Management of infectious encephalitis in adults: Highlights from the French guidelines (short version).

The article highlights the French clinical guidelines for the management of adult patients with acute infectious encephalitis.

MR imaging of adult acute infectious encephalitis.

BACKGROUND: Imaging is a key tool for the diagnosis of acute encephalitis. Brain CT scan must be urgently performed to rule out a brain lesion with mass effect that would contraindicate lumbar puncture. Brain MRI is less accessible than CT scan, but can provide crucial information with patients presenting with acute encephalitis. METHOD: We performed a literature review on PubMed on April 1, 2015 with the search terms "MRI" and "encephalitis". RESULTS: We first described the various brain MRI abnormalities associated with each pathogen of acute encephalitis (HSV, VZV, other viral agents targeting immunocompromised patients or travelers; tuberculosis, listeriosis, other less frequent bacterial agents). Then, we identified specific patterns of brain MRI abnomalies that may suggest a particular pathogen. Limbic encephalitis is highly suggestive of HSV; it also occurs less frequently in encephalitis due to HHV6, syphillis, Whipple's disease and HIV primary infection. Rhombencephalitis is suggestive of tuberculosis and listeriosis. Acute ischemic lesions can occur in patients presenting with severe bacterial encephalitis, tuberculosis, VZV encephalitis, syphilis, and fungal infections. CONCLUSION: Brain MRI plays a crucial role in the diagnosis of acute encephalitis. It detects brain signal changes that reinforce the clinical suspicion of encephalitis, especially when the causative agent is not identified by lumbar puncture; it can suggest a particular pathogen based on the pattern of brain abnormalities and it rules out important differential diagnosis (vascular, tumoral or inflammatory causes).

[Chronic meningitis: differential diagnosis]. / Diagnostic des méningites chroniques.

Chronic meningitis is defined by the association of symptoms of more than 1 month duration and an abnormal cellularity of the cerebrospinal fluid. About 10% of all meningitis are chronic meningitis. The differential diagnosis is wide and relies on anamnestic data, daily life characteristics and activities, immune status, clinical presentation and signs, and systematic search of most frequent causes. The main causes of chronic meningitis are tuberculous, cryptococcal, mainly in immunosuppressed patients, carcinomatous and systemic diseases associated meningitis. The first part of the paper details the overall etiological strategy to be used in the diagnosis of chronic meningitis. The second part is a literature-based review of the common and rare causes of chronic meningitis.

[Anti-NMDA-receptor encephalitis]. / Encéphalites avec anticorps anti-récepteur NMDA.

Anti-NMDA-receptor encephalitis has been described only recently among other causes of paraneoplastic and auto-immune limbic encephalitis. Its frequency is probably underestimated. The very characteristic clinical presentation, the severity of symptoms frequently leading to the intensive care unit, the therapeutic implications of the diagnosis whatever the cause, paraneoplastic or not and, once treated, the possibility of a full recovery or mild sequels in the majority of cases justify a surveillance either in neurology wards or in infectious, psychiatric, intensive care, or pediatric units. The authors review the history of this disease, the available epidemiological data, the characteristic clinical presentation of patients, the differential diagnosis, and the suggested treatment according to an up-to-date literature review.

Posterior reversible encephalopathy syndrome during sunitinib therapy.

A case of posterior reversible encephalopathy syndrome (PRES) occurring in a women treated by sunitinib for an ovarian metastatis of a renal cell carcinoma is described. This is the third case described in the literature. The three cases are very similar except for the delay to onset of the PRES (one week to five months). Both antiangiogenic and prohypertensive effects of sunitinib are probably involved in the pathophysiology of PRES. Physicians should be aware of this potentially life-threatening side-effect of sunitinib easily controlled by withdrawing sunitinib and symptomatic treatment.

[Cerebral vasculitis with aneurysms caused by varicella-zoster virus infection during AIDS: a new clinicoangiographical syndrome]. / Vascularite cérébrale avec sténoses et ectasies due au virus varicelle-zona au cours de l'infection par le VIH : une nouvelle entité compliquant le sida.

We describe three cases of cerebral angiopathy with aneurysms caused by a meningeal varicella-zoster virus infection occurring during AIDS. The clinical picture was rather stereotyped: severe immunocompromission due to HIV infection, ongoing multifocal cerebrovascular disease with territorial infarcts, lymphocytic meningitis with normal glucose content (two cases) or hypoglycorrhachia (one case), multifocal cerebral vasculopathy with narrowings and aneurysms, healing with or without neurological sequelae after intravenous aciclovir treatment. The diagnosis of varicella-zoster virus-induced angiopathy was ascertained by the positive specific PCR in the CSF in the three cases and by the results of the cerebromeningeal biopsy in one case. Although, varicella-zoster virus is already known as a cause of cerebral angiopathy both in the immunocompetent and the immunocompromised, these three cases are the first ever described of a particular angiopathy with narrowings and ectasias complicating AIDS. The infectious treatable cause and the risk of aggravation without treatment require early active oriented investigations in case of a patient with cerebrovascular disease occurring during HIV infection, including a CSF study with varicella-zoster PCR, to allow specific antiviral treatment. In our three cases, aciclovir intravenous treatment (30mg/kg per day) enabled VZ virus clearing from the CSF and stopped the course of the vasculopathy.

[Isoniazid induced neuropathy: consider prevention]. / Neuropathie toxique induite par l'isoniazide: pensez à la prévention.

INTRODUCTION: Antituberculous treatment is effective but has numerous side effects. Among these isoniazid induced neuropathy is easily preventable. CASE REPORT: A female patient of 42 years, infected with HIV, presented with general deterioration associated with an interstitial pulmonary infiltrate and mediastinal lymphadenopathy. Tuberculosis was not confirmed bacteriologically but she responded to antituberculous treatment. Three months later she developed distal leg pains extending proximally. There was superficial sensory impairment up to the groins and loss of the ankle reflexes. The dose of isoniazid was reduced from 5 to 2.5 mg/kg/day on account of slow acetylator status and treatment with pyridoxine 250 mg/day commenced. The clinical signs resolved in a few weeks. CONCLUSIONS: Isoniazid neuropathy develops in the presence of risk factors (HIV, alcoholism, diabetes, renal failure, malnutrition, pregnancy and lactation, neurotoxic medication) and manifests itself initially by burning feet. Pyridoxine is preventative in low dosage and curative in high dosage. The development of symptoms should lead to measurement of acetylator status, and a reduction of the isoniazid dose to 3 mg/kg/day or even less in slow acetylators.

[Treatment of tuberculous meningitis]. / Traitement des tuberculoses cérébro-méningées.

INTRODUCTION: Tuberculous meningitis and brain tuberculomas are currently rare in the western world but remain serious. Improved outcome requires early recognition and treatment of these conditions. STATE OF ART: Treatment is usually begun before diagnostic confirmation. Therapeutic principles are now better defined thanks to recent recommendations and studies. Antituberculous therapy begins with two months of a combination of four drugs: isoniazid, rifampicin, ethambutol and pyrazinamid. Then follows a longer phase of bitherapy with isoniazid and rifampicin, lasting at least four months but usually extended to seven or ten months as a precaution. Patients at risk of toxic neuropathy should receive pyridoxine supplementation. Corticosteroids must be systematically added during the first eight weeks of treatment, beginning with high dose before progressive tapering. Hyponatremia is common, often induced by emesis and cerebral salt wasting syndrome. Therefore saline supply rather than water restriction is required. Non-obstructive hydrocephaly can usually be managed with diuretic therapy including acetazolamid, sometimes complemented by serial lumbar punctures. Neurosurgical interventions are rarely needed. Monitoring of treatment tolerance and efficacy is mainly clinical. Central nervous system imaging and cerebro-spinal fluid analysis are only required to explain clinical deterioration. CONCLUSION: With adequate and prompt anti-tuberculous, anti-inflammatory and supportive treatment, the prognosis of central nervous system tuberculosis can be greatly improved.

[Acute neurological disclosure of B12 avitaminosis induced by folic acid administration]. / Révélation neurologique aiguë d'une avitaminose B12 par l'administration d'acide folique.

A paradigmatic case of acute combined spinal cord degeneration and delirium due to inappropriate administration of folic acid in the context of chronic cobalamin deficiency is described. Rapid improvement was obtained with immediate cessation of folate administration and parenteral cobalamin supplementation. Folic acid and cobalamin prescription rules are recalled. Pathophysiological hypotheses tentatively explaining the neurotoxicity of folic acid in case of vitamin B12 deficiency are summarized.

[Hereditary Creutzfeldt-Jakob disease caused by a mutation at codon 200]. / Maladie de Creutzfeldt-Jakob génétique par mutation du codon 200.

INTRODUCTION: A typical case of genetic Creutzfeldt-Jakob disease in a 39-year-old woman without remarkable familial history is described. CASE REPORT: Initial symptoms were disequilibrium, cerebellar syndrome and complex neurovisual complaints. EEG was pseudoperiodic. NSE and 14-3-3 protein levels were elevated in the CSF. MRI showed anomalies of the anterior parts of the putamen and the caudate nuclei on the MRI T2 FLAIR sequence, mainly on diffusion sequences. A quinacrine test did not yield any effect. Death eventually occurred 8 months after the first symptoms. CONCLUSION: Current data on genetic Creutzfeldt-Jakob disease are briefly reviewed.