It could just be me but I think that laying down flat on the bed when I sleep triggers an attack. And sitting up gets me longer intervals of sleep time. Also, going to bed too late or staying up too long after an episode seems to trigger more.

I think there is something to sleep patterns and frequency and strength of attacks.

For people who get CH overnight I've seen quite a few post that sleeping in a position that isn't quite horizontal can help, so this could be in a reclining chair or something similar. However all you can do is to experiment and see what works for you.

99% of my attacks happen between midnight and 2am. As soon as it wakes me I'm up, down an energy drink and pace until the pain ends. I learned many years ago not to go back to bed. Laying flat in bed will only trigger another attack. I have a very soft, comfortable (read expensive) La-Z-Boy just to finish my cluster night sitting up. In the last 3 and a half years I've probably clocked more hours in the chair than in bed.

YES ,, YES YES YES ,,, my son told me that he started to feel a CH coming on on Saturday night ,, and he stood up and it stopped.  this pushes me even harder wondering if it isn't acid reflux .. (you know the commercials where someone has to tilt the bed to sleep).. He also has such horrible heartburn during the cluster phase...

The current research is showing that CH originates in the hypothalamus area of the brain.

Standing up will alter blood pressure, which could impact it.

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The article you link to only states that there are areas of the brain that show activity because of the pain of the cluster headache.  There is nothing in this article which specifically states that the CH originates in the brain itself.
Note that the headache was induced. Not observed as it occurs naturally which is the real key here. WHY does it occur, not what is reacting to it in our brains after onset.

see excerpt below


Discussion
We observed areas of activation in acute cluster headache that fall into two broad groups: areas known to be involved in pain processing or response to pain, such as cingulate and insula cortex and thalamus; and areas activated specifically in cluster headache but not in other causes of head pain, notably the hypothalamic grey areas. These data suggest that primary headache syndromes share some processing pathways but equally can be distinguished on a functional neuroanatomical basis by areas of activation specific to the clinical presentation.
Studies with PET have repeatedly given results that show activation of the anterior cingulate cortex on the sensation of somatic or visceral pain that are attributed to the emotional response to pain.13, 16 and 17 Activations in the insula have been shown after application of heat,16 and 18 subacutaneous injections of ethanol,19 somatosensory stimulation,20 and during cluster headache.13 Given its anatomical connections, the insula has been suggested as a relay of sensory information into the limbic system and is known to play an important part in the regulation of autonomic responses.21 Painful stimuli are significantly effective in activating the anterior insula, a region closely associated with both somatosensory and limbic systems. Such connections may provide one route through which nociceptive input is integrated with memory to allow full appreciation of the meaning and dangers of painful stimuli. In the acute pain state the thalamus is a site where activations would most be expected. Activation of the contralateral thalamus as a result of pain is known from studies on animals22 and functional imaging studies in human beings.16 and 17 The acute pain in cluster headache, induced activation bilaterally in the cerebellar hemispheres and in the vermis. There seems to be no direct nociceptive input to the cerebellum,23 and there is no clinical evidence that cerebellar lesions or stimulation affect pain sensation in human beings.16 However, there are some PET studies that report an activation in this area during experimental pain.16 and 24
In contrast to migraine,25 no brain stem activation was found during the acute attack compared with the resting state. This finding is remarkable because migraine and cluster headache are often discussed as associated disorders and similar compounds, such as ergotamine and sumatriptan, are used in the acute treatment of both types of headache. These data suggest that while primary headaches, such as migraine and cluster headache, may share a common pain pathway (the trigeminovascular innervation), the underlying pathogenesis differs substantially as might be inferred from the different patterns of presentation and responses to preventive agents.26
Substantial activations ascribable to cluster headache were observed in the ipsilateral hypothalamic grey area when compared with the headache-free state. Just as it is striking that no brain-stem activation occurs, which is in contrast to acute migraine,25 we have seen no hypothalamic activation in experimental pain induced by capsaicin injection into the forehead.27 Injection into the forehead would activate first division (ophthalmic) afferents which traverse the trigeminal division responsible for pain activation in cluster headache. Thus two other types of first division trigeminal nerve pain, while sharing neuroanatomical pathways with cluster headache, do not give rise to hypothalamic activation. Moreover, in the eight control patients who did not experience a headache after taking nitroglycerin, rCBF in the region of the hypothalamic grey area was not increased. This finding implies that the activation we have observed is involved in the pain process in a permissive or triggering manner rather than simply as a response to first division nociception per se. Hypothalamic activation in traumatic nociception has been observed in the hypothalamus proper and is a different more rostral area than we report.19 Moreover, Hsieh and colleagues19 report changes contralateral to the pain, whereas we report changes that are ipsilateral and in the hypothalamic grey area in the region of the circadian pacemaker neurons which is, therefore, an anatomically distinct area on the opposite side of the brain. Given that this area is involved in circadian rhythm and sleep-wake cycling, our data establish an involvement of this area of the hypothalamus as a primum movens in the acute cluster attack.
Cluster headache has been attributed to an inflammatory process in the cavernous sinus and tributary veins.28 Inflammation has been thought to obliterate venous outflow from the cavernous sinus on one side, thus injuring the traversing sympathetic fibres of the intracranial internal carotid artery and its branches. According to this theory, the active period ends when the inflammation is suppressed and the sympathetic fibres partially or fully recover. This theory is based on abnormal findings with orbital phlebography in patients with cluster headache,29 and the fact that nitroglycerin and other vasodilators can induce a cluster attack.5 However, given the circadian rhythmicity and unilaterality of the symptoms, a purely vasogenic cause cannot explain the entire picture of cluster headache.30 Moreover, the frequency and pattern of pathological findings at orbital phlebography in cervicogenic headache, migraine, and tension-type headache is similar to that in cluster headache.31 Given that we have found an increased signal in the region of the cavernous sinus in the patients with acute cluster headache in this study and after capsaicin injection to the forehead in another PET study,27 it seems likely that the vascular changes are an epiphenomenon of activation of the trigeminovascular system.32
A radical reappraisal of the pathophysiology of cluster headache is needed. Our data establish that cluster headache, far from being a primarily vascular disorder, is a condition the genesis of which is to be found in the central nervous system in pacemaker or circadian regions of the hypothalamic grey matter. Further, we suggest that both cluster headache and migraine might usefully be regarded are neurovascular headaches to include the neural contribution to these important clinical syndromes.

and as DUMB as it may sound to everyone ,, we are on Day 3 now ,, no stomach problems .. NO headaches. it may be his Cluster phase is over for now.. I do not know.. as it is all changing .. but in treating his stomach symptoms for the last 3 days ,, his head has improved.

The link between acid reflux and CH has been discussed here before:

Kilowatt3 wrote on Mar 23^rd, 2010 at 10:50am:


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This is the first article I have found to link acid reflux and eustachian tube issues .. my son had many ear infections as a child

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