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Carbon monoxide (CO) inhalation is nowadays the most common cause of fatal poisoning worldwide. CO binds to haemoglobin 230–270 times more avidly than oxygen, thus leading to formation of carboxyhaemoglobin with subsequent reduction of tissue oxygenation. Brain is mainly affected due to its high oxygen requirement. Up to two-thirds of patients who survive the acute phase of this pathology present a delayed leukoencephalopathy, usually in a period ranging from two to 40 days. White matter damage closely relates to long-term prognosis of these patients. On the other hand CO seems to play a fundamental role as a possible neuro-protective agent in ischaemic stroke. Diagnostic imaging, with computed tomography and magnetic resonance imaging, especially magnetic resonance spectroscopy, is very useful to depict the presence and extension of this pathology, in both acute and late phase. Nevertheless, a correlation of imaging studies with clinical history and laboratory data is fundamental to perform the correct diagnosis. The purpose of this article is to highlight the imaging features of brain CO poisoning in acute and late phase, describing a case report of a 56-year-old man found unconscious at home.

Rosai-Dorfman disease (RDD) is a rare, benign, non-Langerhans cells histiocytosis with massive lymphadenopathy of uncertain aetiology. It is commonly characterized by massive, painless, non-tender, bilateral cervical lymphadenopathy. Extra-nodal involvement is usually seen in 50% of patients, with the brain being affected in only 5% of cases, usually as dural-based lesions. Clinical presentation is heterogeneous and strongly dependent on the localization of the lesions. Although the histopathological findings are essential for the final diagnosis, brain magnetic resonance imaging (MRI) currently represents the first-line strategy for the detection of the lesions across the central nervous system (CNS); moreover, it may provide additional elements for the differential diagnosis versus other more common lesions. We performed a case-based literature review to highlight possible aetiologic and pathogenetic theories of this disease, along with imaging features of RDD, with a particular focus on the MRI characteristics of the CNS involvement (CNS-RDD). Finally, we provided a novel insight on the current therapeutic approaches, either surgical or medical.

Background Myasthenia gravis (MG) is an autoimmune disease in which 90% of patients have autoantibodies against the muscle nicotinic acetylcholine receptor (AChR), while autoantibodies to muscle-specific tyrosine kinase (MuSK) have been detected in half (5%) of the remaining 10%. Recently, the low-density lipoprotein receptor-related protein 4 (LRP4), identified as the agrin receptor, has been recognized as a third autoimmune target in a significant portion of the double sero-negative (dSN) myasthenic individuals, with variable frequency depending on different methods and origin countries of the tested population. There is also convincing experimental evidence that anti-LRP4 autoantibodies may cause MG. Methods The aim of this study was to test the presence and diagnostic significance of anti-LRP4 autoantibodies in an Italian population of 101 myasthenic patients (55 dSN, 23 AChR positive and 23 MuSK positive), 45 healthy blood donors and 40 patients with other neurological diseases as controls. All sera were analyzed by a cell-based antigen assay employing LRP4-transfected HEK293T cells, along with a flow cytofluorimetric detection system. Results We found a 14.5% (8/55) frequency of positivity in the dSN-MG group and a 13% frequency of co-occurrence (3/23) in both AChR and MuSK positive patients; moreover, we report a younger female prevalence with a mild form of disease in LRP4-positive dSN-MG individuals. Conclusion Our data confirm LRP4 as a new autoimmune target, supporting the value of including anti-LRP4 antibodies in further studies on Myasthenia gravis.

Although classical trigeminal neuralgia (CTN) is frequently caused by neurovascular contact (NVC) at the trigeminal root entry zone (REZ), both anatomical and MRI studies have shown that NVC of the trigeminal nerve frequently occurs in individuals without CTN. To assess the accuracy of MRI in distinguishing symptomatic from asymptomatic trigeminal NVC, we submitted to high-definition MRI the series of CTN patients referred to our outpatient service between June 2011 and January 2013 (n=24), and a similar number of age-matched healthy controls. Two neuroradiologists, blinded to the clinical data, evaluated whether the trigeminal nerve displayed NVC in the REZ or non-REZ, whether it was dislocated by the vessel or displayed atrophy at the contact site, and whether the offending vessel was an artery or a vein. Our data were meta-analyzed with those of all similar studies published from January 1970 to June 2013. In our sample, REZ contact, nerve dislocation and nerve atrophy were independently associated with CTN (P=.027; P=.005; P=.035 respectively). Compared to a rather low sensitivity of each of these items (alone or in combination), their specificity was high. When REZ contact and nerve atrophy coexisted, both specificity and positive predictive value rose to 100%. Meta-analysis showed that REZ NVC was detected in 76% of symptomatic and 17% of asymptomatic nerves (P