Migraine And Epilepsy
Migraine and epilepsy are comorbid. Andermann and Andermann (1987) reported a median epilepsy prevalence of 5.9% (range 1% to 17%) in migraineurs, which greatly exceeds the population prevalence of 0.5% (Hauser et al., 1991). The reported migraine prevalence in epileptics ranges from 8% to 23% (Olesen, 1993). Methodologic problems make these studies difficult to interpret (Olesen, 1993).
The comorbidity of migraine and epilepsy was studied using Columbia University’s Epilepsy Family Study (Ottman and Lipton, 1994, 1996; Lipton et al., 1994). Among subjects with epilepsy (probands), the prevalence of a migraine history was 24%. Among relatives with epilepsy, 26% had a history of migraine. In control relatives without epilepsy, the prevalence of a migraine history was 15%. The relative risk of migraine in persons with epilepsy was 2.4, for both probands and their epileptic relatives. Migraine risk was not related to age at epilepsy onset (partial vs. generalized) but was highest in post-traumatic epileptics (RR = 4.1).
Using reconstructed cohort methods, migraine risk is elevated both before and after seizure onset; therefore, it cannot be accounted for solely as a cause or solely as a consequence of epilepsy (Ottman and Lipton, 1994, 1996; Lipton et al., 1994). Because migraine risk is particularly elevated in post-traumatic epileptics and head injury is also a risk factor for both disorders, shared environmental risk factors may contribute to their comorbidity (Shechter et al., 1990; Annergers et al., 1980). However, known environmental risk factors cannot fully account for this comorbidity because migraine risk is also elevated in individuals with idiopathic epilepsy. Shared genetic risk factors cannot completely account for comorbidity as migraine risk is elevated in probands with and without a positive family history of epilepsy.
Perhaps an altered brain state increases the risk of both migraine and epilepsy and, thus, accounts for the comorbidity of these disorders (Welch, 1994; Hauser et al., 1991). Genetic or environmental risk factors may increase neuronal excitability or decrease the threshold to both types of attack. A reduction in brain magnesium (Welch et al., 1991) or alterations in neurotransmitters provide plausible potential substrates for this alteration in neuronal excitability (Welch, 1987; Welch et al., 1991; Olesen, 1993).
The association between migraine and epilepsy has implications for clinical practice.
When treating patients for one disorder, it is important to maintain a heightened index of suspicion for the other disorder. Differentiating migraine and epilepsy can be difficult (Andermann and Andermann, 1987; Marks and Ehrenberg, 1993) as both conditions are characterized by episodes of neurologic dysfunction. Headache without other neurologic features is rare as a manifestation of epilepsy. The most difficult diagnostic issue is differentiating migraine with aura from partial complex seizure. If the aura is brief (less than 5 minutes) and associated with alteration of consciousness, automatisms, and other positive motor features (tonic-clonic movements), epilepsy is more likely. If the aura is of long duration (more than 5 minutes) and has a mix of positive (scintillations, tingling) and negative (visual loss, numbness) features, migraine is more likely.
Treatment strategies for patients with comorbid migraine and epilepsy should be governed by the presence of comorbid disease. For example, drugs that lower seizure threshold should be used cautiously. Examples of such drugs include tricyclic antidepressants, selective serotonin reuptake inhibitors, and neuroleptics. However, it is sometimes advantageous to treat both migraine and epilepsy with a single drug, such as divalproex sodium (Jensen et al., 1994), gabapentin, or topiramate.
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Aaron L Shechter
Richard B Lipton
Stephen D Silberstein
Editors: Silberstein, Stephen D.; Lipton, Richard B.; Dalessio, Donald J.