Abstract
Three patients are described who experienced headache from hypertension: one had acute headache from acute hypertension, one had daily, morning headaches from chronic hypertension, and one had acute headache with generalized tonic-clonic seizure from hypertensive encephalopathy. The presumed pathophysiological mechanisms involved in the three hypertensive headache conditions are reviewed.
Keywords
Introduction
It is not uncommon for headache and hypertension to be associated with each other so that determination of the blood pressure is indispensable in the evaluation of the patient with headache. Hypertension can cause headache by itself but it can also aggravate a pre-existing headache condition such as migraine. In this paper, three scenarios involving headache and hypertension are presented: acute hypertension, chronic hypertension and hypertensive encephalopathy. The presumed pathophysiological mechanisms involved in the three hypertensive headache conditions are reviewed.
Acute hypertensive headache
Ten days before consultation, at 06.00, a 49-year-old woman was woken up from sleep by a severe, throbbing headache. The headache was located bilaterally in the back of her head and was associated with vomiting. It had improved 2 days later and she went back to work. However, a day after that, she was again woken up, at 04.00, by a severe, throbbing headache, located in the back of her head. She went to the emergency room and had a cranial computerized tomography without contrast, which was normal and without evidence of haemorrhage. Three days later, she woke up with another severe headache in the back of her head. She went again to the emergency room where her blood pressure was found to be 200/100. She had a lumbar puncture, which was normal except for an elevated protein of 52 mg/dL.
During her consultation with me and while talking about the severe headaches she had experienced for the last 10 days, she became anxious and developed another severe headache in the back of her head. The headache built to its maximum intensity in 5 to 10 min and was associated with restlessness. She could not sit still and did not want to lie down because it aggravated the pain. She was walking the floor while holding her head with both hands; she did not feel nauseated. Her blood pressure was 220/130 and fundoscopic examination was normal.
The blood pressure did not improve over the course of an hour and neither did the headache. She was brought to an emergency room where she received sodium nitroprusside, 0.3 µg/kg/min intravenously, titrated up to 0.6 µg/kg/min. When the blood pressure dropped to 150/80, the headache was relieved and the dose of the sodium nitroprusside was gradually decreased to zero. However, then the blood pressure increased again with diastolic pressures reaching over 110, with return of the headache. The sodium nitroprusside was restarted and she was admitted for further management of the hypertension. This was ultimately accomplished with labetalol, 100 mg twice daily, and captopril, 6.25 mg three times daily. Pheochromocytoma was excluded by 24-h urinalysis and magnetic resonance imaging of the abdomen.
Chronic hypertensive headache
A 50-year-old woman related the onset of headaches a year ago. The headaches occurred daily and were present on awakening in the morning. They were moderately severe in intensity (7–8/10) and located in the back of her head, extending into the posterior vertex. The headaches were associated with severe pain bilaterally in the neck and shoulders, as if an iron rod was stuck through them. They were not associated with nausea or vomiting. The headaches improved immediately upon arising, leaving behind a sore feeling in the back of the head.
On average, once per week she was also woken up at night by headache. The nocturnal headaches were generalized in location, severe in intensity (10/10) and associated with palpitations. They forced her to get up out of bed because they were too intense to allow her to fall back to sleep. Within 20 min after getting up the headaches were relieved to the extent that she could go back to sleep. The physical and neurological examinations were normal, except for an elevated blood pressure of 170/110. Within 2–3 days on atenolol, 25 mg at bedtime, the headaches were relieved and the blood pressure was normalized at 130/80. Due to the relatively mild nature of the hypertension and the fact that it was easily controlled, no further evaluation was undertaken.
Hypertensive encephalopathy
A 50-year-old woman was prescribed mirtazapine, 15 mg at bedtime, for the treatment of depression. A week later she developed a severe headache during orgasm, caused by masturbation, associated with diaphoresis, nausea and protracted vomiting. An hour later, her left arm and hand began to shake, followed in 20–30 s by a generalized seizure with loss of consciousness and tongue bite. The generalized seizure lasted less than a minute; her blood pressure was 180/100.
Cranial computerized tomography and lumbar puncture with spinal-fluid analysis were unremarkable. An electroencephalogram showed bitemporal sharp activity, more pronounced on the left than on the right. A cranial magnetic resonance scan, T2-weighted transverse image, showed multiple, small bright lesions in both occipital lobes, again more prominent on the left than on the right (Fig. 1). The lesions were primarily cortical in location and were associated with patchy enhancement following the administration of gadolinium. On a repeat magnetic resonance scan performed a month later, the occipital lesions had almost completely vanished (Fig. 2).
Cranial magnetic resonance scan, T2-weighted transverse image, showing multiple, small bright lesions in both occipital lobes, more prominent on the left than on the right.
Cranial magnetic resonance scan, T2-weighted image, performed a month after the scan shown in Fig. 1.
Discussion
In relation to headache and hypertension, four conditions can be distinguished: acute and chronic hypertensive headache, malignant hypertension and hypertensive encephalopathy (Table 1). The one of the four that is not necessarily associated with headache and, in fact, often is not, is malignant hypertension. It refers to hypertension associated with papilledema on fundoscopic examination. It is related to chronic hypertension and associated with myointimal proliferation and fibrinoid necrosis of the small arteries and arterioles, due to the chronically elevated blood pressure. It can be associated with the headaches described under chronic hypertensive headache. Acute hypertensive headache and hypertensive encephalopathy are rarely associated with malignant hypertension because of the right-shift in cerebral autoregulation that occurs with chronically elevated blood pressure.
Conditions involving headache and hypertension
Autoregulation is the mechanism by which the brain maintains its perfusion under conditions of changing blood pressure and, thereby, changing perfusion pressures. The regulation occurs at the level of the small cerebral arteries and arterioles, mediated by the sympathetic noradrenergic innervation, which constricts the blood vessels when blood pressure increases and dilates them when it decreases. When blood pressure fluctuates within the normal range, autoregulatory mechanisms control cerebral perfusion over a (mean-arterial) blood pressure range of approximately 50–150 mmHg. Under conditions of chronically elevated blood pressure, the range shifts to the right, making it more actual to the blood pressure fluctuations occurring. At the same time, this protects the patient with chronic hypertension against hypertensive encephalopathy, which occurs when blood pressure increases abruptly beyond the range of autoregulation.
Acute hypertensive headache, as described in the first case study, results from an abrupt increase in blood pressure that remains within the range of cerebral autoregulation. As a result, neurological functioning is intact but the increased resistance created by the constricted small arteries and arterioles increases the transmural pressure in the larger cerebral arteries, which are sensitive to pain. These are the arteries at the base of the brain, mostly located in the posterior fossa, innervated by the cervical nerve roots and referring pain to the back of the head and neck.
In chronic hypertensive headache, as described in the second case study, the headache originates from the decrease in blood pressure that occurs overnight, resulting in compensatory vasodilation. The headache abated as soon as the patient arose because the erect position increased the blood pressure and caused compensatory constriction of the dilated blood vessels.
In the third case study, that of hypertensive encephalopathy, the abrupt increase in blood pressure caused by orgasm exceeded the range of cerebral autoregulation. As a result, the tight endothelial junctions that constitute the blood–brain barrier were disrupted, allowing extravasation of plasma and erythrocytes into brain tissue. The resulting oedema and petechiae disturbed brain function and neurological symptoms ensued, in this particular patient consisting of a simple partial, secondarily generalized, tonic-clonic seizure. The findings on the magnetic resonance scan are typical of hypertensive encephalopathy, not least because of the predominant, posterior location of the lesions. The sympathetic noradrenergic innervation that mediates cerebral autoregulation is more pronounced in the carotid than in the vertebrobasilar system, providing less protection against the impact of an abrupt increase in blood pressure in the posterior-cerebral-artery territories (1).
The hypertensive encephalopathy occurred under treatment with mirtazapine. Antidepressants have a myriad of pharmacological effects, which, almost invariably, include inhibition of the re-uptake and, thereby, inactivation of noradrenaline. As a result, they enhance sympathetically driven responses, like the increase in blood pressure normally occurring with orgasm. The three patients described suffered from migraine headaches but the headaches they experienced related to the hypertension were succinctly different. This was particularly appreciated by the patient in the second case study and caused the anxiety that precipitated the attack I was able to witness and record. Migraine sufferers possibly have an increased risk of developing hypertension (2) and may also be more prone to developing headache as a result of it.