6.1: Acute ischemic cerebrovascular disorder

Pain receptors within the walls of large pain-sensitive arteries may be mechanistically important in the headache that accompanies cerebrovascular diseases. (Raskin, 1988) The supratentorial vessels and dura are innervated by branches of the first division of the trigeminal nerve, so that pain from these areas is usually referred to the forehead, eye, and temple (Feindel et al, 1960). In the infratentorial area pain is commonly referred to the posterior regions of the skull including occiput the ear and behind the ear. The pain-sensitive structures in the posterior fossa are innervated by the upper three cervical nerve roots and the 9th and 10th cranial nerves (Kimmel, 1961). Portenoy et al (1984) and Medina et al (1975) indicate that headache occurs in association with transient ischemic attacks (TIAs) in 25 to 40 percent of patients. It is the presenting complaint in one-third of those with headache (Grindal and Toole, 1974). There is not a good correlation with localization based on angiographic information. Head pain usually begins in association with other neurologic symptoms following the TIA. Rarely, headache heralds the onset of TIA. It is described as pulsatile in about one-third of patients and usually brief lasting 2 hours, but may last a number of days. Bradshaw and McQuaid (1963) indicated that it was often accentuated by stooping or straining. In patients with TIAs or even infarctions in the carotid distribution, headache is usually unilateral and frontal or orbital. In patients with vertebrobasilar TIAs, the headache is commonly occipital in location although as many as one-third indicate that headache may be generalized bifrontal or biparietal. In five cases of transient monocular blindness, Grindal and Toole (1974) found that four had ipsilateral frontal or orbital pain following the visual disturbance.

Because many patients with amarosis fugax report bright lines, sparkles, light flashes, and color (Fisher, 1971; Hoyt, 1970) the differential between amarosis fugax and migraine may sometimes be difficult. The visual phenomena resulting from amarosis fugax is usually obliterated when the eyes are closed, but migrainous visual phenomena persists. In general, temporal profile is quite different with TIAs, flashes are evanescent and in migraine they tend to persist for minutes and spread slowly (Troost, 1998). Prior to the neuroimaging era, it was believed that most lacunar infarctions were painless (Fisher, 1968). However, more recent studies suggest that 10 percent of patients with lacunar infarction report headaches (Gorelick et al, 1986). When there is ischemic distribution of the major arteries such as the internal carotid and middle cerebral vessels, headache occurs in about 25 percent of patients. It is usually lateralized to orbital or frontal region on the side of the occlusions, however, sometimes middle cerebral artery distribution infarct produces non-lateralized bifrontal headache (Gorlick et al, 1986). Occipital headache is unusual in stroke patients even those with posterior circulation infarcts. As with TIA, many patients report that headache is worsened by bending, straining, or jarring ahead. There may be tenderness over the superficial temporal artery or other external carotid arteries on the side of the diseased vessels. Edmeads (1979) noted that temporary compression of the superficial temporal artery on the side of the headache may transiently lessen the discomfort. As with TIAs, headache usually begins at the onset of the neurologic deficit and begins to subside after the peak deficit occurs and rarely lasts for more than 2 days.

Headache with embolic infarction is more common and when the middle cerebral artery distribution is involved the headache is localized to the ipsilateral orbital or frontal region. Fisher (1968), Mohr et al (1978), and Wells (1961) suggested that headache may begin days, or even weeks, prior to embolic or thrombotic infarction. One hypothesis that the headache of occlusive cerebrovascular disease is caused by dilatation of pain-sensitive collateral channels has been tested and no supporting evidence was found (Raskin, 1988). Similarly, hyperprofusion of ischemic brain tissue does not correlate with head pain (Edmeads, 1979). The fact that lacunar infarction results in headache far less frequently than with large infarcts suggests that the larger the zone of ischemia, the more likely there is involvement of pain modulating sending ascending projections to the forebrain (Raskin et al., 1987).

 

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