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Figure 3: Pathophysiology of SUNCT/SUNA and therapeutic targets 1. Posterior Hypothalamus activation causes disinhibition or activation of Trigeminal Cervical Complex and Trigeminal autonomic reflex (in blue) resulting in ipsilateral pain and cranial autonomic symptoms. This disinhibition may be modulated by anti-epileptics (Lamotrigine, Oxcarbazepine, Topiramate and Gabapentin) and Deep Brain Stimulation. 2. In patients with an abbarent vascular loop compressing the Trigeminal nerve, persistent stimulation can cause activation of the posterior hypothalamus via ascending pathways (in orange) and subsequent pain and autonomic symptoms via descending pathways (in purple) This can be modulated by micro vascular decompression of Trigeminal nerve. 3. Increased or decreased traffic in the occipital nerves by means of Greater occipital nerve block or Occipital nerve stimulation can modulate pain and have a therapeutic benefit in SUNHA.

Figure 3: Pathophysiology of SUNCT/SUNA and therapeutic targets 1. Posterior Hypothalamus activation causes disinhibition or activation of Trigeminal Cervical Complex and Trigeminal autonomic reflex (in blue) resulting in ipsilateral pain and cranial autonomic symptoms. This disinhibition may be modulated by anti-epileptics (Lamotrigine, Oxcarbazepine, Topiramate and Gabapentin) and Deep Brain Stimulation. 2. In patients with an abbarent vascular loop compressing the Trigeminal nerve, persistent stimulation can cause activation of the posterior hypothalamus via ascending pathways (in orange) and subsequent pain and autonomic symptoms via descending pathways (in purple) This can be modulated by micro vascular decompression of Trigeminal nerve. 3. Increased or decreased traffic in the occipital nerves by means of Greater occipital nerve block or Occipital nerve stimulation can modulate pain and have a therapeutic benefit in SUNHA.