Reduced Cerebellar Inhibition in Migraine with Aura: A TMS Study

Brighina, Filippo; Palermo, Antonio; Panetta, Maristella; Daniele, Ornella; Aloisio, A.; Cosentino, Giuseppe; Fierro, Brigida

doi:10.1007/s12311-008-0090-4

Cited by 41 publications

(38 citation statements)

References 35 publications

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“…The cerebellum exerts an inhibitory control in the cerebral cortex and thus may play an important role in the filtering of sensory inputs [Strata et al 2009]. A reduction in cerebellar inhibition in migraineurs with aura has been demonstrated [Brighina et al 2009]. …”

Section: Cerebellummentioning

confidence: 99%

Possible sites of action of the new calcitonin gene-related peptide receptor antagonists

Eftekhari

Edvinsson

2010

Ther Adv Neurol Disord

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Migraine is considered a neurovascular disease affecting more than 10% of the general population. Currently available drugs for the acute treatment of migraine are vasoconstrictors, which have limitations in their therapeutic use. The calcitonin gene-related peptide (CGRP) has a key role in migraine, where levels of CGRP are increased during acute migraine attacks. CGRP is expressed throughout the central and peripheral nervous system, consistent with control of vasodilatation and transmission of nociceptive information. In migraine, CGRP is released from the trigeminal system. At peripheral synapses CGRP results in vasodilatation via receptors on the smooth muscle cells. At central synapses, CGRP acts postjunctionally on second-order neurons to transmit pain centrally via the brainstem and midbrain to higher cortical pain regions. The recently developed CGRP-receptor antagonists have demonstrated clinical efficacy in the treatment of acute migraine attacks. A remaining question is their site of action. The CGRP-receptor components (calcitonin receptor-like receptor, receptor activity modifying protein 1 and receptor component protein) are found to colocalize in the smooth muscle cells of intracranial arteries and in large-sized neurons in the trigeminal ganglion. The CGRP receptor has also been localized within parts of the brain and the brainstem. The aim of this paper is to review recent localization studies of CGRP and its receptor components within the nervous system and to discuss whether these sites could be possible targets for the CGRP-receptor antagonists.

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Section: Cerebellummentioning

confidence: 99%

Possible sites of action of the new calcitonin gene-related peptide receptor antagonists

Eftekhari

Edvinsson

2010

Ther Adv Neurol Disord

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“…Abnormalities in visual and motor cortex excitability consistent with a lack of inhibitory effect have been described in migraine. Cerebellar conditioning transcranial magnetic stimulation showed a significant deficit of cerebellar inhibition in migraine patients, compared with controls, 111 suggesting that migraine patients may have a deficit in filtering sensory inputs. The deficit in filtering somatosensory, visual, and auditory inputs may lead to head pain, photophobia, and phonophobia respectively.…”

Section: How Do Cgrp Antagonists Act In Migraine?mentioning

confidence: 99%

CGRP Receptor Antagonism and Migraine

Edvinsson

2010

Neurotherapeutics

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Summary: Calcitonin gene-related peptide (CGRP) is expressed throughout the central and peripheral nervous systems, consistent with control of vasodilatation, nociception, motor function, secretion, and olfaction. ␣CGRP is prominently localized in primary spinal afferent C and A⌬ fibers of sensory ganglia, and ␤CGRP is the main isoform in the enteric nervous system. In the CNS there is a wide distribution of CGRP-containing neurons, with the highest levels occurring in striatum, amygdala, colliculi, and cerebellum. The peripheral projections are involved in neurogenic vasodilatation and inflammation, and central release induces hyperalgesia. CGRP is released from trigeminal nerves in migraine. Trigeminal nerve activation results in antidromic release of CGRP to cause non-endothelium-mediated vasodilatation. At the central synapses in the trigeminal nucleus caudalis, CGRP acts postjunctionally on second-order neurons to transmit pain signals centrally via the brainstem and midbrain to the thalamus and higher cortical pain regions. Recently developed CGRP receptor antagonists are effective at aborting acute migraine attacks. They may act both centrally and peripherally to attenuate signaling within the trigeminovascular pathway.

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“…The cerebellum is also an important site for modulation of cortical inputs, and CGRP is expressed in the cerebellum and Purkinje cells [30,31]. Brighina and colleagues showed in 2009 that a loss of cerebellar inhibition is observed in migraine with aura [32]. The cerebellum has also been shown in PET studies to be active during acute migraine [33].…”

Section: Localisation Of Cgrp Receptors In the Nervous Systemmentioning

confidence: 99%

CGRP Mechanism Antagonists and Migraine Management

Karsan

Goadsby

2015

Curr Neurol Neurosci Rep

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Migraine is a complex disorder of the brain that is common and highly disabling. As understanding of the neural pathways has advanced, and it has become clear that the vascular hypothesis does not explain the disorder, new therapeutic avenues have arisen. One such target is calcitonin gene-related peptide (CGRP)-based mechanisms. CGRP is found within the trigeminovascular nociceptive system widely from the trigeminal ganglion to second-order and third-order neurons and in regulatory areas in the brainstem. Studies have shown CGRP is released during severe migraine attacks and the reversal of the attack with effective triptan treatment normalizes those levels. CGRP administration triggers migraine in patients, and CGRP receptor antagonists have been shown to abort migraine. Here, we review the current state of CGRP mechanism antagonist therapy as its research and development is increasing in migraine therapeutics. We discuss several recent trials, highlighting the evidence base behind these novel drugs, and their potential future contribution to migraine management.

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Reduced Cerebellar Inhibition in Migraine with Aura: A TMS Study

Cited by 41 publications

References 35 publications

Possible sites of action of the new calcitonin gene-related peptide receptor antagonists

Possible sites of action of the new calcitonin gene-related peptide receptor antagonists

CGRP Receptor Antagonism and Migraine

CGRP Mechanism Antagonists and Migraine Management

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