The studies of Ray and Wolff demonstrated that relatively few mechanisms are operative in the genesis of cranial pain. More specifically, intracranial mass lesions cause headache if they deform, displace, or exert traction on vessels and dural structures at the base of the brain, and this may happen long before intracranial pressure rises. In fact, artificially raising the intraspinal and intracranial pressure by the subarachnoid or intraventricular injection of sterile saline solution does not consistently result in headache. This has been interpreted to mean that raised intracranial pressure does not cause headache—a questionable conclusion when one considers the relief of headache in some patients that follows lumbar puncture and lowering of the cerebrospinal fluid (CSF) pressure, particularly after subarachnoid hemorrhage. Actually, most patients with high intracranial pressure complain of bioccipital and bifrontal headaches that fluctuate in severity.
Dilatation of intracranial or extracranial arteries (and possibly sensitization of these vessels), of whatever cause, is likely to produce headache. The headaches that follow seizures and ingestion of alcohol are probably all caused by cerebral vasodilatation. Nitroglycerin, nitrites in cured meats (“hot-dog headache”), and monosodium glutamate in some foods may cause headache by the same mechanism. It is possible that the throbbing or steady headache that accompanies febrile illnesses has a vascular origin as well; it is likely that the increased pulsation of meningeal vessels activates pain-sensitive structures within their walls or around the base of the brain. Febrile headache may be generalized or predominate in the frontal or occipital regions and is relieved on one side by carotid or superficial temporal artery compression and on both sides by jugular vein compression. Like migraine, it is also increased by shaking the head. Certain systemic infectious agents, enumerated further on, have a tendency to cause severe headache.
A similar mechanism may be operative in the severe, bilateral, throbbing headaches associated with extremely rapid rises in blood pressure, as occurs with pheochromocytoma, malignant hypertension, sexual activity, and in patients being treated with monoamine oxidase inhibitors. Mild to moderate degrees of chronic hypertension, however, do not cause headaches despite a popular notion to the contrary. So-called cough and exertional headaches may also have their basis in the distention of intracranial vessels.
For many years, following the investigations of Harold Wolff, the headache of migraine was attributed to dilatation of the extracranial arteries. Now, it appears that this is not a constant relationship and that the headache is of complex intracranial as much as extracranial origin, perhaps related to the sensitization of blood vessels and their surrounding structures. Activation of the trigeminovascular system (the trigeminal nerves and the blood vessels they supply), leading to an inflammatory response that is generated by local neural mechanisms, “neurogenic inflammation,” has also been assigned a role in migraine headache. These and other theories of causation are summarized by Cutrer and discussed further on in this chapter in the section on migraine.