Summary model of the pathophysiology of cluster headache

The performance of orbital phlebograms in cluster headache patients provides evidence of inflammatory processes in the cavernous sinus and in the area of ​​the superior ophthalmic vein . The genesis of these inflammatory processes is still not clear. Inflammation of the venous vessel sections can cause an obstruction to the venous outflow . The inflammatory change in the wall of the cavernous sinus can affect the ipsilateral sympathetic fibers that travel with the internal carotid artery and provide the sympathetic supply to the eyelid, eye, face, orbit, and retroorbital vessels. Surgical greater superficial petrosal nerve or the facial nerve , as well as a trigeminal rhizotomy, completely stop . Based on these observations, it can be concluded that fibers of both the trigeminal and facial nerves significant role in the pathophysiology of cluster headache . The altered pupil response to stimulation of the infratrochlear nerve also suggests involvement of sensory trigeminal fibers. The ipsilateral origin of the pain be explained by the spread of the inflammatory reaction and possible diffusion of the inflammatory neuropeptides ophthalmic nerve passing in the vicinity of the cavernous sinus Due to the close spatial relationship of the sympathetic and sensory fibers and the inflammatory change in the cavernous sinus area, both the sensory and autonomic abnormalities associated with cluster headache attacks can be understood.

Another special feature to note is that in the anatomical area of ​​interest, the internal carotid artery passes through the carotid canal and the vessel is mechanically constricted by a bony coating in the event of possible vasodilation. If an inflammatory process passes from the cavernous sinus to the internal carotid artery, the vessel wall can swell and become edematous and the result is compression of the sympathetic fibers in the carotid canal. The sympathetic fibers are directly irritated mechanically and the activation of sensory nociceptive fibers as well as the deactivation of sympathetic neurons can explain the variety of symptoms of the cluster headache attack. A similar process could play a role in the provocation of cluster headache attacks by nitroglycerin, histamine, alcohol, or hypoxia.

Cluster headaches usually only occur in middle age and older age . The reason for this could be that the elasticity of the vessels decreases in middle age and then, due to the basic physical rule actio = reactio, compression of the sympathetic fibers is caused. The greater vascular elasticity in young people and women compensates for possible compression of the sympathetic fibers . The coarser facial structures may also be present in the area of ​​the skull base and the anatomical formation of the carotid canal could be characterized by a particular narrowness These simple anatomical peculiarities may be the reason why men with special skull structures develop cluster headaches. The strict unilaterality could also be explained by a special anatomy that exists unilaterally .

The latency between the administration of vasodilating substances and the occurrence of the cluster attack after approx. 30 to 40 minutes could be based on the fact that the mechanical irritation of the sympathetic fibers caused by the pulsations of the vessel wall sufficient to cause a corresponding lesion after the summation .

Within the framework of these model ideas, spontaneous cluster attacks could occur if a basal inflammatory reaction persists in the area of ​​the cavernous sinus. During this time, you are vulnerable to cluster attacks. If this inflammatory reaction subsides spontaneously or if corticosteroid therapy is carried out, the remission phase occurs. In the case of a permanent inflammatory reaction in the area of ​​the cavernous sinus, a chronic cluster headache without intervening remission phases can be established.

The rapid relief of the cluster headache attack by vasoconstrictive substances such as sumatriptan could be explained by the fact that there is a rapid vasoconstriction of the carotid artery in the area of ​​the carotid canal and thereby the mechanical irritation of sensory trigeminal fibers and, in addition, the mechanical lesion of the perivascular sympathetic fibers stopped quickly . The same applies to the application of ergot alkaloids and the inhalation of oxygen, which also cause vasoconstriction. The pain-relieving effect after subcutaneous administration of sumatriptan occurs after just five to ten minutes . It is very doubtful that this rapid effect can be caused by an inhibition of an inflammatory process, as blocking an inflammatory reaction within minutes is very unlikely. the , ending simple mechanical irritation the vessel wall in the area of ​​the carotid canal through rapid vasoconstriction is rather obvious and plausible. The same applies to inhalation of pure oxygen, which can cure cluster headaches at a similar rate. The prophylactic administration of corticosteroids can also represent a very safe and reliable prophylactic therapy in patients with cluster headache attacks. An explanation for the effectiveness is given by inhibiting the basal inflammatory reactions The prophylactic administration of ergot alkaloids prevents mechanical irritation.

The individual dependence of cluster headache attacks on the time of day changes in pressure in the cavernous sinus over the course of the day At night , while sleeping in a lying position, there is an increase in venous pressure in the skull area. This is simply due to hydrostatic reasons due to the reduced fluid column when lying down. Venous congestion intensify an existing inflammatory reaction in the area of ​​the cavernous sinus the area of ​​the trigeminal nerve or the internal carotid artery.

The temporal behavior of the cluster headache attack can also be explained in the context of these considerations. Possible mechanical damage to sympathetic fibers in the carotid canal results in disturbed sympathetic activity. The result is a quasi-pathophysiological mechanical sympathicolysis . It is known that in cases of arteriovenous occlusive disease of the extremities, sympatholysis results in a significant improvement in pain and discomfort. Due to the sympathicolysis induced by the pathophysiological conditions in the area of ​​the carotid canal, a reduction in the increased cranial venous pressure be achieved by reducing the sympathetic tone. The pathophysiological process therefore requires a symptom-limiting therapeutic mechanism with a fixed time course, as is typically observed clinically in cluster headache attacks. The refractory period after a cluster attack can now also be explained based on these considerations, since the sympathetic fibers persistently damaged and a renewed excessive increase in intracranial venous tone is initially prevented. Only after a sufficiently long recovery period of sympathetic activity can the pathophysiological process be restarted.