Pathophysiology of Tension Headache

      Tension Headache pathophysiology is still not clearly known. In some of the literature and research results mentioned several circumstances relating to the occurrence of  Tension Headache as follows:
(1) central nervous system dysfunction that is more involved than the peripheral nervous system dysfunction of the peripheral nervous system which leads to more ETTH, whereas central nervous system dysfunction leads to CTTH (Chronic Tension Type Headache) ,
(2) peripheral nerve dysfunction include involuntary muscle contractions and permanently without muscle ischemia,
(3) Tension Headache pain transmission through trigeminocervicalis nucleus pars caudalis, which will sensitization of second order neurons in the trigeminal nucleus and dorsal horn (activation of the NO molecule) thus increasing the input nociceptive pericranial and myofascial tissue and peripheral mechanisms of regulation will occur which will increase muscle pericranial activity. This will increase the release of neurotransmitters in the myofascial tissues,
(4) hyperflexybility central nociceptive neurons in the trigeminal nucleus, thalamus, and cerebral cortex followed hipesensitifitas supraspinal (limbic) on nociception  Pain detection threshold values ​​(pressure, electrical, and thermal) will decrease in the cephalic and extracephalic. In addition, there is also a decrease in supraspinal pain decending inhibit activity,
(5) the filter function abnormalities in brain stem pain causing misinterpretation of information in the brain are interpreted as pain,
(6) there is a relationship between serotonergic and monoaminergic pathways in the brain stem and hypothalamus with occurrence of TTH. Deficiency levels of serotonin and noradrenaline in the brain, and also abnormal platelet serotonin, a decrease in CSF beta- endorphins and exteroceptive emphasis on temporal and masseter muscles,
(7) psychogenic factors (mental stress) and non - physiological state of stress on the motor TTH thus releasing irritating substances which will stimulate the activation of peripheral and supraspinal pain perception structure and central pain modulation . Depression and anxiety will increase the frequency of TTH by maintaining central sensitization of pain transmission lines,
(8) activation of NOS ( Nitric Oxide synthetase ) and NO in the dorsal horn.

In the cases, the presence of stress that triggers headaches. There are several theories to explain it, namely
(1) the existence of physical stress (fatigue) will cause respiratory hyperventilation so that the levels of CO2 in the blood decline that would interfere with acid-base balance in the blood. This will lead to alkalosis which in turn will lead to calcium ions enter the cell and cause excessive muscle contraction headache, so there,
(2) stress activates the sympathetic nerve, causing dilation of the blood vessels of the brain will then activate nociceptors and gamma trigeminal afferent activation will produce neuropeptides (substance P). These neuropeptides will stimulate the trigeminal ganglion (pons) .
(3) stress can be divided into three stages: the alarm reaction, stage of resistance, and the stage of exhausted . Alarm reaction in which stress causes peripheral vasoconstriction which will lead to lack of oxygen and anaerobic metabolism occurs . Anaerobic metabolism will result in a buildup of lactic acid , which stimulates spending bradykinin and proteolytic enzymes which in turn will stimulate the pain pathway . Stage of resistance where the source of energy is derived from glycogen which will stimulate an increase in aldosterone , which will keep the savings aldosterone potassium ion . Stage of exhausted where the source of energy is derived from protein and aldosterone also decreased resulting in the depletion of K + . Depletion of these ions will cause neuronal dysfunction .

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