Introduction: SUNCT belongs to the group of trigeminal-autonomic cephalalgias (TAC) --cluster headache and paroxysmal hemicranias--, since its shares a series of features with them. SUNCT was finally included in this group when the hypothalamus was proved to play a key role in its pathophysiology, an aspect that it has in common with other TAC. However, its clinical resemblance to trigeminal neuralgia of the first branch is notable, although it is accepted that the genesis of the trigeminal neuralgia is peripheral.
Development: The article presents the evidence available to date that has made it possible to associate the hypothalamus with SUNCT, as well as outlining its similarities and differences with respect to other TAC. This evidence is clinical, hormonal, from functional neuroimaging (activation of the posteroinferior hypothalamus) and from therapeutic outcomes (with deep hypothalamic stimulation). Likewise, a detailed description is provided of both the neuroanatomical bases (the hypothalamus as part of the neural networks involved in processes concerned with behaviour, memory, antinociceptive control, waking-sleep control and other circadian rhythms, etc.) and the neurochemical bases (orexins, somatostatin and endogenous opiates) that would support the hypotheses which researchers are attempting to establish to fit the evidence discussed earlier, which would have many points that overlap from one TAC to another.
Conclusions: The question as to whether the hypothalamus is the/a generator of TAC or whether it is an element that allows its development remains open to debate, as does the issue of which would be the most plausible explanation for the phenotypic differences between them. Future studies will allow the enigma of SUNCT and the other TAC to be explained.