Laugh-induced Headache: Clinical Features and Literature Review

Ye Ran, MD; Huanxian Liu, MD; Meichen Zhang, MD; Zhao Dong, MD, PhD; Shengyuan Yu, MD, PhD

Disclosures

Headache. 2017;57(10):1498-1506. 

In This Article

Discussion

LH, or laugh headache, does not appear in the International Classification of Headache Disorders 3β (ICHD-3β). The cases of LH with intracranial disease presented above can be categorized as secondary LH, including the headache attributed to CM-1 as described in the ICHD-3β.[2] Other patients with LHs without an organic basis may be categorized as primary LH. Previously reported cases of LH without intracranial disease were often classified as primary cough headache (PCH) or primary exercise headache (PEH).

Similar to PCH, secondary LH is brought on by and occurs in association with Valsalva maneuvers. However, the secondary LH has closer ties with laugh than does PCH. Like PCH, the attack of LH is usually sudden, reaches its peak immediately, and then subsides within a few minutes.[10] In addition, LH in Patient 2 described above and in the patient in Morales-Asin's report, which we prefer to classify as primary LH, has close relationships with sustained physically strenuous exercise, which is also a precipitating factor of PEH. All these types of headache begin immediately or within seconds after being triggered, reach their peak immediately, and last for a few minutes. Although most cases of PEH are pulsating, LH and PCH are both nonthrobbing. Attacks predominantly affect bilateral and posterior areas of the head in patients with PCH or primary LH.[11] The primary headache may have associated symptoms and responds well to indomethacin. The characteristics of LH, PCH, and PEH are summarized in Table 2.

Secondary LH

After the comparison, we can conclude that secondary LH has many similarities to cough headache (CH). The pathogeny of LH has been reported to include CM-1, GPG, thrombophlebitis, intracranial tumors, posterior arachnoid cysts, intracranial hypotension, and unruptured posterior communicating artery aneurysm.[5,7,12–14] All types of etiologies have influence on the spatial structure of the posterior cranial fossa and cerebrospinal fluid circulation. Correspondingly, the majority etiology of patients with symptomatic CH is also CM-1.[11] Moreover, headache is one of the major symptoms of patients with CM-1 and is reported to occur in 15–75% of these patients.[15]

The mechanism behind the short-lasting headache attacks in CM-1 patients seems to be associated with Valsalva maneuvers, a process that may induce transient pressure dissociation between intracranial and intraspinal compartments.[16] This dissociation probably leads to an impaction of cerebellar tonsils on the foramen magnum, which may press and pull pain-sensitive structures, such as nerves, meninges and vessels, resulting in headache.[17,18] Thus, we speculate that secondary LH and CH are a heterophany of CM-1. However, four of the five patients with cerebellar tonsillar herniation, whom we summarized in Table 1, did not undergo brain surgery to decompress the posterior fossa. Therefore, this hypothesis has yet to be verified.

Primary LH

Although there is no significant change on imaging examinations in some patients with LH, we cannot exclude the possibility of transient intracranial pressure changes associated with Valsalva maneuvers in these patients. According to previous research, retrograde jugular venous flow has been shown to induce intracranial venous congestion that may underlie the pathophysiology of exercise headache.[19,20] Further, some researchers have proposed that activity in the dural branch of the trigeminal nerve or distension of cerebral veins,[21] an increase in brain volume caused by transient elevation of venous pressure,[22] and more crowded posterior cranial fossa[23] may play a role in the pathophysiological process of CH. Thus, we cannot deny that all of these possibilities may also be contributing factors of LH.

In addition, the similarity of good responses in primary LH, PCH, and PEH to indomethacin or prophylactic drugs for treating primary headache compels us to consider that there may be more common pathologies underlying these primary headaches. It is worth mentioning that compared with the other patients, the patient reported by Shatti et al had many characteristics that were similar to those of migraines, including the location, duration, associated symptoms, and drug response. We prefer to speculate that laugh may be a rare trigger of migraine.

Primary LH Associated With Mirthful Laugh

Nevertheless, the suggestive theory of transient intracranial pressure change associated with Valsalva maneuvers cannot explain all aspects of LH. In reports by Levin et al[8] and Shatti et al,[9] patients suffered with headache mainly after mirthful laughing. This is not a unique instance about headache in connection with emotional change. As Blau[24] in 1995 and Evans[25] in 1998 both reported, patients with migraine-like headaches that were precipitated by crying were associated with sadness or emotional upset. However, the headaches could not be triggered by crying from happiness or cutting onions.

The close relationship between emotional laughing and LH suggests that changes of neural function in emotional alteration, rather than just intracranial pressure changes, seem to play a significant role in the production of headaches.[8] In patients with LH, understanding a joke per se does not lead to pain. Thus, it is not a cognitive process but rather an affective experience of mirth that is involved in the triggering process of LH. According to previous reports, the mesolimbic dopaminergic reward system may be involved in the affective processing.[26] Associated corresponding brain areas include the bilateral ventral striatum, nuclei accumbens, ventral tegmenta, hypothalamic region,[26] amygdala, and right medial prefrontal area.[27] To the best of our knowledge, the motor component of laughing includes two partially independent neuronal pathways.[28] The traditional voluntary pathway originates from the motor cortex and passes through the pyramidal tract to the ventral brainstem, whereas the other pathway is an emotionally driven pathway, with participating structures including the amygdala, hypothalamic region, subthalamic region, tegmental brainstem,[28] anterior cingulate cortex,[29] and mesial temporal structures.[30] Therefore, we speculate that the regions of the brain associated with the expression of mirth might be associated with LH (Figure 3). The exact pathophysiological connection between emotional laughing and LH requires further study.

Figure 3.

The possible pathophysiological mechanism of LH.

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