Sir,Roohi et al. recently published their case report on sudden unexpected nocturnal death (SUND) of a 29-year-old with chiari type 1 malformation who received opioid narcotics.[1] The authors present the potential contributory role of altered respiratory and autonomic brainstem centers secondary to local pressure and opioid effect, especially during sleep.Raising issues relating to the risks associated with nonoperated tonsillar decent and chiari 1 is important, however, the title of this single case report is misleading and lacks the fine-tuning of clinical-imaging classification of neurosurgical abnormalitiesThe described case is not an isolated chiari 1 malformation! It is rather, a chiari concurrent with hydrocephalus, significant dilatation of the fourth ventricle, and periventricular edema (on the axial fluid attenuated inversion recovery [FLAIR] image). According to the authors (and the sagittal magnetic resonance imaging [MRI]), the lateral and third ventricles were dilated too. Additionally, the presenting symptoms included headaches, nausea and vomiting, and blurred vision. Despite a near normal neurological (and normal fundoscopic) exam, it seems that this patient presented with symptomatic hydrocephalus. Thus, the basic interpretation of the pathophysiological mechanism in this case is incorrect.Hydrocephalus and chiari may be interrelated. When hydrocephalus is active, and especially when the 4th ventricle is trapped, tonsillar descent may cause respiratory arrest with or without narcotics. Such situations should be taken very seriously and treated promptly.As many people have asymptomatic chiari, and many patients with chiari may have some form of headache, sometime necessitating analgesic treatment, the medico-legal implications of this case report may be very problematic. We encourage the authors and the journal to consider withdrawing this publication.