Skeletomuscular dysfunctions in primary and secondary headaches: part 1. pathogenesis peculiarities and clinical manifestations: a scientific review

Authors:

Sorokin Yuri Nikolaevich – Grand PhD in Medical sciences (Dr. Med. Sci.), Associate Professor; Professor of the Department of Neurology and Restorative Medicine with a course in Osteopathy, Rostov State Medical University, 29 Nakhichevansky Lane, 344022 Rostov-on-Don, Russian Federation; е-mail: sorokin.yuri@bk.ru; https://orcid.org/0000-0002-9185-4073.

Sorokina Elena Yuryevna – senior lecturer at the Department of Foreign Languages with a Latin course, Rostov State Medical University, 29 Nakhichevansky Lane, 344022 Rostov-on-Don, Russian Federation; e-mail: lenoklug@mail.ru.

In the heading: Rewiews

Year: 2025 Volume: 7 Journal number: 4 

Pages: 150-159

Article type: scientific and practical

UDC: 616.857:616.71/.74]-092

DOI: 10.26211/2658-4522-2025-7-4-150-159

Annotation:

The pathogenesis of primary and secondary headaches (HA) is multifactorial, with peripheral and central sensitization mechanisms being of leading importance in the pathophysiology of migraine, tension headache, and cervicogenic HA. Skeletomuscular dysfunctions, myofascial disorders in particular, play a fairly important role in this case and, due to prolonged nociceptive stimulation, cause the development of central sensitization and can provoke the development of HA attack or contribute to the transformation of episodic HA into chronic one. At the same time, central sensitization may cause the formation of myofascial trigger points in pericranial muscles. This ultimately forms a pathologic cycle, when peripheral sensitization supports the central one and vice versa.
Tension headache is likely to be a heterogenous condition, pathogenically and clinically. It may be reflected from myofascial trigger points, may be due to tension of temporal muscles and/or scalp muscles, their tendons and fascia, with the development of local inflammation in the periosteum of skull bones, may result from ischemia of spasmodic muscle or compression of extracranial nerves. During the prolonged course it may be accompanied by intracranial venous dysfunction with difficulty in venous outflow from the cranial cavity.

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