OUTLINE
Definition
Discovery and Description
Differential Diagnosis
Pathogenesis
Basilar Artery Migraine and Stroke
Basilar Artery Migraine and Epilepsy
Treatment
Future Directions
More Information
References


  
Definition
Basilar Artery Migraine (BAM) is a subtype of "migraine with aura" in the new IHS classification scheme. The category now combines the term "basilar artery migraine" with "posterior fossa migraine" under the term "basilar migraine," implying involvement of the basilar artery and its branches to the brainstem as well as the posterior cerebral arteries (Baloh and Harker, 1993). Under the current classification, the migranous episode must meet the criteria for "migraine with aura," and then also meet the following criteria for BAM.

Basilar Artery Migraine: Pt. must have two (2) or more of the following symptoms:

visual symptoms (bilateral temporal and nasal fields) double vision

dysarthria ataxia

vertigo tinnitus

bilateral paresthesia decreased hearing

decreased level of consciousness bilateral paresis

Note that although the headache associated with BAM is almost invariably bioccipital, the patient does NOT have to have a headache to meet the criteria for BAM.
  
Discovery and Description
The term "basilar artery migraine" was coined by E.R. Bickerstaff in 1961 in a paper to the Lancet (Bickerstaff, 1961). Dr. Bickerstaff had noticed several patients with a migraine-type headache whose symptoms were more consistent with the vertebrobasilar circulation of the brain than the internal carotid artery (ICA) circulation. The latter had been deemed by researchers to be the cause of symptoms in most migraine sufferers. Bickerstaff felt that if the ICA could be at fault, the vertebrobasilar circulation could just as easily be affected by whatever process was occuring to cause migraine. He described BAM in 34 patients, 26 of whom were adolescent girls. A typical description from his paper is as follows:

"A 14-year-old girl had been subject for three years to attacks in which vivid flashes of light, developing in both visual fields, would last for fifteen minutes and would be followed by retro-orbital headache lasting an hour. During one of these attacks the flashes of light became so severe as to obscure her vision completely; at the same time she became unsteady on her feet, and rotational vertigo developed. These symptoms lasted about thirty-five minutes, and she then had a severe throbbing occipital headache which persisted for several hours. Her mother had severe migraine. X-rays of the skull, CSF examination immediately following the severe attack, and EEGs were normal (Bickerstaff 1961)."

In addition, in some of the girls the migraine symptoms were temporally related to their menstruation. In the intervals between BAM attacks, patients reported no neurological problems. Twenty-eight patients had a definite family history of migraine. Symptoms lasted from 2 - 45 mintues, then subsided rapidly (with loss of vision a bit slower to resolve). Symptoms described were eight of the 10 of the current definition of basilar migraine (see above). The current description of BAM is basically the same as Bickerstaff’s in 1961.
Other symptoms patients may have include nausea and vomiting, and some of Dr. Troost’s patients have reported experiencing temporal distortion. One paper has described a patient who experienced prolonged coma (from 3 - 10 days) after episodes of BAM, and CT scans repeatedly showed no abnormalties (Frequin et al. 1991). As the patient did not undergo MRI, and the patient had tonic-clonic seizures during some of the episodes, it is unclear if this type of coma is a sequelae of BAM. Cardiac arrhythmia has been described in a 27-year-old (Gilroy and Lerman 1980), as well as transient global amnesia in a 9-year-old (Amit et al. 1986), in two patients described as having basilar migraine, but in both cases the patient as described does not fit the current criteria for BAM.
Bickerstaff noted that most patients with BAM as adolescents find a diminishing of these migraines, replaced with other typical migraine headaches as they age, and other studies have agreed with this (Lapkin and Goldin 1978). However, it is no longer held that BAM strikes only adolescent girls (Caplan 1991b); in a study of 49 cases, the age of onset of BAM ranged from 10 to 63 years and the group was approximately one-third men (Sturzenegger and Meienberg 1985).
  
Differential Diagnosis
The differential diagnosis for BAM includes (Diamond, 1987): tumors of the posterior fossa, thrombosis of basilar or posterior cerebral arteries or cerebral veins, cerebellar or brainstem hemorrhage or infarction, intoxication, temporal lobe epilepsy or other seizure disorder, vertebrobasilar insufficiency, and other types of migraine. In addition, one report cited four cases of psychogenic BAM in which patients either developed basilar migraines or experienced cessation of their migraines with suggestion and saline infusion (Sanchez-Villasenor et al. 1995).
  
Pathogenesis
Although the etiology of migraine is much under debate, it is evident that in some fashion the vertebrobasilar circulation of the brain is involved in the cause of BAM. In BAM, it appears the symptoms are due to ischemia of the posterior circulation of the brain, as they can be explained by lesions to the occipital lobes (blindness), temporal lobes (seizure, time distortion), cerebellum (ataxia), midbrain (gaze palsies and diplopia), pons (hearing decrease, vertigo, and tinnitus), midbrain (dysarthria), and overall brainstem (loss of consciousness, paresis, paresthesias). The cause of the ischemia is still unclear, but several authors have speculated that vasoconstriction is to blame, similarly to other migraines. Caplan offers several theories: severe vasoconstriction, thrombosis due to stasis, endothelial injury leading to platelet adhesion and thrombosis, and dissection of the artery involved (Caplan 1991b). It is also possible that embolism from the venous system (in the case of patent foramen ovale, etc.) or arterial system (plaques, atrial fibrillation, etc.) could be to blame (see below). One study has used SPECT to show that cerebral blood flow was decreased in the areas thought to cause the symptoms of a patient with BAM (Seto et al. 1994), and arteriography has been used in other studies to show occlusion of the vertebrobasilar system (Frequinet al. 1991).
MRI has been used to evaluate BAM, with one study finding mild cortical sulci enlargement and single T2 signal white matter foci in patients with BAM (Jacome and Leborgne 1989), and another study indicating a higher number of signal abnormalities (including white matter hyperintensities) in patients with migraine with aura (including BAM) than migraine without aura (Fazekas et al. 1992). The significance of these findings remains to be seen.
Lastly, it is interesting that BAM has developed in patients with whiplash injury, presumably due to trauma to the basilar or posterior cerebral arteries (Jacome 1986).
  
Basilar Artery Migraine and Stroke
The relationship between migraine and stroke has been reported for some time (Guest and Woolf 1964). The course of most patients with BAM is benign, with no occurence of actual stroke. In the 1985 study by Sturzenegger and Meienberg, of the 49 patients with BAM, 47 never had a stroke, and the two who did both were heavy smokers and took oral contraceptives for years. Because BAM is caused by ischemia to the brainstem, cerebellum, or cerebrum, however, it is thought that patients who have this type of migraine might have a greater risk for actual infarction of brain tissue. Lateral medullary syndrome post BAM has been described in one study (Solomon and Spaccavento 1982); the patient was a nonsmoker without hypertension, diabetes, or known cardiac disease. Another study relates the case of 40 year-old woman who presented with BAM and was found to have cerebellar infarction (McDonald 1990). This patient had been on oral contraceptives for years but had discontinued them four years prior to this event; the study doesn’t mention if the patient was a smoker. Another study denotes a woman who developed locked-in syndrome (tetraparesis and paralysis of the lower cranial nerves that is usually fatal) after what was thought to be BAM; locked-in syndrome is usually do to infarction of the ventral portion of the pons, and it appears this woman who recovered developed transitory ischemia of the pons (Sulkava and Kovanen 1983). This patient also had no known risk factors of cardiovascular disease.
In these patients, if they truly had no stroke risk factors, it is assumed that a process other than atherosclerosis/thrombosis/embolism causes transient occlusion of the posterior circulation in BAM. It is this distinction which differentiates BAM from transient ischemic attack (TIA) (Dichter 1994). Edmeads, in an editorial in 1986, however, wonders if this distinction is so simple clinically. He asks whether stroke patients like those above have actually truly had migraine (as stroke can present with headache), and if they have truly had cardiac risk factors carefully screened for with proper testing (Edmeads 1986). Although it is clear that ischemia can lead to infarction of brain tissue, and that BAM is seemingly a process of transient ischemia, the relationship of stroke and BAM remains unclear. It is important for the physican to realize that stroke is a possibility as outcome of BAM, and that patients should be warned about risk factors for stroke. In addition, the older the patient, the more likely vertebrobasilar insufficency is the diagnosis.
  
Basilar Artery Migraine and Epilepsy
It is beyond the scope of this paper in its current form to discuss the relationship between BAM and epilepsy at length, but a few points are worth noting. Bickerstaff questioned the relationship of BAM and epilepsy in a 1962 paper (Bickerstaff, 1962). In noting several of his patients reported loss of consciousness as a symptom of their BAMs, he wondered if they could actually be experiencing seizures. He felt that one possibility could be that perhaps sometimes BAM occurs in a brain that is potentially epileptic, and that the ischemia of the attack pushes the brain over the seizure threshold. Lees and Watkins in 1963 agreed with this assessment after examining 29 patients with loss of consciousness and migraine. Clinically the entities have been treated as separate, with physicians diagnosing both disorders in the same patient at different times. Both epilepsy and BAM have EEG changes, with the interictal EEG almost always normal in most patients with BAM (Passier et al. 1994), and it can be quite difficult to tell the two disorders apart (Caplan 1991a). The nature of the differences in EEG results and the pathology involved between epilepsy and BAM is still undergoing examination.
  
Treatment
Basilar migraines have been successfully treated with analgesics, cyproheptadine, propranol, tricyclic antidepressants, and calcium channel blockers (Eviatar 1994). In addition, antiepileptics, especially phenytoin, are beneficial to some patients as well (Dichter 1994). There is some question of the use of vasoconstricting agents often used for other migraine as treatment for BAM (Smith and Glass 1989); it is thought that since the circulation is ischemic in these migraines, medicines like ergotamine will only increase ischemia and worsen the attack, possibly even causing stroke (Frequin et al.. 1991). This concern should be taken under consideration when prescribing treatment for BAM.
In addition, a paper by Smith and Glass describes a 14-year-old female patient who had multiple episodes of BAM over the course of several months who did not respond to several medications (mephobarbital, propranolol, probantheline, carbamazepine) but who became headache free with the use of biofeedback techniques, specifically fingertip warming (Smith and Glass 1991).
  
Future Directions
Although many papers elucidating the nature of BAM exist, many questions remain unanswered. Those dilemnas include: (1) Why do some patients have "reversible" ischemia? (2) What is the level of risk of stroke for a patient with BAM? (3) What is the relationship between epilepsy and BAM? and 4) What therapies are most effective in treatment of BAM? Several ideas come to mind for future research about BAM. The advances of SPECT technology will hopefully help answer questions about the pathogenesis of BAM, and the nature of cerebral blood flow. In addition, a study examining risk factors (such as atherosclerosis, lipid levels, smoking and oral contraceptives) of patients with BAM versus patients who develop vertebrobasilar insufficiency and/or infarction would be useful in determining which patients are at risk for stroke. A study comparing the efficacy of various treatments for BAM would also be of use. Lastly, laboratory models will help elucidate factors influencing vasocontriction and reversible ischemia in vasculature that lacks atherosclerosis.
  
More Information
In addition to the references that follow, check out the following web page:
Karyn's Basilar Artery Migraine Page  

  
References
Amit R, Shapira Y, Flusser H, Aker M: Basilar Migraine Manifesting as Transient Global Amnesia in a 9-Year-Old Child. Headache 26:17-18, 1986.
Baloh RW, Harker LA: Central Vestibular System Disorders. in Otolaryngology - Head and Neck Surgery, vol.4, 2nd ed. Mosby-Year Book Inc, 1993.
Bickerstaff ER: Basilar Artery Migraine. Lancet 1:15-17, 1961.
Bickerstaff ER: The Basilar Artery and the Migraine-Epilepsy Syndrome. Proc R Soc Med 55:167-169, 1962.
Caplan LR: Basilar Migraine [letter]. Neurology 41:1707, 1991a.
Caplan LR: Migraine and Vertebrobasilar Ischemia. Neurology 41:55-61, 1991b.
Diamond S:Basilar Artery Migraine: A Commonly Misdiagnosed Disorder. Postgraduate Medicine 84(7): 45-46.
Dichter MA: The Epilepsies and Convulsive Disorders. in Harrison’s Principles of Internal Medicine, 13th ed. McGraw-Hill, 1994, p.2229.
Edmeads J: Stroke in Migraine. Headache 26:149-150, 1986.
Eviatar L: Vertigo. in Pediatric Neurology: Principles and Practice, 2nd ed. Mosby, Inc, 1994.
Fazekas F, et al.: The Prevalence of Cerebral Damage Varies with Migraine Type: A MRI Study. Headache 32:287-291, 1992.
Frequin STFM, et al.: Recurrent Prolonged Coma Due to Basilar Artery Migraine: A Case Report. Headache 31:75-81, 1991.
Gilroy J and Lerman VJ: Cardiac Arrhythmia in Basilar Migraine. Headache 22:140, 1982.
Guest IA, Woolf AL: Fatal Infarction of Brain in Migraine. Brit Med J 1:225-226, 1964.
Hockaday JM: Basilar Migraine in Childhood. Develop Med Child Neurol 21:455-463, 1979.
Jacome DE, Leborgne J: MRI Studies in Basilar Artery Migraine. Headache 30:88-90, 1990.
Jacome DE: Basilar Artery Migraine After Uncomplicated Whiplash Injuries. Headache 26:515-516, 1986.
Lapkin ML, French JH, Golden GS, Rowan AJ: The Electroencephalogram in Childhood Basilar Artery Migraine. Neurology 27:580-583, 1977.
Lapkin ML, Golden GS: Basilar Artery Migraine: A Review of 30 Cases. Am J Dis Child 132: 278-281, 1978.
Lees F, Watkins SM: Loss of Consciousness in Migraine. Lancet 9:647-649, 1963.
McDonald JV: Basilar Artery Migraine: Case Report. J Neurosurg 72:289-291, 1990.
Passier PECA, Vredeveld JW, de Krom MCTFM: Basilar Migraine With Severe EEG Abnormalities. Headache 34:56-58, 1994.
Sanches-Villasenor F, et al.: Psychogenic Basilar Migraine: Report of four cases. Neurology 45:1291-1294, 1995.
Seto H, et al.: Basilar Artery Migraine: Reversible Ischemia Demonstrated by Tc-99m HMPAO Brain SPECT. Clinical Nuclear Medicine 19(3):215-218, 1994.
Smith MS, Glass ST: An Adolescent Girl with Headache and Syncope. Journal of Adolescent Health Care 10:54-56, 1989.
Solomon GD, Spaccavento LJ: Lateral Medullary Syndrome After Basilar Migraine. Headache 22:171-172, 1982.
Sturzenegger MH, Meienberg O: Basilar Artery Migraine: a Follow-up Study of 82 Cases. Headache 25:408-415, 1985.
Sulkava R, Kovanen J: Locked-in Syndrome with Rapid Recovery: a Manifestation of Basilar Artery Migraine? Headache 23:238-239, 1983.
Swanson JW, Vick NA: Basilar Artery Migraine: 12 patients, with an attack recorded electroencephalographically. Neurology 28:782-786.

 

 

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