The pathologic basis of TTH is most likely derived from a combination of personal factors, environmental factors, and alteration of both peripheral and central pain pathways. Peripheral pain pathways receive pain signals from pericranial (around the head) myofascial tissue (protective tissue of muscles) and alteration of this pathway likely underlies episodic tension-type headache (ETTH). In addition to these myofascial tissue pain signals, pericranial muscle tenderness, inflammation, and muscle ischemia have been postulated in headache literature to be causal factors in the peripheral pathophysiology of TTH. However, multiple studies have failed to illustrate evidence for a pathologic role of either ischemia or inflammation within the muscles. Pericranial tenderness is also not likely a peripheral causal factor for TTH, but may instead act to trigger a chronic pain cycle in which the peripheral pain response is transformed over time into a centralized pain response. It is then these prolonged alterations in the peripheral pain pathways that lead to increased excitability of the central nervous system pain pathways, resulting in the transition of episodic tension-type headache into chronic tension type headache (CTTH). Specifically, the hyperexcitability occurs in central nociceptive neurons (the trigeminal spinal nucleus, thalamus, and cerebral cortex) resulting in central sensitization, which manifests clinically as allodynia and hyperalgesia of CTTH.
In difficult cases, "cycloplegic agents are highly favored to break spasm quickly and may be more economical compared to other conventional therapies"Cyclopentolate, Atropine, Tropicamide, and Homatropine are the typical cycloplegic eye drops used once daily to treat spasm of accommodation by relaxing the ciliary muscle. One side effect is blurred vision since these induce dilation. Vision Training
Vision therapy administered by a trained optometrist has shown a success rate of over 70%. Surgery
Multifocal intraocular lens implantation is a new possible treatment involving clear lens extraction and multifocal intraocular lens implantation but it may not be appropriate for patients who have had resistant spasm of accommodation for a long period of time. Research
Experimental Nitroglycerin and Nitric Oxide
Animal studies have found nitroglycerin, a vasodilator used to treat angina, relaxes the ciliary muscle and may hold hope for those suffering from spasm of accommodation. Nitroglycerin is currently being investigated as a treatment for glaucoma, and has shown to decrease intraocular pressure and relax the ciliary muscle. According to Investigative Ophthalmology & Visual Science Journal. "In a nonhuman primate study, topical administration of nitroglycerin at a dose of 0.1% significantly decreased IOP in normotensive animals after 90 minutes". Further, according to Wiederholt, Sturm, and Lepple-Wienhues, "The data indicate (indicates [sic]) that an increase of intracellular cGMP by application of cGMP and organic nitrate or non-nitrate vasodilators induces relaxation of the bovine trabecular meshwork and ciliary muscle". Experimental Perilla frutescens
Since spasm of accommodation is a result of contraction of the ciliary muscle, the goal would be to relax the ciliary muscle.