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lighted the increased risk of ICH among patients with an apoE €2 allele, whereas possession of apoE €4 carries a significant risk for concomitant AD but is not a n independent risk factor for CAArelated ICH. However, how apoE €2 could lead to CAA-related ICH remains undeterminedP J-Ph. al. Apolipoprotein E €4 is associated with the presence and earlier onset of haemorrhage in cerebral amyloid angiopathy. Stroke 1996;27:1333-1337. 4. Nicoll JAR, Burnett C, Love S, et al. High frequency of apolipoprotein E €2 allele in hemorrhage due to cerebral amyloid angiopathy. Ann Neurol 1997;4 1: 7 16 -72 1. 5. Greenberg SM, Hyman BT. Cerebral amyloid angiopathy and apolipoprotein E: bad news for the good allele? Ann Neurol 1997;41:701-702. 6. Davignon J, Gregg RE, Sing CF. Apolipoprotein E polymorphism and atherosclerosis. Atherosclerosis 1988;B:l-21. 7. Premkumar RD, Cohen DL, Hedera P, Friedland RP, Kalaria RN. Apolipoprotein E-€4 alleles in cerebral amyloid angiopathy and cerebrovascular pathology associated with Alzheimer's disease. Am J Pathol 1996; 148:2083-2095. Dopamine and migraineTo the Editor: We read with interest the review by Peroutka on dopamine and migraine.' The author concluded that an increased dopaminergic activity is a key pathophysiologic component of migraine. However, some points are debatable. We agree on the existence of a dopaminergic hypersensitivity in migraine. Our group has described an increased density of dopamine D5 receptors on peripheral blood lymphocytes in previously untreated migraine patients compared with healthy ageand sex-matched controls ( p < 0.05) in a radioligand binding study using [3H]SCH 23390 as a ligand.2 Moreover, we recently demonstrated a lower activation threshold for both pre-and postsynaptic dopamine receptors in migraineurs than in healthy controls ( p < 0.05) in a large and highly selected migraine population by using apomorphine sc at two different doses (2 and 10 Kg/kg), with and without pretreatment with d~m p e r i d o n e .~ Whereas the dose of 10 pgkg induced, at most, yawning and drowsiness (presynaptic symptoms) in controls, the same dose also caused nausea and vomiting (postsynaptic symptoms) in migraineurs. However, in contrast with previous studies cited by Dr. Peroutka in his review, no patient complained of headache following apomorphine administration, nor did any apomorphineinduced symptom resemble those occurring during spontaneous attacks. Furthermore, it is most notable that the occurrence of apomorphine-induced symptoms in each patient was not related to the characteristics or the severity of vegetative symptoms accompanying spontaneous attacks.We believe that clinical, pharmacologic, and biological evidence indicates that dopaminergic hypersensitivity is a specific migraine trait. However, the pharmacologic data currently available seem to be insufficient to hypothesize an involvement of dopamine in the pathophysiology of migraine attack. Dopaminergic drugs are able to unmask the dopaminergic hypersensitivity in migraine but do not act as migrain...
lighted the increased risk of ICH among patients with an apoE €2 allele, whereas possession of apoE €4 carries a significant risk for concomitant AD but is not a n independent risk factor for CAArelated ICH. However, how apoE €2 could lead to CAA-related ICH remains undeterminedP J-Ph. al. Apolipoprotein E €4 is associated with the presence and earlier onset of haemorrhage in cerebral amyloid angiopathy. Stroke 1996;27:1333-1337. 4. Nicoll JAR, Burnett C, Love S, et al. High frequency of apolipoprotein E €2 allele in hemorrhage due to cerebral amyloid angiopathy. Ann Neurol 1997;4 1: 7 16 -72 1. 5. Greenberg SM, Hyman BT. Cerebral amyloid angiopathy and apolipoprotein E: bad news for the good allele? Ann Neurol 1997;41:701-702. 6. Davignon J, Gregg RE, Sing CF. Apolipoprotein E polymorphism and atherosclerosis. Atherosclerosis 1988;B:l-21. 7. Premkumar RD, Cohen DL, Hedera P, Friedland RP, Kalaria RN. Apolipoprotein E-€4 alleles in cerebral amyloid angiopathy and cerebrovascular pathology associated with Alzheimer's disease. Am J Pathol 1996; 148:2083-2095. Dopamine and migraineTo the Editor: We read with interest the review by Peroutka on dopamine and migraine.' The author concluded that an increased dopaminergic activity is a key pathophysiologic component of migraine. However, some points are debatable. We agree on the existence of a dopaminergic hypersensitivity in migraine. Our group has described an increased density of dopamine D5 receptors on peripheral blood lymphocytes in previously untreated migraine patients compared with healthy ageand sex-matched controls ( p < 0.05) in a radioligand binding study using [3H]SCH 23390 as a ligand.2 Moreover, we recently demonstrated a lower activation threshold for both pre-and postsynaptic dopamine receptors in migraineurs than in healthy controls ( p < 0.05) in a large and highly selected migraine population by using apomorphine sc at two different doses (2 and 10 Kg/kg), with and without pretreatment with d~m p e r i d o n e .~ Whereas the dose of 10 pgkg induced, at most, yawning and drowsiness (presynaptic symptoms) in controls, the same dose also caused nausea and vomiting (postsynaptic symptoms) in migraineurs. However, in contrast with previous studies cited by Dr. Peroutka in his review, no patient complained of headache following apomorphine administration, nor did any apomorphineinduced symptom resemble those occurring during spontaneous attacks. Furthermore, it is most notable that the occurrence of apomorphine-induced symptoms in each patient was not related to the characteristics or the severity of vegetative symptoms accompanying spontaneous attacks.We believe that clinical, pharmacologic, and biological evidence indicates that dopaminergic hypersensitivity is a specific migraine trait. However, the pharmacologic data currently available seem to be insufficient to hypothesize an involvement of dopamine in the pathophysiology of migraine attack. Dopaminergic drugs are able to unmask the dopaminergic hypersensitivity in migraine but do not act as migrain...
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