent venlafaxine.


>Also note that the *majority* of studies on SSRI's show a HPA axis normalization after continued use.

HPA axis "normalization" is not necessarily accompanied by clinical improvement of depression:

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TBV-49N9DX7-1&_coverDate=10%2F15%2F2003&_alid=155429854&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=5152&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=a1936fb90f15ac3620f41071d004c766

Psychiatry Research
Volume 120, Issue 3 , 15 October 2003, Pages 257-264

Influence of mirtazapine on urinary free cortisol excretion in depressed patients

Cornelius Schule, Thomas Baghai, Constanze Rackwitz and Gregor Laakmann,
Department of Psychiatry, University of Munich, Nüssbaumstr. 7, Munich 80336, Germany

Mirtazapine has been shown to acutely inhibit cortisol secretion in healthy subjects. In the present study, the impact of mirtazapine treatment on urinary free cortisol (UFC) excretion was investigated in depression. Twenty
patients (six men, 14 women) suffering from major depression according to DSM-IV criteria were treated with mirtazapine for 3 weeks. The patients received 15 mg mirtazapine on day 0; 30 mg mirtazapine on day 1; and 45 mg mirtazapine per day from day 2 to the end of the study (day 21). UFC excretion was measured before treatment (day 1), at the beginning (day 0), after 1 week (day 7) and after 3 weeks (day 21) of treatment with mirtazapine. Urine samples were collected from 08:00 to 08:00 h the following day. On the days of urine sampling, the severity of
depressive symptoms was assessed using the 21-item version of the Hamilton Rating Scale for Depression (21-HAMD). There was a significant reduction of UFC excretion during 3-week mirtazapine therapy, which was already obvious
after the first day of treatment (day 0). However, there were no significant across-subjects correlations between UFC reduction and decrease in 21-HAMD sum scores. Apparently, the mirtazapine-induced rapid reduction of cortisol
secretion in depressed patients is not necessarily correlated with a favorable therapeutic response.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12587193

World J Biol Psychiatry. 2001 Apr;2(2):103-5. Related Articles, Links

Attenuation of HPA axis hyperactivity and simultaneous clinical deterioration in a depressed patient treated with mirtazapine.

Schule C, Baghai T, Zwanzger P, Rupprecht R.

It has been suggested that hypothalamic-pituitary-adrenal (HPA) system dysregulation plays an important role in the pathophysiology of depression and that normalization of HPA axis hyperactivity precedes successful treatment with
antidepressants. We report the case of a 61-year-old patient suffering from a major depressive episode who underwent the combined dexamethasone suppression/CRH stimulation test (DEX/CRH test) before and again after one week of mirtazapine treatment. While the patient showed a marked decrease of cortisol and ACTH secretion during the DEX/CRH test within one week, a pronounced and ongoing deterioration of depressive symptoms with suicidal thoughts occurred that was resistant to antidepressant medication and had to be treated with electroconvulsive therapy. Apparently, mirtazapine rapidly attenuates HPA axis hyperactivity in depressed patients via direct pharmacoendocrinological effects. However, this amelioration of HPA system dysregulation is not necessarily accompanied by clinical
improvement.

> Quite a few people have genes that code for very low MAO-A to begin with. Does this mean that they are born with a brain that poisons itself with serotonin ??? Of course not.
>
> As well, there is a coding for a short allele and long allele (about 40 percent of the population has it) which codes for a 2 fold change in the reputake of serotonin. Do these changes imply natural neurotoxicity.
>
> It is well known that SSRI's *prevent* the axonal dammage due to ecstacy use.
>
> As well paxil prevents the HD neurodenegeration process. Check out www.hdlighthouse.org
>
>
> The *only* studies I have seen linking SSRI's to neuonal dammage were the ones that use 50, and 100 times the maximum human dose of prozac.
> And this could have easily been caused by the harsh dirtyness of prozac to begin with.
>
> My rule of thum is this. Take enough that you feel normal, no more. When this happens it is very likely that your brain is much heathier than with no meds at all.
>
> Also note that the *majority* of studies on SSRI's show a HPA axis normalization after continued use.
>
>
> Linkadge
>
>
>
>


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poster:Marilyn thread:353022
URL: http://www.dr-bob.org/babble/20040602/msgs/353653.html