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Nicergoline is an ergoloid mesylate derivative that is currently being used in the battle to treat senile dementia. Interestingly it has been found to improve mental agility through enhancing clarity and perception.

In this instance it is different to the effects of Hydergine - (which improves oxygen stability, increases mental ability - i.e. it extends the period of useful mental workload, and has been designated as an I.Q. booster with its brain dendrite stimulation).

Nicergoline on the other hand appears to enhance clarity, perception and clear thought.

Dosages for the treatment of senile dementia have been as high as 30mg to 60mg daily, however treatment and protection from ARMD would normally indicate 5mg once, twice or three times daily. Like nearly all nootropics, nicergoline has been shown in clinical trials to be safe when used respectfully.

Side effects include nausea and headache, and is normally an indication of over-dosage or over-stimulation through synergistic combinations. If utilizing nicergoline with other nootropics, always reduce the individual doses and only increase to larger doses over several days. Furthermore as with all nootropic products occasional breaks are recommended (i.e. 1-week per month or 2-days per week).

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Nicergoline (Sermion®)

Tablets: Each tablet contains 5 mg Nicergoline (I.N.N.). Excipients: Sucrose, calcium phosphate, sodium carboxymethyl cellulose, micro-crystalline cellulose, magnesium stearate, gum arabic, titanium dioxide, magnesium carbonate, flora wax, talc and Pal Super orange.
Drops: Each ml (20 drops) of prepared solution contains: 5 mg Nicergoline (I.N.N.), lactose, tartaric acid, methyparaben and water.


Sermion (nicergoline) is a vasoactive pharmaceutical product, synthesized in Farmitalia research laboratories, with alpha-adrenolytic action to activate the brain's metabolism. Sermion (nicergoline) acts on different levels:

On the cerebral level, it prompts a lowering of vascular resistance, an increase in arterial flow and the use of oxygen and glucose. In terms of lung circulation, it lowers vascular resistance. With regard to limb circulation, it brings about an increase in the flow, particularly evident in those patients with insufficient irrigation due to functional arteriopathies.

Studies carried out in vitro and in vivo, both experimental and on human beings, have shown that Sermion (nicergoline) inhibits platelet aggregation. Sermion (nicergoline) has proved to be effective in hospital use, regulating and improving brain disorders caused by metabolic-vascular insufficiency and alterations derived from insufficient arterial irrigation in the limbs. When the therapeutic dosage is administered, Sermion (nicergoline) does not affect arterial tension. In the case of patients suffering from hypertension, it may induce a gradual lowering of tension.

This pharmaceutical product does not induce vomiting.


Acute and chronic cerebral metabolic-vascular disorders (cerebral arteriosclerosis, thrombosis and cerebral embolism, transitory cerebral ischaemia). Acute and chronic peripheral metabolic-vascular disorders (organic and functional arteriopathies of the limbs), Raynaud's disease and other syndromes caused by altered peripheral irrigation.

Migraines of vascular origin

Coadjutant therapy in clinical situations accompanied by platelet hyper-aggregability, arterial tension

Corio-retinal vascular disorders: retinal thromboses, diabetic retinopathy, macular degeneration and retinal angiosclerosis Oto-vestibular problems of a vascular nature: dizziness, auditory hallucinations, hypoacusis.


By mouth: 5-10 mg (1-2 tablets or 20-40 drops) 3 times daily at regular intervals over prolonged periods of time. To facilitate absorption, take this medicine between meals.

The dosage and length of treatment are to be decided by your doctor. At times, the therapeutic effects of Sermion (nicergoline), both subjective and objective, are not immediately noticeable, but will be noted after a certain period of treatment.

Directions For Using Drops

Pour the powder into the vial containing the solvent and shake until completely dissolved.

To measure out Sermion (nicergoline) in drops, use the accompanying syringe, sucking in the amount of liquid required for each dose.


None known.


Although toxicology studies have not shown nicergoline to have any teratogenic effect, the use of this medicine during pregnancy should be limited to those cases where it is absolutely necessary.


None known.


The vasoactivity of Sermion (nicergoline) may heighten the effect of pharmaceutical products that produce hypotension.

Adverse Effects

Although very infrequently, rubeosis, a hot feeling, mild gastric upsets, hypotension and dizziness have been observed. Should you notice any adverse reaction not described, consult your doctor or chemist.

Intoxication And Treatment

The chances of intoxication as a result of taking this product are very remote. Only in certain cases of overdose can the symptoms described under “Adverse Effects” appear. These subside if one stops taking the product.

In cases of overdose or accidental ingestion, consult the Toxicology Information Service.

Available In:

Tablets: 45-tablet container. Drops: Container with 1 vial of powder and 1 bottle of solvent.

Expiry Date

This medicine must not be used after the expiry date printed on the container.

Reconstituted Solution

Drops: Once prepared, the solution is good for 30 days at room temperature.

Keep this and all other medicines safely out of the reach of children.



Saletu B,

Pharmacia & Upjohn


In a double-blind, placebo-controlled study on the therapeutic efficacy and central effects of nicergoline, an ergot alkaloid with metabolic, antithrombotic and vasoactive action, 112 patients with mild to moderate dementia, diagnosed according to DSM III-R criteria (MMS 13-25), living in pensioners' homes, were included. Fifty-six were subdiagnosed as senile dementia of the Alzheimer type (SDAT), 56 as multi-infarct dementia (MID), based on computed tomography and Hachinski scores ( < 49 SDAT, > 7 MID). They received, after 2 weeks' run-in period (placebo), randomized for 8 weeks either 2 x 30 mg nicergoline (NIC) or 2 x 1 placebo (PLAC) orally. The four subgroups (SDAT/NIC, SDAT/PLAC, MID/NIC, MID/PLAC; 4x28 patients) were comparable in regard to age and sex. Only four, four, four and two patients of the respective groups did not finish the study for minor reasons. Confirmatory sta alpha 2 and beta activity and an acceleration of the centriod of the total power spectrum as compared with pretreatment, while opposite changes occurred in PLAC-treated SDAT and MID patients. The differences between PLAC and NIC reached the level of statistical significance. Event-related potential (ERP) recordings demonstrated a significantly shortened P300 latency under NIC treatment in both SDAT and MID patients, while there was a trend towards lengthening under PLAC. Thus, nicergoline improved vigilance and information processing at the neurophysiological level, which leads at the behavioural level to clinical improvement both in degenerative and vascular dementia.


In earlier studies involving clinical and quantitative electroencephalographic (EEG) investigations in dementia patients, we could demonstrate that both senile dementia of the Alzheimer type (SDAT) and multi-infarct dementia (MID) patients demonstrated increased delta/theta and decreased alpha and beta activity, as well as slowing of the dominant frequency and the centroid of the total power spectrum, as compared with normally ageing controls (Saletu et al. 1988, 1991a, 1992; Saletu 1994). These alterations in brain function, evaluated initially by exploratory, and later by confirmatory stastistics, reflected a deterioration in vigilance, as defined first by Head in 1923 as the availability and grade of organization of man's adaptive behaviour, which is dependent upon the dynamic state of the neuronal network. This vigilance decrement results noopsychically in deterioration of intellectual performance and memory, and thymopsychically in decreased drive and affect, which constitute the axial syndrome of dementia, as described in several psychiatric classification systems (Berner 1977; American Psychiatric Association 1987). Indeed, utilizing correlation maps, we could demonstrate that EEG slowing is correlated both to radiological and to psychopathological and psychometric data: the more pronounced the atrophy in computed tomography, the more delta and theta was evident at the neurophysiological level, which in turn was correlated to higher SCAG and lower Mini-Mental State scores at the clinical level, and to a poorer psychometric performance, seen in several tests such as the Digit-Symbol Substitution Test, the Trial-Making Test and the Digit Span Test (Saletu et al. 1991a, b).

With regard to therapeutic efficacy in dementia of the Alzheimer type and vascular dementia, several double-blind studies have been carried out, partly with placebo, partly with active reference substances. However, as some of these early studies have methodological shortcomings in our present scientific methodological understanding, the present study was carried out with a prospective allocation to a degenerative (SDAT) and vascular aetiology (MID), and subsequent randomization of these dementia sub-groups to placebo or verum. The aim of this double-blind, placebo-controlled, parallel-group design study was to assess efficacy, safety and neurophysiological effects of 30 mg nicergoline b.i.d. in mild to moderate dementia of the Alzheimer type (SDAT) and multi-infarct dementia type (MID), utilizing psychometric, computed tomography, EEG and ERP mapping technique.


Of the 112 demented patients included in the study, only 14 dropped out prematurely. In the SDAT/NIC sub-group (n=28) four patients dropped out after week 2 (two patients because they found the study too troublesome. One because she required an antidepressant and one because the moved to live with her daughter in another city). In the SDAT/PLAC sub-group (n=28) four patients left the study in the wash-out period (one because of a venous thrombosis in her legs, two because they found the investigations too troublesome and one because she rejected the idea of taking more pills). IN the MID/NIC sub-group (n=28) four patients with drew from the study (two in the wash-out period, one in week 2 and one in week 4 because they found the study too troublesome). In the MID/PLAC sub-group (n=28), two patients withdrew in the wash-out period because they found it too tiresome to participate.

If one calculates the percentage of responders and non-responders in all four sub-groups, 66.6 per cent of nicergoline-treated SDAT patients showed improvement and 33.3 per cent a non-response, while the placebo-treated SDAT patients exhibited just the opposite findings. Similarly, 70.83 per cent of the nicergoline-treated MID patients were responders, 29.17 per cent non-responders, while of the placebo-treated MID patients 73.08 per cent were non-responders and 26.92 per cent responders. The differences between the groups were significant.


EEG maps -- multi-variate analysis

In order to obtain an answer to the question of whether or not the investigational drug exerted a significant effect on the human brain as compared with placebo, MANOVAs were performed (for each of the 21 electrodes) considering drugs (nicergoline, placebo), times (weeks 0 and 8) and variates (nine absolute power and nine frequency measures). Absolute power values were transformed in In(power) to fulfil the conditions for the MANOVA (homogeneity of variances and co-variances), as well as the symmetrical unimodal distribution (Gasser et al. 1982). Hotelling's T2 values were used to avoid type 1 errors, with inflated df, and were imaged in terms of brain maps (Fig.1). As can be seen, nicergoline induced, as compared with placebo, significant changes in brain function in both SDAT and MID patients.


In the placebo-treated SDAT patients, absolute power increased in the delta/theta and slow alpha, as well as in the superimposed beta frequency range, while opposite changes as well as a decrease of alpha-2 activity occurred in the nicergoline-treated patients (P<0.05, t-test). Thus, inter-drug differences revealed a significant attenuation of delta/theta, alpha-1, but also alpha-2 and beta power, after nicergoline as compared with placebo (P<0.05 t-test).

Relative power increased in the delta/theta and alpha-1 frequency bands of placebo-treated SDAT patients, along with a decrease of alpha-2 and beta activity, while nicergoline-treated patients showed exactly the opposite (P<0.05) (Fig.2). Thus, nicergoline induced, as compared with placebo, an attenuation of delta/theta and slow alpha and an augmentation of alpha-2 and beta activity (P<0.05) (Fig.2). These alterations, reflecting an improvement in vigilance, were most pronounced over the right temporal to frontotemporal and left parietal and temporo-occipital regions.

The centroids became faster in the delta/theta and slower in the alpha, beta and total frequency bands after 8 weeks' placebo in SDAT patients, while an alpha acceleration and acceleration of the total centroid occurred after nicergoline treatment (P<0.05-0.01). Thus, inter-drug differences were characterised by an acceleration of the alpha, beta and total centroid after nicergoline, as compared with placebo, while the delta/theta centroid slowed down (P<0.05).

In MID patients, a decrease in absolute power occurred in the beta band after placebo (P<0.05), while a trend towards an attenuation of delta/theta power was observed after nicergoline. There were no significant inter-drug differences.

Relative power showed an increase in the alpha-1 and decrease in the beta range after placebo administration, while after nicergoline delta/theta attenuation and alpha-1 and -2 augmentation occurred (P<0.05) (Fig.3). Inter-drug differences were characterized by an attenuation of delta/theta power and augmentation of alpha-2 and beta power (P<0.05), thereby signalling an improvement of vigilance (Fig.3).

The centroids showed a slowing in the alpha, beta and total frequency range after placebo (P<0.05), while an opposite trend occurred after nicergoline. Thus, nicergoline induced, as compared with placebo, an acceleration of the alpha centroid and total centroid, while in regard to the beta centroid there was an acceleration over the left parietal and occipito-temporal region and a slowing over the right fronto-temporal region (P<0.05).


While in both SDAT and MID patients nicergoline induced a significant (P<0.05, t-test) shortening of latency of the P300, a trend towards lengthening occurred after 8 weeks of placebo treatment. Differences between verum and placebo were significant (P<0.05) in both sub-types of dementia. Thus, the significantly shortened latency in both sub-types of dementia suggests an improved cognitive information processing under nicergoline.


This double-blind, placebo-controlled study demonstrated that nicergoline improved the clinical symptomatology of both SDAT and MID patients, as compared with placebo. The superior therapeutic efficacy of nicergoline after 8 weeks of treatment with 30 mg b.i.d. over placebo was clearly demonstrated in the confirmatory statistical analysis for the target variable, the clinical global impression, with the clinical relevance of this outcome underlined by the results of the descriptive statistics in the other investigated variables, further by the responder analysis, as well as by the neurophysiological findings underlying the psychopathological changes.

The Clinical Global Impression (CGI) changes were, of course, of small magnitude, with the patients remaining still moderately ill, as far as the severity of illness was concerned. However, item 2 of the CGI showed, on average, a slight improvement in the nicergoline-treated SDAT and MID patients, while there was no change on average after placebo. Moreover, the responder analysis demonstrated that 66.6 per cent of SDAT patients treated with nicergoline improved, while 33.3 per cent did not improve, with just the opposite findings under placebo administration (33.3 per cent improving; 66.6 per cent not improving). Very similarly, with nicergoline treatment of MID patients, 71 per cent improved, 29 per cent did not, while under placebo administration 27 per cent improved and 73 per cent did not. Other nootropic durgs have also been reported to exert similar therapeutic effects in MID and SDAT patients (Saletu et al. 1988, 1992; Fischhof et al. 1989, 1992).

Nicergoline was very well tolerated, as mild side-effects, such as itching, blocked nose, headaches, tachycardia, sweating, insomnia, dry mouth, diarrhoea, constipation and weight loss were mostly observed only in single patients. Oveerall, they were of transient nature and did not warrant any treatment. This low incidence (19 per cent in the nicergoline-treated patients versus 15 per cent in the placebo-treated ones) is in agreement with open-field studies, which also showed a decrease in frequency in virtually all categories of complaints with time (13 per cent in week 4 versus 4.3 per cent in week 24) (Saletu 1991).

Finally, in the light of the significant nicergoline induced improvement observed in the Mini-Mental State in regard to cognition, it seems of interest that the cognitive evoked potential -- the P300 -- showed a significantly shortened latency in nicergoline-treated SDAT and MID patients, while placebo-treated ones exhibited a trend towards lengthening. Several authors such as Squires et al. (1980), Semlitsch et al. (1990, 1992) and Polich (1991) pointed out that the P300 can provide useful information on individual cognitive function. It may possibly be more than a coincidence that the shortening of the P300 latency under nicergoline in SDAT and MID patients (in ms) is the same as the amount by which the latency of the untreated dementia patients deviates from that of normal aged subjects (Saletu 1994). Thus, nicergoline siginificantly improved stimulus evaluation time of cognitive information processing, thereby tending to normalize the former in both SDAT and MID patients.

Acknowledgements :

The authors would like to express their thanks to Drs. E. Kaplan, E. Herchenhan and D.H. Meier from Pharmacia, Germany, and Dr. Ch. De Paolis from Pharmacia, Milan; further to Dr. Wuschitz, H. Saulean and D. Rabel as well as to K. Decker and G. Binder for researach assistance: to Dawn Eckelhart, Secretary; to Helmut Bernhardt, Medical Illustrator and Photographer as well as to the entire of the Division of Pharmacopsychiatry, Department of Psychiatry and the SPECT Laboratory, Department of Neurology, School of Medicine, University of Vienna and the Institute of Neuroimaging, Rudolfinerhaus, Vienna, for their great assistance in this project.

In particular, the authors would also like to thank H. Dinhof, Acting Director of the Kuratorium der Wiener Pensionistenheime and the physicians, staff and patients of the Viennese Old Age Pensioners' Homes, especially the Pensionistenheime Rosenberg and Hetzendorf for their valuable support

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