La depersonnalisation est definie par le DSM-IV comme une experience prolongee ou recurrente d'un sentiment de detachement et d'une impression d'etre devenu un observateur exterieur de son propre fonctionnement mental ou de son propre corps. Elle peut survenir dans le cadre de la pathologie obsessionnelle. La presence dans notre observation de symptomes psychiatriques a type d'obsessions et de depersonnalisation associes a une lesion sous-corticale, de meme que l'evolution extremement pejorative de ce cas clinique, nous ont conduits a faire l'hypothese d'un lien entre les deux phenomenes. La realisation d'explorations complementaires, grâce a l'imagerie morphologique et fonctionnelle, a mis en evidence des anomalies tant sous-corticales que corticales, censees rendre compte de ce tableau et de son aggravation.

La découverte par les méthodes d'imagerie cérébrale morphologique d'anomalies ou de lésions, chez des patients atteints de troubles psychiatriques, a conduit au concept de trouble secondaire. Ce concept est discuté à partir du cas d'une malade atteinte d'un trouble obsessionnel compulsif (TOC) typique, chez laquelle l'IRM a découvert un kyste arachnoïdien temporal gauche qui a été considéré comme une coïncidence probable et une lésion bipallidale, conséquence possible d'une intoxication ancienne à l'oxyde de carbone. Il est proposé que la distinction : formes primaires vs formes secondaires, va s'estomper avec l'apparition de nouvelles méthodes plus performantes d'imagerie cérébrale. Ce nouveau cas de TOC secondaire confirme le rôle de la disjonction ou de la dysfonction (au cours des formes primaires) d'un circuit corticobasal en tant que mécanisme physiopathologique commun des TOC. Des manipulations neurochirurgicales fonctionnelles de ce circuit représentent une nouvelle chance pour la thérapeutique.

Back to table of contents Previous article LetterFull AccessLeft Lenticular Lacuna and SchizophreniaJ-P. Luauté, M.D., K. Rahman, M.D., O. Radu, M.D., J-P. Forray, M.D., P. Dullin, M.D., and E. Sanabria, M.D., J-P. LuautéSearch for more papers by this author, M.D., K. RahmanSearch for more papers by this author, M.D., O. RaduSearch for more papers by this author, M.D., J-P. ForraySearch for more papers by this author, M.D., P. DullinSearch for more papers by this author, M.D., and E. SanabriaSearch for more papers by this author, M.D., Departments of General Psychiatry, Pediatric Psychiatry, and Nuclear Medicine, Centre Hospitalier, Romans-sur-Isère, FrancePublished Online:1 Aug 1998https://doi.org/10.1176/jnp.10.3.367bAboutSectionsView EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail SIR: The application of structural imaging techniques (CT and MRI) in schizophrenia has demonstrated a variety of cerebral lesions. Some were expected on a priori grounds. Other abnormalities, such as midline malformations, were unexpected and were possibly incidental and without etiological significance.The following case report describes the natural history, clinical evolution, and possible functional cortical involvement of a subcortical abnormality.Case ReportA 16-year-old right-handed girl presented with typical early schizophrenic symptomatology of 12 months' duration. Her main symptoms consisted of athymhormia, a syndrome recognized in France that is characterized by a loss of drive and affective responsiveness. She was treated with individual psychoanalytical psychodrama for a year before she had to be admitted to an adult psychiatric ward. The diagnosis of schizophrenia was confirmed, and she was treated with neuroleptics. This reduced her high levels of anxiety and controlled her hallucinatory symptomatology. The results of initial structural (Figure 1) and functional imaging studies were reported as normal.Between the ages of 17 and 23 the patient attended a day hospital. At the age of 24 she was rehospitalized because of a progressive deterioration of her condition, manifested in violent behavior toward her parents, dramatic reduction of speech, prominent auditory hallucinations, incongruous laughter, and autistic withdrawal.A repeat of the previous imaging studies revealed, on CT scan (Figure 2), a 5-mm isolated left lenticular lacuna, which on MRI scan was located at the inferoposterior putamen. Isodense relative to the CFS in a young patient without vascular risk factors or a history of cardiac embolism, it was deemed a type III lacuna resulting from a dilatation of the perivascular (Virchow-Robin) space.1 In retrospect, it could be faintly discerned on the first CT scan and therefore appeared to be evolving. We hypothesize that the major cortical hypoperfusion demonstrated on the second SPECT scan was the result of diaschisis or deafferentation, a depressive metabolic effect exerted on an intact brain region by a distant primary lesion.2,3 This seems particularly plausible in view of the predominantly left ipsilateral cortical hypoperfusion.However, the question remains whether the lacuna is of pathological significance. Such isolated lesions are sometimes discovered accidentally and without any clinical manifestations in elderly subjects, and the cortical hypoperfusion could represent a correlate of the patient's psychotic state.Alternatively, a case could be made for an etiological link between the parallel evolution of the imaged lesion and the patient's clinical condition. The lacuna is situated in a region that has previously been implicated in the pathogenesis of schizophrenia.4 In addition, athymhormia has been observed after acquired basal ganglia lesions.5To conclude, early and repeated structural and functional cerebral imaging studies identified an isolated and evolving lacuna of the left putamen in a case of severe, progressive schizophrenia. Although its origin remains unknown, its pathological significance seems probable. Similar findings may confirm the etiological importance of certain strategically located microlesions in the origin of some psychotic disorders.We thank Professors Derouesné and Poirier for their expert opinions on this case. FIGURE 1. Initial CT scan. In retrospect, a left lenticular lacuna can be faintly discerned (arrow). FIGURE 2. Repeat CT scan 8 years later shows a 5-mm isolated left lenticular lacuna (arrow).References1. Poirier J, Derouesné C: Le concept de lacune cérébrale de 1838 à nos jours. Rev Neurol 1985; 141:3–7Medline, Google Scholar2. Feeney DM, Baron JC: Diaschisis. Stroke 1986; 5:817–830Crossref, Google Scholar3. Luauté JP, Sanabria E, Remy C: Troubles psychiatriques et diaschisis: arguments tirés de l'imagerie cérébrale. Ann Méd-Psychol 1993; 150:168–173.Google Scholar4. Klawans HL, Goetz C, Westheimer R: Pathophysiology of schizophrenia and the striatum. Diseases of the Nervous System 1972; 33:711–718Medline, Google Scholar5. Habib M, Poncet M: Perte de l'élan vital, de l'intérêt et de l'affectivité (syndrome athymhormique) au cours de lésions lacunaires des corps striés. Rev Neurol 1988; 144:571–577Medline, Google Scholar FiguresReferencesCited byDetailsCited ByLe concept français d'athymhormie de 1922 à nos jours1 September 2001 | The Canadian Journal of Psychiatry, Vol. 46, No. 7 Volume 10Issue 3 August 1998Pages 367b-368 Metrics History Published online 1 August 1998 Published in print 1 August 1998

The evolution of some dysthymic states towards dementia is now rarely considered whereas it was well known at the beginning of the century. In French the final stage of this evolution was known as << demence vesanique >>.In recent years it has been noted that a proportion of patients with presenile dementia do not have Alzheimer's disease (AD) but a particular type of cognitive impairment, called dementia of the frontal lobe type (DFT), characterised by clinical and neuropsychological signs of frontal lobe disorder as well as an anterior defect of cerebral perfusion or metabolism. The onset of DFTis insiduous and marked by personality changes and inappropriate affect.It has not yet been reported as starting with true dysthymic disorders.Patients and methods. Ten right handed patients (F/M 9/1) became dysthymic in their fifties (m = 49.8 + 7.6 yr). All initially met the DSM III-R criteria for mood disorders. They were all treated with the standard drugs or ECT. Although initially responsive all the patients relapsed and their dysthymic disorders became less typical in presentation.At a mean age of 63.6 + 2.9 yrs a particular type of dementia became evident. None of the patients had a previous history of mood disorder or a family history of dementia.The demented patients received thorough clinical examinations and 8/10 were tested with the Wechsler Adult Intelligence Scale (WAIS). All had XCT and HMPAO-SPECT scans using a rotating gamma camera. Three patients had a MRI Scan.Results. The main symptoms were apathy and a lack of spontaneity as a result of which the patients were no longer able to live alone. HMPAO-SPECT: All the patients had clear hypoperfusion of the frontal and temporal lobes with seven showing a left predominance. XCT: A moderate degree of cortical atrophy, more pronounced in the frontal lobes, was observed in 6 patients. In 3 of them a previous XCT scan had been normal.MRI: Subcortical white matter hyperintensities were seen in the 3 patients examined.Discussion. Although our patients do not probably form, with regard to a etiology a homogeneous group, they share common characteristics which are very similar to those which differentiates DFT from AD.We postulate that some dysthymic disorders of the presenium might represent the initial stage of this type of dementia.This hypothesis relies on the evidence for frontal dysregulation in mood disorders as demonstrated, for example, by PET studies. In these cases the cortical abnormalities usually disappear as the dysthymia improves and are considered functional phenomena. They may correspond to the mechanism of deafferentation (or diaschisis). This implies a primary lesion, presumably located at a subcortical level (for instance a white matter lesion) producing a disruption of function in a distant (initially) intact brain region. As a supplementary hypothesis we propose that with time, and for as yet unknown reasons, the frontal hypoperfusion in our patients lost its reversibility and that, as a result, a particular type of dementia became manifest. In some cases this diaschisis protractiva may lead to secondary cortical atrophy.Conclusions. A DFT was found in 10 patients who had become dysthymic in their fifties. A pathogenic hypothesis i.e. diaschisis protractiva, is proposed, based on the evidence of neuroimaging studies.

Chez six malades droitiers presentant des troubles schizophreniques, il a ete decouvert par les methodes d'imagerie morphologique une atrophie corticale localisee temporale gauche, qui s'accompagnait a la tomoscintigraphie d'une hypoperfusion de meme siege, souvent plus etendue. Une relation a ete supposee avec des deficits verbaux constates aux tests (WAIS) et avec un trouble formel du langage et de la pensee. Une comparaison avec l'aphasie progressive primaire a permis de degager les points communs et les particularites de ces deux types de troubles sur le plan clinique et en imagerie cerebrale

The evolution of some dysthymic states towards dementia is now rarely considered whereas it was well known at the beginning of the century. In French the final stage of this evolution was known as "démence vésanique". In recent years it has been noted that a proportion of patients with presenile dementia do not have Alzheimer's disease (AD) but a particular type of cognitive impairment., called dementia of the frontal lobe type (DFT), characterised by clinical and neuropsychological signs of frontal lobe disorder as well as an anterior defect of cerebral perfusion or metabolism. The onset of DFT is insiduous and marked by personality changes and inappropriate affect. It has not yet been reported as starting with true dysthymic disorders. PATIENTS AND METHODS. Ten right handed patients (F/M = 9/1) became dysthymic in their fifties (m = 49.8 + 7.6 yr). All initially met the DSM III-R criteria for mood disorders. They were all treated with the standard drugs or ECT. Although initially responsive all the patients relapsed and their dysthymic disorders became less typical in presentation. At a mean age of 63.6 +/- 2.9 yrs a particular type of dementia became evident. None of the patients had a previous history of mood disorder or a family history of dementia. The demented patients received thorough clinical examinations and 8/10 were tested with the Wechsler Adult Intelligence Scale (WAIS). All had XCT and HMPAO-SPECT scans using a rotating gamma camera. Three patients had a MRI Scan. RESULTS. The main symptoms were apathy and a lack of spontaneity as a result of which the patients were no longer able to live alone. HMPAO-SPECT: All the patients had clear hypoperfusion of the frontal and temporal lobes with seven showing a left predominance. XCT: A moderate degree of cortical atrophy, more pronounced in the frontal lobes, was observed in 6 patients. In 3 of them a previous XCT scan had been normal. MRI: Subcortical white matter hyperintensities were seen in the 3 patients examined. DISCUSSION. Although our patients do not probably form, with regard to a etiology a homogeneous group, they share common characteristics which are very similar to those which differentiates DFT from AD. We postulate that some dysthymic disorders of the presenium might represent the initial stage of this type of dementia. This hypothesis relies on the evidence for frontal dysregulation in mood disorders as demonstrated, for example, by PET studies. In these cases the cortical abnormalities usually disappear as the dysthymia improves and are considered functional phenomena. They may correspond to the mechanism of deafferentation (or diaschisis). This implies a primary lesion, presumably located at a subcortical level (for instance a white matter lesion) producing a disruption of function in a distant (initially) intact brain region. As a supplementary hypothesis we propose that with time, and for as yet unknown reasons, the frontal hypoperfusion in our patients lost its reversibility and that, as a result, a particular type of dementia became manifest. In some cases this diaschisis protractiva may lead to secondary cortical atrophy. CONCLUSIONS. A DFT was found in 10 patients who had become dysthymic in their fifties. A pathogenic hypothesis i.e. diaschisis protractiva, is proposed, based on the evidence of neuroimaging studies.