J Neural Transm (2002) 109: 907919

Cycloid psychoses from clinical concepts to biological foundations*

B. E. Jabs1, B. Pfuhlmann1, A. J. Bartsch2, M. G. Cetkovich-Bakmas3, and G. Stber1
2

Department of Psychiatry, and Department of Neuroradiology, Julius-Maximilians-University, Wrzburg, Federal Republic of Germany 3 Department of Mental Health, Buenos Aires, Argentina
1

Received January 21, 2002; accepted February 9, 2002

Summary. The modern concept of cycloid psychoses is primarily based upon the clinical delineation of their phenotypes according to Leonhard. By settling the dilemma of Kraepelinean atypical psychoses, their description may be considered one of the major achievements of clinical psychiatry in the last century. In particular, this had been facilitated by the work of Wernicke and Kleist. Albeit not yet generally recognized, cycloid psychoses have already stimulated great efforts of research yielding remarkable results. In this article, we elucidate the concept of cycloid psychoses and present recent ndings pertaining to their putative biological foundations. Finally, future perspectives for the eld of biological psychiatry are proposed fostering the heuristics of Leonhards nosology. Keywords: Leonhard, nosology, cycloid psychosis, genetics, family study, electrophysiology, functional neuroimaging.
Background Historical and clinical aspects

The development of the concept of cycloid psychoses goes back to the problem of atypical psychoses which arose from Kraepelins dichotomy of endogenous psychoses (Kraepelin, 1923). It concerned the classication of psychoses, which could be assigned neither to dementia praecox nor to manic-depressive illness. One strategy for a solution of this problem was to broaden the concept of schizophrenia as inaugurated by Bleuler (1911).
* Most respectfully dedicated to Prof. Peter Riederer on the occasion of his 60th birthday

908

B. E. Jabs et al. Table 1. Psychoses of the schizophrenic spectrum in Leonhards nosology Psychic system Psychomotility Affect Thought confusional psychosis

Cycloid psychoses

motility psychosis

anxiety-happiness psychosis prognostically favourable

Unsystematic schizophrenias Systematic schizophrenias

prognostically unfavourable periodic catatonia affect-laden cataphasia paraphrenia systematic catatonias hebephrenias systematic paraphrenias

Schizophrenia was then thought to include lots of clinical conditions with entirely different cross-sectional symptomatology, long-term course and outcome, thus considerably reducing the heuristic value of the diagnosis. Furthermore, reliable prognoses became impossible according to Bleulers concepts. Inevitably, the idea was generated that there might be a nosologically independent group of endogenous psychoses in addition to schizophrenias and manic-depressive illness. Based upon the previous work of Wernicke and Kleist (Bartsch et al., 2000a; Leonhard, 1961, 1999), Leonhard further established the concept of cycloid psychoses. Rejecting nosological hybridisation, the independence of these psychoses was emphasized. Representing one of the three main groups in his subdivision of psychoses with schizophreniform symptomatology (Table 1), Leonhard meticulously elaborated on precise clinical diagnostic criteria for cycloid psychoses. Cycloid psychoses are subdivided into three subforms: anxiety-happiness psychosis, excited-inhibited confusional psychosis and hyperkinetic-akinetic motility psychosis. The clinical pictures are polymorphous but nevertheless typical in that they allow establishing the diagnosis of a specic subform for most cases just relying on the cross-sectional presentation of the syndrome. If the differential diagnosis between the subforms is complicated in the acute condition, careful observation of the course further facilitates a reliable diagnosis of the given subsyndromes. A phasic course with favourable outcome is one of the main characteristics of cycloid psychoses. Primary decit or genuine residual syndromes never occur in cycloid psychoses. However, repeated phases of cycloid psychoses may at times result in a purely reactive diminution of psychic functioning. Since cycloid psychoses do remit always completely, even if a given phase may last for a long period of time, one must not misinterpret issues related to coping strategies of the patients as indicating residuum formation. Another general characteristic is the bipolar and polymorphous structure of symptomatology. Mixed states with intrasyndromal bipolarity are not uncommon. Sometimes symptoms from another subform can modify the clinical picture of a specic subsyndrome as well. However, considering the clinical

Cycloid psychoses Table 2. The cycloid psychoses Motility psychosis Hyperkinesia increase in expressive and reactive motions severe distractibility by environmental conditions with continued senseless motor Hypokinesia / akinesia disappearing of reactive motions, stiffness of expressive motions, reduction or standstill of voluntary movements General symptoms incoherent speech, unarticulated sounds of expressive character, or mutism Faculative symptoms mood alterations from anxious to ecstatic hallucinations Confusion psychosis Excitation incoherence of thought with compulsive speech or incoherence of thematic choice or disgressive theme choice Inhibition inhibition of thought, perplexedness ideas of meaning, ideas of reference acustic, visual or somatopsychic hallucinations eeting misrecognitions of persons ideas of reference, eeting hallucinations lability of affect with rapid changes between joy and tearfulness

909

Anxiety-happiness psychosis Ecstacy ecstatic mood with ideas of calling, happiness, reecting an altruistic component of the ecstasy Anxiety severe anxiety with distrust and ideas of reference, ideas of: threat or persecution, anxiously coloured somatic sensations

affect-generated illusory or hallucinatory phenomena

rapid changes of anxiety and ecstatic mood

pictures as a whole with regard to their essential features a precise diagnosis of one subform is nearly always possible (Table 2). Only the diagnosis of a characteristic subsyndrome allows for a valid classication as cycloid psychosis, a fact repeatedly emphasized by Leonhard. Therefore, the assembly of diagnostical criteria for a singular cycloid psychosis as proposed by Perris and Brockington (1981) may be a hazardous over-simplication. This holds true for the ICD-10 classication (WHO, 1991), too. In ICD-10, cycloid psychoses are assigned to a broad spectrum of disorders, such as the acute polymorphous psychotic disorders, the schizoaffective or the schizophrenic psychoses. All of them are characterized by rather arbitrary criteria of duration, no precise differentiation of symptom clusters and a lack of clear prognostic judgement (Harrow et al., 2000; Marneros et al., 2000; Peralta and Cuesta, 1999). For these reasons, it still seems advantageous to use Leonhards original descriptions of these subforms as a diagnostic guideline if one is considering the scientic evaluation of the cycloid psychoses.
Therapeutical implications

The diagnosis of a cycloid psychosis may be of high signicance with respect to therapeutical consequences. Clinical experience has demonstrated that the specic subform may play quite a considerable role for the pharmacotherapeutic approach. The acute therapy of anxiety psychoses usually requires

910

B. E. Jabs et al.

neuroleptic medication, but additional use of anxiolytic substances considerably improves the symptoms including the paranoid ideas basing on serious anxiety. The hyperkinetic expressive and reactive motions of the motility psychosis can be rapidly controlled by neuroleptics in most cases. The therapy of akinetic states is more difcult. Here, neuroleptics can possibly facilitate the development of severe akinetic complications (often mistaken for a malignant neuroleptic syndrome) and may not prove benecial. Thus, the management of akinetic motility psychosis predominantly requires careful clinical observation and additional use of anxiolytic substances (Ungvari et al., 1994). But it should always be kept in mind that the phases also remit spontaneously. In the case of dangerous akinetic complications, electroconvulsive therapy (ECT) may become the therapy of rst choice. Interestingly, Franzek et al. (1994) noticed that 7 out of 9 patients subject to the development of a malignant neuroleptic syndrome suffered from a cycloid psychosis. In the preneuroleptic era, Neele (1944) had already stated that the majority of cases corresponding to Stauders lethal catatonias occur among patients suffering from cycloid psychoses with severe and exhausting hyperkinetic and akinetic features all of them with full recovery following convulsive therapy. It must be stressed that these phasic and completely remitting diseases do not require neuroleptic long-term medication although long-term medication is frequently prescribed to these patients, unfortunately, due to schizophreniform symptomatology according to (Neo-) Schneiderian criteria. However, patients who are well in intervals between phases should not receive such treatment because of the considerable risks for side effects of such medications. Last but not least, an otherwise healthy patient may still be regarded as ill due to some of these side effects (Beckmann et al., 1992). Although studies of sound methodological control are still lacking, clinical experience indicates that for the phasic repetitions prophylactic treatment with lithium or anticonvulsive agents may be superior to neuroleptic maintenance therapy. In his initial studies, Perris (1978) found neuroleptics far less effective than lithium for prophylactic treatment of cycloid psychoses. On the other hand there are indications that after an abrupt discontinuation of long-term neuroleptic treatment of cycloid psychoses the rate of relapse may even increase (Albert, 1986). Though there is no sufcient experience with regards to potential benets of atypical neuroleptics yet, there is some empirical evidence that they might offer distinct advantages compared to typical neuroleptics in terms of the side effects, especially in the acute phase treatment.
Recent results Clinical signicance and prognosis

Additionally to Leonhards own catamnestic studies (von Trostorff and Leonhard, 1990), Beckmann et al. (1990) have demonstrated excellent stability and prognostic validity of cycloid psychoses. In a prospective study they were able to follow up 26 out of 31 patients originally diagnosed by Leonhard as suffering from a cycloid psychosis. In personal examinations as well as using

Cycloid psychoses

911

the Strauss-Carpenter-Scale they found no residual states after a period of 4 years. All but two of the patients, who were actually in an acute phase of their cycloid psychosis, showed complete remission. The diagnosis of cycloid psychoses proved to be stable and there were little shifts between the subforms. In a recent study (Jabs et al., in preparation), 33 patients with cycloid psychoses reported signicantly higher satisfaction with their global quality of life (measured by the German version of the Lancaster quality of life prole) than 44 patients suffering from schizophrenic psychoses according to Leonhard. In both groups the mean duration of illness was about 13 years. Concerning outcome and social functioning, patients suffering from cycloid psychosis also reached signicantly higher scores in the Strauss-Carpenter Outcome-Scale and Global Assessment of Functioning (GAF-) Scale than schizophrenic patients.
Aetiology and genetics

With regard to the aetiology of cycloid psychoses Leonhard (1976, 1999) already postulated a prominent role of somatic factors in these psychoses, which show only low familial loading. He reported a higher number of cycloid psychoses among twins than expected by chance. Frequently, he could nd low birth-weight and other birth complications in the ill twin. Among the cycloid psychoses, high concordance rates (82%) were found only among monozygotic pairs with motility psychoses, but dizygotic index-twins with motility psychoses all had a healthy partner. Franzek and Beckmann (1998, 1999) replicated similar ndings in a systematic twin study including 47 same-sex twin pairs. In pairs with cycloid psychoses, they found nearly the same concordance rate for monozygotic pairs (39%) as for dizygotic pairs (31%), reected by a low heritability index of 0.21. Remarkably, among the concordant monozygotic twins suffering from any psychosis, motility psychosis was the only occurring type of cyloid psychosis (2 out of 14 pairs), whereas the other subforms, anxiety-happinesspsychosis and confusional psychosis, represented the predominant diagnosis (8 out of 8 pairs) in discordant monozygotic pairs. In the latter, the ill twins showed signicantly more frequent and more severe birth complications than their healthy co-twins. In concordant pairs with cycloid psychoses, the more seriously ill twin showed more such complications. There ndings strongly suggest that hereditary inuences even when taking in account some genetic liability in motility psychosis play a subordinate role in the aetiology of cycloid psychoses, whereas somatic inuences seem to be of remarkable importance. Low heredity in patients with cycloid psychoses originally described in Leonhards series (1999) was further substantiated by a recent family study which has been performed satisfying recent methodological standards by personal interviews of the relatives by an experienced psychiatrist blind to the diagnosis of the index cases (Pfuhlmann et al., in preparation). The morbidity risk of rst degree relatives was evaluated in 45 index cases with cycloid

912

B. E. Jabs et al.

psychoses, 32 with manic-depressive illness, and 27 healthy controls. Out of total of 431 rst-degree relatives 353 could be traced and evaluated (82%). Whereas 24.4% of the 45 index cases with cycloid psychoses had at least one rst-degree relative with an endogenous psychosis, the percentage was 62.5% in the 32 manic-depressive probands and 14.8% in the control group. The corresponding cumulative risk for rst-degree relatives to suffer from an endogenous psychosis was 10.8% in cycloid probands vs. 35.2% in manicdepressive probands (p 0.001) and 5.7% in the control group. The latter rate was insignicantly different from cycloid psychoses. These data contradict the thesis of a bipolar affective spectrum and corroborate the nosologic independence of the cycloid psychoses. This corresponds to earlier observations of a morbidity risk of 5.1% for parents, and 4.1% for siblings (Leonhard, 1999). The aetiological importance of exogenous factors, such as exposure to gestational infections and other obstetric complications was the focus of several earlier investigations (Maj et al., 1990; Beckmann and Franzek, 1992; Stber et al., 1997; for review: Franzek and Beckmann, 2000). Seasonality of birth in cycloid psychoses succeeding exposure to annual peaks of acute respiratory infectious diseases in the general population was followed by studies on individual exposure to maternal gestational infections in probands with cycloid psychosis. Mothers of patients with cycloid psychoses had suffered from infectious diseases, particularly inuenza and common cold with fever, predominantly in the rst trimester of gestation. This contrasted to a signicantly increased exposure to mid-gestational infectious diseases in patients with systematic schizophrenias, which show no essential heredity in their aetiology as well. In cycloid psychoses other obstetric complications only showed an insignicant increase compared to controls and seemed to be of no inuence on the age at the onset. This was opposite to subtypes with high genetic loading, like manic-depressive illness or unsystematic schizophrenias, which show no association with any exposure to gestational infections contradicting the double-strike hypothesis of genetic loading and perinatal adverse events in the aetiology of familial endogenous psychoses (Stber et al., 1993). An interesting hint towards the triggering of cycloid psychoses was discovered by a catamnestic study on 39 postpartum psychoses (Pfuhlmann et al., 1998). Here, 54% of the postpartum psychoses turned out to be cycloid psychoses (57% of the latter being motility psychoses), clearly predominating unipolar depressive psychoses (8%), manic-depressive illness (13%), and unsystematic schizophrenias (10%) after a mean follow-up of 12.6 years. An other activating factor for cycloid psychoses may be deduced from a study by Althaus et al. (2000), who determined the menstruational phase in 155 women at the time of admission to the clinic due to an acute non-organic psychiatric disease. Generally, there was no signicant difference between non-psychotic diseases and endogenous psychoses, but women suffering from cycloid psychoses were signicantly more frequently admitted to hospital during the luteal-/menstrual phase than patients with schizophrenia. This may point to an endocrinological factor in the exacerbation of cycloid psychoses.

Cycloid psychoses

913

Electrophysiological ndings

Studies of event-related potentials revealed distinct characteristics in cycloid psychoses (Strik et al., 1996). Signicantly higher amplitudes for the P300 were reported among patients with cycloid psychoses than for age- and sexmatched controls. Both, cycloid psychoses and controls showed a dislocation of the mean P300 peak away from the midline towards the left hemisphere whereas in schizophrenic patients P300 peaks were located within the right hemisphere. Moreover, in schizophrenics amplitudes were signicantly lower than in cycloid psychoses and slightly lower than in controls. During performance of a simple cognitive task (standard oddball paradigm) patients with cycloid psychoses did not exhibit signs of abnormal functional asymmetry of cerebral function as did schizophrenic patients. The right-lateralised peaks in schizophrenics correspond to reduced left hemispheric amplitudes and are possibly related to structural and functional abnormalities of the left temporal lobe.
Morphometric neuroimaging

Franzek et al. (1996) found signicantly more cycloid psychoses among patients with non-specic abnormalities in their cranial computertomographies (cCT), which resulted most plausibly from pre- or perinatal brain damage according to the judgement of an independent neuroradiologist, than among a matched control group of psychotic patients without cCT abnormalities. These ndings corresponded well with preliminary cCT- and magnetic resonance imaging studies (Becker et al., 1995; Falkai et al., 1997) and the results of studies mentioned above, which indicated disturbances in early phases of the development of the central nervous system. Although the described structural abnormalities cannot be viewed as specic for cycloid psychoses, it can be hypothesized that somatic inuences such as gestational infections during the vulnerable rst trimester may disturb the development of structures within the central nervous system. Recently, Jabs et al. (2001) employed neuro(ultra)-sonography as a tool for imaging brain parenchyma to test for differences in the susceptibility to neuroleptic induced parkinsonism related to the echogenicity of the substantia nigra in 79 patients classied according to Leonhard. Here, cycloid psychoses displayed a signicantly larger echogenic area of the substantia nigra than patients with systematic schizophrenia and healthy controls. Echogenicity of the substantia nigra was not correlated to the lifetime intake of neuroleptic agents as estimated by the duration of illness. Generally, a signicant correlation between echogenicity of the substantia nigra and severity of neuroleptic induced parkinsonism could be demonstrated indicating a link to the susceptibility for severe neuroleptic-induced side effects or severe akinetic states in the cycloid psychoses (Franzek et al., 1994).
Functional imaging

There have yet been few but two neuroimaging studies explicitly investigating functional correlates of cycloid psychoses, i.e. global and regional cerebral

914

B. E. Jabs et al.

perfusion at rest (Warkentin et al., 1992; Bartsch et al., 2001; Kck et al., 2001). Warkentin et al. (1992) measured mean hemispheric blood ow and its regional distribution in acute phases of cycloid psychoses as well as after one week of treatment and nally at discharge by 133Xe-inhalation cerebrography. Their results suggested a global hyperactivity during the phasic occurrence of cycloid psychoses favouring occipital on cost of frontal perfusion, particularly on the right side of the brain. On average, initial hyper-perfusion of both hemispheres at admission was found to decrease within a week by more than 10% and in seven out of eight patients under neuroleptic treatment. Thereafter, cerebral perfusion did not differ signicantly from discharge (n 4) and control subjects (n 39). However, an ongoing study at the University of Wrzburg (Bartsch et al., 2001; Kck et al., 2001) using 99mTc-HMPAO-SPECT did not yet yield any evidence for acute elevations of the global perfusion estimator in neither cycloid psychoses (n 8) nor hebephrenias (n 7). Differential diagnoses of non-systematic schizophrenias according to Leonhard as well as the medication history may be crucial in these regards. In contrast to chronic schizophrenias, some cases of cycloid psychoses may present an acute hyperfrontality which is redistributed to occipito-temporo-parietal areas upon their treatment and remission. Notably, statistical parametric mapping revealed corresponding extrastriate clusters of signicantly decreased cortical perfusion in acute as compared to (partially) remitted stages of the cycloid illness. Signicantly increased perfusion was observed in the right dorsolateral prefrontal cortex, the mesocortical cingulum and along the induseum griseum as well as within subcortical regions extending from the ventral and dorsal pallidum to the anterior thalamus. This warrants to reconsider traditional notions about functional brainstem alterations attributed by cycloid psychoses by Kleist (1928/ 1974). In comparison to hebephrenias at admission as well as at their discharge, acute cycloid psychoses presented a signicantly pronounced perfusion of the left dorsolateral prefrontal cortex and within the anterior cingulum. Interestingly, the latter survived a small volume correction centred on the Talairach space coordinates given by Liddle et al. (1992) for maximum positive correlation with schizophrenic disorganisation. Moreover, cycloid psychoses exhibited a signicantly steeper decrease of perfusion than hebephrenias according to Leonhard in the dorsolateral prefrontal cortex bilaterally, along the corpus callosum and in the right anterior cingulum from admission to discharge. Again, the latter survived a small volume correction centred on the Talairach space coordinates given by Liddle et al. (1992) for increasing schizophrenic disorganisation. Therefore, this hypercingularity is either non-specic or even pseudo-schizophrenic in nature.
Future perspectives Differential treatment and prophylaxis

Since controlled studies on acute pharmacological treatment and long-term prophylaxis of cycloid psychoses have not yet been conducted, there is an

Cycloid psychoses

915

urgent need to perform such prospective and appropriately designed studies based on Leonhards criteria with further differentiation into the subtypes motility psychosis, confusional psychosis, and anxiety-happiness-psychosis. The efcacy of atypical neuroleptic agents, benzodiazepines and electroconvulsive therapy should be tested. Considering the observations of potentially disadvantageous effects of neuroleptics in the prophylaxis of cycloid psychoses (Albert, 1986), the application of these drugs and especially of atypical neuroleptics should be compared with lithium and anticonvulsive agents in long-term studies. At the same time, it would be very interesting to detect further somatic (e.g. endocrinological or biorhythmic) factors, which might trigger the psychosis, similar to the mentioned effect of delivery.
Aetiological research

The nding of an elevated echogenicity of the substantia nigra in cycloid psychoses (Jabs et al., 2001) should be replicated with a larger sample and, then, could be the basis to examine patients with severe akinetic episodes by transcranial ultrasonography to establish a potential screening method for these severe complications. Since altered echogenicity in brain parenchyma seems to be caused by an accumulation of minerals, esp. iron (Berg et al., 1999), this question could be answered by other in-vivo imaging techniques. Unfortunately, T2*-weighted magnetic resonance imaging and spectroscopy are difcult to perform accurately in these regions of the brain due to the proximity of the bony as well as air-containing skull base as well as to pulsation of the cerebrospinal uid. Analogies to an impaired iron homeostasis in Parkinsons disease (Double et al., 2000) and psychotic disorders have already been pointed out and discussed in terms of a glutamatergic-dopaminergic imbalance in the brain (Riederer et al., 1992). This trace could also be followed in terms of functional abnormalities in the glutamatergic, dopaminergic, serotonergic, and GABA-ergic neurotransmission, aiming to reveal possible dissimilarities between bipolar affective psychoses, schizophrenias, and cycloid psychoses.
Neuroimaging

So far, computerized neuroimaging has not yet employed voxel-, deformation- or tensor-based morphometry to address the issue of structural cerebral deviations in cycloid psychoses. These may complement and extend previous morphometric ndings in areas of interest. In terms of functional neuroimaging, future investigations will have to segregate medication effects and incorporate psychometric such as Liddles syndromatic dimensions (e.g. Liddle, 1995) in order to differentiate effects related to the nosological categorization from other phenomena. Anatomically guided a priori hypotheses may be derived electrophysiologically, e.g. from altered NoGo-anteriorisations and the variance of functional imaging parameters may be reduced by accounting for genetic modulation effects (Bartsch et al., 2000b; Fallgatter et al., 1999). Cycloid psychoses await further

916

B. E. Jabs et al.

functional differentiation not only from non-cycloid forms but also from each other. In addition, the various poles of cycloid psychoses are likely to represent different conditions of functional segregation and integration. Emerging evidence has pointed towards a phasic hyperfrontocingularity of cycloid psychoses. This emphasises their differentiation from schizophrenias that have been characterized by a variable degree of hypofrontocingularity (Blackwood et al., 1999; Blakemore and Frith, 2000). Any diagnostic overlap between schizophrenias and cycloid psychoses should be avoided as much as the construction of conceptual hybrids such as schizoaffective psychoses. Artifactual and inconsistent nosological stipulations are likely to generate contradictory functional assumptions.
Genetics

The cycloid psychoses appear as complex human diseases which involve multiple genetic and environmental determinants. Thus, major gene effects (as in periodic catatonia) will be unlikely to be established. To successfully search for susceptibility genes in families with increased incidence of the phasic cycloid psychoses, large sets of small to medium sized, multiply affected families or affected sib-pairs would have to be recruited in subgroups with increased familial incidence. On the other hand, the hypothesis of neurodevelopment disturbances in cycloid psychosis may be a focus of DNA microarray analyses to assay gene expression levels in postmortem brain tissue of patients who had suffered from cycloid psychoses. Recent studies in chronic schizophrenia pointed to dysregulations of myelination-related genes in schizophrenia. Additionally, genes involved in GABA signalling, signal transduction, transport function as well as numerous large brain proteins showed aberrant expression patterns (Hakak et al., 2001; Mirnics et al., 2000). Thus, case-control and family-based association analyses of candidate genes with functional polymorphisms may be suitable to detect genes with relatively small albeit signicant contribution to the disorder.
Conclusions

Over the last years, the nosology of Leonhard has been proven to represent a helpful tool for research, both in clinical and in biological psychiatry. Especially, the separation of cycloid psychoses from schizophrenias seems indispensable and should be incorporated into future editions of international diagnostic guidelines. Thus, the heuristics of the Wernicke-Kleist-Leonhard School shall stimulate and guide further clinical and biological research in this eld.
References
Albert E (1986) ber den Einuss von neuroleptischer Langzeitmedikation auf den Verlauf von phasischen remittierenden Unterformen endogener Psychosen. In: Seidel K, Neumrker KJ, Schulze HAF (eds) Zur Klassizierung endogener Psychosen. Hirzel, Leipzig, pp 97107

Cycloid psychoses

917

Althaus G, Pfuhlmann B, Franzek E (2000) Der Einu des Menstruationszyklus auf die Manifestation psychiatrischer Erkrankungen. Fortschr Neurol Psychiatr 68: 357 362 Bartsch AJ, Neumrker KJ, Franzek H, Beckmann H (2000a) Images in Psychiatry: Karl Kleist, 18791960. Am J Psychiatry 157: 703 Bartsch AJ, Hofmann E, Homola G, Schumacher I, Oltmanns F, Jatzke S, Wanninger F, Fallgatter AJ, Pfuhlmann B, Jabs B, Hamelbeck B, Lesch KP, Hoell T, Solymosi L, Beckmann H (2000b) BOLD-contrast functional MRI of higher visual processing and the serotonin transporter promoter polymorphism. Int J Neuropsychopharmacol 3 [Suppl 1]: 381 Bartsch AJ, Seybold S, Koeck PR, Jabs B, Fallgatter AJ, Reiners C, Stber G (2001) Cycloid psychoses in video-demonstrations and 99mTc-HMPAO-SPECT ndings. World J Biol Psychiatry 2 [Suppl 1]: 97 Becker T, Stber G, Lanczik MH, Hofmann E, Franzek F (1995) Cranial computed tomography and differentiated psychopathology are there patterns of abnormal CT-ndings? In: Beckmann H, Neumrker K-J (eds) Endogeneous psychoses. Leonhards impact on modern psychiatry. Ullstein Mosby, Berlin Wiesbaden, pp 230234 Beckmann H, Franzek E (2000) Cycloid psychoses and their differentiation from affective and schizophrenic psychoses. In: Henn et al. (eds) Contemporary psychiatry, vol 3. Springer, Berlin Heidelberg New York Tokyo, pp 387398 Beckmann H, Fritze J, Lanczik M (1990) Prognostic validity of the cycloid psychoses. A prospective follow-up study. Psychopathology 23: 205211 Beckmann H, Fritze J, Franzek E (1992) The inuence of neuroleptics on specic syndromes and symptoms in schizophrenics with unfavourable long-term course. Neuropsychobiology 26: 5058 Berg D, Grote C, Rausch WD, Maurer M, Wesemann W, Riederer P, Becker G (1999) Iron accumulation in the substantia nigra in rats visualized by ultrasound. Ultrasound Med Biol 25: 901904 Blackwood DHR, Glabus MF, Dunan J, OCarroll RE (1999) Altered cerebral perfusion measured by SPECT in relatives of patients with schizophrenia. Correlations with memory and P300. Br J Psychiatry 175: 357366 Blakemore SJ, Frith CD (2000) Functional neuroimaging studies of schizophrenia. In: Mazziotta JC, Toga AW, Frackowiak RSJ (eds) Brain mapping the disorders. Academic Press, San Diego Bleuler E (1911) Dementia praecox oder die Gruppe der Schizophrenien. In: Aschaffenburg G (ed) Handbuch der Psychiatrie. Spezieller Teil, 4. Abteilung, 1. Hlfte. Deuticke, Leipzig Double KL, Gerlach M, Youdim MB, Riederer P (2000) Impaired iron homeostasis in Parkinsons disease. J Neural Transm [Suppl] 60: 3758 Falkai P, Franzek E, Schneider-Axmann T, Blank B, Kleinschmidt A, Steinmetz H (1997) Magnetic resonance imaging ndings in schizophrenic patients diagnosed according to Leonhrads classication: a quantitative morphometric study. In: Franzek E, Ungvari G (eds) Recent advances in Leonhardian nosology I. International Wernicke-Kleist-Leonhard Society, Wrzburg, pp 7788 Fallgatter AJ, Jatzke S, Bartsch AJ, Hamelbeck B, Lesch KP (1999) Serotonin transporter promoter polymorphism inuences topography of inhibitory motor control. Int J Neuropsychopharmacol 2: 115120 Franzek E, Beckmann H (1992) Season-of-birth effect reveals the existence of etiologically different groups of schizophrenia. Biol Psychiatry 32: 375378 Franzek E, Beckmann H (1998) The different genetic background of schizophrenic spectrum psychoses. A twin study. Am J Psychiatry 155: 7683 Franzek E, Beckmann H (1999) Psychoses of the schizophrenic spectrum in twins. Springer, Wien New York

918

B. E. Jabs et al.

Franzek E, Stber G, Beckmann H (1994) Malignes neuroleptisches und akut lebensbedrohlich katatones Syndrom. Eine identische Komplikation im Verlauf von funktionellen Psychosen. Neuropsychiatrie 8: 151158 Franzek E, Becker T, Hofmann E, Flhl W, Stber G, Beckmann H (1996) Is computerized tomography ventricular abnormality related to cycloid psychosis? Biol Psychiatry 40: 12551266 Hakak Y, Walker JR, Li C, Wong WH, Davis KL, Buxbaum JD, Haroutunian V, Fienberg AA (2001) Genome-wide expression analysis reveales dysregulation of myelination-related genes in chronic schizophrenia. Proc Natl Acad Sci 98: 4746 4751 Harrow M, Grossman LS, Herbener ES, Davies EW (2000) Ten-year outcome: patients with schizoaffective disorders, schizophrenia, affective disorders and moodincongruent psychotic symptoms. Br J Psychiatry 177: 421 426 Jabs B, Berg D, Merschdorf U, Pfuhlmann B, Bartsch AJ, Toyka KV, Beckmann H, Becker G (2001) Differences of substantia nigra echogenicity in nosological subtypes within the schizophrenic spectrum a preliminary transcranial ultrasound study. Neuropsychobiology 44: 183186 Kleist K (1928/1974) Cycloid, paranoid, and epileptoid psychoses and the problem of degenerative psychoses [transl by Marshall M from Schweiz Arch Neurol Psychiat (1928) 23: 135]. In: Hirsch SR, Shepherd M (eds) Themes and variations in European psychiatry. An anthology. Wright, Bristol, pp 297331 Kck PR, Bartsch AJ, Seybold ST, Mller TH, Jabs B, Stber G, Reiners C (2001) Cerebrale Tc-99m-HMPAO-SPECT bei zykloiden und chronisch schizophrenen Psychosen im Akutstadium und nach Teilremission. J Funct Mol Imaging 40: A81 Kraepelin E, Lange J (1923) Psychiatrie, vol 3, 8th edn. Johann Ambrosius Barth, Leipzig Leonhard K (1961) Cycloid psychoses endogenous psychoses which are neither schizophrenic nor manic-depressive. J Ment Sci 107: 632648 Leonhard K (1976) Bedeutung der Zwillingsgeburt fr die Entstehung zykloider Psychosen. Psychiat Neurol Med Psychol 28: 8998 Leonhard K (1999) Classication of endogenous psychoses and their differentiated etiology, 2nd, rev. and enlarged ed. Springer, Wien New York Liddle PF (1995) Inner connections within domain of dementia praecox: role of supervisory mental processes in schizophrenia. Eur Arch Psychiatry Clin Neurosci 245: 210 215 Liddle PF, Friston KJ, Frith CD, Hirsch SR, Jones T, Frackowiak RSJ (1992) Patterns of cerebral blood ow in schizophrenia. Br J Psychiatry 160: 179186 Maj M (1990) Cyloid psychotic disorder: validation of the concept by means of a followup and a family study. Psychopathology 23: 196204 Marneros A, Pillmann F, Haring A, Balzuweit S (2000) Acute and transient psychotic discorders. Fortschr Neurol Psychiatr 68 [Suppl 1]: S2225 Mirnics K, Middleton FA, Marquez A, Lewis DA, Levitt P (2000) Molecular characterization of schizophrenia viewed by microarray analysis of gene expression in prefrontal cortex. Neuron 28: 5367 Neele E (1944) Krampftherapie und Differentialdiagnose der bedrohlichen Hyperkinese (flschlich tdliche Katatonie genannt). Z Ges Neurol Psychiat 178: 165189 Peralta V, Cuesta MJ (1999) Diagnostic signicance of Schneiders rst-rank symptoms in schizophrenia. Comparative study between schizophrenic and non-schizophrenic psychotic disorders. Br J Psychiatry 174: 243248 Perris C (1978) Morbidity suppressive effect of lithium carbonate in cycloid psychosis. Arch Gen Psychiatry 35: 328331 Perris C, Brockington IF (1981) Cycloid psychoses and their relation to the major psychoses. In: Perris C, Struwe G, Jansson B (eds) Biological psychiatry. Elsevier, Amsterdam, pp 447450 Pfuhlmann B, Stber G, Franzek E, Beckmann H (1998) Cycloid psychoses predominate among severe postpartum psychiatric disorders. J Affect Disord 50: 125134

Cycloid psychoses

919

Riederer P, Lange KW, Kornhuber J, Danielczyk W (1992) Glutamatergic-dopaminergic balance in the brain. Its importance in motor disorders and schizophrenia. Arzneimittelforschung 42: 265268 Stber G, Franzek E, Beckmann H (1993) Obstetric complications in distinct schizophrenic subgroups. Eur Psychiatry 8: 293299 Stber G, Kocher I, Franzek E, Beckmann H (1997) First-trimester maternal gestational infection and cycloid psychosis. Acta Psychiatr Scand 96: 319324 Strik WK, Fallgatter AJ, Stoeber G, Franzek E, Beckmann H (1996) Specic P300 features in patients with cycloid psychosis. Acta Psychiatr Scand 94: 471 476 Trostorff Sv, Leonhard K (1990) Catamnesis of endogenous psychoses according to the differential diagnostic method of Karl Leonhard. Psychopathology 23: 259262 Ungvari GS, Leung HC, Lee TS (1994) Benzodiazepines and the psychopathology of catatonia. Pharmacopsychiatry 27: 242245 Warkentin S, Nilson A, Karlson S, Risberg J, Franzen G, Gustafson L (1992) Cycloid psychoses: regional cerebral blood ow correlates of a psychotic episode. Acta Psychiatr Scand 85: 2329 World Health Organization (1991) Mental and behavioural disorders (including disorders of psychological development). Clinical descriptions and diagnostical guidelines. In: WHO: International classication of diseases, chapter V (F), 10th edn. WHO, Geneva Authors address: Dr. B. Jabs, Department of Psychiatry, Julius-MaximiliansUniversity, Fchsleinstrasse 15, D-97080 Wrzburg, Federal Republic of Germany, e-mail: burkhard.jabs@mail.uni-wuerzburg.de