Neuroleptic malignant syndrome in a patient treated with clotiapine.

BACKGROUND: Neuroleptic malignant syndrome (NMS), which is linked to the use of antipsychotic medication, is a potentially lethal neurological emergency. The interest of our study is that NMS induced by the use of clotiapine has never previously been described. SUBJECTS AND METHODS: We present the case of a 61-year old man whose sleep disorders were treated with clotiapine 40 mg/day. After 7 days of taking 40 mg clotiapine, the patient presented with a deterioration of his general health which had gradually taken hold, with altered consciousness accompanied by generalised muscle rigidity and hypersalivation. Laboratory blood tests revealed elevated levels of Creatine Phosphokinase (CPK) at 812 U/l. The patient was diagnosed with NMS and treated accordingly. RESULTS: The mechanism that underlies the appearance of NMS remains largely unknown. Clotiapine is a second-generation antipsychotic, first released onto the market in the 1970s, and is available in a few countries, including Belgium. NMS is treated as a medical emergency due to the possibility of morbidity and death. The first step in the treatment of NMS consists in withholding the agent suspected of provoking the symptoms. CONCLUSIONS: NMS is difficult to diagnose due to a great variability in clinical presentations and the absence of specific tests and laboratory results. The use of clotiapine in treating sleep disorders can provoke NMS as a life-threatening side-effect. To our knowledge, this is the first time a case of clotiapine-induced NMS has been published.

An unusual cause of visual loss: involvement of bilateral lateral geniculate bodies.

We report the clinical and radiologic features of a 31-year-old woman who suffered incongruous binasal and bitemporal visual field defects and severe sudden visual loss due to hypoperfusion of bilateral lateral geniculate bodies following anaphylactic shock induced by 500 mg amoxicillin per os. Complete neuroophthalmologic examinations were performed regularly for visual acuity, color vision, pupillary reflexes, and visual fields. Additional testing was performed by means of MR imaging of the brain and CSF analysis. Follow-up was performed for 12 months. Vision loss was acute and severe, its onset bilateral and simultaneous. The patient recovered visual acuity of 1.0 within 7 weeks. Color vision was abnormal in both eyes but gradually improved to normal. Visual fields were characterized by incongruous binasal and bitemporal defects, but they reduced progressively. Cerebral MR imaging confirmed the presence of symmetrical lesions confined exclusively within both lateral geniculate bodies. These lesions were best seen on T1-weighted and fluid-attenuated inversion recovery images as high-signal-intensity areas suggestive of hemorrhagic ischemia. CSF analysis was normal and aseptic. Blood tests and cultures excluded any microbial infection. We conclude that shock may induce a bilateral isolated ischemia of the lateral geniculate bodies, resulting in incongruous binasal and bitemporal visual field defects and severe visual loss. MR imaging is the optimal imaging technique to confirm the diagnosis and for follow-up.