Symptômes psychiatriques d’une encéphalite paranéoplasique à anticorps antirécepteurs NMDA : à propos d’un cas

Foll, Julie Le; Pelletier, A

doi:10.1016/j.encep.2009.06.008

Cited by 8 publications

(3 citation statements)

References 21 publications

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“…Au-delà des aspects réactionnels, on évoquera un épisode dépressif directement lié au processus neurologique ou « syndrome thymique organique » (organic mood syndrom) [9]. Ensuite, compte tenu des antécédents du patient, on évoquera une [8,10] un modèle physiopathologique des troubles psychiatriques : en effet, l'étude du glutamate et des récepteurs aux NMDA avait déjà permis de proposer une hypothèse neurobiologique de la schizophrénie [11]. Un lien entre le récepteur au NMDA et les symptômes thymiques a également été soulevé avec un résultat plus incertain [10].…”

Section: Discussionunclassified

“…Ensuite, compte tenu des antécédents du patient, on évoquera une [8,10] un modèle physiopathologique des troubles psychiatriques : en effet, l'étude du glutamate et des récepteurs aux NMDA avait déjà permis de proposer une hypothèse neurobiologique de la schizophrénie [11]. Un lien entre le récepteur au NMDA et les symptômes thymiques a également été soulevé avec un résultat plus incertain [10]. Les examens réalisés dans le cadre de l'encéphalite limbique de M. H. n'ont pas montré la présence d'autoanticorps.…”

Section: Discussionunclassified

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Syndrome dépressif et encéphalite limbique : à propos d’un cas

Saladini¹,

Gelin²,

Bidault³

et al. 2011

Annales Médico-psychologiques, revue psychiatrique

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Limbic encephalitis is frequently a paraneoplasic disorder. The symptoms are both neurologic and psychiatric such as loss of memory, seizure and depression. We present the case of a sixty years old man in which severe depression, personal and familial history of mood disorders coexists with limbic encephalitis without any neoplasic disorder. In this case, we discuss hypothesis of links between his depression and his limbic encephalitis

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Section: Discussionunclassified

Syndrome dépressif et encéphalite limbique : à propos d’un cas

Saladini¹,

Gelin²,

Bidault³

et al. 2011

Annales Médico-psychologiques, revue psychiatrique

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“…MRI anomalies are known to be nonspecific and present only in 40 % of patients with anti-NMDAR encephalitis (Pollak et al 2020). But some reports of early secondary psychosis described inflammatory lesions in the left precentral and anterior cingulate gyri, the medial temporal lobes and bilateral insular cortices, or in fronto-parietal and bi-occipital gyri (Söylemez et al 2015;Sabbula et al 2020;Le Foll and Pelletier 2010). Diffuse white matter lesions have also been described in settings where isolated psychotic symptoms revealed the onset of neurolupus (Jghaimi, Kabbaj, and Essaadouni 2009) or of demyelinating disorders such as multiple sclerosis (Jongen 2006) and acute disseminated encephalomyelitis (Neeki et al 2016).…”

Section: In Secondary Psychosismentioning

confidence: 99%

Brain anomalies in early psychosis: From secondary to primary psychosis

Iftimovici

Chaumette

Duchesnay

et al. 2022

Neuroscience & Biobehavioral Reviews

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La catatonie

Pot

Lejoyeux²

2015

L'Encéphale

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In the new classification of the DSM-V, catatonia is individualized as a disease of its own. It is defined by presence of at least two out of five criteria: motor immobility, negativism, echolalia or echopraxia, sterile motor activity, atypical movements. The priority is to look first for organic causes: the main ones are neurologic disorders. Intoxication may also be found (illegal drugs or medication), and the role of neuroleptic malignant syndrome in catatonia remains unclear. Among the psychiatric causes, first come bipolar disorders, especially mania; then schizophrenia. Idiopathic forms can also be observed. Epidemiological work on catatonia show highly variable results, highlighting a possible underestimation of the diagnosis. Among the differential diagnoses, which are rare motor syndromes, neuroleptic malignant syndrome and serotonin syndrome are also discussed. The diagnosis of catatonia is clinical and can be obtained using standardized diagnostic scales. The use of zolpidem provides both a diagnostic and therapeutic guidance for the degree of response to drug treatment. The physiopathological hypotheses describe an intracerebral GABAergic, dopaminergic and glutamatergic dysfunction in catatonic patients. The complete mechanisms are still partly unknown. Benzodiazepines are the first treatment of choice. Electroconvulsive therapy is used secondarily or in severe cases. First-generation antipsychotics are prohibited, at the risk of worsening the catatonia in becoming malignant and lethal. The renewed interest in the catatonic syndrome during the past recent years has expanded research on the mechanisms of this syndrome and opened the way to new therapeutic options. The latest works tend to modulate the strict prohibition of antipsychotic in a catatonic patient.

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Symptômes psychiatriques d’une encéphalite paranéoplasique à anticorps antirécepteurs NMDA : à propos d’un cas

Cited by 8 publications

References 21 publications

Syndrome dépressif et encéphalite limbique : à propos d’un cas

Syndrome dépressif et encéphalite limbique : à propos d’un cas

Brain anomalies in early psychosis: From secondary to primary psychosis

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