Trigeminal Nerve Model for Cluster Headache
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Questions and Answers

Which of the following statements about pituitary adenylate cyclase-activating polypeptide (PACAP) is correct based on the information provided?

  • PACAP can induce activation of neurons in regions thought to be involved in cluster headache pathophysiology, such as the superior salivatory nucleus, the sphenopalatine ganglion, and the trigeminal ganglion. (correct)
  • Intravenous administration of PACAP in healthy individuals can induce cluster headache-like symptoms.
  • PACAP is pharmacologically similar to VIP and has been implicated in migraine pathogenesis, but not in cluster headache.
  • PACAP levels have been found to be increased in plasma during acute cluster headache attacks.

    • According to the information provided, which of the following statements about the effects of methylprednisolone on cluster headache pathophysiology is correct?

  • Methylprednisolone can suppress both IL-1β and prostaglandin E2-induced CGRP release from cultured trigeminal ganglia neurons.
  • Pretreatment with methylprednisolone can block cytokine-mediated trigeminal activation, which may mediate its preventive effect on cluster headache pathophysiology. (correct)
  • Methylprednisolone has been shown to have no effect on CGRP release from trigeminal ganglia neurons, but it can reduce plasma CGRP levels in cluster headache patients.
  • The mechanism by which methylprednisolone exerts its preventive effect on cluster headache pathophysiology is not related to its effects on trigeminal ganglia neurons or CGRP release.

    • Based on the evidence presented, which of the following statements is most accurate regarding the role of the trigeminal nerve in cluster headache?

  • Increased levels of calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP) suggest trigeminal nerve and parasympathetic activation, respectively, during cluster headache attacks.
  • Surgical lesioning of the trigeminal nerve is effective in treating cluster headache, indicating a central role.
  • While the trigeminal nerve is involved in cluster headache, its activation alone cannot fully account for the disorder, and other factors are likely involved. (correct)
  • Pretreatment with methylprednisolone can suppress CGRP release from trigeminal ganglia neurons, suggesting a direct effect on the trigeminal nerve.

    • Which of the following statements about calcitonin gene-related peptide (CGRP) is incorrect based on the information provided?

    <p>CGRP levels are decreased in cluster headache patients compared to migraine patients and individuals who have undergone therapeutic lesioning of the trigeminal ganglion.</p> Signup and view all the answers

    Based on the information provided, which of the following statements about the relationship between cluster headache and migraine is correct?

    <p>Cluster headache and migraine share similar pathophysiological mechanisms, and both involve activation of the trigeminal nerve and increased CGRP levels.</p> Signup and view all the answers

    According to the trigeminal nerve model of cluster headache, what mechanism leads to the autonomic symptoms observed in patients?

    <p>Activation of the ophthalmic nerve triggers a reflex activation of the parasympathetic efferents.</p> Signup and view all the answers

    Which statement best describes the role of triptans in the treatment of acute cluster headache attacks according to the information provided?

    <p>Triptans act by inhibiting the release of neurotransmitters from brainstem trigeminal neurons.</p> Signup and view all the answers

    What is the primary controversy regarding the mechanism of action of triptans in the treatment of cluster headache according to the information provided?

    <p>Whether triptans act predominantly through a central nervous system effect in the brainstem or through an effect on peripheral trigeminovascular neurons.</p> Signup and view all the answers

    Based on the information provided, which of the following statements about the role of calcitonin gene-related peptide (CGRP) in cluster headache is most accurate?

    <p>The text does not provide any information about the role of CGRP in the pathophysiology or treatment of cluster headache.</p> Signup and view all the answers

    What is the key evidence provided in the text that supports the trigeminal nerve model of cluster headache?

    <p>The successful use of triptans, which activate postsynaptic 5-HT1B and 5-HT1D receptors, to treat acute cluster headache attacks.</p> Signup and view all the answers

    What evidence suggests that the success of sumatriptan treatment in cluster headache may be due to central effects on the trigeminal nucleus caudalis?

    <p>Increased CGRP levels in patients interictally during a cluster-bout period</p> Signup and view all the answers

    Which neuropeptide is similar to VIP and has been implicated in migraine pathogenesis, inducing migraine-like headaches when administered intravenously?

    <p>PACAP</p> Signup and view all the answers

    What is a marker of parasympathetic activation that is elevated in jugular vein blood samples ipsilateral to cluster headache attacks?

    <p>VIP</p> Signup and view all the answers

    Which finding supports the involvement of PACAP in cluster headache pathophysiology?

    <p>Elevated PACAP levels in plasma during acute cluster headache attacks</p> Signup and view all the answers

    What can be attenuated by sumatriptan injection in patients during nitroglycerine-induced attacks?

    <p>CGRP release induced by prostaglandin E2</p> Signup and view all the answers

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