Les thérapies par anti-TNF alpha (ATA) sont prescrites dans le cadre de certaines maladies inflammatoires rhumatologiques et digestives. Des évènements neurologiques ont été rapportés. La prise en charge de ces épisodes n’est pas standardisée.

Nous avons colligé les patients adressés dans notre service suite à la survenue d’un événement neurologique sous ATA. Pour chaque patient, les caractéristiques cliniques, radiologiques, l’étude du liquide céphalorachidien (LCR) et l’évolution étaient analysées.

Neuf patients ont été colligés (Âge : 49±8ans, sex-ratio : 8/1). Le tableau clinique était d’allure inflammatoire (cinq cas), vasculaire (trois cas) ou une neuropathie périphérique (un cas). L’IRM montrait des hypersignaux T2 suggestifs de pathologie démyélinisante (quatre cas dont un remplissant les critères de Barkhof), vasculaire (deux cas) ou aspécifique (trois cas). L’étude du LCR était normale (quatre cas), montrait des bandes oligoclonales (un cas) ou une méningite lymphocytaire (un cas). Le traitement par ATA a été stoppé dans cinq cas. Le suivi était globalement favorable (huit cas) et a évolué en une sclérose en plaques (SEP) rémittente dans un cas.

Dans notre cohorte, les critères de Barkhof et l’étude initiale du LCR semblent avoir une valeur pronostique sur l’évolution vers une SEP.

Anti-TNF alpha treatments are increasingly prescribed in various rheumatological or gastroenterological inflammatory diseases. Several adverse events, including neurological episodes have been reported in the literature. Relation to treatment is a major concern and guidelines for management of those patients are not available. The aim of our study is to collect and analyze neurological adverse events occurring during anti-TNF alpha therapy, and to propose guidelines for diagnosis of demyelinating-induced diseases.

All patients treated with anti-TNF alpha drug, who were addressed in our department following a neurological event, were collected. We gathered clinical data including previous neurological history and immunosuppressive treatments. Paraclinical data included brain and spinal MRI, CSF study and outcome after anti-TNF therapy was collected.

Nine patients were included in this study. Sex ratio was eight and mean age was 49±9 years. One patient had previous history of subarachnoïdian hemorrage. All the patients previously received immunosuppressive drugs, including methotrexate (nine) and leflunomide (four). Three patients had a brain MRI before initiation of anti-TNF treatment, which was normal. Clinical episode was stroke-like in three cases, clinically isolated syndrome (CIS) in five cases, and peripheral neuropathy in one case. MRI showed lesions suggestive of demyelinating T2 hyperintensities in four cases, vascular infarcts in two cases, and non-specific T2 hyperintensities in three cases. Barkhof and Tintore criteria were fulfilled in one of the four CIS cases. CSF study was available for six patients. It was normal (four cases), showed oligoclonal bands (one case) and lymphocytic meningitis (one case). Anti-TNF alpha discontinuation was decided in five cases. Outcome was favorable for eight patients. One patient, whom MRI fulfilled Barkhof and Tintore criteria, and CSF showed oligoclonal bands, further developed relapsing remitting multiple sclerosis.

Our study is compatible with data found in the literature. Barkhof and Tintore criteria and CSF study are useful in clinical practice to diagnose a first demyelinating event. Standardized paraclinical neurological explorations should be proposed to physicians who are in charge of anti-TNF treated patients.