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Dabigatran etexilate (DE) is a direct thrombin inhibitor, which has been approved for the treatment of non-valvular atrial fibrillation (AF), and for the prevention and treatment of venous thromboembolism (VTE). Despite large randomized clinical trials and independent observational studies providing robust data concerning DE safety and efficacy, some physicians still perceive mild-to-moderate renal impairment and old age as a relative contraindication to its use. In this article, we review the available scientific evidence supporting the use of DE in these clinical situations. Patients with AF and chronic kidney disease (CKD) are per se at high risk of stroke, bleeding and mortality. Although there is evidence of clinical benefit of anticoagulation in these patients, anticoagulant therapy requires caution and demands careful clinical monitoring, regardless of the drug used. In patients with no contraindication to its use, the clinical benefit of DE versus warfarin is independent of renal function. The elderly with AF are frequently undertreated because of the perception of high bleeding risk and limited clinical benefit. However, the clinical benefit of anticoagulation is independent of patient age, and age per se should not represent a contraindication to anticoagulation. DE has been extensively studied in the elderly, both in randomized clinical trials and in observational studies: DE 150 mg BID should not be used in patients 80 years of age or older, while DE 110 mg BID is as safe as warfarin. Intracranial haemorrhages reduction by DE compared with warfarin is preserved in the elderly. Therefore, mild and moderate CKD and being elderly should not deter physicians from prescribing DE. Furthermore, the availability of a specific antidote is expected to improve the safety of the use of DE in clinical practice.

The Glasgow Coma Scale (GCS) is the most widely accepted tool for the evaluation of consciousness, despite several reported shortcomings. A new coma scale, named Full Outline of UnResponsiveness (FOUR) score, is now available. The aim of the present study is to provide and validate the Italian version of the FOUR score. The Italian version of the FOUR score was developed according to a standardized protocol, and thereafter validated in a series of patients with acute neurological illness. For each patient, the FOUR and the GCS scores were recorded by two physicians randomly selected. The inter-rater agreement for the FOUR and the GCS scores was evaluated using the weighted kappa (κ(w)). The receiving operating characteristic curve was also calculated to determine the ability of the scales to predict outcome. Eighty-seven consecutive patients with an acute brain injury were enrolled. The inter-rater agreement was excellent both for the FOUR (κ(w) = 0.953; P 0.0001) and the GCS (κ(w) = 0.943; P 0.01). The area under the curve for mortality was 0.935 for the FOUR and 0.953 for the GCS. The FOUR score provides greater neurological details than the GCS. Our data indicate that the Italian version of the FOUR score is a valid predictor of outcome, yielding reproducible findings across raters independent of their expertise.

Aortic dissection is an uncommon cause of stroke in young patients, and can lead to a severe prognosis, especially if not promptly diagnosed and adequately treated. Among the etiologies that can underlie an arterial dissection in the young, there are heritable connective tissue disorders (HCTDs) with increased vascular fragility [1]. Among them, the Loeys–Dietz syndrome (LDS) is a recently defined aortic aneurysm syndrome, inherited as an autosomal-dominant disease, and caused by heterozygous mutations in various proteins of the transforming growth factor beta (TGF-b) pathway [2]. We report a case of a young woman with LDS, which had been unrecognized until the patient presented to the emergency department (ED) with focal neurological symptoms due to an acute ischemic stroke secondary to aortic dissection. The diagnosis of LDS type 2, confirmed at the molecular level, offered the opportunity to describe and discuss several causes of arterial dissection in the young, and focus on the underlying diseases, particularly focusing on this recently described HCTD.

Different types of hyperkinetic movement disorders, such as hemiballism, hemichorea, dystonia and tremor, have been reported in patients with basal ganglia lesions due to ischemic or hemorrhagic stroke. Hemiballism, defined as a severe, violent, dysrhythmic and flinging excursion of a limb from a proximal joint, is one of the most distinctive signs of a vascular basal ganglia lesion [1]. The involuntary movements in hemiballism commonly involve the arm and the leg, as well as the facial muscles in about half of the cases. This relatively rare movement disorder has been classically ascribed to a lesion of the subthalamic nucleus (STN). However, the increasing use of neuroimaging in the last 20 years has highlighted the association between hemiballism and lenticular, caudate and even cortical lesions, usually involving the parietal lobe [1]. Stroke accounts for 50–75 % of cases of this disorder, which usually consist of lacunar infarctions or, less often, of hemorrhage. Other rarer vascular causes include arteriovenous malformations, venous angioma and subarachnoid hemorrhage. In addition, brief episodes of hemiballism may be a manifestation of a transient ischemic attack, involving either the carotid or vertebrobasilar territories. Neuroimaging studies have shown that several of these transient episodes are based on permanent infarcts [2]. A 74-year-old right-handed man, with a previous history of hypertension and dyslipidemia, presented a left motor disorder upon arrival at the emergency department (ED) of our hospital. The clinical examination highlighted slow, random, mostly proximal, involuntary movements involving the left arm and leg, associated with some grimacing on the homolateral side of the face. A cerebral computed tomography scan, performed 2.5 h after symptom onset, revealed mild signs of chronic vascular leucoencephalopathy. Although the patient had a National Institutes of Health Stroke Scale (NIHSS) score of zero [3], it was decided, on the basis of the clinical signs and after the exclusion of other possible causes for the hyperkinetic disorder (e.g. marked hypoglycemia, drugs), that he should undergo off-label thrombolysis with alteplase (67.6 mg iv), which was administered 3.5 h after stroke onset. Within 2 h of treatment, the involuntary movements were less pronounced, being limited to the left arm, mainly distal and of lower amplitude. A brain magnetic resonance imaging (MRI) examination performed the following day revealed a recent ischemic lesion of the right capsula extrema and insular cortex and the integrity of both subthalamic nuclei (Fig. 1). Another smaller lesion was found in the right temporal–parietal cortex. The patient’s symptoms resolved completely within 3 days without any symptomatic therapy. Hemiballism may be caused by a lesion in the contralateral STN, but, several studies have demonstrated that lesions outside the STN region, as in the present case, may be responsible for up to 85 % of the cases of hemiballism [4]. STN lesions reduce the striato-pallidal inhibitory influences along the basal ganglia circuit. This leads to reduced excitatory projection from the STN to the pars interna of the globus pallidus, which in turn disinhibits the thalamus and cortex, resulting in an involuntary movement. The somatosensory cortex also projects to the putamen, and may influence this basal ganglia circuit. It has been suggested that hemiballism caused by lesions of the STN is more severe than that caused by lesions located elsewhere, A. Correnti D. Toni C. Colosimo (&) Department of Neurology and Psychiatry and Neurovascular Unit, ‘‘Sapienza’’ University of Rome, v.le dell’Universita 30, Rome, Italy e-mail: carlo.colosimo@uniroma1.it