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Atypical migraine presenting with meningeal signs
Atypical Migraine Presenting With Meningeal Signs ATA ULHAQ, MD, WALID MASSARWEH,
MD
A case of atypical or complicated migraine is presented with signs and symptoms of meningeal irritation, projectile emesis NS obtundation, and unresponsiveness. The patient is a 19-year-old diabetic on insulin who had a mild episode of upper respiratory tract symptoms with severe headache and was found unresponsive and brought to the emergency department. After a work-up for meningitis was negative (as well as computerized tomography and magnetic resonance imaging) he recovered totally in 3 days with no residual signs or symptoms and was discharged from the hospital. (Am J Emerg Med 1994;12:88-87. Copyright 0 1994 by W.B. Saunders Company) A 19-year-old known diabetic, who is insulin dependent, was doing well until a few days before a visit to the emergency department (ED) when he started to have upper respiratory tract symptoms of cough and congestion. The day before his ER visit he had stopped at a fast food restaurant to have some orange juice and food. Soon afterwards he experienced severe headache bilaterally, and after coming home, went to sleep. After waking up the headache was still present and he developed multiple episodes of emesis. Soon afterwards he became extremely disoriented, with a mental status that was waxing and waning. According to his mother, he was first alert and awake and then became delirious. He was brought into the ED by the ambulance and was found slightly obtunded. Because there was a history of diabetes, the patient was given dextrose 50% with no change of the mentum. In the ED, he responded only to painful stimuli (moving all his extremities and awakening). However, he was nonresponsive to verbal questioning or stimulus. A complete and thorough neurological examination was negative initially. Pupils and eye grounds were negative and the neck was supple initially. Chest, including lungs and heart, showed no signs of focal pathology and the abdomen was extremely supple. The extremities were devoid of any pathology. The cranial nerves were grossly intact. Pupils were mid-sized, slug-
gish to react, and eye grounds were devoid of pathology. Venous pulsation was noted and disk margins were slightly blurred. Plantars reflexes were downgoing bilaterally. Sensory was intact to pinprick. The patient was moving all his extremities. Deep tendon reflexes were slightly hyperactive. A complete blood cell count obtained initially show a white blood cell count of 15,000 with 5.3 red blood cells, hemoglobin, 15; hematocrit, 46; mean corpuscular volume, 86; mean corpuscular hemoglobin, 29; mean corpuscular hemoglobin concentrations. 34; and platelets of 367. Initial chemistries were obtained and showed a blood sugar of 235 and blood urea nitrogen of 10. Blood glucose drawn before the squad giving him D50 was 86. After D50 blood sugar was 235 in the ED with blood urea nitrogen of 10 and creatinine clearance of 1. Serum sodium was 137: potassium was 3.7:
From the Ashtabula County Medical Center, Ashtabula, OH. Manuscript received February 17, 1993; revision accepted July 25, 1993. Address reprint requests to Dr Ulhaq. Ashtabula County Medical Center, 2420 Lake Ave, Ashtabula, OH 44004. Key Words: Headache, meningeal signs, obtundation, bitemporal headaches, waxing and waning mental status, CAT scan, MRI Copyright 0 1994 by W.B. Saunders Company 0735-6757/94/l 201-0021$5.00/O 66
chloride was 100; CO2 was 26. and acetone was less than IO. The drug screen for amphetamines, barbiturates, benzodiazepines, cocaine, and opiates was negative. The THC screening showed less than 100 ngimm of the substance: PCP was not detected. Ethanol/ alcohol level was less than IO. Chest x-ray showed no acute pathology; urinalysis was also negative. The patient’s mentation waxed and waned. This time, neck examination showed meningismus. A computed axial tomography (CAT) scan was negative for any internal bleed. The spinal tap was traumatic but on spinning, the cerebral spinal fluid (CSF) totally cleared without any xanthochromia. CSF chemistries and the cell count were within normal limits. Arterial blood gases obtained initially showed a ph of 7.4, Pco? of 36, PO? of 143 on 2 L nasal cannula. also a saturation of 98%. By the time the patient was seen by a neurologist. the neck was definitely rigid. With an impression of meningitis. the patient was started on antibiotics. However, a repeat spinal tap performed was also benign and was not suggestive of infection. Magnetic resonance imaging (MRI) was performed to entertain a diagnosis of aneurysm with subarachnoid bleed. but that was also negative and benign. The next day the patient was more alert. Cultures returned sterile and all antibiotics were stopped. The patient was discharged on the fourth hospital day and was followed-up by his private medical doctor. The final diagnosis. based on exclusion, was atypical or complicated migraine.
DISCUSSION Migraine is a term referred to periodic hemicranial pain with associated gastrointestinal (GI) symptoms. ie, nausea and vomiting, beginning at early childhood, adolescence of adulthood, or at any time during this period. They are recurring in intensity as the age increases. More commonly found in females, migraines or vascular headaches can present in many different forms. The four classic forms are (I) classic migraines; (2) common migraines; (3) complicated migraines; and (4) cluster headaches. Women are affected about three times more than men, mostly during their premenstrual period. Classic migraines sometimes begin with a prodrome of neurological symptoms, such as visual disturbance and photophobia. Classic migraine is also associated with prodrome of symptoms such as elated feeling, excessive energy, food cravings, and other central nervous system symptoms. At other times, the patient is depressed and no warning whatsoever may be associated with this syndrome. The disturbance of vision is followed by homonymous hemianopsia field effects, and sometimes even total blindness, In common migraines there is unheralded onset of headaches associated with GI symptoms. Both classic and common migraines respond to preparations. Complicated migraine, however, is associated with neurological symptoms that are preceded by headache. There is numbness and a tingling sensation of the face and extremities. Often the patient is paralyzed on one side, mimicking a CVA. The numbness or weakness spreads from one part of
ULHAQ AND MASSARWEH
n MIGRAINE
PRESENTING
WITH MENINGEAL
the body to another part, in minutes to hours. Full recovery usually occurs, usually within minutes or hours and sometimes days. However, permanent deficits (hemianopsia and lesions going into the basilar artery) may occur. Ophthalmoplegia, usually of the third nerve, may be present. “Basilar migraine” is associated with bilateral paresthesias and visual disorders, and it is also sometimes accompanied by confusion, rarely stupor, and excessive outbursts of visual disturbances. The full syndrome is infrequent; however, partial syndromes are found in approximately 30% to 40% of the individuals. It is more common in children. Neurological syndromes occurring in migraines are not always followed by headaches. In children, abdominal pain, vomiting, and other cyclical problems may occur without headaches. Such migraine occurrence may be manifested by thorax, pelvis, and other discomfort. Cluster headaches, which are more common in males, usually onset within 2 to 3 hours after falling asleep. It can be unilateral and tends to spread during the phase of rapid eye movement. The pain is intense and nonthrobbing with lacrimation. There is also nasal congestion and rhinorrhea and sometimes mild ptosis. Flushing and edema of the cheeks is present approximately 1 to 2 hours in the cephalgia. It tends to occur and recur nightly for several weeks or months (hence the term “clusters”). The pain of a given attack may leave as rapidly as it begins, often involving the same orbit in each cluster. Occasionally, alcohol, nitroglycerin, and thiamine-containing food precipitate the attack. The relationship of cluster headaches or migraines remains unclear. Most headaches are based on vascular dilatation, and the mechanics of their initiation and pathophysiology is based on changes in platelet and serotonin levels, which are shown to decrease during the attack, accompanied with increased excretion of serotonin, S-hydroxyindoleacetic acid. Also, neural transmitters found in the nerve fibers that innervate blood vessels show activity causing vasodilatation that may affect the vascular tone. Although the factors that trigger migraine attacks vary from individual to individual, alcohol, chocolate, coffee, tea, and other agents have been implicated.
a7
SIGNS
meningeal lesions and migraines remain as diagnoses by exclusion. REFERENCES Barbiroli R, Montagna P, Cortelli P, et al: Complicated migraine studied by phosphorus magnetic resonance spectroscopy. J Cephal 1990;10:263-272 Bruyn G, Ferrari M: Migraine, Tolosa-Hunt syndrome and plaocytosis: correlation or coincidence? J Clin Neurol Neurosurg 1984;86:33-41 Cole AL J, Auba M: Migraine with vasospasm and delayed intracerebral hemorrhage. Arch Neurol 1990;47:53-56 Fitzsimons R, Wolfenden W: Migraine coma. Meningitic migraine with cerebral edema associated with a new form of autosomal dominant cerebellar ataxia. Brain 1965;106:555-577 Harper AM, MacKenzie ET, McCulloch J, et al: Migraine the blood brain barrier. Lancet 1977;1:1034 Jacome DF, Leborgne I: MRT studies graine. Headache 1990;30:66-90 Malmgren R: The central 1990;10:199-204
serotoninergic
Norris JW, Hackinski VC, Cooper blood flow during a migraine attack.
in basilar system.
and
artery
mi-
Cephalalgia
PW: Changes in cerebral Br Med J 1975;3:676
Olesen J: Pathophysiological implications of migraine and symptomatology. In Olesen J, Edvinsson L (eds): Basic Mechanisms of Headache: Pain Research and Clinical Management, Vol 2. Elsevier, Amsterdam 1966, p 353 Olesen J: Regional tacks by xenon-133 Brain 1964;107:447
cerebral blood flow during migraine atinhalation and emission tomography.
Pfaffenrath V, Kaube H: Diagnostics ache. Funct Neurol 1990;5:159-164 Raskin NH: Migraine in Diseases Asbury AK, McKhann GM, McDonald Saunders, 1966, p 961
of cervicogenic
head-
of the Nervous System. In WI (eds). Philadelphia, PA,
Roldan-Montaud A, Jimenez-Jimenez EL, Zancada F, et al: Neurobrucellosis mimicking migraine. J Eur Neurol 1991;31:3032 Spierings in migraine
F: Angiographic changes suggestive of vasospasm complicated by stroke. Headache 1990;30:727-728
CONCLUSION
Stamboulis F, Spengos M, Rombos A, et al: Aseptic inflammatory meningeal reaction manifesting as a migrainous syndrome. Headache 1987;27:439-441
Although meningeal signs should first direct a physician to workup meningitis, subarachnoid hemorrhage and other
Vinken PJ, Bruyn GW (eds): Handbook of Clinical vol 5: Headache and Cranial Neuralgias. Amsterdam, land, 1966
Neurology, North Hol-
MD
A case of atypical or complicated migraine is presented with signs and symptoms of meningeal irritation, projectile emesis NS obtundation, and unresponsiveness. The patient is a 19-year-old diabetic on insulin who had a mild episode of upper respiratory tract symptoms with severe headache and was found unresponsive and brought to the emergency department. After a work-up for meningitis was negative (as well as computerized tomography and magnetic resonance imaging) he recovered totally in 3 days with no residual signs or symptoms and was discharged from the hospital. (Am J Emerg Med 1994;12:88-87. Copyright 0 1994 by W.B. Saunders Company) A 19-year-old known diabetic, who is insulin dependent, was doing well until a few days before a visit to the emergency department (ED) when he started to have upper respiratory tract symptoms of cough and congestion. The day before his ER visit he had stopped at a fast food restaurant to have some orange juice and food. Soon afterwards he experienced severe headache bilaterally, and after coming home, went to sleep. After waking up the headache was still present and he developed multiple episodes of emesis. Soon afterwards he became extremely disoriented, with a mental status that was waxing and waning. According to his mother, he was first alert and awake and then became delirious. He was brought into the ED by the ambulance and was found slightly obtunded. Because there was a history of diabetes, the patient was given dextrose 50% with no change of the mentum. In the ED, he responded only to painful stimuli (moving all his extremities and awakening). However, he was nonresponsive to verbal questioning or stimulus. A complete and thorough neurological examination was negative initially. Pupils and eye grounds were negative and the neck was supple initially. Chest, including lungs and heart, showed no signs of focal pathology and the abdomen was extremely supple. The extremities were devoid of any pathology. The cranial nerves were grossly intact. Pupils were mid-sized, slug-
gish to react, and eye grounds were devoid of pathology. Venous pulsation was noted and disk margins were slightly blurred. Plantars reflexes were downgoing bilaterally. Sensory was intact to pinprick. The patient was moving all his extremities. Deep tendon reflexes were slightly hyperactive. A complete blood cell count obtained initially show a white blood cell count of 15,000 with 5.3 red blood cells, hemoglobin, 15; hematocrit, 46; mean corpuscular volume, 86; mean corpuscular hemoglobin, 29; mean corpuscular hemoglobin concentrations. 34; and platelets of 367. Initial chemistries were obtained and showed a blood sugar of 235 and blood urea nitrogen of 10. Blood glucose drawn before the squad giving him D50 was 86. After D50 blood sugar was 235 in the ED with blood urea nitrogen of 10 and creatinine clearance of 1. Serum sodium was 137: potassium was 3.7:
From the Ashtabula County Medical Center, Ashtabula, OH. Manuscript received February 17, 1993; revision accepted July 25, 1993. Address reprint requests to Dr Ulhaq. Ashtabula County Medical Center, 2420 Lake Ave, Ashtabula, OH 44004. Key Words: Headache, meningeal signs, obtundation, bitemporal headaches, waxing and waning mental status, CAT scan, MRI Copyright 0 1994 by W.B. Saunders Company 0735-6757/94/l 201-0021$5.00/O 66
chloride was 100; CO2 was 26. and acetone was less than IO. The drug screen for amphetamines, barbiturates, benzodiazepines, cocaine, and opiates was negative. The THC screening showed less than 100 ngimm of the substance: PCP was not detected. Ethanol/ alcohol level was less than IO. Chest x-ray showed no acute pathology; urinalysis was also negative. The patient’s mentation waxed and waned. This time, neck examination showed meningismus. A computed axial tomography (CAT) scan was negative for any internal bleed. The spinal tap was traumatic but on spinning, the cerebral spinal fluid (CSF) totally cleared without any xanthochromia. CSF chemistries and the cell count were within normal limits. Arterial blood gases obtained initially showed a ph of 7.4, Pco? of 36, PO? of 143 on 2 L nasal cannula. also a saturation of 98%. By the time the patient was seen by a neurologist. the neck was definitely rigid. With an impression of meningitis. the patient was started on antibiotics. However, a repeat spinal tap performed was also benign and was not suggestive of infection. Magnetic resonance imaging (MRI) was performed to entertain a diagnosis of aneurysm with subarachnoid bleed. but that was also negative and benign. The next day the patient was more alert. Cultures returned sterile and all antibiotics were stopped. The patient was discharged on the fourth hospital day and was followed-up by his private medical doctor. The final diagnosis. based on exclusion, was atypical or complicated migraine.
DISCUSSION Migraine is a term referred to periodic hemicranial pain with associated gastrointestinal (GI) symptoms. ie, nausea and vomiting, beginning at early childhood, adolescence of adulthood, or at any time during this period. They are recurring in intensity as the age increases. More commonly found in females, migraines or vascular headaches can present in many different forms. The four classic forms are (I) classic migraines; (2) common migraines; (3) complicated migraines; and (4) cluster headaches. Women are affected about three times more than men, mostly during their premenstrual period. Classic migraines sometimes begin with a prodrome of neurological symptoms, such as visual disturbance and photophobia. Classic migraine is also associated with prodrome of symptoms such as elated feeling, excessive energy, food cravings, and other central nervous system symptoms. At other times, the patient is depressed and no warning whatsoever may be associated with this syndrome. The disturbance of vision is followed by homonymous hemianopsia field effects, and sometimes even total blindness, In common migraines there is unheralded onset of headaches associated with GI symptoms. Both classic and common migraines respond to preparations. Complicated migraine, however, is associated with neurological symptoms that are preceded by headache. There is numbness and a tingling sensation of the face and extremities. Often the patient is paralyzed on one side, mimicking a CVA. The numbness or weakness spreads from one part of
ULHAQ AND MASSARWEH
n MIGRAINE
PRESENTING
WITH MENINGEAL
the body to another part, in minutes to hours. Full recovery usually occurs, usually within minutes or hours and sometimes days. However, permanent deficits (hemianopsia and lesions going into the basilar artery) may occur. Ophthalmoplegia, usually of the third nerve, may be present. “Basilar migraine” is associated with bilateral paresthesias and visual disorders, and it is also sometimes accompanied by confusion, rarely stupor, and excessive outbursts of visual disturbances. The full syndrome is infrequent; however, partial syndromes are found in approximately 30% to 40% of the individuals. It is more common in children. Neurological syndromes occurring in migraines are not always followed by headaches. In children, abdominal pain, vomiting, and other cyclical problems may occur without headaches. Such migraine occurrence may be manifested by thorax, pelvis, and other discomfort. Cluster headaches, which are more common in males, usually onset within 2 to 3 hours after falling asleep. It can be unilateral and tends to spread during the phase of rapid eye movement. The pain is intense and nonthrobbing with lacrimation. There is also nasal congestion and rhinorrhea and sometimes mild ptosis. Flushing and edema of the cheeks is present approximately 1 to 2 hours in the cephalgia. It tends to occur and recur nightly for several weeks or months (hence the term “clusters”). The pain of a given attack may leave as rapidly as it begins, often involving the same orbit in each cluster. Occasionally, alcohol, nitroglycerin, and thiamine-containing food precipitate the attack. The relationship of cluster headaches or migraines remains unclear. Most headaches are based on vascular dilatation, and the mechanics of their initiation and pathophysiology is based on changes in platelet and serotonin levels, which are shown to decrease during the attack, accompanied with increased excretion of serotonin, S-hydroxyindoleacetic acid. Also, neural transmitters found in the nerve fibers that innervate blood vessels show activity causing vasodilatation that may affect the vascular tone. Although the factors that trigger migraine attacks vary from individual to individual, alcohol, chocolate, coffee, tea, and other agents have been implicated.
a7
SIGNS
meningeal lesions and migraines remain as diagnoses by exclusion. REFERENCES Barbiroli R, Montagna P, Cortelli P, et al: Complicated migraine studied by phosphorus magnetic resonance spectroscopy. J Cephal 1990;10:263-272 Bruyn G, Ferrari M: Migraine, Tolosa-Hunt syndrome and plaocytosis: correlation or coincidence? J Clin Neurol Neurosurg 1984;86:33-41 Cole AL J, Auba M: Migraine with vasospasm and delayed intracerebral hemorrhage. Arch Neurol 1990;47:53-56 Fitzsimons R, Wolfenden W: Migraine coma. Meningitic migraine with cerebral edema associated with a new form of autosomal dominant cerebellar ataxia. Brain 1965;106:555-577 Harper AM, MacKenzie ET, McCulloch J, et al: Migraine the blood brain barrier. Lancet 1977;1:1034 Jacome DF, Leborgne I: MRT studies graine. Headache 1990;30:66-90 Malmgren R: The central 1990;10:199-204
serotoninergic
Norris JW, Hackinski VC, Cooper blood flow during a migraine attack.
in basilar system.
and
artery
mi-
Cephalalgia
PW: Changes in cerebral Br Med J 1975;3:676
Olesen J: Pathophysiological implications of migraine and symptomatology. In Olesen J, Edvinsson L (eds): Basic Mechanisms of Headache: Pain Research and Clinical Management, Vol 2. Elsevier, Amsterdam 1966, p 353 Olesen J: Regional tacks by xenon-133 Brain 1964;107:447
cerebral blood flow during migraine atinhalation and emission tomography.
Pfaffenrath V, Kaube H: Diagnostics ache. Funct Neurol 1990;5:159-164 Raskin NH: Migraine in Diseases Asbury AK, McKhann GM, McDonald Saunders, 1966, p 961
of cervicogenic
head-
of the Nervous System. In WI (eds). Philadelphia, PA,
Roldan-Montaud A, Jimenez-Jimenez EL, Zancada F, et al: Neurobrucellosis mimicking migraine. J Eur Neurol 1991;31:3032 Spierings in migraine
F: Angiographic changes suggestive of vasospasm complicated by stroke. Headache 1990;30:727-728
CONCLUSION
Stamboulis F, Spengos M, Rombos A, et al: Aseptic inflammatory meningeal reaction manifesting as a migrainous syndrome. Headache 1987;27:439-441
Although meningeal signs should first direct a physician to workup meningitis, subarachnoid hemorrhage and other
Vinken PJ, Bruyn GW (eds): Handbook of Clinical vol 5: Headache and Cranial Neuralgias. Amsterdam, land, 1966
Neurology, North Hol-