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What was
formerly known as “basilar artery migraine” or “basilar migraine” is now termed
“basilar-type migraine” and is listed as 1.2.6 in the new IHS classification.1
A description of this condition is listed in Table 6. Basilar-type attacks
are mostly seen in young adults. While originally the terms “basilar artery
migraine” or “basilar migraine” were used, the involvement of the basilar artery
territory was uncertain, and therefore, it is now preferred to use the term
“basilar-type migraine.”145,146
Bickerstaff147
introduced the concept of "basilar artery migraine," with symptomatology
including bilateral disturbance of vision, ataxia, dysarthria, vertigo,
tinnitus, and face or limb paresthesias, followed by severe throbbing headache
usually in the occipital region. While a definite diagnosis of migraine was
impossible to prove, the mode of onset, the associated headache, the relatively
brief duration of the attack, the family history of migraine, the occurrence of
other attacks more typically migrainous, and the absence of all neurologic
abnormality between episodes made the diagnosis of migraine most likely.
Twenty‑six of 34 described patients were adolescent girls. The symptoms lasted
from 2 to 45 minutes with rapid disappearance of symptoms; however, if there had
been complete loss of vision, this symptom disappeared more gradually with a
period of "graying" of vision. The attacks occurred infrequently but tended to
be associated with menses in the young girls; the episodes subside over ensuing
years and are replaced by more common varieties of migraine.
The visual
symptoms described included vivid flashes of light throughout the entire visual
field, intense enough to obscure vision completely, and sudden bilateral visual
loss occurring over seconds and persisting up to 15 minutes, with a gradual
return of vision to normal. None of these patients had their symptoms of
brainstem ischemia accompanied by the characteristic fortification spectra of
classic migraine.
Later,
Bickerstaff148 described a group of patients in whom
consciousness was impaired during attacks of migraine, and he suggested that
the mechanism was transient ischemia of the
reticular activating system of
the brainstem secondary to vasomotor disturbance in the distribution of the
basilar artery. Loss of consciousness in migraine was reviewed by Lees and
Watkins,149 with particular reference to the association of migraine
and epilepsy. Basser,150 in an analysis of 1,800 migraine patients
demonstrated an increased incidence of epilepsy when compared with a control
group. Bickerstaff151 suggested that two mechanisms could lead to
loss of consciousness in migraine: 1) brainstem ischemia of the reticular
activating system and, 2) ischemia producing seizure in a potentially epileptic
brain, the latter being much less common.
Basilar-type migraine is regarded as a rare but definite clinical variant of
the migraine spectrum, with signs and symptoms similar to those seen in
transient ischemic attacks of the posterior circulation as observed in
elderly individuals with cerebrovascular disease. This syndrome occurs
primarily in young women and usually has a benign prognosis. However, one
reported fatality with migraine was probably due to a complicated basilar
artery attack.152
Basilar
artery migraine was reviewed by Swanson and Vick.153 Ten of the
12 patients reported were female with age of onset from 8 to 46 years. All
but one had onset before age 25. Symptoms included typical classic migraine
visual auras, diplopia, ptosis, ataxia and brief (1‑10 min.) episodes of
unconsciousness. One illustrative case is abstracted as follows:
The
patient had cyclic vomiting and car‑sickness as a young girl. At age 20 she
had episodes of bilateral loss of vision associated with vertigo, but no
headaches or other migrainous symptoms. At age 21, and twice at age 23, she
became unconscious without warning. Two attacks occurred in a brightly
lighted environment while she was standing at the foot of an upward moving
elevator. The third attack occurred at home while she was reading quietly.
In each attack she suddenly lost vision and quickly became unconscious,
slumping to the floor. Upon awakening she had severe, generalized throbbing
headache, nausea, and vomiting. Truncal ataxia was severe and lasted 15
minutes. Her father had common migraine and her mother had classic
migraine. At age 24, photic stimulation during an EEG induced a fourth
attack similar to the others.
Therapy for
these patients included ergonovine maleate, propranolol, phenytoin, and
primidone. It is of interest that anticonvulsants were effective in half
the patients.
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