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Torre Annunziata, Italy

Anticoli S.,Stroke Unit | Pezzella F.R.,Stroke Unit | Pozzessere C.,Stroke Unit | Gallelli L.,University of Catanzaro | And 3 more authors.
Journal of Stroke and Cerebrovascular Diseases | Year: 2015

Background Acute ischemic lesions on diffusion-weighted magnetic resonance imaging (DWI-MRI) are reliable predictors of recurrent stroke at 90 days. However, to date, limited information on transient ischemic attack (TIA) patients with positive DWI lesions for stroke risk from 1 to 5 years is available. In this study, we evaluated the role of positive DWI lesions and vascular risk factors on stroke, cardiovascular death, and mortality at 90 days (T0), 1 year (T1), and 5 years (T2). Moreover, we also evaluated the association between stroke risk and the presence of DWI lesions. Methods We performed an observational study on consecutive patients admitted to the emergency department of San Camillo-Forlanini Hospital, Rome, Italy, from January 2007 to November 2012. Over the study period, 4300 patients with TIA or ischemic stroke were examined by stroke specialists in an emergency room setting within 1 hour from admittance. Results In 510 of 4300 patients (11.86%), a TIA was diagnosed, and 445 patients satisfy the study inclusion criteria. For all 445 patients, the mean ABCD2 score was 4.35 ± 1.30. Using DWI-MRI, we identified acute ischemic lesions in 185 patients (41.57%). We did not observe any correlation between duration of symptoms, ABCD2 score, and positive or negative DWI lesions. Positivity for DWI was not associated with the presence of diabetes mellitus, hypertension, smoking habit, or age; however, an association with weakness was observed. We documented a time-dependent increase in the absolute risk of stroke: T0: 1.35% (95% confidence interval [CI],.81-2.8); T1: 4.78% (95% CI, 2.88-7.47); T2: 9.02% (95% CI, 4.66-5.70). We did not record any difference in stroke risk in patients with positive DWI lesions: T0: hazard ratio [HR], 1.43; 95% CI,.35-5.88; log-rank P =.60; T1: HR, 1.04; 95%CI,.42-2.61; log-rank P =.91; T2: HR,.83; 95% CI,.25-2.67; log-rank P =.86. Conclusions This long-term follow-up study in TIA patients documents that both positive and negative DWI patients treated with fast-track had similar long-term risks of stroke. © 2015 National Stroke Association. Source


Siniscalchi A.,Annunziata Hospital | Bonci A.,U.S. National Institute on Drug Abuse | Mercuri N.B.,University of Rome Tor Vergata | De Siena A.,Dependance Unit | And 4 more authors.
Current Neurovascular Research | Year: 2015

Cocaine abuse remains a devastating medical problem for our society. Current concepts suggest that both hemorrhagic and ischemic stroke, particularly in young people, can result as a consequence of cocaine exposure. We provide an analysis of mechanisms of injury and a discussion of the pharmacological management of stroke following cocaine use. Preclinical research suggests that the cause of cocaine-mediated stroke is multifactorial and involves vasospasm, changes in cerebral vasculature, and platelet aggregation. We suggest that drugs able to induce vasospastic, thrombogenic, or neurotoxic effects of cocaine could be suitable as therapeutic agents. In contrast caution should be exerted when using anti-platelet and thrombolytic agents in cocaine users with stroke. Source


Siniscalchi A.,Annunziata Hospital | Gallelli L.,University of Catanzaro | De Sarro G.,University of Catanzaro
Clinical Drug Investigation | Year: 2013

Dysaesthetic pain is a common neuropathic pain in patients with multiple sclerosis. Both tricyclic antidepressants (i.e., amitriptyline and duloxetine) and antiepileptic drugs (i.e., carbamazepine, gabapentin and pregabalin) represent first-line treatment of neuropathic pain. However, topiramate, an antiepileptic drug, also demonstrated clinical efficacy in these patients. In this report we describe the case of a 42-year-old woman with an 8-year history of multiple sclerosis who developed dysaesthetic pain in the lower limbs, and was successfully treated with topiramate at a final dose of 150 mg/day. About 8 months after beginning topiramate treatment, the patient had not shown any dysaesthetic pain, and no adverse events related to topiramate had been recorded. © 2012 Springer International Publishing Switzerland. Source


Siniscalchi A.,Annunziata Hospital | Iannacchero R.,Regional Headache Research Center | De Sarro G.,University of Catanzaro | Gallelli L.,University of Catanzaro
Current Vascular Pharmacology | Year: 2016

Stroke is an acute condition characterized by a sudden decrease in blood flow to brain tissue, resulting in immediate deprivation of both glucose and oxygen. Different mechanisms are involved in the pathogenesis of stroke, but increasing evidence suggests that one of the processes worsening clinical outcome is inflammation with the synthesis and the release of pro-inflammatory cytokines that activate several cells contributing to the progression of brain injury. Monoclonal antibody therapy has proved useful and safe for the treatment of several systemic diseases. In contrast, the evidence is limited for the treatment of stroke. More studies are needed in order to standardize the method of treatment and establish if it is safe and effective. © 2016 Bentham Science Publishers. Source


Siniscalchi A.,Annunziata Hospital | Gallelli L.,University of Catanzaro | Tolotta G.A.,University of Catanzaro | Loiacono D.,University of Catanzaro | De Sarro G.,University of Catanzaro
Clinical Therapeutics | Year: 2010

Background: Improvement of fatigue in patients with multiple sclerosis (MS) who were given bupropion has been previously reported, but scales for lethargy and depression were not used.Objective: This letter describes the course of chronic fatigue in a patient with MS who received off-label treatment with bupropion.Methods: A 47-year-old white woman (weight, 56 kg) with a 7-year history of relapsing-remitting MS (Ex- panded Disability Status Scale score of 3), without previous use of medication for MS, presented with a complaint of irritability and chronic fatigue. The Fatigue Severity Scale (FSS) documented the presence of fatigue related to MS (score of 7). The Beck Depression Inventory scale excluded an association between depression and fatigue (score of 8; possible range, 0-24); both the Pittsburgh Sleep Quality Index (score of 4; possible range, 0-21) and the Epworth Sleepiness Scale (score of 6; possible range, 0-24) excluded nighttime and daytime sleep disturbances. The patient was started on amantadine (100 mg/d), with an increase to 100 mg every 12 hours 2 weeks later, for the persistence of fatigue. Three months later, the absence of clinical response was noted (FSS score of 7). Amantadine was discontinued and bupropion therapy was initiated at 300 mg/d.Results: A repeat clinical evaluation conducted after 3 months of bupropion treatment indicated an improvement in fatigue (FSS score of 4) without changes in Beck Depression Inventory, Pittsburgh Sleep Quality Index, or Epworth Sleepiness Scale scores. The discontinuation and reinitiation of bupropion confirmed the effective- ness of bupropion for improving chronic fatigue in this patient. At the time of writing this report, 13 months after the resumption of bupropion treatment, the patient had experienced no further episodes of fatigue, and no adverse events had been reported.Conclusion: This patient with relapsing-remitting MS experienced improvements in chronic fatigue (as measured by FSS) after treatment with bupropion, but properly designed, randomized, active- and placebo-controlled clinical trials are needed to evaluate the efficacy and safety of bupropion in more patients with MS and fatigue. © 2010 Elsevier HS Journals, Inc. Source

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