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Biomedical subjects

Iacopo Cancelli

Publications and source records attributed to Iacopo Cancelli.

5 recordsLinked to original sources
PubMed2006

Detection of anti-brain serum antibodies using a semi-quantitative immunohistological method.

The number of autoimmune disorders that may involve the nervous system is increasing. The diagnosis of neurological involvement in the context of systemic diseases may be helped by the detection of autoantibodies reacting against neural autoantigens. If the autoantigen is not known but the target tissue is suspected, immunohistochemistry is one of the main techniques used to certify the presence of autoantibodies. Autoreactive antibodies are also present in the healthy population but in low quantity compared to patients with such diseases. Quantification of such autoantibodies could help to discriminate between disease and healthy states. We have developed a densitometric immunohistological method for the evaluation of human serum anti-neural reactivity. Using a densitometric analysis of rat brain sections incubated with the serum from 107 healthy subjects, we have defined the baseline of natural anti-neural autoreactivity, and the cut-off for subsequent quantification of anti-neural reactivity in patients with neurological involvement in the context of autoimmune diseases, including systemic lupus erythematosus, paraneoplastic cerebellar degeneration, and stiff person syndrome. The test sensitivity was 81% with a positive predictive value of 52%, a specificity of 89% with a negative predictive value as high as 97%. In conclusion, this standardised semi-quantitative procedure makes immunohistochemistry a reliable diagnostic test for autoimmune neuropathologies and represents an excellent exclusion test for anti-neural autoimmunity.

Animals↗
PubMed2006

Sensory gating deficit assessed by P50/Pb middle latency event related potential in Alzheimer's disease.

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.

Acoustic Stimulation↗
PubMed2005

Sleep disorders in patients with end-stage renal disease undergoing dialysis therapy.

BACKGROUND: Many patients with end stage renal disease (ESRD) undergoing dialysis therapy suffer from sleep disturbances. The aim of this study was to investigate the prevalence of sleep disorders in a large population of uraemic patients recruited from 20 different dialytic centres in Triveneto. METHODS: 883 patients on maintenance dialysis were enrolled in the study. Demographic, lifestyle, renal and dialysis data were recorded. Renal parameters were compared with the database of the Veneto Dialysis Register. Using a self-administered questionnaire we assessed the presence of the following sleep disorders: insomnia, restless leg syndrome (RLS), obstructive sleep apnoea syndrome (OSAS), excessive daytime sleepiness (EDS), possible narcolepsy, sleepwalking, nightmares and possible rapid eye movement behaviour disorders (RBD). Moreover, in order to determine the prevalence of sleep disturbances and the possible effect of demographic or clinical data on sleep, we divided our population into two groups: with (SLEEP+) and without (SLEEP-) sleep disorders. RESULTS: The questionnaire revealed the presence of insomnia (69.1%), RLS (18.4%), OSAS (23.6%), EDS (11.8%), possible narcolepsy (1.4%), sleepwalking (2.1%), nightmares (13.3%) and possible RBD (2.3%). Eighty percent demonstrated SLEEP+, having at least one sleep disorder. Independent risk factors for sleep disorders were advanced age (P<0.001), excessive alcohol intake (P<0.04), cigarette smoking (P<0.006), polyneuropathy (P<0.05) and dialysis shift in the morning (P<0.001). CONCLUSIONS: The questionnaire showed a high presence of sleep disruption in dialytic populations. Awareness by Italian nephrologists regarding sleep disruption seems to be insufficient. Our data might help nephrologists to deal with uraemic patients with possible sleep disorders. Concerning the high prevalence of possible narcolepsy, further studies using polysomnographic records are necessary to confirm our results.

Adolescent↗
PubMed2004

Factors associated with complex visual hallucinations during antidepressant treatment.

Published case reports on complex visual hallucinations (CVH) occurring during antidepressant (AD) treatment were reviewed. Thirteen cases of CVH associated with SSRI treatment, 16 cases during tricyclic drug treatment and seven cases with other AD drug treatments were found. Nine patients were taking concomitant drugs while on therapy with SSRIs and four had a neurological disease in addition to depression. The cholinergic impoverishment occurring in dementia states or during concomitant therapy with anticholinergic drugs could increase the sensitivity to serotonergic agonists, triggering the manifestation of CVH. During tricyclic drug treatment, half of the reports were of hypnopompic or hypnagogic hallucinations and this can be associated with the effects of tricyclics (TCA) on sleep architecture. It is likely that the potent anticholinergic effect of amitriptyline was potentiated in a situation of a rapidly changing state of consciousness. In general, the review supports the view that an imbalance between serotonin and acetylcholine systems is at the root of AD-induced CVH, with a profile defined by a cholinergic hypoactivity and a serotonergic hyperactivity. Caution is needed when administering a combination of serotonergic and anticholinergic AD in the treatment of the demented population and in other already compromised patients because there is a risk of precipitating CVH.

Acetylcholine↗