Primary headache disorders and neuro-ophthalmologic manifestations

Abstract

Headache is an extraordinarily common complaint presenting to medical practitioners in all arenas and specialties, particularly primary care physicians, neurologists, and ophthalmologists. A wide variety of headache disorders may manifest with a myriad of neuro-ophthalmologic symptoms, including orbital pain, disturbances of vision, aura, photophobia, lacrimation, conjunctival injection, ptosis, and other manifestations. The differential diagnosis in these patients is broad and includes both secondary, or symptomatic, and primary headache disorders. Awareness of the headache patterns and associated symptoms of these various disorders is essential to achieve the correct diagnosis. This paper reviews the primary headache disorders that prominently feature neuro-ophthalmologic manifestations, including migraine, the trigeminal autonomic cephalalgias, and hemicrania continua. Migraine variants with prominent neuro-ophthalmologic symptoms including aura without headache, basilar-type migraine, retinal migraine, and ophthalmoplegic migraine are also reviewed. This paper focuses particularly on the symptomatology of these primary headache disorders, but also discusses their epidemiology, clinical features, and treatment.

Secondary Headache: Current Update

“…Acute headache following ischemic stroke is more commonly associated with infarction of the posterior than the anterior cerebral circulation. Moreover, subcortical and lacunar infarctions are the least associated with acute headache compared to cortical strokes 16,17 . Previous studies have reported that vessels in the posterior circulation are more richly innervated by nociceptive afferents than in the anterior circulation 17‐20 .…”

“…Moreover, subcortical and lacunar infarctions are the least associated with acute headache compared to cortical strokes 16,17 . Previous studies have reported that vessels in the posterior circulation are more richly innervated by nociceptive afferents than in the anterior circulation 17‐20 . Pain signals from the circle of Willis are transmitted through the trigeminal nerve, whereas vasculature structures of the posterior fossa are innervated by the cervical plexus, vagus, and trigeminal nerve 18,20,21 .…”

“…Hemorrhagic and edematous complications resulting from ischemic infarction have been suggested to cause headache by stretching pain‐sensitive intracranial structures such as the dura; however, small infarcts without hemorrhage or edema have been accompanied by headache as well. Furthermore, studies have shown that the occurrence of headache and its severity is not correlated with the size of cerebral infarction 17,22,23 . Young age and female sex appear to be additional risk factors for headache due to ischemic stroke 15 …”

Retinal migraine

“…Substance P, nitrous oxide, calcitonin generated peptides have been suspected as chemical effectors in the possible pathophysiological mechanisms of retinal migraine, by exercising a non-desired effect leading to the plasma extravasation, neurogenic inflammation, vasodilatation. Other neuro-ophthalmological structures involved are: periaqueductal gray (PAG), locus coeruleus (LC), dorsal Raphe nucleus (DRC), retinal vasculature, and activation of the retinal-thalamic-visual pathway [ 3 ].…”

<p>The Psychophysical Assessment of Hierarchical Magno-, Parvo- and Konio-Cellular Visual Stream Dysregulations in Migraineurs</p>

“…Although there is a strong consensus that migraine begins with cortical hyperexcitability followed by spreading waves of compensatory inhibition throughout the cortical surface,1 evidence also points to the trigeminovascular system and its associated subcortical and neuro-ophthalmologic manifestations as the etiological source for migraine 2–7. Whether vasogenic or neurogenic in origin, numerous studies have investigated visual pathway operations in an attempt to identify the pathogenesis of migraine through its characteristic visual symptoms such as triggers, visual snow, halos, phosphenes, paliopsia, and photophobias 7. Interestingly, many of the hallucinatory symptoms have been identified as stable geometric fortifications (ie, Kluver’s forms8) that scale out to the same hexagonally packed cortical hypercolumns of the cortex 9.…”