Elvira Ventura Spagnolo

Neurological aspects of medical use of cannabidiol

BACKGROUNDnCannabidiol (CBD) is among the major secondary metabolites of Cannabis devoid of the delta-9-tetra-hydrocannabinol psychoactive effects. It is a resorcinol-based compound with a broad spectrum of potential therapeutic properties, including neuroprotective effects in numerous pathological conditions. CBD neuroprotection is due to its antioxidant and antiinflammatory activities and the modulation of a large number of brain biological targets (receptors, channels) involved in the development and maintenance of neurodegenerative diseases.nnnOBJECTIVEnThe aim of the present review was to describe the state of art about the pre-clinical research, the potential use and, when existing, the clinical evidence related to CBD in the neurological field.nnnMETHODnCollection of all the pre-clinical and clinical findings carried out investigating the effects of CBD alone, not in combination with other substances, in the neurological arena with the exclusion of studies on neuropsychiatric disorders.nnnRESULTSnLaboratory and clinical studies on the potential role of CBD in Parkinsons disease (PD), Alzheimers disease (AD), multiple sclerosis (MS), Huntingtons disease (HD), amyotrophic lateral sclerosis ALS), cerebral ischemia, were examined.nnnCONCLUSIONnPre-clinical evidence largely shows that CBD can produce beneficial effects in AD, PD and MS patients, but its employment for these disorders needs further confirmation from well designed clinical studies. CBD pre-clinical demonstration of antiepileptic activity is supported by recent clinical studies in human epileptic subjects resistant to standard antiepileptic drugs showing its potential use in children and young adults affected by refractory epilepsy. Evidence for use of CBD in PD is still not supported by sufficient data whereas only a few studies including a small number of patients are available.

Cardiac rupture caused by traffic accident: Case reports and a literature review

The commonest cause of blunt cardiac injuries is from traffic accidents followed by violent falls, sport activities, accidents or a fight but rupture of the heart is rare and lethal. The precise incidence of cardiac injury after a blunt chest trauma is unknown as rates vary greatly in the literature from between 7% and 76% of cases. Autopsy studies have shown that the right ventricle is the most frequently ruptured, followed by the left ventricle, right atrium, intraventricular septum, left atrium and interatrial septum with decreasing frequency. Post-mortem imaging is a rapidly advancing field of post-mortem investigations of trauma victims. The available literature dealing with the comparison of post-mortem computed tomography results with forensic autopsy indicates that conventional autopsy remains superior for the detection of organ and soft tissue injuries in all body regions.

Forensic tools for the diagnosis of electrocution death: Case study and literature review:

Diagnosis of death by electrocution may be difficult when electric marking is not visible or unclear. Accordingly, the body of a man who appeared to have died from accidental electrocution was carefully forensically analysed. Macroscopic and microscopic analysis of the current mark was carried out using a variable-pressure scanning electron microscope equipped with energy dispersive X-ray microanalyser to highlight skin metallisation, indicating the presence of iron and zinc. The histological findings of electrocution myocardial damage were supported by the results of biochemical analysis which demonstrated the creatine kinase-MB and cardiac troponin I elevation. The effects of electric current flow were also highlighted by perforations of endothelial surface of a pulmonary artery using scanning electron microscope, and all the results were analysed by the main tools suggested in the literature.

Analysis on sarcoglycans expression as markers of septic cardiomyopathy in sepsis-related death

The post-mortem assessment of sepsis-related death can be carry out by many methods recently suggested as microbiological and biochemical investigations. In these cases, the cause of death is a multiple organ dysfunction due to a dysregulated inflammatory response occurring after the failure of infection control process. It was highlighted also that the heart can be a target organ in sepsis which determines the so-called septic cardiomyopathy characterized by myocardial depression. Several mechanisms to explain the pathophysiology of septic cardiomyopathy were suggested, but very few studies about the structural alterations of cardiac cells responsible for myocardial depression were carried out. The aim of this study was to evaluate whether sarcoglycans (SG) were involved in septic cardiac damage analyzing their expression in sepsis-related deaths and, particularly, if these proteins can be used as markers of septic myocardial dysfunction. Cases of septic-related death confirmed by clinical and autopsy records were investigated and compared to a control group of traumatic deaths. Indirect immunofluorescence analysis was performed to analyze α-SG, β-SG, δ-SG, ζ-SG, ε-SG, and γ-SG. Decrease of fluorescence staining pattern for all tested sarcoglycans was observed in the septic-related deaths compared to normal fluorescence staining pattern of control group. These results provide new findings about the myocytes structural alterations due to sepsis and suggest that these proteins could be used in forensic assessment of septic cardiomyopathy.

Immunohistochemical study on dystrophin expression in CAD-related sudden cardiac death: a marker of early myocardial ischaemia

The aims of this study were to assess if dystrophin can be a tool for the forensic evaluation of sudden cardiac death due to coronary atherosclerotic disease (CAD) and particularly if it can be a marker of early myocardial ischaemia. Then in this investigation, the dystrophin was compared to C5b-9 and fibronectin to analyze if there are some differences in the expression of these proteins. Two groups of CAD-related sudden cardiac death, respectively the group 1 with gross and/or histological evidence and the group 2 with no specific histological signs of myocardial ischaemia were used. A third group formed by cases of acute mechanical asphyxiation was used as a control. The immunohistochemical staining by dystrophin, C5b-9 and fibronectin antibodies was performed. Loss of sarcolemmal dystrophin was observed in different degrees according to more or less significant histological evidence of myocardial ischaemia. Moreover, the comparison between loss of dystrophin expression and fibronectin positivity showed significant differences in group 2. The results suggested that dystrophin can be used in forensic diagnosis of CAD-related sudden cardiac death and as marker of early myocardial ischaemia.

Allele frequencies distribution of 16 forensic STR loci in a Western Sicilian population sample

The PowerPlex® ESI 17 Fast and ESX 17 Fast Systems represent faster cycling versions released by Promega® to follow the requirements of ENFSI and EDNAP groups’ for new STR genotyping systems in Europe. Allele frequencies and forensic parameters were estimated in a population sample of 120 unrelated healthy individuals living in Sicily (Western Sicilian population sample) using PowerPlex® ESI 17 Fast and PowerPlex® 17 Fast Systems. Full concordance of the results for both systems was observed. No significant deviation from Hardy-Weinberg equilibrium was detected. The observed heterozygosity changed from 0.85833 for FGA to 0.95 for TH01. The combined power of discrimination for the 16 loci was >0.999999.

An unusual fatal case of overdose of Vinblastine and review of literature

The pharmacological treatment of neoplasia is based on the use of chemotherapeutic substances. Chemotherapeutic agents can cause acute and chronic toxicity even at therapeutic doses. For this reason their overdose puts a patient’s life at severe risk. This work presents an unusual fatal case of overdose subsequent to an accidental massive administration of Vinblastine (90 mg instead of 9 mg), slow bolus (five minutes), to a 33-year-old woman who suffered from Hodgkin’s Lymphoma. The administration of the massive dose was due to a transcription error of the therapeutic treatment plan and miscommunication between the health professionals which caused the use of the wrong dose. The forensic investigation showed the systemic macroscopic and histological changes due to the toxic effect of Vinblastine on the body, by offering a realistic example of the microscopic tissue changes caused by the antineoplastic agent to different organs. Such evidence shows the importance of being very accurate when writing the therapeutic treatment plans and of counting on adequately-trained health care staff.