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Keywords:

  • Migraine;
  • Epilepsy

Abstract

  1. Top of page
  2. Abstract
  3. CASE REPORT
  4. CONCLUSIONS
  5. REFERENCES

Summary:  Migraine and epilepsy are common neurological conditions that may share a pathophysiologic and genetic basis. The following case is presented to illustrate key aspects of their relationship.

The coexistence of migraine and epilepsy has been a subject of intense interest for more than a century, and intrigued both Jackson and Gowers. Jackson discussed the spectrum of these disorders and analyzed their relationship (1), whereas Gowers concluded that any relationship was rare, indirect, and frequently constituted “a source of error” (2). Over a hundred years later, there is still not consistent agreement on the pathophysiologic and genetic relationship between these disorders. The three main possibilities are well reviewed by Andermann (3): (i) both migraine and epilepsy are relatively common and will co-occur by chance; (ii) there is a shared pathophysiological or genetic basis; and (iii) they are causally related, with one leading to the other. The third possibility encompasses the condition termed “migralepsy” by Lennox, wherein a classic migraine attack evolves into an epileptic seizure (4).

CASE REPORT

  1. Top of page
  2. Abstract
  3. CASE REPORT
  4. CONCLUSIONS
  5. REFERENCES

A 22-year-old right-handed college student with migraine headaches and epilepsy was transferred to our institution for treatment of status epilepticus. Birth and development had been normal. At 12 years of age, she began having 2–3 min episodes of fluorescent-colored flashing lights, black spots, and squiggly lines. At age 13, the visual symptoms began to be followed by bifrontal headaches and nausea lasting half an hour, with a catamenial component. At age 15, she had her first convulsion. It occurred in the context of worsened headaches after she had been struck in the head by a car door several weeks previously. The day of the convulsion, she had had her typical migraine, with left visual field scintillations. Though she would typically have rested to minimize the headache, on this occasion, she did not want to miss her softball game. While playing, she lost vision and then had a convulsion; she was admitted to the local hospital. Examination showed left facial weakness and saccadic pursuit movements to the left. EEG and MRI were normal. She began taking valproic acid. Over the next 4 years, she had 1–2 secondarily generalized seizures a year, on and off valproic acid, all preceded by the identical visual aura. Compliance with valproate treatment was variable in part because of associated weight gain. At 19 years of age, her regimen was changed to topiramate and perimenstrual acetazolamide.

Past medical history included sinus surgery and counseling for depression and anxiety. Socially, she was a senior in college with good grades and many friends, and was active in religious organizations. Family history included many maternal relatives who had migraine with visual aura (mother, grandmother, aunt, uncle, two nieces). Her only sibling, a brother, did not have migraines. Nobody else in the family had ever had a seizure, and there was no family history to suggest mitochondrial dysfunction, such as myopathy, short stature, hearing loss, gastrointestinal disorders, or strokes.

One week prior to transfer to our institution, she had an episode of severe perimenstrual migraine with waxing and waning spatial disorientation. Topiramate was increased and methylprednisolone was started. She left college to stay with her parents due to the severity of her headache and disorientation. During the night, she had a cluster of three convulsions and was admitted to the local hospital. While there, she was observed to have 2–3 focal seizures per hour, each consisting of muteness, thrashing, left adversion, and unresponsiveness for about 1 min. CT and MRI were normal. Phenytoin was added and transfer arranged.

On arrival, she had repeated episodes of left head and eye deviation, left facial twitching, and thrashing/clonic movements lasting 1–2 min. She was drowsy but oriented between events. CSF showed five white blood cells, with normal protein and glucose. Herpes simplex virus-PCR was negative, as were serum and urine toxic screens. A limited emergency EEG, using a technique modified from Bridgers and Ebersole (5) showed right greater than left posterior fast activity followed by bilateral rhythmic theta and delta with intermixed spikes (Fig. 1). Valproic acid was added to topiramate and phenytoin. Her seizures were controlled by day 2. Examination showed mild left neglect and constructional apraxia resolving over days. She also had postictal psychosis with paranoid features, improving over days to weeks. MRI and ECD-SPECT were normal. MRS showed mildly decreased NAA in R > L temporal lobes. EEG showed right posterior delta and frontal intermittent rhythmic delta activity (Fig. 2). Depakote was withdrawn 10 days after admission.

imageimageimage

Figure 1. “Below the hairline” emergency EEG performed the night of transfer. Technique and montage modified from Bridgers and Ebersole (5). Fp1/2 and F7/8 approximate the electrode positions in the 10–20 system, while T3/4 and T5/6 are located more inferiorly. (A) Right > left mid-posterior temporal low voltage beta superimposed on delta. (B) After 10 s, tracing obscured by muscle artifact. (C) 1.5 min later, muscle artifact has subsided and there is bilateral 2–3 Hz delta with intermixed spikes and polyspikes. Sensitivity 7 uV/mm, low frequency filter (LFF) 1 Hz, high frequency filter (HFF) 35 Hz, 60 Hz filter on.

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Figure 2. EEG performed 4 days after admission shows loss of the posterior rhythm and presence of irregular theta and delta on the right, along with bilateral frontal intermittent rhythmic delta (FIRDA). Sensitivity 10 uV/mm, LFF 1 Hz, HFF 70 Hz, 60 Hz filter on.

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One year later, she takes topiramate 325 mg a day (level 4 mg/dl) and phenytoin 425 mg a day (level 14 mg/dl). She has infrequent, mild left visual field scintillations with or without headache. She has had no further episodes of altered awareness or involuntary movements. Repeat MRI was normal 6 months after discharge, while MRS was normal in the left temporal lobe but still showed decreased NAA in the right temporal lobe. EEG showed mild right posterior theta slowing and no discharges (Fig. 3).

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Figure 3. EEG 5 months after discharge shows only decreased alpha amplitude on the right, with intermixed irregular theta. Sensitivity 7 uV/mm, LFF 1 Hz, HFF 70 Hz, 60 Hz filter off.

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CONCLUSIONS

  1. Top of page
  2. Abstract
  3. CASE REPORT
  4. CONCLUSIONS
  5. REFERENCES

This case demonstrates a close relationship in this young woman between migraine and epilepsy. She had migraines with visual aura and a catamenial component for 3 years. At that time, a minority of the typical auras began to be followed by convulsions. She has a strong family history of classic migraine, all on the maternal side, but no other family members have had seizures.

There is an increased risk of migraine in individuals with epilepsy (6). Marks and Ehrenberg showed that patients with catamenial epilepsy and patients with migraine with aura were at an increased risk for an association between these two disorders (7). Of their 395 adult patients with epilepsy, 79 (20%) had both migraine and epilepsy, and 13 (3%) had seizures during or immediately following a migraine aura, such as in our case. In this small but significant proportion of patients, the pathophysiology responsible for migraine may predispose to seizures.

During the individual attacks of classic migraine auras, reduced regional cerebral blood flow, demonstrated by several investigators (7–9), may concomitantly reduce the seizure threshold. In our patient, the right posterior hemisphere is the likely origin of both the left visual field migraine aura and the left adversive seizures. On a chronic level, repeated episodes of migraine in combination with other genetic or environmental factors may lead to focal cortical injury and reorganization, resulting in a tendency toward recurrent seizures. However, in most patients with both conditions, as in the present case, there is no evidence of cerebral infarction, even though stroke may rarely result from migraine and commonly causes epilepsy.

What determines which patients with migraine develop migralepsy? Despite the absence of a family history of epilepsy in many such patients, including ours, a genetic explanation is raised by the complex pattern of inheritance that appears to underlie many of the common epilepsy syndromes, as well as migraine. Although a shared genetic mechanism remains elusive and was not demonstrated by Ottman and Lipton (10), the observed association between the two conditions could be explained by a shared subset of predisposing genes and/or by environmental factors leading to increased neuronal excitability.

REFERENCES

  1. Top of page
  2. Abstract
  3. CASE REPORT
  4. CONCLUSIONS
  5. REFERENCES
  • 1
    Gowers WR. The borderland of epilepsy: faints, vagal attacks, vertigo, migraine, sleep symptoms and their treatment. London : Churchill , 1907.
  • 2
    Jackson JH. Hospital of the epileptic and paralyzed: case illustrating the relation betwixt certain cases of migraine and epilepsy. Lancet 1875;2: 2445.
  • 3
    Anderman F. Clinical features of migraine-epilepsy syndromes. In: AndermanF, LugaresiE, eds. Migraine and epilepsy. Boston : Butterworths, 1987, p. 3.
  • 4
    Lennox WG, Lennox MA. Epilepsy and related disorders. Boston : Little, Brown, 1960, p. 451.
  • 5
    Bridgers SL, Ebersole JS. EEG outside the hairline: detection of epileptiform abnormalities. Neurology 1998;38: 1469.
  • 6
    Ottman R, Lipton RB. Comorbidity or migraine and epilepsy. Neurology 1994;44: 210510.
  • 7
    Marks DA, Ehrenberg BL. Migraine-related seizures in adults with epilepsy, with EEG correlation. Neurology 1993;43: 247683.
  • 8
    Flippen C, Welch KM. Imaging the brain of migraine sufferers. Curr Opin Neurol. 1997;10: 22630.
  • 9
    Olesen J, Friberg L, Olsen TS, et al. Timing and topography of cerebral blood flow, aura, and headache during migraine attacks. Ann Neurol 1990;28: 7918.
  • 10
    Ottman R, Lipton RB. Is the comorbidity of epilepsy and migraine due to a shared genetic susceptibility? Neurology 1996;47: 91824.