# completely dysfunctional and troubled



## York (Feb 26, 2008)

My anxiety gets worse and worse. I thought for a while I was getting better, but the last two weeks have been absolute Hell.
I'm really starting to wonder if this is DP, or if I am about to develop DID or schizophrenia. Not to forget my fear of becoming psychotic, which sends me into one panic-attack after another. I can't seem to recognize anything around me. I can't take it!
The doctors I've spoken to does nothing besides lowering my benzo-dose, and I get more and more wrapped up in my own head as a result. Is this really anxiety? I just don't believe it. I have not one moment during the day where I feel even close to normal, I only feel slightly less insane if I take 3 benzo's and curl up in a ball in my bed. Does anyone have any words of encouragement? Anyone recovered from feeling like this???


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## DownTheRabbitHole (May 30, 2009)

only speaking from my own experience, i would advise not to take any meds etc.

as i have no idea what they can do to you, i feel we all must face our problems ourselves, and we will have a better chance of getting thorugh them.

if its a chemical imbalance that causes DP, then fair enough, meds may help if they are changing that.

gtg il post the rest later, friends waiting on me outside!

x


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## Surfingisfun001 (Sep 25, 2007)

NumbNeo said:


> only speaking from my own experience, i would advise not to take any meds etc.


People who have suffered long term and have been using medications long term cannot just decide to "not take their meds" without facing horrible experiences.


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## Conjurus (Oct 25, 2008)

surfingisfun001 said:


> NumbNeo said:
> 
> 
> > only speaking from my own experience, i would advise not to take any meds etc.
> ...


I agree with what my surfing friend has said. From my own experience I'd also like to add that even if you've only been on medications for a short time, you could still have horrible experiences.


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## Surfingisfun001 (Sep 25, 2007)

Conjurus said:


> I agree with what my surfing friend has said. From my own experience I'd also like to add that even if you've only been on medications for a short time, you could still have horrible experiences.


I'd also like to add I agree with what my Conjuras friend has said.


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## Guest (May 30, 2009)

Hang in there Anny, Im in the same boat, if it werent for my benzos, I think I would never leave my bed. Although I can barely function with them. We prolly feel the exact same way, maybe you could try this like me. Im gonna do it.

Report this postReply with quoteNaloxone for depersonalization study - a success!!!
by Deja_vu_256 on Thu May 07, 2009 9:17 pm

Effect of naloxone therapy on depersonalization: a pilot study

Yuri L. Nuller, Marina G. Morozova, Olga N. Kushnir and Nikita Hamper
Bekhterev Psychoneurological Research Institute. St-Petersburg, Russia.

To test the hypothesis of the role for the opioid system in the pathogenesis of depersonalization, the effect of
naloxone (an opioid receptor blocker) on the symptoms and corticosteroids secretion was studied in
patients with depersonalization syndrome. Fourteen depersonalization patients were treated with
naloxone: 11 patients received single doses (1.6 or 4 mg i.v.) and three others received multiple infusions,
with the maximal dosage being 10 mg, and the effect of naloxone on symptom severity was determined. In
eight patients, the cortisol, cortisone and corticosterone content in the blood plasma was determined prior
to and after the 4 mg naloxone infusion. A reversed-phase microcolumn high-performance liquid
chromatography with ultraviolet detection was applied for assessment of glucocorticoids. In three of 14
patients, depersonalization symptoms disappeared entirely and seven patients showed a marked
improvement. The therapeutic effect of naloxone provides evidence for the role of the endogenous opioid
system in the pathogenesis of depersonalization.
Key words: depersonalization; glucocorticoids; naloxone

Introduction
Depersonalization is a change of self-awareness such that the
person feels unreal. It is characterized by the loss of emotional
perception or a blunted feeling of one?s own body and its functions,
etc. Patients with this condition find it difficult to describe, often
speaking of being detached from their own experience and unable
to feel emotion. A similar change in relation to the environment is
called derealization. Depersonalization can manifest itself as a
symptom in the structure of various psychopathological syndromes
or as an independent syndrome. In the latter case, where the
depersonalization syndrome is unrelated to any other mental
disease, it is defined as a depersonalization disorder (Nuller, 1982;
American Psychiatry Association, 1994).
Depersonalization syndrome often has a long, lingering course
which is resistant to therapy (Shader, 1994). Antidepressants,
neuroleptics and electroconvulsive therapy usually fail to produce
any therapeutic action. Only very large doses of benzodiazepines
produce a therapeutic effect in some patients (Nuller, 1982; Gelder
et al., 1989). In cases where depersonalization lasts for months and
years, no psychotropic therapy has documented efficacy. When
depersonalization is a part of another mental disorder, it is most
often a major depression. In such cases, depression can become
resistant to therapy and have a lingering course.
An effective medical treatment of depersonalization is impaired
by the lack of data on the biochemical mechanisms of this disorder.
Depersonalization usually develops as a reaction to severe
emotional stress, or can emerge from acute anxiety and tension in
various mental illnesses. The fact that anxiety is involved in its
genesis is confirmed by the therapeutic efficacy of large doses of
anxiolytics in the acute depersonalization syndrome (Nuller, 1982;
Nuller and Mickalenko, 1988). Stress can be accompanied by
secretion of endogeneous opioids, mostly beta-endorphins. This
helps to explain the hypoalgesia or total analgesia found in
depersonalization (Nuller and Mikhalenko, 1988; Moroz et al.,
1990; Abugova, 1996) as well as a less pronounced pupil reaction
to morphine (Nuller and Mikhalenko, 1988). These observations
led us to suggest that disturbance in the opioid system such as the
increased endorphin secretion and/or a change in the sensitivity of
opioid receptors play an important role in the pathogenesis of
depersonalization. To verify this hypothesis, we investigated the
effect of naloxone ? an opioid receptor blocker. Stress is also
characterized by changes in secretion of corticoids. Therefore it
was of interest to determine the levels of corticoids under
depersonalization.

Methods
Subjects

Fourteen patients (nine females and five males, mean age 32 years)
were assigned to treatment with naloxone. In six patients,
depersonalization was the only manifestation of a mental illness
and they met the DSM-IV criteria for depersonalization disorder.
Eight patients had mixed depersonalization and depressive
symptoms with dominating depersonalization syndrome. In three
patients, the duration of the disease was less than 1 year, in seven
patients, it ranged from 1?5 years; in two patients, from 5?10 years
and in two patients, 14 and 16 years.
The control group for plasma corticosteroids included 36 healthy 
volunteers whose age ranged from 25?45 years and whose
corticosteroid level in the blood plasma was determined twice for
two subsequent days.

Naloxone administration

Naloxone (Polfa) was injected i.v. at 12 in the afternoon in a
single-blind placebo controlled design, with placebo always first.
The patients had one dose of naloxone, which was followed by
further doses if they did not respond. Eleven patients had one
infusion, the doses were 4 mg in nine patients and 1.6 mg in two
patients. Three patients had multiple naloxone infusion: in one
case, 2 mg infusions within 3 days (6 mg total) and, in two other
cases, multiple infusions with doses increasing from 2 mg to 10 mg
every 2 or 3 weeks (50 mg total). The maximal number of
infusions administered was 10. Between the naloxone infusions,
these two patients received tranquilizers (lorazepam, 6 mg per day;
phenazepam, 8 mg per day; hydroxyzine, 200 mg per day) and
antidepressants (paroxetine, 60 mg per day; mianserine, 90 mg per
day).

Biochemical methods

The cortisol, cortisone and corticosterone content in the blood
plasma was determined in eight patients prior to and after the
naloxone infusions. Blood was taken from a catheter inserted into
the ulnar vein, and kept open with heparin. The first sample was
taken at 11.00 h immediately after the catheter was inserted; the
second at 11.30 h, after 10 ml of physiological solution (placebo)
was infused iv.; the third at 12.00 h, then the infusion of 0.4 mg of
naloxone (1 ml of naloxone solution and 9 ml of the physiological
solution) was made; the fourth at 12.15 h before the 4 mg naloxone
infusion (10 ml of the solution) and the fifth at 12.30 h.
For measurement of glucocorticoids, a reversed-phase microcolumn
HPLC with ultraviolet (UV) detection was applied. A
150 ? 1 mm column filled with Separon SGX C18 5? and linear
gradient elution (70 : 30 to 35 : 65 water-acetonitrile for 30 min)
was used. The technique allowed a good baseline separation of
aldosterone, cortisol, cortisone and corticosterone (Gamper et al.,
1996). The detection limit (UV detection at 254 nm) was
approximately 5 ng/ml. Serum protein electrophoresis was used to
extract the substances of interest from the serum.

Results

Efficacy was assessed using the depersonalization scale (Nuller
and Mikhalenko, 1988) and subjective response. The depersonalization
scale was administered before the naloxone infusion and
after 4 h (peak effect). In three of 14 patients, depersonalization
symptoms disappeared entirely. Seven patients showed a marked
improvement: with symptoms reduced by more than 50% on the
depersonalization scale. One patient showed moderate improvement
and, in two patients, the improvement was short and
insignificant, one patient showed no positive effect.
Thus, 10 of 14 patients showed a considerable therapeutic
effect, which is undoubtedly a success considering the therapeutic
resistance of the depersonalization syndrome. In addition, the
subsequent benzodiazepine therapy (lorazepam, 6 mg per day;
phenazepam, 8 mg per day; hydroxyzine, 200 mg per day within
4 weeks) resulted in a fast and complete reduction of depersonalization
in three patients (two demonstrated considerable and one
moderate improvement), although, in two of these patients, the
same drugs were not effective prior to the naloxone therapy.
After reduction of depersonalization, four patients showed no
evidence of any mental disorder except for the personality traits
they had had in the premorbid period; five patients continued to
express the symptoms of major depressive disorder, which was less
severe than before the depersonalization had manifested itself and
responded quickly to the antidepressants; one patient was found to
be deluded with intense anxiety. This condition showed a good
response to antipsychotic therapy.
In most cases, the first signs of improvement were recorded
soon after the naloxone infusions (within 20?40 min) and the
patients? perception of the world was marked by greater brightness.
A complete reduction or disappearance of depersonalization
occurred within the interval of 1?4 h and, in some patients, continued
for as long as 12?24 h. This was followed by some
deterioration, although the depersonalization never recurred to the
initial level. Five patients showed evidence of a stable improvement.
Two patients had considerable but not total reduction of depersonalization
due to the naloxone therapy. Immediately thereafter,
they received long-term benzodiazepine treatment. The impression
was that benzodiazepines stabilize the improvement that was
reached as a result of the naloxone therapy.
No side-effects were recorded when naloxone was
administered.
Table 1 presents the corticosteroid data. The depersonalization
patients have a very low initial cortisol level compared to the
control. The cortisone level also decreased, but to a smaller degree,
whereas the corticosterone content appeared to be slightly higher.
Upon 4 mg naloxone infusion, the cortisol content was found to
reliably increase compared to its post-placebo level. With respect
to cortisone, it increased but not as drastically and the corticosterone
content remained unchanged.

Table 1 Plasma corticosteroids concentration (ng/ml) in normal controls and depersonalization patients
Cortisol Cortisone Corticosterone
Control group (n = 36)
After catheter insertion 30.5 ? 2.65 22.48 ? 3.24 9.61 ? 1.69
Depersonalization group (n = 
After catheter insertion 13.98 ? 0.95*** 16.77 ? 2.54 13.90 ? 2.66
30 min after catheter insertion 11.91 ? 1.36 14.45 ? 2.63 10.45 ? 2.01
15 min after placebo infusion 10.21 ? 1.09 13.84 ? 2.22 9.16 ? 1.10
15 min after naloxone infusion (0.4 mg) 11.53 ? 2.55 15.90 ? 2.56 7.97 ? 1.20
15 min after naloxone infusion (4 mg) 18.64 ? 3.35 20.33 ? 3.17 9.93 ? 2.01

Discussion
Previous attempts to use naloxone for treating mental disorders
proved to be unsuccessful (Abrams et al., 1978; Volavka et al.,
1982; Keuler et al., 1996) and an insignificant positive effect of
short duration was recorded only in case of mania (Janowsky et al.,
1983). The opioid system seems to play an insignificant role in the
pathogenesis of the endogeneous depression (Banki and Araio,
1987). As mentioned above, we used indirect data which suggested
the importance of the opioid system in the pathogeneses of
depersonalization, i.e. some depersonalization symptoms resemble
the effect of morphine and depersonalization arises as a reaction to
an acute emotional stress, which causes endorphin secretion.
The positive therapeutic effect of the opioid receptor blocker,
naloxone, offers some evidence for the implication of the opioid
system in the pathogenesis of depersonalization. This role is also
confirmed by the influence of naloxone on the cortisol secretion in
depersonalization patients: the low level of cortisol in depersonalization
patients could be explained by the fact that endogeneous
opioids inhibit CRF secretion. By blocking the action of
endorphins, naloxone increases the cortisol secretion (Delitala
et al., 1994). The depersonalization patients were found to have
a much lower cortisol content in plasma, which was drastically
increased by naloxone. The increase of cortisol level coincided
in time with the therapeutic effect of naloxone. There was a
reduction of depersonalization symptoms without any signs of
anxiety.
Our data do not provide sufficient evidence to conclude whether
the therapeutic effect of naloxone is only related to the blockade of
the opioid receptors or to some other factors that affect the opioid
system. In most patients, the positive action of naloxone developed
during the first hours after the infusion and, in many, the
improvement lasted more than 24 h. Because the half-life of
naloxone is approximately 60 min, this suggests that naloxone
increased the patients? therapeutic sensitivity to the drugs that were
previously not very effective for these particular patients.
One naloxone infusion was sufficient to entirely eliminate or
considerably reduce all the symptoms of depersonalization in four
patients who had a relatively recent depersonalization syndrome.
However, some symptoms recorded prior to depersonalization
reappeared and were easily treated by conventional medicine. Our
previous data on the positive effect of large doses of benzodiazepines
on depersonalization (Nuller, 1982) are evidence for the
close relationship between depersonalization and anxiety. In most
cases of chronic depersonalization, syndrome reduction was not
accompanied by manifestation of affective symptoms. Here,
depersonalization seems to be unrelated to anxiety and might
become autonomous. The change of sensitivity in opioid receptors
may be important in cases of chronic depersonalization.
In conclusion, some clinical manifestations of depersonalization,
such as analgesia, the suppression of corticosteroid
secretion and especially the positive therapeutic effect of the opioid
receptor blocker, naloxone, offer evidence for the implication of
the opioid system in the pathogenesis of depersonalization.

Address for correspondence
Professor Yuri L. Nuller
The Psychopharmacological Department
Bekhterev Psychoneurological Research Institute
3 Bekhterev St
St-Petersburg 193019
Russia
Email: [email protected]
References
Abrams A, Braff D, Janowsky D S, Holl S, Segal D S (1978)
Unresponsiveness of catatonic symptoms to naloxone.
Pharmakopsychiatry 11: 177?179
Abugova M A (1996) Indices of pain threshold as a method of
objective assessment of depersonalization therapy efficacy.
Bekhterev Rev Psychiatry Med Psychol 4: 120?122
American Psychiatric Association (1994) DSM-lV: diagnostic and
statistical manual of mental disorders, 4th edn. American
Psychiatric Association, Washington DC
Banki C V, Araio M (1987) Multiple hormonal responses to
morphine: relationship to diagnosis and dexamethasone
supression. Psychoendocrinology 12: 3?11
Delitala G, Trainer P S, Oliva O, Fanciully G, Grossman A B (1994)
Opioid peptide and alpha-adrenoreceptor pathways in the
regulation of the pituitary?adrenal axis in man. Endocrinology
141: 163?168
Gamper N L, Velicanova L I, Korolyova N M (1996) Determination
of six corticosteroids in human serum by reversed phase
microcolumn HPLC. Proceedings of the 18th International
Symposium on capillary chromatography V111, pp. 1655?1663
Gelder M, Gath D, Mayou R (1989) Oxford textbook of psychiatry,
2nd edn. Oxford University Press, Oxford
Janowsky D S, Judd L L, Huey L Y, Rish S C, Segal D S (1983)
Behavioral effects of opioid receptor antagonists in
psychopathological states. Psychiatry Clin North Am 6: 403?414
Keuler D J, Altemus M, Michelson D, Greenberg B, Murphy D L
(1996) Behavioral effects of naloxone infusion in
obsessive?compulsive disorder. Biol Psychiatry 40: 154?156
Moroz B T, Nuller Y L, Ustimova I N, Andreev B V (1990) Study of
pain sensitivity based on the indicators of electroodontometry
in patients with depersonalization and depressive disorders.
Zhurnal Nevropatologii Psichiatrii 90: 81?82
Nuller Y L (1982) Depersonalisazion ? symptoms, meaning, therapy.
Acta Psychiatr Scand 66: 451?458
Nuller Y L, Mickalenko I N (1988) Affective psychoses. Meditsina,
Leningrad
Shader R I (1994) Manuel of psychiatric therapeutics, 2nd edn.
Little, Brown and Company, Boston
Volavka J, Anderson B, Koz G (1982) Naloxone and naltrexone in
mental illness and tardive dyskinesia. Ann NY Acad Sci 97?102Deja_vu_256 
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Posts: 21
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## York (Feb 26, 2008)

Problem is, I live in Norway, where they'll give you a band-aid if you've shot your head off, just in case you'd enjoy it too much if they stitched it back on.


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## Guest (May 30, 2009)

york said:


> Problem is, I live in Norway, where they'll give you a band-aid if you've shot your head off, just in case you'd enjoy it too much if they stitched it back on.


Damn :evil:


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## Guest (May 30, 2009)

If they keep lowering your benzos its no wonder you feel worse and you will until they stop adjusthng them BUT it will get easier. I can really only reasure you that you aren't going crazy. I never had any normal moments when I had Dpd and was convinced it was something worse and not what everyone else had. Remember Dp makes you feel and think alotta things but thoughts and feelings won't kill us, remember logic, you know Dpd is a liar. Hope you feel better soon.


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## Guest (May 30, 2009)

Spirit said:


> If they keep lowering your benzos its no wonder you feel worse and you will until they stop adjusthng them BUT it will get easier. I can really only reasure you that you aren't going crazy. I never had any normal moments when I had Dpd and was convinced it was something worse and not what everyone else had. Remember Dp makes you feel and think alotta things but thoughts and feelings won't kill us, remember logic, you know Dpd is a liar. Hope you feel better soon.


EXACTLY!!!!! Anny believe that. :wink:


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## Garjon (Apr 4, 2009)

i just wanted to tell you (if it helps at all) that what you originally wrote is exactly what i am thinking/feeling/experiencing right now. I have convinced myself that even the people on this forum are suffering from something different than i am. so in a way its scary, and in another way it's good to know that at least someone else feels like they might have something else which means that we probably have what everyone else here has and nothing more. Probably just overanalyzing and thinking our way into a pit of despair. If i can find a ladder big enough i'll climb out and help you get back up too. let's both hang in there!


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## Guest (May 31, 2009)

Get on a opiod receptor blocker. I plan to very soon because I had a natural birth and am taking placenta pills and I still have DP very bad. I thought that would have been my "cure" but it wasn't but it did open my mind more ina better direction. So yeah that is my last resort to start to feel better. I hear you about the anxiety stuff! I'm post-partum by 4 weeks now and I feel like I have post partum depression but I still take good care of myself and baby but I'm extremely depressed. I'm going to a hollistic health place to get treatments soon including hypnosis and Eye Movement Dessensitization & Reprocessing therapy. I'm done with mainstream psychiatry it has nothing to offer me but a prison paradigm of treatments and options.

You will feel better don't hope it just know it!


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## Guest (May 31, 2009)

MassagePatriot said:


> Get on a opiod receptor blocker. I plan to very soon because I had a natural birth and am taking placenta pills and I still have DP very bad. I thought that would have been my "cure" but it wasn't but it did open my mind more ina better direction. So yeah that is my last resort to start to feel better. I hear you about the anxiety stuff! I'm post-partum by 4 weeks now and I feel like I have post partum depression but I still take good care of myself and baby but I'm extremely depressed. I'm going to a hollistic health place to get treatments soon including hypnosis and Eye Movement Dessensitization & Reprocessing therapy. I'm done with mainstream psychiatry it has nothing to offer me but a prison paradigm of treatments and options.
> 
> You will feel better don't hope it just know it!


YEP What she said, im doing the naloxone thing too. YYYYAAAAAAAAYYYYYYYY


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## Surfingisfun001 (Sep 25, 2007)

We should have a webcam party of us all shooting up naloxone. It's pretty pathetic that people have discovered how to build and fly rockets to the moon yet people who suffer from DP are resorting to posing as drug addicts to obtain naloxone to experiment with due to the failure rate of available treatments.



MassagePatriot said:


> I'm done with mainstream psychiatry it has nothing to offer me but a prison paradigm of treatments and options.


Good quote.


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## Surfingisfun001 (Sep 25, 2007)

double post


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## peachy (Feb 9, 2008)

surfingisfun001 said:


> We should have a webcam party of us all shooting up naloxone. It's pretty pathetic that people have discovered how to build and fly rockets to the moon yet people who suffer from DP are resorting to posing as drug addicts to obtain naloxone to experiment with due to the failure rate of available treatments.


for real. 
well said


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## Guest (Jun 1, 2009)

peachyderanged said:


> surfingisfun001 said:
> 
> 
> > We should have a webcam party of us all shooting up naloxone. It's pretty pathetic that people have discovered how to build and fly rockets to the moon yet people who suffer from DP are resorting to posing as drug addicts to obtain naloxone to experiment with due to the failure rate of available treatments.
> ...


agreed completley


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