Publications by authors named "Martina Bracaglia"

14 Publications

  • Page 1 of 1

Acute inflammatory demyelinating polyneuritis in association with an asymptomatic infection by SARS-CoV-2.

J Neurol 2020 Nov 25;267(11):3166-3168. Epub 2020 Jun 25.

Neurology Unit, Medical Oncological Department, S. Maria Della Scaletta Hospital, 40026, Imola, BO, Italy.

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http://dx.doi.org/10.1007/s00415-020-10014-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7315403PMC
November 2020

The function of the lateral inhibitory mechanisms in the somatosensory cortex is normal in patients with chronic migraine.

Clin Neurophysiol 2020 04 3;131(4):880-886. Epub 2020 Feb 3.

Sapienza University of Rome Polo Pontino, Department of Medico-Surgical Sciences and Biotechnologies, Latina, Italy; IRCCS Neuromed, Pozzilli, IS, Italy.

Objective: To study lateral inhibition and habituation/sensitization in the somatosensory cortex of patients with chronic migraine (CM) and to identify correlations with clinical migraine features.

Methods: Sixteen patients with CM without medication overuse, and 17 healthy volunteers (HVs) received somatosensory evoked potentials (SSEPs) elicited by separate electrical stimulation of the right median (M) and ulnar (U) nerves at the wrist and by simultaneous nerve stimulation (MU). We measured the N20-P25 amplitudes and calculated the lateral inhibition (LI) percentage using the formula {100-[MU/(M + U) * 100]}. We also calculated sensitization (SSEP amplitude during block 1) and delayed habituation to M-nerve stimulation.

Results: The percentage of LI did not differ between the groups (40.2% in HV, 47.4% in CM, p = 0.276) and was negatively correlated with the monthly headache-day number (r = -0.532, p = 0.034). Patients showed a generalized increase in SSEP amplitudes compared to HVs and habituated normally.

Conclusions: We showed a pattern of somatosensory response in CM similar to that observed during attacks of episodic migraine.

Significance: In the transition process between episodic migraine and CM, LI attempts to physiologically counteract the mounting increase in attack frequency, but this is insufficient to allow patients to exit the chronic phase.
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http://dx.doi.org/10.1016/j.clinph.2020.01.009DOI Listing
April 2020

A ketogenic diet normalizes interictal cortical but not subcortical responsivity in migraineurs.

BMC Neurol 2019 Jun 22;19(1):136. Epub 2019 Jun 22.

Department of Medico-Surgical Sciences and Biotechnologies, "Sapienza" University Rof Rome Polo Pontino, Latina, Italy.

Background: A short ketogenic diet (KD) treatment can prevent migraine attacks and correct excessive cortical response. Here, we aim to prove if the KD-related changes of cortical excitability are primarily due to cerebral cortex activity or are modulated by the brainstem.

Methods: Through the stimulation of the right supraorbital division of the trigeminal nerve, we concurrently interictally recorded the nociceptive blink reflex (nBR) and the pain-related evoked potentials (PREP) in 18 migraineurs patients without aura before and after 1-month on KD, while in metabolic ketosis. nBR and PREP reflect distinct brain structures activation: the brainstem and the cerebral cortex respectively. We estimated nBR R2 component area-under-the-curve as well as PREP amplitude habituation as the slope pof the linear regression between the 1st and the 2nd block of 5 averaged responses.

Results: Following 1-month on KD, the mean number of attacks and headache duration reduced significantly. Moreover, KD significantly normalized the interictal PREP habituation (pre: + 1.8, post: - 9.1, p = 0.012), while nBR deficit of habituation did not change.

Conclusions: The positive clinical effects we observed in a population of migraineurs by a 1-month KD treatment coexists with a normalization at the cortical level, not in the brainstem, of the typical interictal deficit of habituation. These findings suggest that the cerebral cortex may be the primary site of KD-related modulation.

Trial Registration: ClinicalTrials.gov NCT03775252 (retrospectively registered, December 09, 2018).
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http://dx.doi.org/10.1186/s12883-019-1351-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6588932PMC
June 2019

O025. Excitability of the motor cortex in migraine changes with the distance from the last attack.

J Headache Pain 2015 Dec;16(Suppl 1):A158

Department of Medico-Surgical Sciences and Biotechnologies, "Sapienza" University of Rome Polo Pontino, Latina, Italy.

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http://dx.doi.org/10.1186/1129-2377-16-S1-A158DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759334PMC
December 2015

Cortical functional correlates of responsiveness to short-lasting preventive intervention with ketogenic diet in migraine: a multimodal evoked potentials study.

J Headache Pain 2016 31;17:58. Epub 2016 May 31.

Department of Medico-Surgical Sciences and Biotechnologies, "Sapienza" University of Rome Polo Pontino, Latina, Italy.

Background: Here, we aim to identify cortical electrofunctional correlates of responsiveness to short-lasting preventiveintervention with ketogenic diet (KD) in migraine.

Methods: Eighteen interictal migraineurs underwent visual (VEPs) and median nerve somatosensory (SSEPs) evokedpotentials before and after 1 month of KD during ketogenesis. We measured VEPs N1-P1 and SSEPs N20-P25 amplitudes respectively in six and in two sequential blocks of 100 sweeps as well as habituation as theslope of the linear regression between block 1 to 6 for VEPs or between 1 to 2 for SSEPs.

Results: After 1-month of KD, a significant reduction in the mean attack frequency and duration was observed (all P< 0.001). The KD did not change the 1st SSEP and VEP block of responses, but significantly inducednormalization of the interictally reduced VEPs and SSEPs (all p < 0.01) habituation during the subsequentblocks.

Conclusions: KD could restore normal EPs habituation curves during stimulus repetition without significantly changing theearly amplitude responses. Thus, we hypothesize that KD acts on habituation regulating the balancebetween excitation and inhibition at the cortical level.
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http://dx.doi.org/10.1186/s10194-016-0650-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4887398PMC
October 2016

Visual evoked potentials in subgroups of migraine with aura patients.

J Headache Pain 2015 2;16:92. Epub 2015 Nov 2.

Department of Medical and Surgical Sciences and Biotechnologies, "Sapienza" University of Rome Polo Pontino, Latina, Italy.

Background: Patients suffering from migraine with aura can have either pure visual auras or complex auras with sensory disturbances and dysphasia, or both. Few studies have searched for possible pathophysiological differences between these two subgroups of patients.

Methods: Methods - Forty-seven migraine with aura patients were subdivided in a subgroup with exclusively visual auras (MA, N = 27) and another with complex neurological auras (MA+, N = 20). We recorded pattern-reversal visual evoked potentials (VEP: 15 min of arc cheques, 3.1 reversal per second, 600 sweeps) and measured amplitude and habituation (slope of the linear regression line of amplitude changes from the 1st to 6th block of 100 sweeps) for the N1-P1 and P1-N2 components in patients and, for comparison, in 30 healthy volunteers (HV) of similar age and gender distribution.

Results: VEP N1-P1 habituation, i.e. amplitude decrement between 1st and 6th block, which was obvious in most HV (mean slope -0.50), was deficient in both MA (slope +0.01, p = 0.0001) and MA+ (-0.0049, p = 0.001) patients. However, VEP N1-P1 amplitudes across blocks were normal in MA patients, while they were significantly greater in MA+ patients than in HVs.

Conclusions: Our findings suggest that in migraine with aura patients different aura phenotypes may be underpinned by different pathophysiological mechanisms. Pre-activation cortical excitability could be higher in patients with complex neurological auras than in those having pure visual auras or in healthy volunteers.
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http://dx.doi.org/10.1186/s10194-015-0577-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4630240PMC
May 2016

Lateral inhibition in the somatosensory cortex during and between migraine without aura attacks: Correlations with thalamocortical activity and clinical features.

Cephalalgia 2016 May 6;36(6):568-78. Epub 2015 Oct 6.

"Sapienza" University of Rome Polo Pontino Department of Medical and Surgical Sciences and Biotechnologies, Italy INM Neuromed IRCCS, Italy.

Background: We studied lateral inhibition in the somatosensory cortex of migraineurs during and between attacks, and searched for correlations with thalamocortical activity and clinical features.

Participants And Methods: Somatosensory evoked potentials (SSEP) were obtained by electrical stimulation of the right median (M) or ulnar (U) nerves at the wrist or by simultaneous stimulation of both nerves (MU) in 41 migraine without aura patients, 24 between (MO), 17 during attacks, and in 17 healthy volunteers (HVs). We determined the percentage of lateral inhibition of the N20-P25 component by using the formula [(100)-MU/(M + U)*100]. We also studied high-frequency oscillations (HFOs) reflecting thalamocortical activation.

Results: In migraine, both lateral inhibition (MO 27.9% vs HVs 40.2%; p = 0.009) and thalamocortical activity (MO 0.5 vs HVs 0.7; p = 0.02) were reduced between attacks, but not during. In MO patients, the percentage of lateral inhibition negatively correlated with days elapsed since the last migraine attack (r = -0.510, p = 0.01), monthly attack duration (r = -0.469, p = 0.02) and severity (r = -0.443, p = 0.03), but positively with thalamocortical activity (r = -0.463, p = 0.02).

Conclusions: We hypothesize that abnormal migraine cycle-dependent dynamics of connectivity between subcortical and cortical excitation/inhibition networks may contribute to clinical features of MO and recurrence of attacks.
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http://dx.doi.org/10.1177/0333102415610873DOI Listing
May 2016

Lateralized nociceptive blink reflex habituation deficit in episodic cluster headache: Correlations with clinical features.

Cephalalgia 2015 Jun 16;35(7):600-7. Epub 2014 Sep 16.

IRCCS-Neuromed, Pozzilli (IS), Italy.

Background: We previously observed impaired habituation mechanisms of the conventional blink reflex (BR) in patients with episodic cluster headache (ECH) during the bout, studying only the affected side. Here, we have studied the nociceptive-specific BR (nBR) both on the affected and non-affected sides, and in relation to clinical features.

Participants And Methods: We recorded nBR in 18 ECH patients during the bout, and in 18 healthy volunteers (HVs). We compared pain threshold, area, and habituation of the nBR, recorded both for the affected and non-affected sides.

Results: In patients, the pain threshold on the affected side was lower than that of the non-affected side (p = 0.009), and lower than in HVs (p = 0.038). Reflex area was decreased on both sides (p < 0.05) compared with HVs, whereas habituation was significantly impaired only on the affected side (p = 0.025 vs. HVs; p = 0.003 vs. non-affected). The habituation slope was positively correlated with the number of days since the onset of the bout and the daily attack frequency.

Conclusions: Our data reflect lateralized pathological variations in craniofacial nociception in ECH patients over the course of the cluster period. We hypothesized that this is due to malfunctioning of mechanisms that regulate hypothalamic activity and descending aminergic controls.
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http://dx.doi.org/10.1177/0333102414550418DOI Listing
June 2015

Diet transiently improves migraine in two twin sisters: possible role of ketogenesis?

Funct Neurol 2013 Oct-Dec;28(4):305-8

The ketogenic diet is a high-fat, low-carbohydrate diet long used to treat refractory epilepsy; ketogenesis (ketone body formation) is a physiological phenomenon also observed in patients following lowcarbohydrate, low-calorie diets prescribed for rapid weight loss. We report the case of a pair of twin sisters, whose high-frequency migraine improved during a ketogenic diet they followed in order to lose weight. The observed time-lock between ketogenesis and migraine improvement provides some insight into how ketones act to improve migraine.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3951260PMC
http://dx.doi.org/10.11138/FNeur/2013.28.4.305DOI Listing
November 2014

Response to letter to the editor.

Pain 2014 Mar 12;155(3):644-645. Epub 2013 Dec 12.

IRCCS Neuromed, Pozzilli (IS), Italy "Sapienza" University of Rome, Department of Medico-surgical Sciences and Biotechnologies, Neurology Section, Rome, Italy "Sapienza" University of Rome, Department of Medico-surgical Sciences and Biotechnologies, Latina, Italy G.B. Bietti Foundation-IRCCS, Department of Neurophysiology of Vision and Neurophthalmology, Rome, Italy.

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http://dx.doi.org/10.1016/j.pain.2013.12.013DOI Listing
March 2014

Electrophysiological correlates of episodic migraine chronification: evidence for thalamic involvement.

J Headache Pain 2013 Sep 9;14:76. Epub 2013 Sep 9.

G,B, Bietti Foundation IRCCS, Department of Neurophysiology of Vision and Neurophthalmology G,B, Bietti Foundation-IRCCS, Via Livenza 3, Rome 00198, Italy.

Background: Episodic migraine is characterized by decreased high-frequency somatosensory oscillations (HFOs), reflecting thalamo-cortical activity, and deficient habituation of low-frequency (LF-) somatosensory evoked potentials (SSEPs) to repetitive sensory stimulation between attacks. Here, we study conventional LF-SSEPs and HFOs in episodic migraineurs who developed chronic migraine (CM).

Methods: Thirty-four episodic (15 interictally [MOii], 19 ictally [MOi]) and 19 CM patients underwent right median nerve SSEPs. The patient groups were compared to a group of 20 healthy volunteers (HV) of comparable age and gender distribution. We measured the N20-P25 LF-SSEP 1st amplitude block and habituation, and, after applying a band-pass filter (450-750 Hz), maximal peak-to-peak latency and the amplitudes of the early and late HFOs.

Results: Reduced early HFOs, lower 1st block LF-SSEPs and deficient habituation characterize MOii. Initially higher SSEP amplitudes and late normal habituation characterize both CM and MOi patients. After the digital filtration, both patient groups showed shortened latency peaks and normalization of early HFO amplitudes with increased late HFOs. When data of MO and CM patients were combined, the monthly number of days with headache negatively correlated with the LF-SSEP slope (r = -0.385, p = 0.006), which in turn negatively correlated with the 1st amplitude block (r = 0.568, p < 0.001).

Conclusions: Our results show abnormalities in chronic migraine that are also reported during attacks in episodic migraineurs, namely early response sensitization and late habituation. The HFO analysis suggests that this sensory sensitization may be explained by an increase in the strength of the connections between the thalamus and cortex compared to episodic migraine between attacks. Whether this electro-functional behaviour is primary or secondary to daily headache, thus reflecting an electrophysiological fingerprint of the somatosensory system central sensitization process, remains to be determined.
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http://dx.doi.org/10.1186/1129-2377-14-76DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3844625PMC
September 2013

Abnormal sensorimotor plasticity in migraine without aura patients.

Pain 2013 Sep 18;154(9):1738-1742. Epub 2013 May 18.

IRCCS Neuromed, Pozzilli (IS), Italy "Sapienza" University of Rome, Department of Medicosurgical Sciences and Biotechnologies, Neurology Section, Rome, Italy "Sapienza" University of Rome, Department of Medicosurgical Sciences and Biotechnologies, Latina, Italy G.B. Bietti Foundation-IRCCS, Department of Neurophysiology of Vision and Neurophthalmology, Rome, Italy.

The period between migraine attacks is characterized by paradoxical responses to repetitive sensory and transcranial magnetic stimulation (TMS). Abnormal long-term cortical functional plasticity may play a role and can be assessed experimentally by paired associative stimulation (PAS), in which somatosensory peripheral nerve stimuli are followed by TMS of the motor cortex. Changes in motor-evoked potential (MEP) amplitudes were recorded in 16 migraine without aura patients (MO) and 15 healthy volunteers (HV) before and after PAS, which consisted of 90 peripheral electrical right ulnar nerve stimulations and subsequent TMS pulses over the first dorsal interosseous (FDI) muscle activation site with a delay of 10 ms (excitability depressing) or 25 ms (excitability enhancing). As a control experiment of the 31 subjects studied, 8 (4 MO and 4 HV) also underwent PAS10 earlier, the recording of somatosensory high-frequency oscillations (HFOs) reflecting thalamocortical activation (early HFOs). Although PAS10 reduced MEP amplitudes in HV (-17.7%), it significantly increased amplitudes in MO (+35.9%). Although in HV MEP amplitudes were significantly potentiated (+55.1) after PAS25, only a slight, nonsignificant increase was observed in MO (+18.8%). In the control experiment, performed on 8 subjects pooled together, Pearson's correlation showed an inverse relationship between the percentage of MEP amplitude changes after PAS10 and early HFO amplitudes (r=-0.81; P=.01). Because we observed that the more deficient the long-term PAS-induced change, the more the thalamocortical activation decreased, we hypothesize that the abnormalities in long-term cortical plasticity observed in the interictal period between migraine episodes could be due to altered thalamic control.
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http://dx.doi.org/10.1016/j.pain.2013.05.023DOI Listing
September 2013

Drug-induced changes in cortical inhibition in medication overuse headache.

Cephalalgia 2011 Sep 22;31(12):1282-90. Epub 2011 Jul 22.

Department of Medical-Surgical Sciences and Biotechnologies, A. Fiorini Hospital, Terracina, LT, Sapienza University of Rome Polo Pontino, Italy.

Background: We investigated whether chronic headache related to medication overuse (MOH) is associated with changes in brain mechanisms regulating inhibitory cortical responses compared with healthy volunteers and episodic migraineurs recorded between attacks, and whether these changes differ according to the drug overused.

Subjects And Methods: We studied 40 MOH patients whose symptoms were related to triptans alone, non-steroidal anti-inflammatory drugs (NSAIDs) or both medications combined, 12 migraineurs and 13 healthy volunteers. We used high-intensity transcranial magnetic stimulation over the primary motor cortex to assess the silent period from contracted perioral muscles.

Results: In MOH patients the cortical silent period differed according to the type of headache medication overused: in patients overusing triptans alone it was shorter than in healthy volunteers (44.7 ± 14.2 vs. 108.1 ± 30.1 ms), but similar to that reported in migraineurs (59.9 ± 30.4 ms), whereas in patients overusing NSAIDs alone or triptans and NSAIDs combined duration of silent period was within normal limits (80.6 ± 46.4 and 103.8 ± 47.2 ms).

Conclusions: Compared with episodic migraineurs, MOH patients overusing triptans have no significant change in cortical inhibition, whereas those overusing NSAIDs have an increase in cortical inhibitory mechanisms. We attribute these changes to medication-induced neural adaptation promoted by changes in central serotonin neurotransmission.
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http://dx.doi.org/10.1177/0333102411415877DOI Listing
September 2011