CASE REPORT
EFFORT HEADACHE WITH CEREBRAL INFARCTION Don F. Seelinger, M.D. Gene C. Coin, M.D. Thomas J. Carlow, M.D. From the University of New Mexico School of Medicine Department of Neurology, 1007 Stanford N.E. Albuquerque, New Mexico 87131. Submitted for Publication 3-14-75 Accepted 4-25 75 SYNOPSIS A 26 year old man ran a distance of 11/2 miles in 12 minutes. Soon after this effort he developed visual disturbances in the right field of vision and left-sided clumsiness associated with left frontal headache, nausea and vomiting. Four vessel arteriography and skull x-rays were normal but examination of the visual fields showed a right superior quadrantic field defect and the electroencephalogram a left posterior temporal slow focus. EMI scan performed a few days later showed an infarct in the left inferior occipital pole. No known risk factors for stroke were present. It is suggested that the cerebral infarction associated with headache was related to effort at altitude and most importantly to lack of physical training. HEADACHE OCCURRING immediately .after exhaustive exercise has previously been reported. It is often associated with nausea and vomiting and has many features which suggest that it is migrainous. The headache might be pounding, it is aggravated by altitude, heat and high humidity. Effort migraine has many features in common with altitude headache and it has been suggested that the pathogenesis of both types of headache might be similar. In altitude headache cerebral edema and transient focal neurologic deficits have been recognized. To our knowledge effort migraine has not been associated with permanent neurologic deficits. We report a case of headache induced by unaccustomed exertion at moderate altitude and infarction of the brain demonstrated by computerized axial tomography. CASE HISTORY The patient is 26 years old and has no pertinent past history nor family history of migraine or other headache. On the morning of February 8, 1975, he ran a mile and one half in 12 minutes to qualify for flight duties. Prior to the run he omitted breakfast. He prepared for the test by running shorter distances at an unknown speed once or twice per week for a total of about eight times. After completing the run he did not feel unwell or fatigued and 15 to 20 minutes later he consumed 3 or 4 beers with some friends. He then drove a distance of one mile to get some more beer and developed visual disturbances. These consisted of a squiggly luminous line which was imbedded in an area that looked like water dripping on a window pane situated in the lower half of the right visual field. Despite his visual problem he returned to the track with the beer. While driving back his visual disturbance progressed to the horizontal meridian and towards the midline of the visual field. When he reached his friends he felt light headed and noticed clumsiness and lack of control of his left upper limb. He became nauseated but did not vomit. There was no headache at that time. After about 5 minutes a peculiar clammy feeling appeared in his left upper limb. The left-sided difficulties then disappeared but some visual disturbance remained. He returned to his home, by car. While driving back his vision suddenly closed in on him and he was left with tunnel vision only. The light headedness returned and he thought that his left arm was shaking uncontrollably. Nevertheless, he was able to drive safely and as he reached his home the vision "opened out again" but he was left with a right superior quadrantic visual deficit. About an hour and a half after completion of his test run he developed pain over the left eye. This he described as sharp spreading down into the eye and back to the
occiput. The headache had a tendency to exacerbations and remissions lasting about 30 minutes. This pain lasted for 7 hours. It was unlike any headache he had ever had before. He drove to the base hospital where examination showed right upper quadrantic field defect and slight residual weakness of the left upper limb. Because the headache was still present and he was nauseated and vomiting he was given Ergot tablets, which had no effect. An internist examined him about an hour later and was unable to detect any neurologic deficits apart from the visual field cut. Four days later repeat examination showed only a right upper quadrantic homonomous hemianopia (Fig. 1). In retrospect his neurologic deficits clearly pointed to a posterior circulatory disturbance because of left sided motor dysfunction and right visual field defect. INVESTIGATIONS Normal findings were reported on x-rays of his skull, chest and neck. The brain scan and electrocardiogram were normal. A vertebral arteriogram showed the left vertebral
to fill well and satisfactory reflux into the right vertebral artery. There were no abnormalities in the posterior inferior cerebellar arteries or branches of the basilar artery. An electroencephalogram showed a left temporal slow focus and a computer axial tomographic scan showed a left occipital inferior pole infarction (Fig. 1). DISCUSSION This patient suffered a cerebral infarction in association with unaccustomed effort. This was accompanied by severe ipsilateral headache in the first division of the trigeminal nerve. An analysis of 60 cases of infarcts in the supply territory of the posterior cerebral artery showed that headache occurred concomitantly with the stroke in 29 but was rare preceding the cerebral vascular accident. Commonly the headache was frontal and ipsilateral and, like in our patient it usually started in the supraorbital region often radiating to the occipital area. However, posterior cerebral artery territory strokes accompanied by headache were usually large infarcts with major persisting neurologic deficits. Many patients had with the headache scintillations and some persistent headache when the neurologic deficit was resolving. The pain was often throbbing and sometimes accompanied by nausea and vomiting.1 Because of these clinical features it is understandable that an erroneous diagnosis of vascular headache of the migrainous type could be made in the face of an impending vascular accident. Most patients with small infarcts do not complain of headache. Our patient was treated with Ergot because he was thought to have migraine related to effort. Effort migraine has been described and editorialized in these pages.2 Migraine after effort is more frequent at altitude or when the temperature and humidity are high. Lack of training is now recognized as a major precipitating cause of effort migraine. In our patient, though the temperature and humidity were low, the exercise did take place at an altitude of approximately 5,000 feet and there was undoubtedly an absence of appropriate training for the effort required. To our knowledge, however, the occurrence of a cerebral infarction with persistent neurologic deficits after effort migraine has not been demonstrated. Headache is prominent in acute mountain sickness, but exposure to altitude of 8,000 feet or above is usually necessary for mountain sickness to appear. The headache of mountain sickness is aggravated by exertion, coughing, straining, a sudden jolt to the head and by lying down. Curiously it is temporarily alleviated by the intake of cold fluids and carbohydrates are said to have a protective effect.3 There are a number of similarities between effort migraine and the headache of acute mountain sickness. In both situations cerebral vasoconstriction edema and perhaps anoxia might be responsible for part of the syndrome. Hyperventilation which occurs both at altitude and during exercise produces hypocapnia. This might remove an important dilator stimulus to the cerebral blood vessels. It has been postulated that a rapid loss of carbon dioxide may cause cerebral vasoconstriction and initiate the aura of migraine.2 Subsequent extracranial vasodilatation and headache might be aggravated by an elevated blood pressure which occurs during exertion and also at altitude. Some experiments have been carried out on the retinal circulation in man. In this vascular bed, with similar reactivity to the cerebral circulation, exposure to altitude for some 9 days leads to a decrease in flow when compared to values obtained immediately after altitude exposure. After some days at high altitude retinal and probably cerebral vessels become reset at the prevailing CO2 tension and altitude hypoxia becomes the predominant controlling factor in regulating retinal and probably also cerebral blood flow.4 Our patient omitted breakfast prior to the run. Hunger has been associated with headache and in some patients it is capable of triggering a migraine attack. Hypoglycemia is one of many predisposing causes in the genesis of some strokes particularly in diabetic patients. During exercise there is marked vasodilatation in active muscles. The skin blood vessels usually constrict. Alcohol has a vasodilator effect on many vascular beds. The ingestion of alcohol soon after exhaustive exercise may lead to significant hypotension because of vasodilatation in resistance vessels resulting in global cerebral ischemia and fainting. Whether relative hypotension induced by the beer in our patient contributed to the stroke remains, however, speculative. Though many factors could have contributed to the appearance of an infarct in this young man some well known risk factors for stroke were not present. The patient did not have hypertension, diabetes, syphilis, evidence of vascular disease, or an identifiable source of emboli in the heart or blood vessels. We believe, therefore, that his undoubted cerebral infarct associated with headache and suggestive of migraine was the result of an unfavorable combination of circumstances; moderate altitude, effort, perhaps hypoglycemia in addition to alcohol intake and most importantly lack of physical training,
REFERENCES 1.
Fisher, C.M.: Headache in cerebrovascular disease in Handbook of Clinical Neurology 5:124-156, Viken, P.J. and Bruyn, G.W. Editors. Horth-Holland Publishing Co., Amsterdam, 1968.
2.
Dalessio, D.J.: Effort migraine. Headache 14:53, 1974.
3.
Appenzeller, O.: Altitude headache. Headache 12:126-129, 1972.
4.
Frayser, R., Gray, G.W. and Houston, C.S.: Control of the retinal circulation at altitude. J. Appl. Physiol. 37:302-304, 1974.
Reprint requests to: Don F. Seelinger, M.D. 1010 Las Lomas, N.E. Albuquerque, New Mexico 87102
EFFORT HEADACHE WITH CEREBRAL INFARCTION Don F. Seelinger, M.D. Gene C. Coin, M.D. Thomas J. Carlow, M.D. From the University of New Mexico School of Medicine Department of Neurology, 1007 Stanford N.E. Albuquerque, New Mexico 87131. Submitted for Publication 3-14-75 Accepted 4-25 75 SYNOPSIS A 26 year old man ran a distance of 11/2 miles in 12 minutes. Soon after this effort he developed visual disturbances in the right field of vision and left-sided clumsiness associated with left frontal headache, nausea and vomiting. Four vessel arteriography and skull x-rays were normal but examination of the visual fields showed a right superior quadrantic field defect and the electroencephalogram a left posterior temporal slow focus. EMI scan performed a few days later showed an infarct in the left inferior occipital pole. No known risk factors for stroke were present. It is suggested that the cerebral infarction associated with headache was related to effort at altitude and most importantly to lack of physical training. HEADACHE OCCURRING immediately .after exhaustive exercise has previously been reported. It is often associated with nausea and vomiting and has many features which suggest that it is migrainous. The headache might be pounding, it is aggravated by altitude, heat and high humidity. Effort migraine has many features in common with altitude headache and it has been suggested that the pathogenesis of both types of headache might be similar. In altitude headache cerebral edema and transient focal neurologic deficits have been recognized. To our knowledge effort migraine has not been associated with permanent neurologic deficits. We report a case of headache induced by unaccustomed exertion at moderate altitude and infarction of the brain demonstrated by computerized axial tomography. CASE HISTORY The patient is 26 years old and has no pertinent past history nor family history of migraine or other headache. On the morning of February 8, 1975, he ran a mile and one half in 12 minutes to qualify for flight duties. Prior to the run he omitted breakfast. He prepared for the test by running shorter distances at an unknown speed once or twice per week for a total of about eight times. After completing the run he did not feel unwell or fatigued and 15 to 20 minutes later he consumed 3 or 4 beers with some friends. He then drove a distance of one mile to get some more beer and developed visual disturbances. These consisted of a squiggly luminous line which was imbedded in an area that looked like water dripping on a window pane situated in the lower half of the right visual field. Despite his visual problem he returned to the track with the beer. While driving back his visual disturbance progressed to the horizontal meridian and towards the midline of the visual field. When he reached his friends he felt light headed and noticed clumsiness and lack of control of his left upper limb. He became nauseated but did not vomit. There was no headache at that time. After about 5 minutes a peculiar clammy feeling appeared in his left upper limb. The left-sided difficulties then disappeared but some visual disturbance remained. He returned to his home, by car. While driving back his vision suddenly closed in on him and he was left with tunnel vision only. The light headedness returned and he thought that his left arm was shaking uncontrollably. Nevertheless, he was able to drive safely and as he reached his home the vision "opened out again" but he was left with a right superior quadrantic visual deficit. About an hour and a half after completion of his test run he developed pain over the left eye. This he described as sharp spreading down into the eye and back to the
occiput. The headache had a tendency to exacerbations and remissions lasting about 30 minutes. This pain lasted for 7 hours. It was unlike any headache he had ever had before. He drove to the base hospital where examination showed right upper quadrantic field defect and slight residual weakness of the left upper limb. Because the headache was still present and he was nauseated and vomiting he was given Ergot tablets, which had no effect. An internist examined him about an hour later and was unable to detect any neurologic deficits apart from the visual field cut. Four days later repeat examination showed only a right upper quadrantic homonomous hemianopia (Fig. 1). In retrospect his neurologic deficits clearly pointed to a posterior circulatory disturbance because of left sided motor dysfunction and right visual field defect. INVESTIGATIONS Normal findings were reported on x-rays of his skull, chest and neck. The brain scan and electrocardiogram were normal. A vertebral arteriogram showed the left vertebral
to fill well and satisfactory reflux into the right vertebral artery. There were no abnormalities in the posterior inferior cerebellar arteries or branches of the basilar artery. An electroencephalogram showed a left temporal slow focus and a computer axial tomographic scan showed a left occipital inferior pole infarction (Fig. 1). DISCUSSION This patient suffered a cerebral infarction in association with unaccustomed effort. This was accompanied by severe ipsilateral headache in the first division of the trigeminal nerve. An analysis of 60 cases of infarcts in the supply territory of the posterior cerebral artery showed that headache occurred concomitantly with the stroke in 29 but was rare preceding the cerebral vascular accident. Commonly the headache was frontal and ipsilateral and, like in our patient it usually started in the supraorbital region often radiating to the occipital area. However, posterior cerebral artery territory strokes accompanied by headache were usually large infarcts with major persisting neurologic deficits. Many patients had with the headache scintillations and some persistent headache when the neurologic deficit was resolving. The pain was often throbbing and sometimes accompanied by nausea and vomiting.1 Because of these clinical features it is understandable that an erroneous diagnosis of vascular headache of the migrainous type could be made in the face of an impending vascular accident. Most patients with small infarcts do not complain of headache. Our patient was treated with Ergot because he was thought to have migraine related to effort. Effort migraine has been described and editorialized in these pages.2 Migraine after effort is more frequent at altitude or when the temperature and humidity are high. Lack of training is now recognized as a major precipitating cause of effort migraine. In our patient, though the temperature and humidity were low, the exercise did take place at an altitude of approximately 5,000 feet and there was undoubtedly an absence of appropriate training for the effort required. To our knowledge, however, the occurrence of a cerebral infarction with persistent neurologic deficits after effort migraine has not been demonstrated. Headache is prominent in acute mountain sickness, but exposure to altitude of 8,000 feet or above is usually necessary for mountain sickness to appear. The headache of mountain sickness is aggravated by exertion, coughing, straining, a sudden jolt to the head and by lying down. Curiously it is temporarily alleviated by the intake of cold fluids and carbohydrates are said to have a protective effect.3 There are a number of similarities between effort migraine and the headache of acute mountain sickness. In both situations cerebral vasoconstriction edema and perhaps anoxia might be responsible for part of the syndrome. Hyperventilation which occurs both at altitude and during exercise produces hypocapnia. This might remove an important dilator stimulus to the cerebral blood vessels. It has been postulated that a rapid loss of carbon dioxide may cause cerebral vasoconstriction and initiate the aura of migraine.2 Subsequent extracranial vasodilatation and headache might be aggravated by an elevated blood pressure which occurs during exertion and also at altitude. Some experiments have been carried out on the retinal circulation in man. In this vascular bed, with similar reactivity to the cerebral circulation, exposure to altitude for some 9 days leads to a decrease in flow when compared to values obtained immediately after altitude exposure. After some days at high altitude retinal and probably cerebral vessels become reset at the prevailing CO2 tension and altitude hypoxia becomes the predominant controlling factor in regulating retinal and probably also cerebral blood flow.4 Our patient omitted breakfast prior to the run. Hunger has been associated with headache and in some patients it is capable of triggering a migraine attack. Hypoglycemia is one of many predisposing causes in the genesis of some strokes particularly in diabetic patients. During exercise there is marked vasodilatation in active muscles. The skin blood vessels usually constrict. Alcohol has a vasodilator effect on many vascular beds. The ingestion of alcohol soon after exhaustive exercise may lead to significant hypotension because of vasodilatation in resistance vessels resulting in global cerebral ischemia and fainting. Whether relative hypotension induced by the beer in our patient contributed to the stroke remains, however, speculative. Though many factors could have contributed to the appearance of an infarct in this young man some well known risk factors for stroke were not present. The patient did not have hypertension, diabetes, syphilis, evidence of vascular disease, or an identifiable source of emboli in the heart or blood vessels. We believe, therefore, that his undoubted cerebral infarct associated with headache and suggestive of migraine was the result of an unfavorable combination of circumstances; moderate altitude, effort, perhaps hypoglycemia in addition to alcohol intake and most importantly lack of physical training,
REFERENCES 1.
Fisher, C.M.: Headache in cerebrovascular disease in Handbook of Clinical Neurology 5:124-156, Viken, P.J. and Bruyn, G.W. Editors. Horth-Holland Publishing Co., Amsterdam, 1968.
2.
Dalessio, D.J.: Effort migraine. Headache 14:53, 1974.
3.
Appenzeller, O.: Altitude headache. Headache 12:126-129, 1972.
4.
Frayser, R., Gray, G.W. and Houston, C.S.: Control of the retinal circulation at altitude. J. Appl. Physiol. 37:302-304, 1974.
Reprint requests to: Don F. Seelinger, M.D. 1010 Las Lomas, N.E. Albuquerque, New Mexico 87102
