Sulpiryd, Solian itp. - jak to z nimi jest ?

[lolo76]

No właśnie. Jak to jest z tymi lekami w leczeniu depresji ?

Informacje na ich temat mnie bardzo zainteresowały. Jakiś czas temu miałem
zdiagnozowaną dystymię ( przewlekłą depresję ), na którą podobno te leki
bardzo dobrze działają. Depresja u mnie objawiała się obniżonym nastrojem i
ciągłym b. silnym wyczerpaniem i zmęczeniem psychofizycznym. Ani jeden ani
drugi lekarz u którego byłem ani słowem nie wspomniał o możliwości leczenia
wspomnianymi substancjami ? Dlaczego ?

Obecnie od 4 miesięcy nie biorę leków ( wcześniej brałem przez pół roku
Seronil ) i moja sytuacja wygląda tak że obecnie cały czas nastrój jest
całkiem ok. Brak przygnębiających myśli, pesymizmu itd. typowych dla depresji.

Niestety po zaprzestaniu leczenia mimo dobrego nastroju, powróciło nieustanne
zmęczenie i wyczerpanie. Wszystko mnie męczy. Nie potrafie znaleźć w sobie
siły do pracy. Mimo niewielkiej liczby obowiązków i niewielkiej ilośći
pracy "ledwo wyrabiam". Dużo spię, budzę się zmęczony, dosypiam popołudniami.
Parę godzin pracy totalnie mnie wypruwa z i tak niewielkiej energii :( Do
pracy bardzo ciężko mi się zabrać ( ale trzeba więc się biorę ) a po pracy
jestem tak wyczerpany że nie mam już ochoty na jakakolwiek aktywność. Należy
tutaj dodać że nie jest to praca ani super intensywna ani wielogodzinna ...
wręcz przeciwnie :(

Byłem miesiąc temu u psychiatry i pani powiedziała mi że na razie nie da mi
antydepresantów. Dała na sen Hydroksyzynę i zaleciła intensywny wysiłek
fizyczny, wczesne wstawanie itd. Na pytanie o leki które pobudzają
psychofizycznie, dodają energi itd. odpowiedziała że takie "efekty" to tylko
dają właściwie narkotyki :(

I co z tym począć ???

lolo76

[mr_hyde]

lolo76 napisał:

> No właśnie. Jak to jest z tymi lekami w leczeniu depresji ?
>
> Informacje na ich temat mnie bardzo zainteresowały. Jakiś czas temu miałem
> zdiagnozowaną dystymię ( przewlekłą depresję ), na którą podobno te leki
> bardzo dobrze działają. Depresja u mnie objawiała się obniżonym nastrojem i
> ciągłym b. silnym wyczerpaniem i zmęczeniem psychofizycznym. Ani jeden ani
> drugi lekarz u którego byłem ani słowem nie wspomniał o możliwości leczenia
> wspomnianymi substancjami ? Dlaczego ?
>


Dlatego,że to leki neuroleptyczne stosowane do leczenia ciężkich psychoz i
schizofrenii.Nie licz,że one by cię pobudziły hehe raczej bardzo mocno
otępiły bo takie mają działanie.Ale może kiedyś doigrasz się schizofrenii
to wtedy będziesz je brać na pewno.

[nadja]

Ja biore Sulpiryd a nie choruje na schizofrenie.
Ale fakt - chetnie poznam opinie Pani doktor na temat tego leku,
czy rzeczywiscie jest tak silny. Nie zgodze sie z opinia,
ze oglupia, bo tak nie jest. Ma raczej pobudzac
(i tutaj bywa roznie ), ale nie oglupia.
pozdrawiam.
n.

[bradcure]

)Dlatego,że to leki neuroleptyczne stosowane do leczenia ciężkich psychoz i
)schizofrenii.Nie licz,że one by cię pobudziły hehe raczej bardzo mocno
)otępiły bo takie mają działanie.Ale może kiedyś doigrasz się schizofrenii
)to wtedy będziesz je brać na pewno.

I po co wypisujesz takie bzdury? Nie wiesz nic w temacie dysthymii to nie zabieraj glosu. Oto badania, ktore wykazaly skutecznosc amisulpridu (Solian) w depresji/dystymii:

#1

The substituted benzamides and their clinical potential on dysthymia and on the negative symptoms of schizophrenia.

Mol Psychiatry 2002;7(3):247-53
Pani L, Gessa GL.
Center for Neuropharmacology, National Research Council, Neuroscienze Scarl, via Porcell 4, 09124-I Cagliari, Italy. [e-mail]

In this paper the historical and scientific background that led to the use of substituted benzamides in two apparently unrelated clinical conditions namely dysthymic disorder and schizophrenia will be reviewed, in order to understand if a common mechanism of action may support this dual therapeutic indication. The dopaminergic antidepressant action of substituted benzamides such as sulpiride, has been proposed, since the late 1970s, by several authors and extensively explored in preclinical experiments by our group. In Italy the first marketing authorization obtained for the new substituted benzamide amisulpride, was with the sole indication of dysthymia and therefore a solid clinical experience exists in the use of substituted benzamides in mild forms of depression, with more than 1,000,000 patients being treated in the last 7 years. The proposed mechanism of action of substituted benzamides implies a selective modulation of the dopaminergic system in the mesocorticolimbic area, important for cognitive processing of internal and external cues, related to survival. The selective antagonism of dopamine D2-D3 receptors has been evoked to explain, in small to moderate doses (ie 50-100 mg day(-1)), the antidepressant effect and, in moderate to medium doses (100-400 mg day(-1)), the reported efficacy on negative symptoms of schizophrenia. Thus, substituted benzamides could represent the first class of atypical antipsychotics successfully employed for both depressive states and schizophrenia. Interestingly, recent evidence in the literature suggests that depressive episodes belonging to the bipolar spectrum are among "alternative indications" of other atypical antipsychotics such as olanzapine and risperidone

#2

The mesolimbic dopamine system as a target for rapid antidepressant action.

Willner P
Department of Psychology, University of Wales, Swansea, UK.
Int Clin Psychopharmacol, 12 Suppl 3():S7-14 1997 Jul

Chronic treatment with antidepressant drugs produces a variety of changes in dopaminergic neurotransmission, most notably a sensitization of behavioural responses to agonists acting at dopamine D2/D3 receptors within the nucleus accumbens. Evidence from animal models of depression (the forced swim test and the chronic mild stress procedure) indicates that these effects are crucial for the therapeutic effect of antidepressants in these models. Antidepressant-like effects in animal models are also seen with drugs that act directly on the dopaminergic system. Because of its prolonged time-course, the chronic mild stress procedure can be used to examine onset latencies. Some dopamine-active drugs (e.g. the catechol-O-methyltransferase inhibitor tolcapone; D2/D3 agonists administered intermittently) are active in this procedure but have a time-course comparable to that of conventional antidepressants. Other dopamine-active drugs may have a more rapid onset; the evidence to date suggests this possibility for the D2/D3 agonist pramipexole and the preferential presynaptic antagonist amisulpride. In clinical studies, rapid-onset latencies have been claimed for the D2/D3 agonist roxindole, the preferential presynaptic antagonist sulpiride and the relatively selective dopamine-uptake inhibitor amineptine. The mechanisms that might give rise to a rapid onset of dopamine-mediated antidepressant effects are discussed.

#3

Amisulpride vs amitriptyline in the medium-term treatment of dysthymia: A safety study

M. C. Jori1, C. Natale1, B. M. Cesana2 and L. Ravizza3

1 Synthélabo S.p.A.-Medical Department Milan Italy
2 Epidemiologic Unit, Hospital Maggiore, IRCCS Milan Italy
3 Neuroscience Department, University of Turin Turin Italy

European Neuropsychopharmacology, Volume 7, Supplement 2, September 1997, Page S154

A six-month, double-blind study was set up to evaluate safety and efficacy of medium-term treatment with amisulpride 50 mg/day vs amitriptyline 25-75 mg/day in patients with a diagnosis of dysthymia according to the DSM-III-R. Two hundred and fifty patients were recruited in 26 Italian Psychiatric centres, 165 allocated to amisulpride and 85 to amitriptyline (2:1 randomization).

The two groups were well balanced for age ( ? SD: 47 ? 12.6), sex (female/male ratio in both groups: 1.8) and baseline symptom severity (MADRS: 21.2 ? 2.7, HAM-A: 19.6 ? 5.9).

A total of 130 patients (93 amisulpride, 46 amitriptyline) completed the study with no statistical differences in reasons for premature termination between groups (drop-outs due to: adverse event: 14% amisulpride, 13% amitriptyline; lack of efficacy: 9.6% amisulpride, 3.5% amitriptyline; uncooperativeness: 8.4% amisulpride, 15.3% amitriptyline).

Proportion of patients with at least one treatment emergent adverse event was higher with amitriptyline (72.9%) than with amisulpride (64.2%, NS). In the amitriptyline group a statistically significantly higher incidence of CNS and autonomic nervous system disorders was observed (41.2% and 44.7%, respectively vs 23.6% and 15.8% for amisulpride).

As expected, endocrine disorders were more frequent with amisulpride (17.6% vs 7.1%) and mostly confined to females of fertile age.

Results of the symptom rating scales indicate that both drugs were equally effective: 60% and 63% of patients under amisulpride and amitriptyline, respectively, achieved a 50% reduction of the MADRS at 6 months. Mean total score of the MADRS at last assessment was 10.2 ? 8.3 for amisulpride and 10.1 ? 8.4 for amitriptyline; corresponding values for the HAM-A were 9.3 ? 7.6 and 9 ? 7.3. Comparable results were seen on the item "global improvement" of the CGI: 67% and 68.3% of patients were rated as "very much" or "much improved" for amisulpride and amitriptyline, respectively.

In conclusion, results of the present study, in a large sample, support the safe use of amisulpride in the medium-term treatment of dysthymia.

#4

A comparison of paroxetine and amisulpride in the treatment of dysthymic disorder

Paola Rocca, Valeria Fonzo, Luigi Ravizza, Giuseppe Rocca, Monica Scotta, Enrico Zanalda and Filippo Bogetto
Department of Neuroscience, Psychiatric Section & Department of Gastroenterology, University of Turin, via Cherasco 11, 10126, Torino, Italy
Journal of Affective Disorders, Volume 70, Issue 3, August 2002, Pages 313-317

Background: The purpose of this study was to provide preliminary data on the effects of paroxetine and amisulpride on depressive dimensions, analyzed by factor analysis, in dysthymic patients. Methods: One hundred and eighteen patients with DSM IV criteria for DD without concurrent major depression were enrolled in this 8-week, open study, and 100 completed it. Symptom dimensions were identified by principal components analysis with the SAS Factor procedure. Results: Results of the symptom rating scales indicated that both drugs were equally effective. Response rate was 65% both in the paroxetine and the amisulpride group and the proportions of patients achieving a final HRSD score 7 were 46.7 and 55%, respectively. MADRS factor analysis identified two factors at baseline: the first corresponding to the global severity of depression and the second to somatic

[bradcure]

#5

Faster response on amisulpride 50 mg versus sertraline 50-100 mg in patients with dysthymia or double depression: a randomized, double-blind, parallel group study.

Amore M; Jori MC
Institute of Psychiatry, University of Parma, Ugolino Hospital, Italy; Collective Name: AMISERT Investigators.
Int Clin Psychopharmacol 2001 Nov;16(6):317-24 (ISSN: 0268-1315)

Amisulpride (50 mg o.d.) was compared with sertraline (50-100 mg o.d.) for 12 weeks in a double-blind, parallel-group study in 313 outpatients with dysthymia (DSM-IV +/- episode of major depression). Full response rate [> or = 50% decrease in Hamilton Depression Rating Scale (HAMD) total score] was higher with amisulpride after 4 weeks (63% versus 50%, P < 0.02) and 8 weeks (82% versus 69%, P < 0.009). Time to initial improvement (> or = 25% decrease in HAMD total score) and to > or = 50% HAMD decrease were significantly shorter with amisulpride (P < 0.0033 and P < 0.0080, respectively). A faster response was also present in the subgroup of patients with pure dysthymia. The improvement in HAMD, Montgomery and Asberg Depression Rating Scale and Social and Occupational Assessment Scale total scores, as well as Clinical Global Impression improvement, was significantly greater with amisulpride after 4 weeks. Both drugs were equally effective at week 12. The tolerability of both drugs was satisfactory. Amisulpride is significantly more effective than sertraline during the first weeks of treatment in dysthymia.

#6

Amisulpride versus amineptine and placebo for the treatment of dysthymia.

Boyer P; Lecrubier Y; Stalla-Bourdillon A; Fleurot O
Unit´e INSERM 302, H^opital Salp^etri`ere, Paris, France.
Neuropsychobiology, 39(1):25-32 1999

Amisulpride, a selective antagonist for D2 and D3 dopamine receptors, acts preferentially on presynaptic receptors increasing dopaminergic transmission at low doses. In a multicentre, 3-month, placebo-controlled study, amisulpride (50 mg/day) was compared to amineptine (200 mg/day) in the treatment of primary dysthymia. A total of 323 patients were enrolled. Amisulpride and amineptine were found to be statistically superior to placebo (p < 0.0001) on the Clinical Global Impression (item 2): 63, 64 and 33% responders, respectively; improvement of Montgomery-Asberg Depression Rating Scale and Scale for the Assessment of Negative Symptoms scores following amisulpride or amineptine treatment was twice as high as with placebo (p < 0.0001). The adverse event profile of amisulpride was similar to that of placebo except for endocrine symptoms in female patients; amineptine showed mainly events linked to psychic activation (insomnia, nervousness). Results show that amisulpride can improve symptoms of chronic depression in dysthymia.

#7

Amisulpride versus imipramine and placebo in dysthymia and major depression.
Amisulpride Study Group. Lecrubier Y; Boyer P; Turjanski S; Rein W
Unit´e INSERM 302, H^opital Salpetri`ere, Paris, France.
J Affect Disord, 43(2):95-103 1997 Apr

Amisulpride, a selective antagonist of D2 and D3 dopamine receptors, acts preferentially on presynaptic receptors increasing dopaminergic transmission at low doses. In a multicentre, 6 months, placebo-controlled trial, amisulpride (50 mg/daily) was compared to imipramine (100 mg/daily) in the treatment of patients with DSM-III-R criteria for primary dysthymia, dysthymia with major depression or major depression in partial remission. A total of 219 patients were included. Both analyses (intention-to-treat and "per protocol' analysis) detected significant differences between groups (active treatment vs. placebo) on all main rating scales (CGI, MADRS, ERD, and SANS). The number of patients reporting at least one adverse event was higher in the imipramine group than in the two other, mainly due to anticholinergic effects. Endocrine symptoms were more frequent in female patients treated with amisulpride. These results confirm the interest of a drug acting on dopaminergic transmission such as amisulpride in the treatment of depressed patients.

[bradcure]

Jak pokazaly badania w poprzednich moich postach 50-100mg Amisulpridu (Solian) ma dzialanie anty-depresyjne poprzez bezposrednia blokade receptorow dopaminowych D2 oraz D2 -> i posrednio przez to zwiekszenia transmisji presynaptycznej. Badania pokazuja naprawde niski prog skutkow ubocznych. W celach anty-dep cena jest w normie (50-100mg to 50-100zl), natomiast wspolczuje schizofrenikom ktorzy biora 400mg = 500 zl (!) bez refundacji.
Obecnie sam stosuje z wielkim powodzeniem 50mg/dziennie i polecam kazdemu komu dolega dystymia/melancholijna depresja/atypowa depresja.

[f.qu]

Lolo76 opisany przez Ciebie problem to idealne odbicie mojego problem mam
dokładnie to samo. Chodzę to pracy na 4 godz. dziennie a i tak ciągle jestem
zmęczony i nie mogę rano wstać. Mnie psychiatra zalecił lerivon i sulpiryd.
Jestem obecnie podleczony choć nie wyleczony do końca.
Sam sulpiryd mnie aktywizuje i nie ma prawie żadnych skutków ubocznych. Na
ulotce wyraźnie pisze że ma działanie przeciwdepresyjne. Jedyny problem to to
że z czasem się człowiek przyzwyczaja do jego działanie i trzeba zwiękaszać
dawkę. I jeszcze jedno jest chyba w 100 % refundowany. :)

[novika7]

Ja zażywam Sulpiryde z powodu mojej schizofemi od 1,5 roku i czuję się całkiem
dobrze. Czasami mam tylko objawy mani prześladowczej albo rozdwojenie jaźnii.
Ogólnie jest to lek dobrze tolerowany i dość tani. Chyba kosztuje 0 zł. za
opakowanie czy coś takiego. Polecam go gorącą wszystkim schizfremikom.

Sulpiryd=do bani

[zyg_zak]

sulpiryd jest niezbyt dobrym lekiem,tyje się po nim
i często nie trzyma moczu,brałam to 1 miesiac,przytyłam 10 kg
i zmienilam leki,obecnie biorę asentrę, która jest b. dobrym lekiem

[nadja]

Nie zgodze sie. Ja przytylam ok20kg po innych lekarz
(nie wiem po ktorych, bo mialam czesto zmieniane i w rezultacie
nie mam pojecia...) a juz na pewno nie pomogla mi zupelnie
asentra. Sulpiryd natomiast sprawil, ze czuje sie choc troszke
lepiej. I nie tyje.
pozdrowienia
n.