Psychoses are probably the main concern of adolescent psychiatrists and the obsession with their clinical observations. In fact, adolescence poses, in a crucial way, difficult diagnostic questions in the presence of noisy or more discrete symptoms which, without a close or compulsory correlation with a proven mental pathology, express polymorphically the psychic suffering frequent at this age. At a time of profound mutation, adolescence is indeed a period of development where, from a psychodynamic point of view, mechanisms of archaic or psychotic defenses can be activated in order to respond to the psychological difficulties that can be induced by the adolescent process itself and vital crisis “that it provokes.
Added to this is the fact that adolescence is also the preferred age for the outbreak of most psychiatric diseases with chronic potential, since they do not initially have the clinical characteristics that will make them later easier recognizable.
In adolescence, more than at any other period of life, the clinician is led to question the psychopathological dimension of the symptoms that he / she sees and their diagnostic and prognostic value, with a main fear, the entry into the schizophrenia of which it is the age of election.
This should not make us forget the frequency of deceptive psychotic signs in other pathologies emerging during this period of development.
Finally, questioning psychoses in adolescence today also raises the question of the value of the premorbid manifestations appearing at this age: factors of vulnerability or prodromes of the disease with consequent treatment modalities and prevention which can be very different.
These diagnostic issues have become even more important since recent schizophrenia data advocate early diagnosis and multifocal treatment as it appears that the greatest risk of a deficit is in the first two years of the disease, whereas the prognosis seems unfavorably affected by the duration of untreated psychosis (DUP).
Advances in the field of pharmacotherapy (the emergence of chemotherapeutic treatments more adapted to thymic disorders and the development of new antipsychotic medications better tolerated and more effective on negative signs) further increase the stakes of early diagnosis and renew the clinical interest of old questions: when and how should these new molecules be prescribed? In the face of syndromes entirely constituted or in front of prodromes, even premises or signs of vulnerability? With what aims and for what duration?
Conversely, it is not possible to underestimate the potentially iatrogenic effect of an over-diagnosis of a chronic psychiatric disorder, which can lead to long-term drug prescriptions, side effects, and profoundly change the subject’s relationship to himself and others.
The first question that arises is that which affects the recognition of psychotic symptoms in adolescence according to a point of view that is rather a dimensional approach.
In practice, we consider as psychotic signs in adolescence all the signs which, in nosographic classifications, must evoke schizophrenia, that is to say essentially the characteristic symptoms which we shall evoke below.
Such a position can be relevant only if it is assumed that the presence of any of these signs does not necessarily mean the diagnosis of schizophrenia.
As noted in the Diagnostic and Statistical Manual of Mental Disorders (DSM) -IV: “No isolated symptom is pathognomonic of schizophrenia, the diagnosis of which involves the recognition of a constellation of signs and symptoms associated with social and occupational dysfunctions . “
Whatever the theoretical currents adopted, there is currently an international consensus on this point.
The psychotic symptoms in adolescents are therefore identical to those of adults and group (DSM-IV):
• the following characteristic symptoms:
* delusions, (mental automatism, delusions with persecutory themes or polymorphic and non-systematized megalomaniacs);
* psychosensory hallucinations (verbal but also cenesthetic, olfactory or visual auditory);
* disorganized discourse (looseness of associations, incoherence, poverty of the content of discourse, neologisms, perseverations, blockage, echolalia, associations by assonances);
* grossly disorganized or catatonic behavior (indecision of gesture, indeterminacy of attitudes, automatic movements, mannerisms of presentation and gestures, paramimy, stereotypy, even catalepsy, stiffness, hyperkinesia, etc.);
* negative symptoms (such as emotional loss, loss of bonds or loss of will);
• symptoms associated with social dysfunction or activities, ie, during a significant part of the time since the onset of the disruption one or more major areas of functioning such as work, interpersonal relationships, or personal care is significantly worse than it was before the disruption occurred.
The occurrence of psychotic symptoms in adolescence, however, has specific characteristics that induce the diagnostic difficulties already mentioned. For example, the criterion of the level of interpersonal achievement for children and adolescents in the school setting or in other activities should be approached with caution. Indeed, it is sometimes difficult to distinguish disorders with an insidious onset, a long history of developmental disturbances and personality disorders. Cultural, developmental and intellectual factors must be taken into account before a relevant symptomatic description can be claimed.
Moreover, it is not uncommon for psychotic symptoms to be more torpid or misleading: with predominance of signs that can be considered as negative psychotic signs (see below Prodromal symptoms). In some cases, this means that they are only recognized on the occasion of their consequences, particularly on conduct. The risk of suicide must be particularly feared because the encounter of psychotic symptoms with the tendency to act, frequent in adolescence, significantly increases the occurrence of conduct and behavioral disorders. All data show that this risk is significantly increased in the presence of a psychotic process, particularly in the first year after the first acute episode. A not uncommon eventuality is that the suicide attempt is inaugural or revealing symptoms previously neglected.
Regarding the frequency of psychotic disorders in adolescence, the only data we have available relate to patients hospitalized or followed in psychiatry.
Thus, 5 to 20% of adolescent patients consulting or hospitalized in psychiatry have psychotic symptoms.
The diagnostic approach approaches very differently according to whether one is faced with an acute psychotic state or a more torpid or deceptive symptomatology.
In the first situation, the acute delirium puff (BDA) syndrome, the description of which corresponds fairly closely to DSM-IV schizophreniform disorders, acute and transient psychotic disorders of the International Classification of Diseases (ICD) 10 , and to the acute psychoses of the French Classification of Mental and Childhood Disorders (CFTMEA).
The advantage of the concept of BDA in adolescence is not to anticipate the place of this syndrome in the spectrum of schizophrenia. As a syndromic diagnosis, it leaves the problem of categorical diagnosis, which can only be carried on in a second stage. In other words, the ambiguity introduced by the term BDA seems well adapted to the diagnosis of psychosis in adolescence, of which it respects the prognostic uncertainties.
In practice, before a first BDA, the differential diagnosis is made between:
• diagnosis of isolated BDA;
• an entry into schizophrenia;
• a first thymic episode in a bipolar disorder;
• a first atypical thymic episode of dysthymic schizophrenia;
• an acute psychotic episode occurring in the course of a personality disorder and more specifically of a borderline condition;
• an acute psychotic episode in the evolution of a childhood psychosis;
• an acute psychotic episode secondary to a toxic or an organic cause.
In the face of a more torpid or deceptive picture, the distinction between the normal and the pathological is often complex, and we are led to add to this series the differential diagnosis with a crisis of adolescence which we must try not to confuse with premises or prodromes of a psychosis declared without renouncing nevertheless to take into account its symptomatic value.
We will consider successively each of the disorders mentioned above and describe their connection with adolescence and psychoses.
Acute delusional puffiness:
In classical French nosology, the acute delusional puff has been described for the first time a hundred years ago and continues to be a widely used category. It includes all psychotic pathologies lasting less than 6 months and therefore includes various disorders. Its borders are blurred, which is both its limitations and its interest.
Ey uses this category to differentiate it from schizophrenia, the whole problem being for him to determine whether it is the “madness of an instant” or the “madness of an existence”; he stresses the complexity of this differentiation: “the signs that qualify in this respect the diagnosis and the prognosis are hardly usable”.
The DSM-IV describes two acute and sub-acute pathologies. The short psychotic disorder, lasting less than 1 month, with a complete return to the premorbid functioning level after the psychotic episode (a distinction is made according to whether or not the disorder occurs after a marked episode of stress), and schizophreniform disorder , which is distinguished from schizophrenia only by two criteria, that of duration: it must last more than 1 month but less than 6 months (criteria C of schizophrenia), and that of the degradation of social functioning or activities that is not required (Criterion B of schizophrenia).
Carlson et al. find that schizophreniform disorders occur in 45% of cases before 20 years. They progressed in 58% of cases to schizophrenia and 18.3% of cases to bipolar disorders, for the group of adolescent subjects (having a start before the age of 20 years).
It remains the central diagnostic issue in the face of psychotic disorders in adolescence. To repeat, this diagnosis, sometimes too rapidly evoked, is a syndromic diagnosis and must imperatively meet a set of criteria in order to be retained.
Schizophrenia appears very rarely during childhood and early adolescence. Then, the incidence increases during adolescence: 13.5% of schizophrenia occurs before 20 years (and 47.3% occurs between 21 and 30 years) the incidence increasing considerably especially between 15 and 17 years.
McClellan et al. estimate between 12 and 20% the prevalence of early-onset schizophrenia (ie, before 18 years of age).
Regarding the sex ratio, studies show either an equal proportion of girls and boys or, more often than not, a preponderance of boys.
Personality disorders of moderate to severe intensity are frequently found in personal histories.
A history of acute episodes (39% of cases in the Halfon study) and a family history of schizophrenia (0-17%) and mood disorders (17-29%) are common.
Diagnostic criteria (according to DSM-IV) are the same as in adults with permanent signs of persistent perturbation for at least 6 months as a criterion for duration. This duration criterion is even more important at adolescence than at other ages, with several long-term studies showing that the diagnosis of schizophrenia in acute episodes is not subsequently confirmed in a non-negligible number of patients. (29.8% of whom half will be borderline and antisocial personality disorders).
With regard to symptomatology, there are the classic positive and negative signs and the most frequent forms of schizophrenia are the undifferentiated form and the paranoid form.
In the schizophrenia of children and adolescents, psychotic symptoms most often found are auditory hallucinations, delirium and disorders in the course of thought. However, none of these symptoms is systematically reported.
We note also the presence of thymic disorders, classically variable, labile and discordant. They are present in 52% of cases.
The classically accepted idea was that early-onset schizophrenia had an unfavorable prognosis. However, follow-up of early-onset patients, schizophrenia suggests that fate would be the same as for later onset schizophrenia.
We will see in the following paragraphs the difficulties posed by the exclusion of thymic disorders (DSM-IV criterion D) and disorders related to the abuse of toxic substances (criterion E).
All the authors today emphasize the frequency of an onset of these disorders in adolescence.
Kraepelin (quoted by Carlson) acknowledged the occurrence of manic disorders in 3% of cases before 15 years and at least 20% before 20 years.
This observation, a forgotten time, has been reactivated by data from the current literature which finds that thymic disorders occur in 20 to 30% of cases in subjects less than 20 years old.
The average age at onset of thymic disorders in adolescence ranges from 13.9 years to 15.3 years.
High rates (67%) of a history of personality disorders have been found by some authors. They are mostly anxious / dysthymic and are more common in mood disorders with psychotic symptoms.
A family history of thymic disorders is also common.
ICD-10 and DSM-IV agree that psychotic symptoms may occur more frequently in adolescence than in adulthood in a major depressive episode, a manic episode or a mixed episode.
The most frequent psychotic symptoms in mood disorders with psychotic manifestations are delirious ideas then auditory hallucinations and finally disorders in the course of thought.
The disorders of the course of thought, such as the relaxation of associations, incoherence, the poverty of the content of discourse, neologisms, perseverations, blockage, echolalia, associations by assonances, are no more pathognomonic of schizophrenia than auditory hallucinations. can frequently be found in bipolar disorders, especially in adolescence.
This explains the frequency of schizophrenia diagnosis errors in patients with bipolar disorder.
Thus, in the Werry study cited above, half of bipolar patients between the ages of 13 and 17 are falsely considered schizophrenic at the time of the first diagnosis (observation made at 5 years). In the Joyce study, 72% of the manic patients whose disorder began before 20 years versus 24% of the manic patients whose disorders began after 30 years were initially diagnosed with schizophrenia. This means the difficulty of meeting DSM-IV criteria for schizophrenia (ie exclusion of schizoaffective disorders and mood disorders).
The concept of dysthymic psychosis or schizophrenia, according to French terminology (CFTMEA in particular), or schizoaffective disorders, according to international terminology, raises the problem of the boundaries between schizophrenia and thymic disorders.
CIM 10 and DSM-IV do not comment on the specificity of these disorders in adolescence, but indicate that they may occur at this age.
In personal histories, personality disorders are more frequent; with respect to family history, there is more history of affective disorder but less history of schizophrenic disorder than in schizophrenia itself.
In the adolescent, psychotic symptoms can also occur outside a diagnosis of psychosis, during personality disorders and more particularly during borderline states.
Altman et al. find that hallucinations and delusions can be found in patients with borderline and schizotypical personalities, but also in post-traumatic stress disorder and dissociative disorders.
McClellan and Werry frequently find these psychotic symptoms in borderline, antisocial, schizoid and schizotypical personalities.
Thomsen shows that 10 years later, 21% of a group of children and adolescents who have been diagnosed with schizophrenia have a personality disorder (12.4% borderline type) and not a schizophrenia. He concludes that about half of the patients who are wrongly diagnosed with schizophrenia actually suffer from personality disorders, particularly an antisocial or borderline disorder.
However, the association between personality disorder and psychosis is not limited to this symptomatic overlap, it is more complex. Indeed, some psychotic patients previously presented with a personality disorder. For example, in a study of children and adolescents with psychotic disorders, McClellan et al. find a 60% history of personality disorders.
These authors also point out that adolescents with psychotic symptoms in personality disorders function as disturbedly as schizophrenics in the degree of dependence, general functioning, and chronicity following a follow-up of several years.
So that it seems reasonable to propose to distinguish at adolescence:
• structured or systematized boundary states, sufficiently “stable in instability”, a concept whose internal coherence appears only through the psychopathological point of view;
• waiting limit states where the issue of the adolescent crisis remains open despite sometimes the severity of symptomatic manifestations.
This position assumes that we refer to a classification which, like the CFTMEA, does not oppose the diagnosis of disease (axis I of the DSM) and that of personality (axis II of the DSM).
Johnson shows that it is very difficult for adolescents to evaluate a psychiatric disorder without reference to the personality on which it occurs.
Autism, childhood psychoses and adolescent-related disorders:
In the context of infantile psychoses, psychotic symptoms in adolescence are found either in the context of the evolution of aged infantile psychoses, or in real schizophrenic pictures. The DSM-IV provides a criterion of duration (at least 1 month of delusions or pronounced hallucinations) to retain a diagnosis of schizophrenia in association with an invasive developmental disorder.
For children with childhood psychosis, adolescence is accompanied, in half of the cases, by a temporary or permanent worsening of pre-existing symptoms (withdrawal, stereotypies, epilepsy, hyperactivity, aggression). More productive tables are found in 5 to 10% of cases, the figures varying according to the diagnostic framework and the overall level of functioning. They are generally atypical clinical pictures because of the association of psychotic symptoms of very variable pace and symptoms related to developmental disorders that are to be sought after a thorough history (early language disorders, intellectual development, of relational skills). The identification of psychotic symptoms can therefore be difficult because developmental disorders modify their expression. For example, a significant language disorder interferes with the expression of a disorder in the course of thought or delirious content; a low intellectual level inevitably modulates the richness of the symptomatic picture. There are nevertheless real delusions, hallucinatory and dissociative paintings. The next question is whether these are old psychotic symptoms or new, evolving symptoms.
Conventional epidemiological data report the same prevalence rates of schizophrenia in children with developmental disorders as in the general population. It appears that the frequency is actually higher, especially for early-onset schizophrenia often associated with more pronounced premorbid symptoms. Studies of the fate of Asperger syndrome demonstrate that schizophrenia is more frequently found in the development of these patients, perhaps because of a better ability to manifest positive psychotic symptoms. In any case, there is the question of the links between schizophrenia and the spectrum of autistic disorders.
Hallucinogenic substances or toxic substances (cannabis, ecstasy, cocaine, lysergic acid diethylamide [LSD]) used by adolescents for an addictive purpose may be responsible for either confusion or psychotic symptoms. It is sometimes difficult to distinguish between a toxic effect and the presence of an associated psychotic pathology. Indeed, during an initial psychotic episode, adolescent smoking is common (54% co-morbidity in the McClellan study). In other words, DSM-IV criterion E for schizophrenia (the absence of toxic substances) is often difficult to demonstrate in adolescence, which increases the need for caution in this diagnosis.
The recommendations are as follows: if the psychotic symptoms persist for more than 1 week despite the cessation of substance use, the clinician will evaluate whether it is a first psychotic episode rather than a psychotic disorder due to the consumption of a toxic. However, these products act more often by exacerbating (or even triggering) rather than being a major etiologic agent of psychotic disorders.
Certain organic disorders, such as drunkenness, poisoning, brain or general affections, can cause acute psychotic symptoms. For adolescents with psychotic symptoms, this requires a medical and neurological assessment, with, if necessary, further examination.
Period of teenage rebellion:
This notion, which we have already mentioned, covers multiple disorders of behavior and affects, which appear in some adolescents and disappear with the end of adolescence. The ambiguous notion between normal and pathological was used to avoid a categorization too rapid for adolescents whose troubles did not yet seem to correspond to the criteria retained by the nosography. This concern can only be considered legitimate if it does not serve as an alibi for a therapeutic abstention that is harmful to the patient.
At the present time, it is stressed that this crisis must at least be considered as symptomatic of psychological difficulties which must be the subject of therapeutic treatment without delay, even if their nosographic status remains in question.
Initiation and Vulnerability:
From the point of view of psychosis, the main characteristic of adolescence is the fact that it generally marks the transition from premorbid symptoms to prodromes and from these to the declared disease. It is this characteristic which makes all the difficulty of the psychiatric diagnoses at this period of life and the interest of individualizing the study.
Recent studies suggest that in a significant proportion of cases the complete expression of the psychotic illness is preceded by clinical or neurofunctional premorbid dysfunctions from childhood and non-specific symptoms in adolescence. Identifiable early on, these dysfunctions could be found in all areas of development (cognitive, affective, perceptivomotor). The problem then is that of the predictive value of these indicators. Retrospective studies and cohort studies have shown that although there are many biological and behavioral precursors of schizophrenia, none of them are specific to schizophrenia. For example, Fish’s pandysmaturation, which has a specificity of 95% and a sensitivity of 90%, is able to predict correctly the development of schizophrenia only with a probability of 0.15. At least 85% of children with this predictive sign will not develop schizophrenia. Thus, the possibility of predicting the onset of disease on an individual basis is still a long way off. None of the premorbid precursors appears to be predictive in terms of disease progression and prognosis.
Little is known about the prodromal symptoms that precede the onset of schizophrenia. Individuals in the prodromal phase do not exhibit florid psychotic symptoms but are characterized by a number of nonspecific behavioral changes and specific attenuated psychotic elements. The onset of the first changes is often imperceptible as well as the gradual transition between non-psychotic symptoms and frankly psychotic symptoms.
According to studies of early episodes, the most frequently described prodromal elements are non-specific neurotic symptoms such as anxiety, hypochondriacal ideas, depressive syndromes, affective changes such as anhedonia (ie, loss of pleasure), apathy, irritability, withdrawal, suspicion, lack of initiative, sleep disorders, changes in experience, perception, volition and motor functions.
In practice, differentiation between the premorbid, prodromal and psychotic phases of the disease is often impossible.
As for the adolescent crisis, we have seen that its ambiguity made it possible to consider it as a manifestation of adolescence, a prodromal symptom or a sign of vulnerability to psychosis.
Vulnerability model and / or neurodevelopmental assumptions:
Two hypotheses are currently attempting to account for these pre-disease signs:
• the neurodevelopmental hypothesis;
• the vulnerability model.
According to the classical model of vulnerability, some subjects would have genetically determined neurocognitive dysfunctions that would make them susceptible to developing psychotic symptoms under certain conditions of environmental stress. These markers of biological or neuropsychological vulnerability could be demonstrated in schizophrenic patients in active phase (state markers), but also out of access (trait markers), as well as in related relatives of genetically related schizophrenics.
According to the concept of vulnerability, therefore, schizophrenia, although a temporally defined disorder, does not appear ex nihilo, but is preceded and facilitated by certain psychological and biological factors necessary for its development.
In this model, the genetic inheritance may or may not appear to be the indispensable aetiological factor on which environmental factors play a more or less modulatory role, essential for the expression of the disease. Only some of the vulnerable individuals will develop schizophrenic psychosis if they are exposed to stressors while the others will remain asymptomatic or show only subclinical manifestations. In this model, schizotypic disorders are a direct manifestation of vulnerability and are considered premorbid states of schizophrenia. Schizophrenic psychosis would result from decompensation of a schizotypic disorder due to additional environmental or genetic factors. However, there is still no way to disprove the idea that, beyond conventional biological vulnerability, there is also a psychopathological vulnerability (within what we might call an “extended model of vulnerability”), would give an equivalent etiological status to the psychological, biological and environmental determinants.
This is not the case for the neurodevelopmental hypothesis that makes neurocognitive anomalies found in subjects belonging to the spectrum of schizophrenia, a neurological abnormality resulting from cerebral instability during gestational life due to intrauterine or perinatal viral or nutritional nature or obstetric complications, in subjects with a predisposed genetic background. In childhood, these lesions are manifested by the non-specific premorbid signs mentioned above. In adolescence, specific symptoms of the psychotic registry are expressed by an alteration of the usual phenomenon of corticocortical synaptic pruning, which in these patients goes beyond its usual developmental limits.
The psychiatric community is thus currently undergoing a debate on the etiopathogenesis of psychoses. This debate opposes:
• early schizophrenic patients, even if their classic symptomatic revelation is only realized after puberty (neurodevelopmental hypothesis);
• and those who consider this pathology to be the common final pathway for several convergent vulnerability factors, the summation of which ultimately leads to adoles- cents with the qualitative changes that characterize schizophrenia (the “wider” model of vulnerability).
In this context, there is the question of the value to be given to the warning signs of psychotic pathology: is it an emerging form of a psychosis already constituted or risk factors likely to increase vulnerability to psychosis (“Mental state at risk”)?
Current psychopathological studies focus on:
• the plurifactorial character of the etiopathogenesis of psychotic disorders in adolescence and they no longer oppose psychogenesis to other approaches, especially biological;
• the articulation between factors of vulnerability and pathology constituted, from a developmental perspective that leaves room for prognostic uncertainties;
• the influence of puberty and the adolescent process on the onset of the disorder.
In this respect, many authors converge more or less directly towards the idea that there would be a psychotic risk associated with adolescence itself directly or through the depressive risk that would be linked to it.
The question that arises then is the future of these psychotic ruptures beyond the forms they take in adolescence: a temporary rupture linked to this period of development and passing with it or a lasting rupture, inscribed as a structured issue, freed from the adolescence which precipitated the onset?
Starting from the common psychodynamic foundations which make adolescence the second phase of the development of human sexuality and the process of separation-individuation, the numerous psychodynamic works on this theme are schematically grouped into two tendencies.
Oedipus and genitalia:
A first trend emphasizes the new sexuation of the body that results from the puberty. Represented in particular by M. and E. Laufer or P. Gutton, the works belonging to this tendency insist on the psychic effects of puberty, which makes the body the incarnation of the Oedipus.
For the adolescent, it is a question of being able to “modify the image of his body by including efficient sexual organs”, the possibilities of this change being “dependent on the transformation of the incestuous Oedipal desires that must be displaced by Oedipal parents “.
It is the failure of this process which is at the root of the stops of development which appear as resistance to Oedipal resolution.
For the Laufer, it is the non-resolution of the Oedipus, with the consequence of the impossibility of managing the anxiety of castration, which would be at the origin of the alteration of the relation to the reality and the external objects , a characteristic alteration of the developmental stops which, according to these authors, always take on a more or less psychotic dimension.
Psychopathology of links:
The second trend will focus on the consequences of this resexualization movement on the relationship with others.Concerning psychotic disorders in adolescence, the works of this tendency (embodied by P. Jeammet) lead to the following considerations.
Adolescence is the source of an imbalance narcissicoobjectal that creates the conditions of an antagonism between investment of self and investment of the other. If it is too important, this antagonism directly threatens the sense of continuity of the subject, the investment of the other taking the value of hemorrhage for self-investment.
This puts the adolescent face an intensification of his needs for the object of external reality and thus facing an increased vulnerability to the relationship with the other, which increases the potential risk (abandonment, intrusion, seduction, dependence) .
The psychotic disinvestment of the bond can then become “the ultimate narcissistic defense of a self submerged and threatened with a life of total surrender to the object whose syndrome of influence and mental automatism are the most complete expression “.
This necessity is all the more likely to be imposed because the compensatory mechanisms that the subject has put in place in his early childhood to counter relational insecurity, an otherwise unavoidable anguish and precociously threatening representations are important. Adolescence is therefore a potential revelation of what remains of an earlier vulnerability.
Among these early factors, we must mention those related to the problem of attachment, of which we are interested in becoming in adolescence. This work suggests that, through the internal operating models that underlie them, attachment models can, through their effects on the internal safety of the subjects, constitute factors of vulnerability or protection to support the constraints of the adolescent process .
Faced with these constraints, we must emphasize the importance that external reality assumes for the adolescent who exports, in his “expanded psychic space”, the conflictuality that he can no longer contain in his inner psychic space.When the expanded psychic space is no longer sufficient, certain cultural, social or media overinvestments can take over and ensure an antipsychotic function by relying on the idealization they induce.
General principles :
The plurifocality of the treatment of schizophrenia patients is the subject of a broad professional consensus. The same principles are also applicable for the treatment of psychoses in adolescence:
• based on the model of vulnerability and data from psychopathology, treatment is not only concerned with treating psychotic manifestations and containing its disorganizing effects, but also with reducing the summation of factors that may be at risk, result in an irreversible psychotic rupture;
• Treatment focuses primarily on the reduction of psychotic symptoms (positive and negative symptoms) which are considered to be psychotic factors, the prolongation of which may exacerbate the prognosis of the disorder.
The difficulty here is to avoid the negative effects of these therapeutic interventions when they lead, for example, to a too rapid categorization of the disorder, which can have serious consequences for the adolescent and his entourage.
A drug prescription with too aggravating effects on negative symptomatology can also contribute to increasing evolutionary risks.
In view of the diagnostic and prognostic uncertainties of which we have seen the peculiarities in adolescence, we must adapt the therapeutic approach to the clinical context: first acute psychotic episode or, on the contrary, torpid symptomatology dominated by negative psychotic symptomatology.
Another therapeutic issue specific to adolescence is the question of the premorbid symptoms and the therapeutic or preventive interventions to which they can give rise.
The therapeutic approach must, in any case, always be global, considering generally the combination of drug treatment and an institutional dimension, as well as a psychotherapeutic approach, individual and family.
Drug prescription is indicated in case of obvious psychotic symptoms. Recall that this is a symptomatic treatment that does not require that the syndromic diagnosis be made beforehand.
The first-line use of atypical neuroleptics (risperidone, olanzapine, amisulpiride) is recognized. They are preferred over conventional neuroleptics because of their better tolerance (reduced extrapyramidal and cognitive effects) and their effect on negative symptomatology. However, these treatments have negative effects on the adolescent (weight gain, sexual problems) and are only symptomatic. Moreover, the use of classical neuroleptics can sometimes not be avoided in acute psychotic episodes very florid.
In the case of mood stabilizers, they must be prescribed in the presence of any suspicion of bipolar disorder, the diagnosis of which must be largely evoked in adolescence.
This prescription is also recommended in case of depressive syndrome in proven schizophrenia. Some authors even recommend using a mood stabilizer in all acute psychotic tables in adolescence.
Prolonged treatment over 6 months to 1 year after an acute episode reduces rates of psychotic recurrence. Spun doses or a progressive reduction of neuroleptics are preferred by some to a complete stop even in the event of total clinical remission. Others advocate a full stop after a gradual reduction over 6 months in the absence of worrying signs. Prolonged follow-up is, in any case, indispensable.
It can intervene at differential times of the disease. It aims at:
• first to contain psychotic symptoms in an acute episode;
• then to allow a reinvestment of the internal and external reality thanks to the support provided by the accompanying daily life and the various therapeutic mediations that are offered to patients from workshops that call upon the shared creativity of patients and caregivers. These mediations first create the conditions for the team to supplement imaginary and elaborate failures of the patient before favoring the latter a process of internalization of this elaborative approach thanks to the intermediate space that they reactivate.
In some cases, the peculiarities of adolescence impose the prolongation of residential treatments to accompany the process of maturation of the patient. In these cases, socio-educational and psychosocial rehabilitation needs to be addressed early on by care, which may be based on adapted vocational training or the resumption of studies within the framework of specific educational schemes or not.
The establishment and maintenance of individual or family psychotherapy are often favorable prognostic factors regardless of the technique used. They participate in the system aimed at helping the adolescent and his family to regain their previous functioning and to accompany them in the formalization and the elaboration of the conflicts that the acute episode brought to light. They require caution and experience.
The approaches are multiple, individual or not, psychoanalytic, systemic or cognitive-behavioral. The analytic psychodrama is particularly indicated in adolescents as long as they are sufficiently stabilized and in any case emerged from the acute episode.
Conclusion: strategy for the detection and prevention of schizophrenia
With neurodevelopmental and vulnerability assumptions, prevention finds new legitimacy. It now consists in better identifying and studying premorbid symptoms, markers of vulnerability and prodromes of schizophrenic disease.However, the use of vulnerability markers is currently reserved for the field of research, especially in the field of prevention.
Nevertheless, early intervention programs are beginning to be put in place.
While these research directions appear to be promising, clinicians must remain alert to the ethical risks of such procedures that have not proven their effectiveness and may lead to patient stigmatization and inadequate therapeutic voluntarism.