P040: THE USE OF PTERYGOPALATINE GANGLION BLOCK FOR POSITIONAL HEADACHE AND NAUSEA SECONDARY TO IATROGENIC CSF LEAK
Sindhuja R Nimma, Cameron R Smith, MD, PhD, Andre Boezaart, MD, PhD; University of Florida
Case Report: A 64 year old male presented at outside hospital for lumbar hemilaminectomy. Anesthesia was uneventful and he was discharged to the floor and home on POD2. On the 3rd day he presented with severe positional headache (PH), nausea and vomiting (N&V). CT angiography of his head was normal. He was readmitted and received epidural blood patch (EBP) with immediate relief. Severe PH returned the next day with N&V. Surgical notes reported accidental intraoperative durotomy, and next day EBP was repeated without improvement. On POD9 he was discharged with persistent severe PH and N&V. Three months later he presented to our institution with persistent severe PH and N&V. MRI revealed chronic intracranial hypotension, and EBP was considered but pterygopalatine ganglion (PPG) block was offered instead, resulting in immediate and complete symptom resolution. He was discharged the following day without return of PH, but required monthly PPG block for N&V, which also completely relieved the symptoms for 3 to 4 weeks. PPG neuromodulation or transcutaneous vagal nerve stimulation were considered as potential permanent solution, but the symptoms completely disappeared after 12 monthly PPG blocks.
Discussion: The PPG parasympathetic root reaches the PPG via the Vidian nerve. It originates in the superior salivary nucleus in the medulla. Recent research has highlighted the important role of the PPG in cerebrovascular autonomic physiology1, in the pathophysiology of vascular headaches, and in conditions such as stroke and cerebral vasospasm2. The general key step of pathogenesis of various craniofascial pain syndromes, including primary headaches (tension-type headache, migraine, cluster headache and postdural puncture headache (PDPH)3 is activation of the trigeminal nerve, which is followed by the formation of an ascending nociceptive flow along the trigemino-thalamo-cortical pathway. Therefore interrupting the transmission of this pathway with a combination of local anesthetic and steroid has shown to help with PH as well as N&V. Another proposed mechanism for etiology of the headache is global cerebral vasodilation that occurs to compensate for loss of CSF volume. With the PPG block, the parasympathetic supply to the vessels, above the tentorium and in the dura, is inhibited leading to vasoconstriction and resolution of headache. As there are no alpha receptors in the brain, the PPG block is an effective way to combat the global vasodilation and eliminate the PH and N&V.
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