Tracking patients with chronic occipital headache after occipital nerve decompression surgery: A case series.

BACKGROUND: The therapeutic benefit of nerve decompression surgeries for chronic headache/migraine are controversial. AIM: To provide clinical characteristics of headache type and treatment outcome of occipital nerve decompression surgery. METHODS: A retrospective review of clinical records. Inclusion criteria were evidence of chronic occipital headache with and without migrainous features and tenderness of neck muscles, occipital allodynia, and inadequate response to prophylactic drugs. RESULTS: Surgical decompression of the greater and lesser occipital nerves provided complete and extended (3-6 years) relief of new daily persistent headache in case 3 (46 year old female), and of chronic post-traumatic headache in cases 4 and 6 (35 and 30 year old females, respectively), partial relief of chronic headache/migraine in cases 1 and 2 (41 year old female and 36 year old male), and no relief of episodic (cases 3 and 4) or chronic migraine (case 5, 52 year old male), or chronic tension-type headache (case 7, 31 year old male). CONCLUSIONS: As a case series, this study cannot test a hypothesis or determine cause and effect. However, the complete elimination of new daily persistent headache and post-traumatic headache, and the partial elimination of chronic headache/migraine in two patients - all refractory to other treatment approaches - supports and justifies the effort to continue to generate data that can help determine whether decompression nerve surgeries are beneficial in the treatment of certain types of chronic headache.

Extracranial origin of headache.

PURPOSE OF REVIEW: To summarize recent clinical and preclinical studies on extracranial pathophysiologies in migraine. It challenges the opinion-based notion that the headache phase of migraine occurs without input from peripheral nociceptors or is caused solely by activation of intracranial nociceptors supplying dural and cerebral vasculature. RECENT FINDINGS: Data that support a scenario by which migraine can originate extracranially include the perception of imploding headache that hurts outside the cranium, the existence of a network of sensory fibers that bifurcate from parent axons of intracranial meningeal nociceptors and reach extracranial tissues such as periosteum and pericranial muscles by crossing the calvarial bones through the sutures, the discovery of proinflammatory genes that are upregulated and anti-inflammatory genes that are down regulated in extracranial tissue of chronic migraine patients, and evidence that administration of OnabotulinumtoxinA to peripheral tissues outside the calvaria reduces frequency of migraine headache. SUMMARY: These findings seeks to shift clinical practice from prophylactically treating chronic migraine solely with medications that reduce neuronal excitability to treating irritated nociceptors or affected tissues. The findings also seeks to shift current research from focusing solely on central nervous system alterations and activation of meningeal nociceptors as a prerequisite for studying migraine.

Upregulation of inflammatory gene transcripts in periosteum of chronic migraineurs: Implications for extracranial origin of headache.

OBJECTIVE: Chronic migraine (CM) is often associated with chronic tenderness of pericranial muscles. A distinct increase in muscle tenderness prior to onset of occipital headache that eventually progresses into a full-blown migraine attack is common. This experience raises the possibility that some CM attacks originate outside the cranium. The objective of this study was to determine whether there are extracranial pathophysiologies in these headaches. METHODS: We biopsied and measured the expression of gene transcripts (mRNA) encoding proteins that play roles in immune and inflammatory responses in affected (ie, where the head hurts) calvarial periosteum of (1) patients whose CMs are associated with muscle tenderness and (2) patients with no history of headache. RESULTS: Expression of proinflammatory genes (eg, CCL8, TLR2) in the calvarial periosteum significantly increased in CM patients attesting to muscle tenderness, whereas expression of genes that suppress inflammation and immune cell differentiation (eg, IL10RA, CSF1R) decreased. INTERPRETATION: Because the upregulated genes were linked to activation of white blood cells, production of cytokines, and inhibition of NF-κB, and the downregulated genes were linked to prevention of macrophage activation and cell lysis, we suggest that the molecular environment surrounding periosteal pain fibers is inflamed and in turn activates trigeminovascular nociceptors that reach the affected periosteum through suture branches of intracranial meningeal nociceptors and/or somatic branches of the occipital nerve. This study provides the first set of evidence for localized extracranial pathophysiology in CM. Ann Neurol 2016;79:1000-1013.