Summary model of the pathophysiology of cluster headache
Orbital phlebograms performed on cluster headache patients reveal evidence of inflammatory processes in the cavernous sinus and the superior ophthalmic vein . The origin of these inflammatory processes remains unclear. Inflammation of the venous segments can obstruct venous outflow . Inflammatory changes in the cavernous sinus wall can affect the ipsilateral sympathetic fibers that run with the internal carotid artery and supply the eyelid, eye, face, orbit, and retro-orbital vessels. greater superficial petrosal nerve or the facial nerve, trigeminal rhizotomy, can completely cessation . Based on these observations, it can be concluded that fibers of both the trigeminal and facial nerves significant role in the pathophysiology of cluster headaches . The altered pupillary response to stimulation of the infratrochlear nerve also suggests the involvement of sensory trigeminal fibers. origin of the pain can the spread of the inflammatory reaction and the possible diffusion of inflammatory neuropeptides in the region of the cavernous sinus to the ophthalmic nerve, . Due to the close spatial relationship of the sympathetic and sensory fibers and the inflammatory changes in the region of the cavernous sinus, both the sensory and autonomic abnormalities associated with cluster headache attacks can be understood.
Another important point to note is that in the relevant anatomical area, the internal carotid artery passes through the carotid canal, and the vessel is mechanically constricted by a bony sheath during potential vasodilation. If an inflammatory process spreads from the cavernous sinus to the internal carotid artery, the vessel wall can become edematous and inflamed, resulting in 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 diverse symptoms of a 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 typically in middle and later life . This could be because vascular elasticity decreases in middle age, leading to compression of sympathetic fibers Greater vascular elasticity in youth and in women compensates for this potential compression coarser facial structures described in patients with cluster headaches may also be present in the area of the skull base, and the anatomical structure of the carotid canal be characterized by a particular narrowness in cluster headache sufferers men with specific skull structures are more likely to develop cluster headaches. The strict unilaterality of the could also be explained by a unilaterally specific anatomy of the carotid canal.
The latency between the administration of vasodilating substances and the occurrence of the cluster attack after approximately 30 to 40 minutes could be based on the fact that the mechanical irritation of the sympathetic fibers by the pulsations of the vessel wall only sufficient to cause a corresponding lesion after the summation of a large number of vessel pulsations.
According to this model, spontaneous cluster attacks could occur if a persistent basal inflammatory reaction in the cavernous sinus persists. During this time, susceptibility to cluster attacks is present. If this inflammatory reaction subsides spontaneously or if corticosteroid therapy is administered, the remission phase begins. In the case of a permanent inflammatory reaction in the cavernous sinus, chronic cluster headache without intervening remission phases can be diagnosed.
The rapid relief of cluster headache attacks with vasoconstrictive substances such as sumatriptan could be explained by the rapid vasoconstriction of the carotid artery in the region of the carotid canal , which quickly stops the mechanical irritation of sensory trigeminal fibers and, furthermore, the mechanical damage to the perivascular sympathetic fibers . The same applies to the administration of ergot alkaloids and the inhalation of oxygen, which also cause vasoconstriction. The pain-relieving effect after subcutaneous administration of sumatriptan occurs within five to ten minutes . It is highly doubtful that this rapid effect can be attributed to the inhibition of an inflammatory process, as blocking an inflammatory reaction within minutes is very unlikely. The cessation of simple mechanical irritation of the vessel wall in the region of the carotid canal by rapid vasoconstriction, on the other hand, is more plausible. The same applies to the inhalation of pure oxygen, which can alleviate cluster headaches with a similar speed. Prophylactic administration of corticosteroids can also be a very safe and reliable prophylactic therapy for patients with cluster headache attacks. Inhibition of the basal inflammatory reactions in the area of the cavernous sinus explains its effectiveness. Prophylactic administration of ergot alkaloids prevents mechanical irritation.
The individual diurnal pattern of cluster headache attacks could be explained changes in pressure day During sleep, lying down leads to an increase in venous pressure in the skull. This is due to hydrostatic pressure alone, caused by the reduced fluid volume in the skull. Venous congestion exacerbate an existing inflammatory reaction in the cavernous sinus , potentially spreading the inflammatory response from the sinus to the sensory autonomic fibers in the trigeminal nerve or the internal carotid artery.
The temporal pattern of cluster headache attacks can also be explained within this framework. Possible mechanical damage to sympathetic fibers in the carotid canal leads to impaired sympathetic activity. This results in a quasi-pathophysiologically induced mechanical sympatholysis . It is well known that in arteriovenous occlusive disease of the extremities, sympatholysis leads to a significant improvement in pain and symptoms. The sympatholysis induced in the carotid canal under these pathophysiological conditions reduces sympathetic tone and thus lowers elevated cranial venous pressure . This pathophysiological process therefore simultaneously establishes a symptom-limiting therapeutic mechanism with a fixed time course, as is typically observed clinically in cluster headache attacks. The refractory period following a cluster attack can also be explained by these considerations, as the sympathetic fibers remain 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.