Aim: Trigeminal neuropathies are a group of clinical disorders that involve injury to primary first-order neurons within the trigeminal nerve. We review the spectrum of etiologies underlying both painful and non-painful trigeminal neuropathies, with attention to particularly dangerous processes that may elude the clinician in the absence of a meticulous evaluation. Complications and management issues specific to patients with trigeminal neuropathy are discussed. Methods: Retrospective literature review. Results: Facial or intraoral numbness, the hallmark of trigeminal neuropathy, may represent the earliest symptomology of malignancy or autoimmune connective tissue disease as sensory neurons are destroyed. Such numbness, especially if progressive, necessitates periodic evaluation and vigilance even years after presentation if no diagnosis can be made. Conclusions: In the routine evaluation of patients with facial pain, the clinician will inevitably be confronted with secondary pathology of the trigeminal nerves and nuclei. The appearance of numbness, even when pain continues to be the most pressing complaint, necessitates clinical assessment of the integrity of all aspects of the trigeminal pathways, which may also include neurophysiologic, radiographic, and laboratory evaluation.

Recurrent episodes of transient focal neurologic symptoms, known as aura, occur in association with migraine headache in about 11.9 million people in the United States. At present, the International Headache Society has recognized 3 "typical" auras: visual, sensory, and language. Increasing evidence from investigations in human subjects suggests that typical auras may be the clinical manifestation of a cortical spreading depression (CSD)-like phenomenon. Other studies have shown altered reactivity and processing within the cortices of migraineurs who experience an aura, which might render them more vulnerable to CSD-like events. Recent investigations also support the hypothesis that events intrinsic to the cerebral cortex are capable of activating trigeminal nociceptive neurons and of affecting the caliber of vascular structures innervated by them. A better understanding of the mechanisms underlying the aura may potentially lead to more effective therapies, which will aim at preventing migraine headaches before they start.

Our understanding of migraine pathophysiology is a work in progress. As more is learned about migraine, it seems that the probability of identifying a single unifying explanation for this common disorder becomes less and less. Although the neuroanatomy and elements of pain physiology underlying migraine attacks are probably shared pathophysiologic elements, the emerging complexity of migraine genetics suggests that the acute attack may be the final common expression of more than one type of initiating abnormality. After a brief summary of the neuroanatomic structures involved in the generation of migraine attacks and the traditional theories of migraine, the author focuses on the current understanding of migraine genetics and reviews recent data from the neuroimaging and the neurophysiology of migraine.

Migraine is a common and disabling disorder. Fibromyalgia has been shown to be commonly comorbid in patients with migraine and can intensify disability. The aim of this study was to determine if patients with co-morbid fibromyalgia and migraine report more depressive symptoms, have more headache related disability, or report higher intensity of headache as compared to patients with migraine only. Cases of comorbid fibromyalgia and migraine were identified using a prospectively maintained headache database at Mayo Clinic Rochester. One-hundred and fifty seven cases and 471 controls were identified using this database and the Mayo Clinic electronic medical record. Depressive symptoms as assessed by PHQ-9, intensity of headache, and migraine related disability as assessed by MIDAS were primary measures used to compare migraine patients with comorbid fibromyalgia versus those without. Patients with comorbid fibromyalgia reported significantly higher PHQ-9 scores (OR 1.08, p < .0001) and headache intensity scores (OR 1.149, p = .007). There was no significant difference in migraine related disability (OR 1.002, p = .075). Patients with fibromyalgia were more likely to score in a higher category of depression severity (OR 1.467, p < .0001) and more likely to score in a higher category of migraine related disability (OR 1.23, p = .004). Patients with comorbid fibromyalgia and migraine report more depressive symptoms, higher headache intensity, and are more likely to have severe headache related disability as compared to controls without fibromyalgia. Clinicians who care for patients with migraine may consider screening for comorbid fibromyalgia particularly in patients with moderate to severe depressive symptoms, high headache intensity and/or high headache related disability. This is the first matched study to look at these characterisitcs, and it replicates previous findings from unmatched studies.