Background and Purpose: We aimed to investigate the rate of hospital admissions for cerebrovascular events and of revascularization treatments for acute ischemic stroke in Italy during the coronavirus disease 2019 (COVID-19) outbreak. Methods: The Italian Stroke Organization performed a multicenter study involving 93 Italian Stroke Units. We collected information on hospital admissions for cerebrovascular events from March 1 to March 31, 2020 (study period), and from March 1 to March 31, 2019 (control period). Results: Ischemic strokes decreased from 2399 in 2019 to 1810 in 2020, with a corresponding hospitalization rate ratio (RR) of 0.75 ([95% CI, 0.71–0.80] P <0.001); intracerebral hemorrhages decreased from 400 to 322 (hospitalization RR, 0.81 [95% CI, 0.69–0.93]; P =0.004), and transient ischemic attacks decreased from 322 to 196 (hospitalization RR, 0.61 [95% CI, 0.51–0.73]; P <0.001). Hospitalizations decreased in Northern, Central, and Southern Italy. Intravenous thrombolyses decreased from 531 (22.1%) in 2019 to 345 in 2020 (19.1%; RR, 0.86 [95% CI, 0.75–0.99]; P =0.032), while primary endovascular procedures increased in Northern Italy (RR, 1.61 [95% CI, 1.13–2.32]; P =0.008). We found no correlation ( P =0.517) between the hospitalization RRs for all strokes or transient ischemic attack and COVID-19 incidence in the different areas. Conclusions: Hospitalizations for stroke or transient ischemic attacks across Italy were reduced during the worst period of the COVID-19 outbreak. Intravenous thrombolytic treatments also decreased, while endovascular treatments remained unchanged and even increased in the area of maximum expression of the outbreak. Limited hospitalization of the less severe patients and delays in hospital admission, due to overcharge of the emergency system by COVID-19 patients, may explain these data.
Between January 2007 and March 2008, we prospectively studied all patients operated on for intracranial tumours in our Department of Neurosurgery. Preoperatively, all patients were interviewed by a neurologist to collect headache characteristics. Measurements of tumour and oedema volume were made using dedicated software for magnetic resonance imaging studies. Tumour histopathology was established by histological examination postoperatively. If headache improved postoperatively, a diagnosis of 'headache attributed to intracranial neoplasm' was made, according to the 2004 International Classification of Headache Disorders (ICHD-II). A multivariate logistic regression model was used to evaluate the association of headache with potential risk factors. We studied 206 subjects. The prevalence of tumour headache was 47.6%. Intracranial tumour headache was non-specific and in most cases could not be classified by current ICHD-II diagnostic criteria for primary headache syndromes. Its prevalence varied depending on volume, location and type of tumour, as well as on the patient's previous headache history.
Sensory gating is defined as the brain's ability to inhibit repetitive and irrelevant incoming sensory stimuli and is supposed to be related to cholinergic transmission. Indeed, Alzheimer's disease (AD) is characterized by a cholinergic deficit that is believed to be involved in cerebral cortex hyperexcitability and short latency afferent inhibition deficit. Therefore, a sensory gating deficit may be supposed present in AD within the frame of cortex hyperexcitability and loss of cortex modulation of sensory inputs. The authors investigated whether a sensory gating deficit may be present in AD and whether this deficit may be related to the presence of neuropsychiatric symptoms (NPS) and reversed by donepezil treatment. Sensory gating was evaluated using a paired-stimulus auditory P50 event-related potential paradigm. Eighteen drug-naïve probable AD patients (mean age 76.1 years; SD 5.6 years; 13 females and 5 males) and 15 healthy elderly controls (mean age 74.2 years; SD 5.4 years; 10 females and 5 males) were recruited. Sensory gating was evaluated in AD patients before starting therapy and after 1 and 3 months of donepezil treatment. Auditory P50 sensory gating was impaired in AD patients but no correlation was found between gating deficit and NPS. Moreover, AD patients displayed increased P50 amplitude when compared with healthy elderly subjects. Donepezil treatment did not improve P50 sensory gating in AD patients but decreased P50 amplitude. Patients with AD displayed an augmented P50 amplitude, in accordance with previous studies, suggesting increased cortex excitability. Donepezil does not affect P50 sensory gating but reduces P50 amplitude. Donepezil may induce P50 amplitude reduction by means of enhanced dopamine release. Indeed, it has been demonstrated that donepezil induces dopamine release "in vitro." The findings suggest that AD patients have a sensory gating impairment but the link with both NPS and the cholinergic deficit is doubtful.
Emerging evidence suggests that psychosis in persons with Alzheimer's disease (AD) may be linked to the cholinergic deficit associated with the disease. This study sought to evaluate whether anticholinergic (ACH) drugs could be a risk factor for psychosis onset. A total of 230 patients affected with probable AD were recruited. Data on behavioral and psychological symptoms were collected using the Neuropsychiatric Inventory, and diagnosis of psychosis was performed. Patients were divided into those who used ACH drugs and those who used non-ACH drugs. Those using ACH drugs (18.3%) were more likely to have psychosis than those using non-ACH drugs (odds ratio (OR)=2.52; 95% confidence interval (CI), 1.27-5.00); this association remained significant even after adjusting for potential confounding variables (OR=2.13; 95% CI, 1.03-4.43). Our data suggest that patients with AD are frequently treated with ACH drugs and that ACH drug intake should be regarded as a potential risk factor for psychosis.
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