86,620 research outputs found
Patologia del mediastino. Aspetti neurologici. Approfondimento: Miastenia Gravis.
Seconda Edizion
Central pontine myelinolysis:diagnosis by computed tomography, magnetic resonance and evoked potentials
Psychiatric onset and late chorea in a patient with 41 CAG repeats in the TATA-binding protein gene
[No abstract available
Intracerebral hemorrhage after cranioplasty: an unpredictable treacherous complication due to reperfusion or possible systemic inflammatory response syndrome
Introduction: In case of malignant cerebral infarction and progressive neurological
worsening, decompressive craniectomy is the surgical option that is recommended
when medical therapies fail. The occurrence of an intracerebral hemorrhage after
reconstruction of the bone defect is extremely rare. This is an extremely rare
complication, with only four cases reported thus far in the literature.
Case Report: A 54-year-old male suffered a malignant cerebral infarction and
progressive neurological worsening requiring decompressive hemicraniectomy. Three
months later, an autologous cranioplasty was performed. Postoperatively, the patient
experienced a generalized epileptic seizure and a hemorrhage in the left cerebellar
hemisphere on control CT scan. After surgical removal the patient did not improve, and
CT revealed the occurrence of further cerebellar, mesencephalic, and intraventricular
hemorrhages. Systemic inflammatory response syndrome was suspected, but death
occurred 72 hours after cranioplasty.
Conclusions: The reperfusion-hyperperfusion mechanism after cranioplasty might favor
intracerebral hemorrhages limited to the ischemic tissue, which is unable to support the
cerebral blood perfusion pressure. When diffuse atypical hemorrhages far from the
surgical site occur after cranioplasty, a systemic inflammatory response syndrome is
supposed
Diffusion MRI Findings in Encephalopathy Induced by Immunosuppressive Therapy after Liver Transplantation
Neurological complications are common after liver transplantation, as they affect up to one-third of the transplanted patients and are associated with significant morbidity. The introduction of calcineurin inhibitors, cyclosporine A and tacrolimus, in immunosuppressive regimens significantly improved the outcome of solid-organ transplantation even though immunosuppression-associated neurotoxicity remains a significant complication, particularly occurring in about 25% of cases after liver transplantation. The immunosuppressant cyclosporine A and tacrolimus have been associated with the occurrence of major neurological complications, diffuse encephalopathy being the most common. The biochemical and pathogenetic basis of calcineurin inhibitors-induced neurotoxicity are still unclear although several mechanisms have been suggested. Early recognition of symptoms could help reduce neurotoxic event. The aim of the study was to evaluate cerebral changes through MRI, in particular with diffusion-weighted images (DWI) and apparent diffusion coefficient (ADC) maps, in two patients undergoing liver transplantation after immunosuppressive therapy. We describe two patients in which clinical pictures, presenting as a severe neurological condition, early after orthotopic liver transplantation during immunosuppression therapy, showed a different evolution in keeping with evidence of focal-multifocal lesions at DWI and ADC maps. At clinical onset, DWI showed hyperintensity of the temporo-parieto-occipital cortex with normal ADC values in the patient with following good clinical recovery and decreased values in the other one; in the latter case, MRI abnormalities were still present after ten days, until the patient's exitus. The changes in DWI with normal ADC may be linked to brain edema with a predominant vasogenic component and therefore reversible, while the reduction in ADC is due to cytotoxic edema and linked to more severe, nonreversible, clinical picture. Brain MRI and particularly DWI and ADC maps provide not only a good and early representation of neurological complications during immunosuppressant therapy but can also provide a useful prognostic tool on clinical outcome of the patient
Overt and covert effects of cognitive fatigue on attention networks
Background and aims
Cognitive fatigue refers to a variation of the psychophysiological state during or after prolonged periods of mental activity that requires work efficiency, and could lead to temporary deterioration of attentional functioning, especially top-down attention and cognitive control. The present study aims to verify the effects of cognitive fatigue on attention in the context of the three attentional networks described by Posner, by using behavioral and psychophysiological measures, to detect variations in overt and covert responses respectively.
Methods
Thirty young healthy subjects were enrolled in the study, 15 in the “fatigue” and 15 in the control group. Cognitive fatigue was provoked by a continuous arithmetic task lasting 1 h, and the EEG recordings were conducted before and after the task, while subjects were performing the attention network test. The N1, N2 and P3 components were analyzed for the alerting, orienting and conflict networks, in conformity with behavioral analysis.
Results
No difference emerged between groups in networks' efficiency scores and in N1 and P3 amplitudes related to the alerting network. As regards the orienting network, P3 amplitude was significantly reduced in the fatigue group alone (p = 0.02), while no differences emerged in N1 amplitude. As regards the conflict network, both N2 and P3 amplitudes were significantly reduced in the fatigue group alone and selectively for the incongruent target (p < 0.001; p = 0.001 respectively).
Conclusions
Our results suggest that, in young healthy subjects, cognitive fatigue interferes with goal-driven attention especially when the task demand is higher, sparing the bottom-up attention control mechanisms and in absence of any overt observable effect
Author correction to: l-acetyl-carnitine in patients with carpal tunnel syndrome: effects on nerve protection, hand function and pain
Background and Aim: L-Acetyl-carnitine (LAC) exerts an energetic effect on nerves and muscles. Recently, preclinical experiments have demonstrated a central anti-nociceptive action.
Objective: Our objective was to assess the effects of LAC on neuroprotection, pain, and function in carpal tunnel syndrome (CTS), a very frequent chronic compressive neuropathy.
Methods: In a multicentre, examiner-blinded, clinical and neurophysiological 4-month study, we enrolled 82 patients and examined 120 hands with CTS of mild to moderate severity. Patients were assessed at baseline and 10, 60 and 120 days after treatment with LAC 500 mg twice daily (BID). All patients underwent a conduction study of the median nerve, the Boston Carpal Tunnel Questionnaire (BCTQ) and the Neuropathic Pain Symptom Inventory(NPSI). The primary endpoint was the sensory conduction velocity (SCV) of the median nerve.
Results: The primary endpoint was met, with significant improvement of the SCV (P\0.0001). All sensory neurophysiological measures also significantly improved. BCTQ score changed significantly (P\0.0001), with a greater improvement in the symptom component. Nine of the NPSI types of pain, particularly squeezing and pressure pain and pain evoked by pressure, showed a significant reduction (P\0.0001).
Conclusions: Our clinical and neurophysiological study indicated that 4 months of treatment with LAC exerted a neuroprotective effect. LAC reduced pain in patients with mild and moderate CTS, a result that is possibly due to both its neuroprotective action and its central anti-nociceptive properties.
Clinical Trials Registration code: EudraCT 2014-002289-62
Pearl and pitfalls in brain functional analysis by event–related potentials: position statement of Italian Psychophysiology and Cognitive Neuroscience Society on methodological limits and clinical reliability. Part 1.
124. Pearl and pitfalls in brain functional analysis by event–related potentials: a narrative review by Italian Psychophysiology and Cognitive Neuroscience Society on methodological limits and clinical reliability- Part II.
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