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SSRI Discontinuation?

Discussion in 'Psychiatry' started by pschmom1, Dec 20, 2005.

  1. pschmom1

    pschmom1 Senior Member
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    Does anyone have any advice as how to relieve the overall discomfort when discontinuing SSRIs? Mainly Paxil. Any advice would be helpful. I think the book "Feeling Good" by David Burns MD might help emotionally, what do you all think?
     
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  3. OldPsychDoc

    OldPsychDoc Senior Curmudgeon
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    We can't provide psychological advice either, but we can give book plugs!

    FG is a good "do-it-yourselfer's" basic intro to CBT. It is useful in many situations. I would recommend it.
     
  4. Poety

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    "poppa can you hear me, poppa can you see me?" <sung in Barbara Streisand voice. "oh poppa" :scared:
     
  5. Anasazi23

    Anasazi23 Your Digital Ruler
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    SSRI discontinuation can be a large issue, or a non-issue with patients, it seems. I've seen 80 year old ladies quit large doses of Effexor cold turkey with no problem whatsoever. I've also seen people not willing/able to get out of get out of bed from 'withdrawal' from very low dose Paxil. I've also heard from an attending of a withdrawal case so bad it was associated with violent flu-like symptoms and autonomic instability.

    If a patient is experienceing SSRI discontinuation, there are a few ways in which you can relieve the discomfort, the easiest of which is to titrate the drug in a slower, more deliberate fashion - sometimes leaving the dose a 3/4 of what is was for week or more before again lowering the dose. In this way, it could take a month or more to d/c the drug completely. Another trick is to give on the last dose a prescription for one pill of Fluoxetine. This can be taken after the other ssri or snri has been d/c'd, and the longer t1/2 will make a smooth transition off.

    There are also cross-taper strategies and the use of non-ssri's in the use of symptom-management in discontinuation syndromes.

    In the above extreme case I was referring to, the person was titrated down over the course of a year, and was so exquisitely sensitive to the reduction of serotonin, that she required small fractions of pills crushed and taken with water for some time
     
  6. PublicHealth

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    How will pharmacogenomics inform prescribing of psychotropics?
     
  7. Anasazi23

    Anasazi23 Your Digital Ruler
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    Little blurb from the Oxford Journal of Medicine:Volume 93, Number 7 Pp. 391-423
    "Neuropsychiatry

    Psychiatrists must usually rely on complex clinical symptoms and diagnostic schemes that although highly reliable, have no obvious biological criteria. Thus, the question of whether our modern definitions of clinical syndromes (considered as phenotypes) accurately reflect underlying genetic substrates (genotypes) remains. Genetic analysis of some psychiatric disorders might be improved by the identification of basic phenotypes for which a more homogeneous aetiology might be expected. The identification of these phenotypes could be achieved by two complementary strategies: the description of the affected subjects and the identification of vulnerability traits in non-affected relatives of affected individuals. By studying the core symptoms of an illness, the clinical phenotype will be more aetiologically homogeneous. The extent to which genetic mapping is simplified by restriction of the phenotype redefinition can be assessed by measuring the recurrence risk for a relative of an affected person, divided by the risk in the general population.5

    Factors such as genetic polymorphisms, age at onset, disease severity and family history can be helpful in the identification of homogeneous subtypes. Early onset is associated with increased familial risk in schizophrenia, bipolar affective disorder, major depressive disorder and obsessive-compulsive disorder.66–68 The study of associated symptoms and co-morbid conditions has also proved helpful in the identification of subgroups. Increased familial risk can also provide a key in the identification of subgroups that have a genetic basis. In schizophrenia, a study of genetic polymorphism for drug metabolism (CYP2D6) and tardive dyskinesia suggests that heterozygous carriers of 2D6 mutated alleles may show an increased susceptibility to developing dyskinesia.69 In Alzheimer's disease, point mutations in the gene encoding the amyloid precursor protein (chromosome 21), the gene encoding presenilin 1 (chromosome 14) and the gene encoding presenilin 2 (chromosome 1) were identified only after early-onset familial cases that showed an autosomal dominant pattern of inheritance were recognized. Furthermore, subdivision according to age at onset and mode of inheritance has been particularly useful in the clarification of genetic heterogeneity in dementias of the Alzheimer type."

    More...
    "Disorders of ion channels (channelopathies) are increasingly being identified, making this a significant expanding area of neurology. Ion channel function may be controlled by changes in voltage (voltage-gated), chemical interaction (ligand-gated), or by mechanical perturbation and it has become obvious that genetic defects of both ligand- and voltage-gated ion channels can cause diverse neurological disease.72–74 A channelopathy may cause an abnormal gain of function (e.g. myokymia, myotonia, and epilepsy) or an abnormal loss of function (e.g. weakness or numbness) depending on whether change of channel function leads to excessive membrane excitability or inexcitability. The impact of these recent discoveries is that it is now understood that genetic channelopathies could affect nerves as well as muscles, and that they may also represent rare forms of more common disorders such as migraine and epilepsy.75

    The first diseases recognized as channelopathies were the voltage-gated channelopathies causing inherited muscle diseases (the non-dystrophic myotonias and familial periodic paralyses). Paramyotonia congenita is due to mutations in the gene coding for the 1 subunit of the sodium channel (SCN4A), while Thomsen's disease (autosomal dominant myotonia congenita) and Becker's disease (autosomal recessive myotonia congenita) are allelic disorders associated with mutations in a gene coding for skeletal muscle chloride channel (CLCN1). Familial hyperkalaemic periodic paralysis is due to mutations in the same sodium channel gene (SCN4A) as that affected in paramyotonia congenita, while familial hypokalaemia periodic paralysis results from mutations in the gene coding for the 1 subunit of a skeletal muscle calcium channel (CACNL1A3). DNA-based diagnosis of periodic paralyses is now decreasing the need for time-consuming and hazardous provocative testing.76 Malignant hyperthermia is now known to be a disorder of regulation of skeletal muscle calcium and that mutations in the ryanodine receptor gene (RYR1) may cause malignant hyperthermia in some families.77,78 Ryanodine receptor gene mutation analysis can now be used to identify those at risk of malignant hyperthermia in families with a known mutation in this gene.

    One of the most intriguing recent discoveries in genetic channelopathies is that mutations in the same gene (CACNL1A4) can cause three different autosomal dominant disorders such as familial hemiplegic migraine, episodic ataxia type 2 and spinocerebellar degeneration type 6.79 It is unclear how different mutations of the same gene can give rise to such different phenotypes. A CACLN1A4 mutation in a case of ‘non-hemiplegic’ migraine suggests also that such mutations may associate with commoner forms of migraine.80 The abnormalities on EEG which are noted in patients with familial hemiplegic migraine and episodic ataxia type 2 together with the recent observations of mouse models have led to the question of whether the gene CACLN1A4 is relevant to epilepsy in humans.81 In the case of myotonia congenita and familial hyperrekplexia, point mutations in the same gene can result in either autosomal recessive or dominant inheritance.

    Ligand-gated channelopathies that have recently been described include familial startle disease, which is due to mutations of the 1 subunit of the glycine receptor, and dominant nocturnal frontal lobe epilepsy, which is due to mutations of the 4 subunit of the nicotinic acetylcholine receptor.82,83 A gene for familial paroxysmal choreoathetosis has been mapped to a region of chromosome 1p where a cluster of potassium channel genes is located.84

    The benefits of recent genetic findings are an improved classification of these neurological disorders and the availability of DNA-based diagnosis. Such findings will certainly bring novel treatment interventions issued from pharmacogenomics research with the likely possibility of linking treatments to specific genotypes and modes of ion channel impairment. "
     
  8. Poety

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    "Poppa can you hear me? Poppa do you see me?" :laugh:

    and to Sazi's blurb above: They actually did a study (don't remember which one) where they took specific taste elements and found that those that could not taste the substance were at higher risk of developing schizophrenia, as schizophrenics could not taste it - also, the closer a relative with schizophrenia, they noticed less tasting ability as well.
     
  9. pschmom1

    pschmom1 Senior Member
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    Thanks sazi. I've heard a lot about cutting back very slowly and that seem to be the best way to go. I'ts hard to see my friend go through the withdrawl symptoms. She just wants a baby and it seem so hard for her. :(
     

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