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Headache is one of the most common neurological diseases. It is well known that there are differences in the perception and in the management of pain in various populations. Immigrants represent a growing portion between neurology outpatients. We analyzed the epidemiological characteristic of headache in immigrants come to our attention, in comparison with Italians. Data collected included age at immigration, age of onset of headache, headache's type (HIS criteria), and psychiatric comorbidities. There were not substantial differences in the incidence of headache subtypes: migraine was the most frequent diagnosis in both groups, followed by tension-type headache. The incidence of depression was similar, while anxiety was significantly less frequent in immigrants. Studies on neurological diseases in immigrants are few. The data available seem to show no differences in the incidence, but rather in treatment. Our study confirms the evenness of two populations, local and foreign, afferent in a Headache Unit, according to the single similar study, except for anxiety, maybe related to language difficulties or cultural background. [ABSTRACT FROM AUTHOR]

The association between Amyotrophic Lateral Sclerosis (ASL) and FrontoTemporal Dementia (FTD) is well known. Most of reports describing ASL-FTD cases show a strong association between ALS and the behavioural form of FTD. Conversely, the association between ALS and pure Semantic Dementia or Progressive Non-Fluent Aphasia (PNFA) is extremely rare, ranging from 1 to 3%. A clinical phenotype characterized by a rapidly progressive aphasic dementia and motoneuron disease (MND) has been described in few case reports; since the updating of PNFA diagnostic criteria in 2011, no clinical report has been related. We want to describe a case of patient presented, at the onset, as PNFA who developed, one year later, ALS with bulbar onset. The patient was screened for the main genes causing or associated with MND and/or dementia but no variants with a pathogenetic effect were observed. [ABSTRACT FROM AUTHOR]

We discuss the Boussinesq system with the stationary time t5 within a general framework of stationary flows of n-Gel'fand-Dickey hierarchies. A careful use of the bi-Hamiltonian structure can provide a set of separation coordinates for the corresponding Hamilton-Jacobi equations. [ABSTRACT FROM AUTHOR]

We suggest a method to extend the theory of recursion operators to integrable Hamiltonian systems in two-space dimensions, like KP systems. The approach aims to stress the conceptual unity of the theories in one and two space dimensions. A sound explanation of the appearance of bilocal operators is also given. [ABSTRACT FROM AUTHOR]

In surgery around brainstem for preservation of swallowing function, monitoring of the corticobulbar tract of the X cranial nerve – and not only vagal rootlets – is needed. A few researchers have studied intraoperative monitoring of the vagus nerve corticobulbar pathway. In the past, X nerve has been monitored using needle or hook-wire electrodes, endoscopically or laryngoscopically placed in the vocal fold. Because of their complexity and invasiveness, these techniques have not been widely used. New studies with vagal MEPs have been recently published, although they required needle insertion into the vocal cord. Reports with non-invasive methods are still lacking. In this work we report our series of vagal nerve motor evoked potentials using endotracheal adhesive electrode in surgery around brainstem. In 26 patients who have undergone surgery around brainstem vocal cord MEPs were recordable in about 70% of cases. Correct electrode placement is the main issue to obtain signals. Latencies varied from 14 to 20 msec and amplitude from 40 to 200 uv. In 3 cases there was MEP loss and the patients suffered of post operative dysphagia. MEP recorded with endotracheal tube adhesive electrodes is a safe, effective and reliable method to monitor corticobulbar vagal tract. [ABSTRACT FROM AUTHOR]

The pathophysiology of migraine with or without aura (MA, MO) is still a matter of debate. We thus studied patients with MA and MO by means of paired-pulse flash-visual evoked potentials (paired F-VEPs). This technique analyses the overall excitability of visual system as detected from the cortical occipital signal. We enrolled 13 adult patients with MO and 13 with MA. Twenty-two normal subjects served as controls. Stimuli were single flashes, intermingled at random to flash pairs at critical interstimulus intervals (ISIs, 16.5–125 ms) with closed and open eyes. The “single” (unconditioned) F-VEP was split into a “main complex” (50–200 ms after the flash) and a “late response” (200–400 ms). As for paired stimulation, the “test” F-VEP emerged from electronic subtraction of the “single” F-VEP to the “paired” F-VEP. In the MA group, the “main complex” of the “test” F-VEP did not show the size reduction (at ISIs 50–62.5 ms) which was typical among the control and MO groups in the “eyes-closed” state. Paired F-VEPs document a defective neural inhibition in the visual system of patients with MA and may warrant future clinical studies, aiming to evaluate its potential role in the pathophysiology and management of MA. [ABSTRACT FROM AUTHOR]

Objective The pathophysiology of migraine with or without aura (MA, MO) is still a matter of debate. We thus studied patients with MA and MO by means of paired-pulse flash-visual evoked potentials (paired-F-VEPs). This technique analyzes the overall excitability of visual system as detected from the cortical occipital signal. Methods We enrolled 13 adult patients with MO and 13 with MA. Twenty-two normal subjects acted as controls. Stimuli were single flashes, intermingled at random to flash pairs at critical interstimulus intervals (ISIs, 16.5–125 ms) with closed and open eyes. The “single”(unconditioned) F-VEP was split into a “main complex” (50–200 ms after the flash) and a “late response” (200–400 ms). As for paired stimulation, the “test” F-VEP emerged from electronic subtraction of the “single” F-VEP to the “paired” F-VEP. Results In the MA group, the “main complex” of the “test” F-VEP did not show the size reduction (at ISIs 50–62.5 ms) which was typical among the control and MO groups in the “eyes-closed” state. Conclusions Paired-F-VEPs document a defective neural inhibition in the visual system of patients with MA and may warrant inclusion in future clinical studies, to evaluate its potential role in the pathophysiology and management of MA. [ABSTRACT FROM AUTHOR]

Question Focal epilepsies (FEs) arise from a lateralized network. In generalized epilepsies (GEs) there is a bilateral network involvement from the outset. The corpus callosum is the anatomical substrate for interhemispheric spread, although its detailed physiological role is uncertain. We used transcranial magnetic stimulation (TMS) to explore the physiology of the corpus callosum in patients with FE and idiopathic GE (IGE), as compared to healthy subjects (HS). Methods We studied 16 patients with FE, 17 with IGE, and 17 HS of similar age and sex. We used TMS to measure the interhemispheric inhibition (IHI) from left-to-right primary motor cortex (M1) and viceversa. A conditioning stimulus (CS) was given to one M1 10 and 50 ms before a test stimulus delivered to the contralateral M1. Statistics was based on ANOVAs. Results Across HS, IHI was reproducible, since a contralateral CS suppressed MEPs at ISIs of 10 and 50 ms ( p < 0.05). Similar effects occurred in IGE patients ( p < 0.05). FE patients behaved differently, since IHI was significantly ( p < 0.05) reduced bilaterally. Conclusions FE patients had a bilateral defective inhibitory response. We suggest that it may represent one key factor for the contralateral spread of focal discharges, and seizure generalization. [ABSTRACT FROM AUTHOR]

Focal epilepsies (FEs) arise from a lateralized network. In generalized epilepsies (GEs) there is a bilateral network involvement from the outset. The corpus callosum is the anatomical substrate for interhemispheric spread, although its detailed physiological role is uncertain. We used transcranial magnetic stimulation (TMS) to explore the physiology of the corpus callosum in patients with FE and idiopathic GE (IGE), as compared to healthy subjects (HS). We studied 16 patients with FE, 17 with IGE, and 17 HS of similar age and sex. We used TMS to measure the interhemispheric inhibition (IHI) from left-to-right primary motor cortex (M1) and viceversa. A conditioning stimulus (CS) was given to one M1 10 and 50 ms before a test stimulus delivered to the contralateral M1. Statistics was based on ANOVAs. Across HS, IHI was reproducible, since a contralateral CS suppressed MEPs at ISIs of 10 and 50 ms ( p < 0.05). Similar effects occurred in IGE patients ( p < 0.05). FE patients behaved differently, since IHI was significantly ( p < 0.05) reduced bilaterally. In conclusion, FE patients had a bilateral defective inhibitory response. We suggest that it may represent one key factor for the contralateral spread of focal discharges, and seizure generalization. [ABSTRACT FROM AUTHOR]

Abnormal cortical plasticity has been hypothesized to play a crucial role in the pathogenesis of juvenile myoclonic epilepsy (JME). We used an excitatory paired associative stimulation (PAS) paradigm to study motor cortex plasticity in patients with JME. Twelve adult patients with JME were compared with 13 healthy subjects (HS) of similar age and sex. PAS consisted of 180 electrical stimuli of the right median nerve paired with a single transcranial magnetic stimulation (TMS) stimulus over the hotspot of right abductor pollicis brevis (APB) at an ISI of 25 ms (PAS25). We measured motor evoked potentials (MEPs) before and after each intervention for up to 30 min. Data entered repetitive measure ANOVAs. In HS the PAS25 protocol was followed by a significant increase of the MEP amplitude (p < 0.001). In patients with JME, the MEP amplitude did not change. We suggest that a defective motor cortex plasticity may play a role in the pathogenesis of JME and it may be involved in the development of myoclonus in these patients. [ABSTRACT FROM AUTHOR]

Visual and motor cortex are involved in the origin/propagation of the photoparoxysmal response (PPR), a stronghold for the diagnosis of generalized photosensitive epilepsies. The study of the functional connection between these two distant cortical areas with transcranial magnetic stimulation (TMS), could help clarify the pathophysiology of photosensitivity. Eleven patients with idiopathic generalized epilepsy and photosensitivity were compared to 11 healthy subjects. We measured the resting motor threshold of the left hand motor area and the phosphene threshold. The paradigm consisted in a conditioning stimulus (CS) delivered over the phosphene hotspot of the visual cortex and followed at random interstimulus intervals (15–40 ms) by a test stimulus over the left motor cortex to evoke a motor evoked potential (MEP) of ∼1 mV from the right FDI. The conditioned-MEP was expressed as a percentage of the unconditioned-MEP amplitude. In healthy subjects the CS over the visual cortex produced significant inhibitory changes on the corticospinal excitability with a time course between 18 and 40 ms. Patients with IGE and photosensitivity showed a failure of the physiological inhibition. In photosensitive patients the alteration of the normal visuo-motor functional connectivity could be responsible for the origin/propagation of the PPR from the hyper-excitable visual cortex to the motor cortex. [ABSTRACT FROM AUTHOR]

Objective Abnormal cortical plasticity has been hypothesized to play a crucial role in the pathogenesis of juvenile myoclonic epilepsy (JME). To study the motor cortical plasticity we used paired associative stimulation (PAS). When a repetitive electrical stimulus to the median nerve is paired with a transcranial magnetic stimulus (TMS) pulse over the controlateral motor cortex with at an interstimulus interval (ISI) of 25 ms, a long-term potentiation (LTP)-like synaptic plasticity is induced in the corticospinal system. Aim of this study was to investigate the motor cortex LTP-like synaptic plasticity by means of PAS in patients with JME. Methods Twelve adult patients with JME were compared with 13 healthy subjects of similar age and sex. PAS consisted of 180 electrical stimuli of the right median nerve paired with a single TMS over the hotspot of right APB at ISI of 25 ms (PAS25). We measured motor evoked potentials (MEPs) before and after each intervention for up to 30 min. Results In healthy subjects the PAS25 protocol was followed by a significant increase of MEP amplitude. On the contrary, in patients with JME, the MEP amplitude did not change. Conclusions Defective motor cortex plasticity may be involved in the pathogenesis of JME. [ABSTRACT FROM AUTHOR]

Objective Visual and motor cortex are involved in the origin/propagation of the photoparoxysmal response (PPR), a stronghold for the diagnosis of generalized photosensitive epilepsies. The study of the functional connection between these two distant areas with transcranial magnetic stimulation (TMS), could help clarify the pathophysiology of photosensitivity. Methods Eleven patients with idiopathic generalized epilepsy and photosensitivity were compared to 11 healthy subjects. We measured the resting motor threshold of the left hand motor area and the phosphene threshold. The paradigm consisted in a conditioning stimulus (CS) delivered over the phosphene hotspot of the visual cortex and followed at random interstimulus intervals (15–40 ms) by a test stimulus over the left motor cortex to evoke a motor evoked potential (MEP) of ∼1 mV from right FDI. The conditioned-MEP was expressed as a percentage of the unconditioned-MEP amplitude. Results In healthy subjects the CS over the visual cortex produced significant inhibitory changes on the corticospinal excitability with a time course between 18 and 40 ms. Patients with IGE and photosensitivity showed a failure of the physiological inhibition. Conclusions In photosensitive patients the alteration of the normal visuo-motor functional connectivity could be responsible for the origin/propagation of the PPR from the hyper-excitable visual cortex to the motor cortex. [ABSTRACT FROM AUTHOR]