Middle Cerebral Artery Dissection: A Report of Two Cases With Treatments and Outcomes.

In the present report, we describe two cases of right-sided M1 segment middle cerebral artery dissection in a 51-year-old Asian female and in a 28-year-old Caucasian male patient with no previous history of ischemic stroke or known intracranial atherosclerosis presenting with acute unilateral headache progressing to severe multifocal hemispheric infarction with nearly complete one-sided motor paralysis. In both patients, a middle cerebral artery dissection was detected on angiography; they were given exclusively medical therapy: patient 1 was not eligible to reperfusive therapies and was treated with a three-month course of acetylsalicylic acid and clopidogrel combined with low-dose enoxaparin, while patient 2 was initially treated with intravenous alteplase with no hemorrhagic complications and was later shifted to single antiplatelet therapy. Despite an initial worsening of clinical severity and an extensive ischemic lesion in both patients, neurologic function improved over time, eventually allowing recovery of unaided gait. Therefore, in the absence of signs of hemorrhage, intravenous thrombolysis or dual antiplatelet regimens could be considered in strokes related to middle cerebral artery dissection.

Multiple Sclerosis: Inflammatory and Neuroglial Aspects.

Multiple sclerosis (MS) represents the most common acquired demyelinating disorder of the central nervous system (CNS). Its pathogenesis, in parallel with the well-established role of mechanisms pertaining to autoimmunity, involves several key functions of immune, glial and nerve cells. The disease's natural history is complex, heterogeneous and may evolve over a relapsing-remitting (RRMS) or progressive (PPMS/SPMS) course. Acute inflammation, driven by infiltration of peripheral cells in the CNS, is thought to be the most relevant process during the earliest phases and in RRMS, while disruption in glial and neural cells of pathways pertaining to energy metabolism, survival cascades, synaptic and ionic homeostasis are thought to be mostly relevant in long-standing disease, such as in progressive forms. In this complex scenario, many mechanisms originally thought to be distinctive of neurodegenerative disorders are being increasingly recognized as crucial from the beginning of the disease. The present review aims at highlighting mechanisms in common between MS, autoimmune diseases and biology of neurodegenerative disorders. In fact, there is an unmet need to explore new targets that might be involved as master regulators of autoimmunity, inflammation and survival of nerve cells.

A Case of Anti-Leucine-Rich Glioma-Inactivated Protein 1 (Anti-LGI1) Encephalitis With an Unusual Frontomesial Motor Cortex T2 MRI Hyperintensity.

Anti-leucine-rich glioma-inactivated protein 1 (anti-LGI1) encephalitis is a rare autoimmune disorder, classified within limbic encephalitides, and characterized by seizures and subacute cognitive-behavioral impairment, mainly affecting short-term memory and usually involving temporo-mesial lobe structures. We present a case of anti-LGI1 encephalitis characterized by focal right lower limb motor seizures and pyramidal signs and responsive to high-dose methylprednisolone. The patient developed an atypical left frontal lobe parasagittal T2 hyperintense lesion on MRI within one month of hospital admission, which has not been described previously in this disease to the best of our knowledge.

Diffusion-weighted imaging in the early diagnosis of intraventricular rupture of a brain abscess.

Brain abscess is a potentially fatal injury that must be treated promptly to avoid complications that require neurosurgery such as intraventricular rupture. Patients with brain abscess may exhibit a multiple variety of nonspecific symptoms, simulating the presence of neurological diseases such as ischemic stroke or intracranial tumor masses. Early radiological diagnosis with adequate subsequent treatment improves the patient's chances of recovery. We report the case of a 48-year-old male patient with brain abscess complicated by an initial rupture into the ventricle. Magnetic resonance imaging with diffusion-weighted images, and apparent diffusion coefficient maps made it possible to diagnose an intraventricular rupture of the abscess with consequent appropriate neurosurgical treatment.

Cut-off point of CT-assessed epicardial adipose tissue volume for predicting worse clinical burden of SARS-CoV-2 pneumonia.

OBJECTIVE: To identify a cut-off value of epicardial adipose tissue (EAT) volume quantified by CT associated with a worse clinical outcome in patients with SARS-CoV-2 pneumonia. MATERIALS AND METHODS: In this retrospective study, sixty patients with a diagnosis of laboratory-confirmed COVID-19 pneumonia and a chest CT exam on admission were enrolled. Based on a total severity score (range 0-20), patients were divided into two groups: ordinary group (total severity score < 7) and severe/critical group (total severity score > 7). Clinical results and EAT volume were compared between the two groups. RESULTS: The severe/critical patients, compared to the ordinary ones, were older (66.83 ± 11.72 vs 58.57 ± 16.86 years; p = 0.031), had higher body mass index (27.77 ± 2.11 vs 25.07 ± 2.80 kg/m2; p < 0.001) and higher prevalence of comorbidities. EAT volume was higher in severe/critical group, compared with the ordinary group (151.40 ± 66.22 cm3 vs 92.35 ± 44.46 cm3, p < 0.001). In severe/critical group, 19 (73%) patients were admitted in intensive care unit (ICU), compared with 6 (20%) patients in the ordinary group (p < 0.001). The area under the ROC curve (AUC) is equal to 0.781 (p < 0.001) (95% CI: 0.662-0.900). The cut-off found, in correspondence with the highest value of the Youden Index, is 97 cm3: the sensitivity is equal to 83.3%, while the specificity is equal to 70% for predicting a worse outcome. The risk (odds ratio) of belonging to the severe/critical group in this population due to EAT ≥ 97 cm3 is 11.667 (95% CI: 3.384-40.220; p < 0.001). CONCLUSION: An EAT volume of 97 cm3 has good sensitivity and specificity to predict a greater extent of pulmonary involvement and therefore a worse clinical outcome in patients with SARS-CoV-2 pneumonia.

Cerebrospinal Fluid α-Calcitonin Gene-Related Peptide: A Comparison between Alzheimer's Disease and Multiple Sclerosis.

Alzheimer's disease (AD) and Multiple Sclerosis (MS) represent an emerging health problem on a global scale, as they are responsible for a significant contribution to the burden of disability in Western countries. Limited numbers of cerebrospinal fluid (CSF) diagnostic markers are available for each disease (amyloid and tau deposition markers for AD and oligoclonal bands for MS) representing mostly state markers that provide few, if any, clues about the severity of the clinical phenotype. α-CGRP is a neuropeptide implied in nociception, vasodilation, synaptic plasticity and immune functions. This neuropeptide is expressed in encephalic regions connected to memory, attention, autonomic and behavioral functions and is also expressed by spinal motor neurons. The present work confronted α-CGRP levels between 19 AD, 27 MS and 17 control subjects using an ELISA/EIA assay. We measured higher CSF α-CGRP contents in control subjects with respect to AD, as shown in previous studies, as well as in MS patients in comparison to AD. The control subjects and MS patients did not significantly differ between each other. We did not observe a relationship between CSF protein content, albumin quotient and α-CGRP. We also describe, retrospectively, an association between higher CSF CGRP content and higher MRI overall lesion count in MS and between lower α-CGRP and worse attention and visuo-perceptual skills in AD. We speculate that α-CGRP could be differentially involved in both disabling diseases.

Association between homocysteine levels and cognitive profile in Alzheimer's Disease.

BACKGROUND: Growing evidence suggests that hyperhomocysteinemia (HHcy) constitutes a risk factor for Alzheimer's Disease (AD). The impact of HHcy on cognitive functions has mainly been investigated using screening neuropsychological tests that provide general, unspecific measures of cognitive level. Since an association between HHcy and temporo-mesial atrophy has been documented, we predicted that a fine-grained analysis of neuropsychological performance should show stronger Hcy effects on memory scores than on other cognitive scores. OBJECTIVE: To determine the influence of Hcy level on cognitive profile evaluated with specific, sensitive neuropsychological tests in a wide AD cohort. METHODS: 323 patients with AD were enrolled in a cross-sectional study and underwent a neuropsychological examination exploring several cognitive domains (memory, language, visuoperception, visuospatial abilities, executive function, constructional praxis, ideomotor praxis). The effects of Hcy levels and other risk factors (including cholesterol, smoking habits, triglycerides, apoEε4 allele) were analysed. RESULTS: Generalized Linear Model detected a significant drop in performance with increasing Hcy in 6/19 measures of cognitive functions, namely, in memory performance tasks as well as in Luria's motor planning test, with effect sizes ranging 1.4%-2.8% (Eta-squared), partialling out effects of other predictors. CONCLUSIONS: HHcy was associated with poor performance in short and long-term spatial and verbal memory more than with other cognitive dysfunctions. These results support the hypothesis that medial temporal networks might be vulnerable to HHcy, consistently with data from neuroimaging studies suggesting a link in AD between temporal atrophy and HHcy; the effect on Luria's motor planning task suggests further involvement of frontal structures.

Vasoactive neuropeptides and Alzheimer's disease: a systematic review focusing on calcitonin gene-related peptide.

Vasoactive peptides constitute a heterogenous family of mediators exerting various physiological functions, mostly studied for their vasotropic effects and role as peripheral neurotransmitters/neuromodulators, mainly involved in nociceptive transmission modulation. They have been divided into vasodilatory or vasoconstrictive peptides, according to their predominant effects on vascular tone. Recent research has shown in the Central Nervous System effects as transmitters and "growth factor-like" signals. Therefore, deregulation of their signaling systems has been thought to play a role in neural cell death and in the pathogenesis of neurodegenerative disorders, including Alzheimer's disease, since these peptides can regulate neuronal stress signaling, survival cascades, synaptic plasticity. This review considers evidence about the implication of neuropeptide systems in Alzheimer's disease while focusing mainly on calcitonin gene-related peptide-alpha. In vitro and in vivo studies have shown potential implications in its pathogenesis. It has been possibly proposed as a neuroprotective agent, considering not only its pleiotropic actions on blood vessels, neurovascular coupling, energy metabolism, but also its potential actions on neuronal, glial, and immune system stress signaling, which might also derive from its structural homology to amylin. Amylin signaling is thought to be disrupted in Alzheimer's disease, and amylin itself takes part in the composition of senile plaques. Calcitonin gene-related peptide-containing systems seem more closely related to Alzheimer's disease pathogenesis than other neuropeptidergic systems, and their regulation might represent an interesting mechanism in developing novel therapeutic approaches.