Publications by authors named "Bonavita V"

Headache is the most frequent and often the most severe symptom of idiopathic intracranial hypertension (IIH) clinical presentation, although pain characteristics are very variable among sufferers and the pain may even lack in some cases. Whatever the headache features, refractoriness to treatments, pain worsening in the recumbent position, and frequent awakenings with severe headache late in the night are the specific complains of such patients. However, a migraine or probable migraine headache, mostly with a chronic headache pattern, can be diagnosed in about 2/3 of the cases.

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Available evidences suggest that a number of known assumption on idiopathic intracranial hypertension (IIH) with or without papilledema might be discussed. These include (1) the primary pathogenetic role of an excessive dural sinus collapsibility in IIH, allowing a new relatively stable intracranial fluids pressure balance at higher values; (2) the non-mandatory role of papilledema for a definite diagnosis; (3) the possibly much higher prevalence of IIH without papilledema than currently considered; (4) the crucial role of the cerebral compliance exhaustion that precede the raise in intracranial pressure and that may already be pathologic in cases showing a moderately elevated opening pressure; (5) the role as "intracranial pressure sensor" played by the trigeminovascular innervation of dural sinuses and cortical bridge veins, which could represent a major source of CGRP and may explain the high comorbidity and the emerging causative link between IIHWOP and chronic migraine (CM). Accordingly, the control of intracranial pressure is to be considered a promising new therapeutic target in CM.

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Most of the data in this review have been already reported by the authors in Neurological Science, but the goal of the present paper is to realize an integrated lecture of all the available data and look to the last achievements in pain cognition, with a special focus on migraine and chronic migraine. According to the proposed integrated perspective, migraine can be viewed as an adaptive behavioral response with evolutionistic advantages.

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Two critical functions for the control of intracranial fluids dynamics are carried on the venous side of the perfusion circuit: the first is the avoidance of cortical veins collapse during the physiological increases of cerebrospinal fluid (CSF) pressure in which they are immersed. The second, is the generation of an abrupt venous pressure drop at the confluence of the cortical veins with the dural sinuses that is required to allow a CSF outflow rate balanced with its production. There is evidence that both of these effects are ensured by a Starling resistor mechanism (a fluid dynamic construct that governs the flow in collapsible tubes exposed to variable external pressure) acting at the confluence of cortical veins in the dural sinus.

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Background: A previous phase 2 trial has suggested that statins might delay brain atrophy in secondary progressive multiple sclerosis.

Objectives: The objective of this study was to evaluate the effect of atorvastatin add-on therapy on cerebral atrophy in relapsing-remitting multiple sclerosis.

Methods: This randomised, placebo-controlled study compared atorvastatin 40 mg or placebo add-on therapy to interferon β1b for 24 months.

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The hypothesis that central sensitization/allodynia is the common final mechanism responsible for the progression of migraine pain is supported by the possibility of tracing back to allodynic mechanisms the action of the main risk factors for chronic migraine validated by the recent literature. The comorbidity between migraine and idiopathic intracranial hypertension without papilledema is emerging as a new, commonly overlooked risk factor for migraine progression whose putative mechanism might also converge on the sensitization of central pain pathways. If headache progression always occurs at the end of a pathogenetic sequence typical of an individual susceptibility to allodynia, then the primary character of chronic migraine might be debated.

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To assess the prevalence and possible pathogenetic involvement of raised intracranial pressure in patients presenting with unresponsive chronic migraine (CM), we evaluated the intracranial opening pressure (OP) and clinical outcome of a single cerebrospinal fluid withdrawal by lumbar puncture in 44 consecutive patients diagnosed with unresponsive chronic/transformed migraine and evidence of sinus stenosis at magnetic resonance venography. The large majority of patients complained of daily or near-daily headache. Thirty-eight (86.

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Data in the literature show that migraine tends to improve during pregnancy in most migrainous women. The aim of this Internet survey was to obtain the most likely cross section of the situation in the general population with respect to the presence and course of migraine in pregnancy. All women who participated were asked to answer questions pertaining to their history of pregnancy and headache.

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The role of the cortical spreading depression (CSD)-dependent trigeminovascular activation in migraine etiopathogenesis, long considered paradigmatic, has remained substantially unproven in humans. The parallel advancement of functional neuroimaging techniques promoted the extensive exploration of the brain networks involved in pain processing in search of a possible central migraine generator. However, despite initial enthusiasms, it has not been possible to clarify whether the functional central "markers" of pain observed in primary headaches could be considered as causative or just the neural correlates of the ongoing pain.

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The recently advanced hypothesis that idiopathic intracranial hypertension without papilledema (IIHWOP) is a powerful risk factor for the progression of pain in individuals prone to episodic primary headache implies that IIHWOP is much more prevalent than it is believed to be in the general population and that it can run almost asymptomatic in most of the affected individuals. In this review, we discuss the evidence available supporting that: (a) sinus venous stenosis-associated IIHWOP is much more prevalent than believed in the general population and can run without symptoms or signs of raised intracranial pressure in most of individuals affected, (b) sinus venous stenosis is a very sensitive and specific predictor of intermittent or continuous idiopathic intracranial hypertension with or without papilledema, even in asymptomatic individuals, (c) in primary headache prone individuals, a comorbidity with a hidden stenosis-associated IIHWOP represents a very common, although largely underestimated, modifiable risk factor for the progression and refractoriness of headache.

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Data from two recent studies strongly support the hypothesis that idiopathic intracranial hypertension without papilledema (IIHWOP) could represent a powerful risk factor for the progression of pain in primary headache individuals. The first study highlights that an asymptomatic IIHWOP is much more prevalent than believed in the general population and occurs only in central venous stenosis carriers. In the second study, about one half of a large consecutive series of unresponsive primary chronic headache patients shows significant sinus venous stenosis.

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A panel of Italian neurologists of the Italian Society for the study of Dementias (SINDEM) discussed the recently proposed new lexicon for Alzheimer disease (AD) and the related diagnostic criteria for the different phases of the disease (Preclinical AD, prodromal AD and Alzheimer's dementia) (Dubois et al. in Lancet Neurol 6:734-746, 2007; in Lancet Neurol 9:1118-1127, 2010). The aim of this discussion was to reach a consensus, among the Italian neurologists involved in the study and care of persons with dementia, in particular in reference to the potential use of the proposed diagnostic criteria in clinical practice.

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In the field of so-called chronic daily headache, it is not easy for migraine that worsens progressively until it becomes daily or almost daily to find a precise and universally recognized place within the current international headache classification systems. In line with the 2006 revision of the second edition of the International Classification of Headache Disorders (ICHD-2R), the current prevailing opinion is that this headache type should be named chronic migraine (CM) and be characterized by the presence of at least 15 days of headache per month for at least 3 consecutive months, with headache having the same clinical features of migraine without aura for at least 8 of those 15 days. Based on much evidence, though, a CM with the above characteristics appears to be a heterogeneous entity and the obvious risk is that its definition may be extended to include a variety of different clinical entities.

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This lecture is not a historical lecture, but rather a journey through the "story" of neurology in Italy from its "prehistoric" beginning in the 19th century. The birth of a neurological school is that magical moment in which a founder attracts disciples: the more capable this founder is of transmitting methodology and allowing his pupils intellectual freedom, the longer his memory will live on. On the basis of this idea, the scientific biography of a few leading Italian neurologists of the 20th century is outlined, starting from Leonardo Bianchi, founder of the Italian Neurological Society in 1907.

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Reported prevalence of idiopathic intracranial hypertension without papilledema (IIHWOP) in series of patients with chronic or transformed migraine is significantly higher than expected; yet, IIHWOP is not included among the risk factors for migraine progression. However, several studies provided evidences suggesting that IIHWOP could represent a possible, largely underestimated, risk factor for progression of pain in migraine and, possibly, in other primary headaches. Data from two recent studies, albeit aimed to different end-points, strongly support this hypothesis.

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The proposed title "Pain as an evolutionary necessity" could lead to a broad debate with implications covering many chapters of the medicine and particularly of clinical neurology. In the present perspective, the discussion will focus on migraine and cluster headache chosen as elective examples of biological and not only clinical conditions, that unveil the bond between pain and necessity. Migraine, cluster headache, and perhaps other primary headaches begin to be depicted in terms of recurrent activation of innate bio-behavioral specific patterns, with a crucial and highly conserved evolutionarily adaptive significance.

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The identification of predictive factors of NAbs development might have a relevant impact on clinical practice. Our objective is to look after predictive factors of NAbs development in MS IFN Beta-1b-treated patients. Database was screened for patients on IFN Beta-1b treatment with an Expanded Disability Status Scale (EDSS) at a baseline between 1 and 3.

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In the light of the pathophysiologic knowledge acquired in recent years, a tentative redefinition of some types of headache, until now defined as primary, is now possible. Chronic migraine is proposed here as the consequence of "processes" to be ascribed to mechanisms activated by comorbid conditions. The observations supporting the possibility that allodynia represents the process leading to pain progression, which occurs in some migraineurs, are discussed.

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Idiopathic intracranial hypertension is consistently associated with venous outflow disturbances. Sinus venous stenosis are found at magnetic resonance venography in the large majority of IIH patients and may have various conformations, ranging from functional smooth narrowings of sinus segments associated or not with definite flow gaps, to segmental hypoplasia or aplasia of one or more central venous collectors. Stenosis are currently believed to be a consequence of a primary altered cerebrospinal fluid (CSF) pressure since it may normalize after CSF subtraction with lumbar puncture or shunting procedures.

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The association of chronic migraine (CM) with an idiopathic intracranial hypertension without papilledema (IIHWOP), although much more prevalent than expected in clinical series of CM sufferers, is not included among the risk factors for migraine progression. We discuss the available evidence supporting the existence of a pathogenetic link between CM and idiopathic intracranial hypertensive disorders and suggest a causative role for IIHWOP in migraine progression.

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In the light of the pathophysiologic knowledge acquired in the recent years, a tentative redefinition is now possible of some types of headache until now defined as idiopathic, and indistinctly described as primary headaches. Cluster headache and trigeminal neuralgia are known examples of diseases classified as primary, which are, in contrast, well-defined diseases to be distinguished from headaches without any recognized anatomic site of lesion or pathogenesis. Another still debated condition, chronic migraine, is proposed here as the consequence of "processes" to be ascribed to mechanisms activated by other comorbid conditions.

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