Lateralizing value of peri-ictal headache: A study of 100 patients with partial epilepsy
A. Bernasconi, MD;,
F. Andermann, MD, FRCP(C);,
N. Bernasconi, MD;,
D.C. Reutens, MD, FRACP; and
F. Dubeau, MD FRCP(C)
From the Departments of Neurology and Neurosurgery, McGill University, and Montreal Neurological Institute and Hospital, Quebec, Canada.
Address correspondence and reprint requests to Dr. Frederick Andermann, Montreal Neurological Institute and Hospital, 3801 University Street, Montreal H3A 2B4, Quebec, Canada.
To determine the lateralizing value of peri-ictal headache,the authors conducted a standardized interview of 100 patientswith partial epilepsy, 60 with temporal lobe epilepsy (TLE)and 40 with extratemporal epilepsy (ETE). Peri-ictal headacheoccurred in 47 of 100 (47%) patients. Peri-ictal headache wasmore likely to be ipsilateral to the seizure onset in TLE (27of 30 = 90%) than in ETE (two of 17 = 12%; p< 0.001). Forboth groups, peri-ictal headache usually conformed to the diagnosticcriteria for common migraine (18 of 30 = 60% in TLE; 7 of 17= 41% in ETE).
Postictal headache is a common feature of generalized tonic-clonicseizures. In a study of 100 epileptic patients,1 postictal headachewas found in approximately 50% of patients, and seizures provokeda syndrome similar to migraine in 50% of them. Unilateral cephalicpain of epileptic origin was reported in few patients and wasfound to be associated with temporal or occipital EEG epilepticdischarges. However, the pain did not colocalize with the EEGabnormalities.2 Exceptionally, headache represents the onlyictal symptom. Studies with intracerebral depth electrode recordings3,4showed that such headache is ipsilateral to an epileptic dischargearising from the amygdala and the hippocampus.
Despite the evidence for occurrence of peri-ictal headache,there have been only few and contradictory data about its lateralizingvalue in partial epilepsy. The purpose of this study was todetermine the lateralizing value of peri-ictal headache as aclinical symptom in patients with pharmacologically intractablepartial epilepsy.
A standardized interview was used to determine the prevalence,lateralization, and characteristics of headaches in 100 consecutivepatients (45 men; mean age, 33 years) undergoing presurgicalevaluation for refractory partial epilepsy.
Type and seizure focus lateralization was determined by a comprehensiveevaluation including video-EEG telemetry and high-resolutionMRI, and by response to surgical treatment (68%). Twenty-sixpatients (26%) underwent invasive recording from stereotacticmultiple intracranial depth electrodes, because extracranialEEG recordings did not provide clear lateralization of the seizureonset. Of the 60 patients with temporal lobe epilepsy (TLE),52 had unilateral epileptic discharges (left TLE, n = 27; rightTLE, n = 25), and eight had seizures originating in both temporallobes. Seizures in the 40 patients with extratemporal epilepsy(ETE) emanated from the frontal lobe (n = 13), centroparietalregion (n = 19), and the occipital lobe (n = 8). Two patientshad bifrontal epileptic foci.
The standardized interview was administered during the patients’stay in the telemetry unit by one of the authors (A.B.), a neurologist( table 1). The interview began with a verbatim record of thedescription of the headache by the patient. Interictal headachewas defined as not temporally related to the seizures. Peri-ictalheadache was defined as headache temporally related to the attacks.Peri-ictal headache included preictal and postictal headache.For each headache type, subsequent questions inquired aboutheadache localization, premonitory neurologic symptoms and signs,and general symptoms, as well as headache quality. Migrainouscharacter of the headache was determined according to the diagnosticcriteria of the International Headache Society (IHS).5 Familyhistory of recurrent headache or migraine was documented accordingto the criteria when possible.
Table 1. Interview for peri-ictal and interictal headaches in patients with refractory partial epilepsy
We analyzed differences between patients with TLE and ETE byuse of Fisher’s exact test for categorical data and pairedStudent t-test for numerical data. Significance was assumedwhen p < 0.05.
Overall, 59 patients (59%) reported recurrent headaches. Itoccurred in 37 of 60 (62%) patients with TLE and in 22 of 40(55%) patients with ETE (p = 0.53).
Peri-ictal headache.
Results are summarized in table 2. Peri-ictal headache wasreported by 47 of 100 (47%) patients. Eleven had preictal headache,and 44 patients had postictal headache. Eight patients had bothpreictal and postictal headache.
Table 2. Peri-ictal headache in 100 patients with partial epilepsy
Peri-ictal headache was reported by 30 of 60 (50%) of patientswith TLE and by 17 of 40 (43%) patients with ETE. There wasno difference in the proportion of patients with peri-ictalheadache between the two groups (p = 0.54).
The most severe pain was located in the anterior part of thehead in most individuals with peri-ictal headache (29 of 47= 62%). This was true for patients with TLE (19 of 30 = 63%)as well as those with ETE (11 of 17 = 65%; p = 1.0).
In patients with TLE, peri-ictal headache was ipsilateral tothe focus in 27 patients, bilateral in two, and contralateralto the focus in one. In patients with ETE, peri-ictal headachewas ipsilateral to the focus in two patients, bilateral in 12,and contralateral to the focus in three. We found a strong associationbetween peri-ictal headache and seizure focus lateralizationin patients with TLE (27 of 30 = 90%), but not in patients withETE (2 of 17 = 12%; p < 0.0001). This was true both for preictalheadache (TLE: 9 of 10; ETE: 0 of 1) and postictal headache(TLE: 24 of 27 = 89%; ETE: 2 of 17 = 12%; p < 0.0001).
Peri-ictal headache conformed to the diagnostic criteria formigraine without aura (common migraine) of the IHS5 in 18 of30 (60%) patients with TLE and in 7 of 17 (41%) of those withETE (p = 0.24). The others had insufficient clinical featuresfor migrainous headache as defined by the IHS.
Interictal headache.
Interictal recurrent headaches or migraine were found in 31of 100 (31%) patients and were reported by 20 of 60 (33%) patientswith TLE and 11 of 40 (27%) with ETE (p = 0.66). Twenty-ninepatients (29 of 100 = 29%) had a positive family history ofrecurrent headaches or migraine. Two patients reported migrainewith aura. One patient with TLE who had no peri-ictal headachereported scintillating scotomatas preceding migrainous headaches.Another patient with right TLE reported episodes of scintillatingscotomatas with paresthesias of the left hand followed by frontalheadache. She also had preictal prodromal headache characterizedby throbbing pain in the right temple with nausea and photophobialasting many hours and never preceded by visual symptoms. Theothers had insufficient clinical features for migrainous headacheas defined by the IHS. No patient described symptoms compatiblewith cluster headaches or other craniofacial algias.
In our population of 100 consecutive patients with pharmacologicallyrefractory partial epilepsy, we found a strong association betweenthe side of peri-ictal headache and seizure focus lateralizationin patients with TLE, but not in patients with partial epilepsyof extratemporal lobe origin. Of the three TLE patients withperi-ictal headache that was not colocalized with the seizurefocus, two had bilateral headache, and only one had contralateralpain. Thus, we believe that peri-ictal headache, used in conjunctionwith other electroclinical and radiologic data, should be consideredas a reliable and valuable clinical symptom in the lateralizationof the epileptic focus in patients with TLE. However, evidenceavailable about headache laterality is not sufficient to resolvediscrepancies between other types of lateralizing informationor strong enough that invasive monitoring might not be required.
The pathophysiology of peri-ictal headache is unclear. However,the migrainous character of the peri-ictal headache in approximatelyhalf of our patients and 60% of those with TLE suggests a similaritybetween the pathophysiologic mechanism of peri-ictal pain andthat of primary headache syndromes, namely, a neurovascularorigin. Studying the exposed human cerebral cortex during epilepticseizures, Penfield and Jasper6 observed widespread vasodilationand reactive prolonged postictal hyperemia in large pial veinsover the discharging epileptic focus. Therefore, local vasodilatationof pain-producing large cranial vessels and dura mater, andconsequent stimulation of the trigeminal sensory nervous painpathways, seems to be a key mechanism underlying the generationof headache associated with epileptic seizures. Individual susceptibilityfor activation of this system could explain why only approximatelyhalf of patients with partial epilepsy have peri-ictal headache.
The reason that patients with TLE have mainly unilateral painas opposed to those with ETE is probably multifactorial. Differentsites of seizure origin and, consequently, different patternsof dural stimulation could provide a plausible explanation forthis clinical observation. Feindel et al.7 observed that manipulationof the sinuses adjacent to the tentorium during temporal lobectomyproduced pain, which is felt behind the eye on the same sideof the stimulation. In contrast, unilateral dural stimulationover the hemispheres can elicit bilateral or contralateral pain,probably because of the bilateral termination of the dural nervesnear the midline.8-10 These observations could explain, at leastin part, why patients with seizures originating in mesial temporalstructures more frequently experience unilateral headache.
The difference between the pattern of referred pain in patientswith TLE and those with ETE also could be explained by the tendencyof epileptic activity in seizures originating outside the temporallobe to be more diffuse and therefore lead to more widespreadinvolvement of pial vessels. Furthermore, well-localized unilateralictal pain generally occurs contralateral to an epileptic focusin the postcentral gyrus or neighboring parietal lobe.2
Acknowledgments
Supported by the Savoy Foundation for Epilepsy Research, St.Jean-sur-Richelieu, Quebec, Canada (A.B.).
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Received April 7, 2000.
Accepted in final form August 29, 2000.
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