Secondary cluster headache due to a contralateral demyelinating periaqueductal gray matter lesion

Abstract

Although not generally considered as a symptom of multiple sclerosis (MS), headache is reported to be more frequent in patients with MS than in the general population. 1 Tension-type headache and migraine without aura are the most common primary headaches in people with MS, whereas cluster headache (CH) can be considered exceptional. Generally, neuroimaging is normal in patients with CH. However, in a few cases, this disorder is associated with intracranial pathology (e.g., tumors, aneurysms, arteriovenous malformations, infections, etc.). 2 There have so far been six cases in the literature regarding CH associated with MS, all of them showing a brainstem lesion ipsilateral to the pain, [3][4][5][6][7] with a possible exception. Mijajlović et al. 8 described a case in which brainstem lesions were found both ipsilaterally (brachium pontis) and contralaterally (dorsolateral region of the pons) to the pain. Only one case of CH as the initial and unique clinical manifestation of MS has been described. 8 The location of demyelinating lesions could be strategic in these cases, involving areas interacting with the trigeminovascular system. 1 This report describes the case of a 54-year-old woman with a right-sided CH as the initial manifestation of an inflammatory demyelinating disease of the central nervous system and showing a left dorsal brainstem lesion on magnetic resonance imaging (MRI). C A S E REP ORTWe report the case of a 54-year-old Caucasian woman with a history of 2-year severe/unbearable (8-10 on numeric rating scale for pain) lancinating pain strictly located in the right maxillary-zygomatic region prior to admission at our hospital in 2019. The attacks lasted about 30-60 min (both untreated and treated with nonsteroidal

Altered metabolites in the periaqueductal gray of COVID-19 patients experiencing headaches: a longitudinal MRS study

“…Both take part in ascending and descending projections and modulate the 'ON' (facilitating the activity of neurons responding to noxious stimuli) and 'OFF' (ceasing firing immediately, inhibiting nociceptive responses) cells in the rostral ventromedial medulla to control nociceptive processing (20)(21)(22). Stimulation of the PAG can induce analgesic effects, while lesions in the PAG have been associated with causing headaches (13,23). Glutamate and glutamine are typically quantified together as the glutamate/glutamine complex (Glx) due to their spectral overlap, making it challenging to separate their individual signals.…”

Pathophysiology of cluster headache: From the trigeminovascular system to the cerebral networks

“…This would explain why patients with other primary headaches, like migraine, may also experience activation of the parasympathetic reflex during pain (35,36). The evidence in clinical cases of CH attacks even after complete sectioning of the trigeminal nerve (37) or attacks secondary to lesions of deep brain structures (38,39), further complicates the pathophysiological picture of CH, suggesting that peripheral activation of the trigeminal nerve is not sufficient to explain the pain in CH. These data were considered in favour of the hypothesis of multiple central permissive anatomico-functional factors underlying the pain and recurrence of cluster headache.…”