Trigeminal Nerve Model for Cluster Headache

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15 Questions

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.

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

Pretreatment with methylprednisolone can block cytokine-mediated trigeminal activation, which may mediate its preventive effect on cluster headache pathophysiology.

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

While the trigeminal nerve is involved in cluster headache, its activation alone cannot fully account for the disorder, and other factors are likely involved.

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

CGRP levels are decreased in cluster headache patients compared to migraine patients and individuals who have undergone therapeutic lesioning of the trigeminal ganglion.

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

Cluster headache and migraine share similar pathophysiological mechanisms, and both involve activation of the trigeminal nerve and increased CGRP levels.

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

Activation of the ophthalmic nerve triggers a reflex activation of the parasympathetic efferents.

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

Triptans act by inhibiting the release of neurotransmitters from brainstem trigeminal neurons.

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

Whether triptans act predominantly through a central nervous system effect in the brainstem or through an effect on peripheral trigeminovascular neurons.

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?

The text does not provide any information about the role of CGRP in the pathophysiology or treatment of cluster headache.

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

The successful use of triptans, which activate postsynaptic 5-HT1B and 5-HT1D receptors, to treat acute cluster headache attacks.

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

Increased CGRP levels in patients interictally during a cluster-bout period

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

PACAP

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

VIP

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

Elevated PACAP levels in plasma during acute cluster headache attacks

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

CGRP release induced by prostaglandin E2

Learn about the trigeminal nerve model of cluster headache, which involves the activation of the ophthalmic nerve by various triggers leading to severe unilateral headache. Explore how this activation results in the reflex activation of parasympathetic efferents.

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