C A S E REPORT
Reversible Quantitative EEG Changes in a Case of Cyclic Vomiting: Evidence for Micrraine Equivdent Sondra A. Jernigan Lucile M . Ware
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Medical experts have debated whether cyclic vomiting is a manifestation of epilepsy (Hoefer et al. 1951, Livingston 1951, Babb and Eckman 1972, Jay 1982) or a migraine equivalent (Gascon and Barlow 1970, Hammond 1974, Rabe 1974, Prensky 1976, Brown 1977, Weitz 1982, Lanzi et al. 1983a, b). The syndrome involves intermittent attacks of vomiting lasting several hours t o several days and occurring at intervals of weeks or months, with behavioural symptoms including withdrawal, irritability and aggression. This paper presents quantitative EEG data supporting interpretation of cyclic vomiting as a migraine equivalent, even when headache is not a symptom. EEG examinations of patients with cyclic vomiting should clarify the issue, but few such studies have been done. Millichap et al. (1955) reported EEG abnormalities consistent with epilepsy, but the study is compromised by the presence of seizures in some patients, and brain damage in many. Davenport et al. (1972), in a report describing patients' behaviour problems, briefly mentioned EEG results consisting of diffuse slowing during vomiting episodes, but improved or normal EEGs between episodes. Hoyt and Stickler (1960) found no evidence of
convulsive disorder. Douglas and White (1971) proposed that true cases of abdominal epilepsy should manifest epileptiform EEG changes, and Mitchell et al. (1983) concluded that true abdominal epilepsy is rare. In studies examining the EEG patterns of migraine patients, the most common abnormality is an increase in localized or diffuse slow waves (Selby and Lance 1960, Camp and Wolff 1961, Smythe and Winter 1964, Slatter 1968, Hockaday and Whitty 1969, Walser and Isler 1982). EEG studies of basilar artery migraine (BAM) in children and adults have also typically shown slow waves (Lapkin et al. 1977, Sturzenegger and Meienberg 1985, Ganji 1986). Most EEG studies have been conducted between episodes rather than during a migraine attack, but a few studies with serial EEGS have noted increased slowing during the migraine and a normal EEG when patients were asymptomatic (Lapkin et al. 1977, Walser and Isler 1982, Ganji 1986). Quantitative EEG (QEEG) measures provide additional information which is not detected by visual inspection (Gotman et al. 1975, Isaksson et al. 1976, Colon et al. 1977, Jonkman et al. 1985), and in serial evaluations provide an objective
baseline from which t o measure change (Matousek er al. 1979). The few studies using QEEG methods for migraine patients (Jonkman and Lelieveld 1981, Simon et al. 1983, Polich et al. 1986, Drake et al. 1987) examined patients only between episodes rather than during attacks, and the measures varied between studies, so conclusions regarding migraine cannot yet be determined from the QEEG measures. The present case is of interest for several reasons. Few studies describe cyclic vomiting with abnormal behaviour but without a history of seizures or headaches. Few studies have systematically compared EEG patterns during and between episodes, and no study has used QEEG measures both during and between episodes to compare differences in a n objective, statistical manner against ageappropriate norms.
Case report Hisrory This I?-year-old female patient’s first episode of cyclic vomiting occurred at about 5 % years of age. From then until age 17 she had more than 20 such episodes, 19 of which resulted i n admission to hospital. Nausea a a s birtually always the first symptom. Headache was noted in only one episode, lasting for a day before onset of vomiting. The patient never complained of abdominal pain or visual disturbances during the episodes. Dizziness and vertigo did precede several episodes, but a neurologist interpreted these symptoms as secondary to ear infections. Each episode typically lasted between four and seven days, during which time her behaviour and affect markedly changed. She would become agitated, withdrawn and uncommunicative for days, not responding to questions and appearing ‘nearly autistic’. Regressive behaviours included drooling, biting herself and others, picking at herself, incontinence and masturbation. She was often unco-operative and aggressive, even combative. Because she was receiving psychiatric treatment for emotional problems, the cyclic vomiting was regarded as psychosomatic and selfserving, and her unco-operative behaviour was viewed as an extension of her attention-seeking and jealous anger. Neurological evaluations were normal, as were two standard EEGs done during different episodes. A brain scan and skull X-rays at age six, when the episodes were most frequent, showed no evidence of abnormality. She had been born three weeks prematurely, but showed no developmental delays or gross problems other than multiple ear infections, for which tubes were placed at age four. She had no gross CNS abnormality on standard neurological examination, but psychological testing revealed gross and fine motor clumsiness, visualmotor integration difficulties, and a certain literalness in her thinking.
The family history included migraines on the maternal side, and the father described himself as having had frequent episodes of childhood vomiting, which sometimes lasted for two days.
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Testing The patient was first referred for an evaluation to include QEEG and evoked potentials at age nine, following admission to hospital for her twelfth episode of cyclic vomiting. Laboratory tests showed her WBC, H b , electrolytes, including serum ammonia, PCOz and pH, to be within the normal range. The C T scan was normal. In the wake of numerous tests (on days one and two) that had all proved negative, she was referred for QEEG to determine whether there was any other physiological basir for the episode; i.e. whether the vomiting episodes had an organic basis or, as had been suggested, were psychosomatic. Testing was done during the episode (on day three) and again nine weeks later. Six years later a second evaluation was completed during the patient’s eighteenth episode (on day four) and at follow-up five weeks later. Again, laboratory studies were unremarkable, except for a slighty elevated WBC ( 1 4 . 4 ~109/L, with 89 per cent segmented neutrophils on admission, which subsided to normal by day four. Hb was stable. Repeated pH and PCOZ remained normal. Serum electrolytes were normal on admission. There was a mild drop of serum potassium to 3.3mmol/L on day two, which responded to IV fluid correction and returned to normal by day four. Otherwise repeated electrolytes, including serum ammonia, remained within the normal range. During the two vomiting episodes she was taking no medication that would affect the QEEG and evoked potentials. The neurometric assessment battery (John er al. 1977, 1980, 1983; Ahn er a/. 1980; Prichep er a/. 1983) uses a computer-controlled data acquisition system to record artifact-free quantitative EEG and evoked potential data. Electrodes are placed according to the standardized 10-20 system. Eight bipolar EEG derivations are computed from monopolar recordings for central, temporal, parieto-occipital and fronto-temporal regions referenced to linked ears. The EEG data are divided into a frequency spectrum consisting of four bands: delta (1.5-3.5Hz), theta (3.5-7.5Hz), alpha (7.5-12.5Hz) and beta (12.5-25Hz). The relative (percent) power is calculated for each frequency in each region, and the data are compared statistically with standardized normative data based on derived age-regression equations (John et a/. 1980, 1983). Using these age-regression equations, z-transformations express the degree to which the values obtained from an individual patient depart from values expected in normally functioning individuals of the same age. Hemispheric differences are computed, using coherence and amplitude asymmetry measures. Visual and auditory evoked potentials form part of the neurometric battery, but the present paper will be limited to presentation and discussion of the QEEG results only. QEEG data were recorded while the patient was resting, awake but with eyes closed, seated in a semidarkened room. The EEG was sampled at a rate of 100Hz, and 60 seconds of artifact-free data were
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TABLE 1 Z Scores during and after vomiting episodes
Episode 1
2
During Delta Alpha
Brain region Central left Central right Temporal left Temporal right Parieto-occipital Parieto-occipital Fronto-temporal Fronto-temporal Central left Central right Temporal left Temporal right Parieto-occipital Parieto-occipital Fronto-temporal Fronto-temporal
left right left right
2.4* 1.6 1.7 2.6** 4.0t 2.9** - 1.2 -0.6
- 1-7 - 1.7 -2.7** - 3.47 -4.0t -2.9** -2.0* -2.0*
left right left right
2.3* 2.2* 4.lt 4.lt 3.9t 2.8** 2.4* 1.7
-2.5' -3.57 -3.87 -5.4t -6.lt -4.9t - 2.3* -2.7**
After Delta Alpha 0.1
0.8 0.5
0.8 0.5
0.7 -0.4 0.2
0.2 -0.4 -0.2 -0.6 -0.4 -0.9 0.8 0.5
-1.3
1.4
-1.5
1.0
0.3 -0.1 0.7 0.3 -2.5* -2.6**
-0.7 -2.2* -2.3* -2.1* 0.7 2.4*
Positive numbers indicate an excess, negative numbers a deficit of relative power within a specific frequency band. *p
Reversible Quantitative EEG Changes in a Case of Cyclic Vomiting: Evidence for Micrraine Equivdent Sondra A. Jernigan Lucile M . Ware
m 'A m 0 m
h
B
80
Medical experts have debated whether cyclic vomiting is a manifestation of epilepsy (Hoefer et al. 1951, Livingston 1951, Babb and Eckman 1972, Jay 1982) or a migraine equivalent (Gascon and Barlow 1970, Hammond 1974, Rabe 1974, Prensky 1976, Brown 1977, Weitz 1982, Lanzi et al. 1983a, b). The syndrome involves intermittent attacks of vomiting lasting several hours t o several days and occurring at intervals of weeks or months, with behavioural symptoms including withdrawal, irritability and aggression. This paper presents quantitative EEG data supporting interpretation of cyclic vomiting as a migraine equivalent, even when headache is not a symptom. EEG examinations of patients with cyclic vomiting should clarify the issue, but few such studies have been done. Millichap et al. (1955) reported EEG abnormalities consistent with epilepsy, but the study is compromised by the presence of seizures in some patients, and brain damage in many. Davenport et al. (1972), in a report describing patients' behaviour problems, briefly mentioned EEG results consisting of diffuse slowing during vomiting episodes, but improved or normal EEGs between episodes. Hoyt and Stickler (1960) found no evidence of
convulsive disorder. Douglas and White (1971) proposed that true cases of abdominal epilepsy should manifest epileptiform EEG changes, and Mitchell et al. (1983) concluded that true abdominal epilepsy is rare. In studies examining the EEG patterns of migraine patients, the most common abnormality is an increase in localized or diffuse slow waves (Selby and Lance 1960, Camp and Wolff 1961, Smythe and Winter 1964, Slatter 1968, Hockaday and Whitty 1969, Walser and Isler 1982). EEG studies of basilar artery migraine (BAM) in children and adults have also typically shown slow waves (Lapkin et al. 1977, Sturzenegger and Meienberg 1985, Ganji 1986). Most EEG studies have been conducted between episodes rather than during a migraine attack, but a few studies with serial EEGS have noted increased slowing during the migraine and a normal EEG when patients were asymptomatic (Lapkin et al. 1977, Walser and Isler 1982, Ganji 1986). Quantitative EEG (QEEG) measures provide additional information which is not detected by visual inspection (Gotman et al. 1975, Isaksson et al. 1976, Colon et al. 1977, Jonkman et al. 1985), and in serial evaluations provide an objective
baseline from which t o measure change (Matousek er al. 1979). The few studies using QEEG methods for migraine patients (Jonkman and Lelieveld 1981, Simon et al. 1983, Polich et al. 1986, Drake et al. 1987) examined patients only between episodes rather than during attacks, and the measures varied between studies, so conclusions regarding migraine cannot yet be determined from the QEEG measures. The present case is of interest for several reasons. Few studies describe cyclic vomiting with abnormal behaviour but without a history of seizures or headaches. Few studies have systematically compared EEG patterns during and between episodes, and no study has used QEEG measures both during and between episodes to compare differences in a n objective, statistical manner against ageappropriate norms.
Case report Hisrory This I?-year-old female patient’s first episode of cyclic vomiting occurred at about 5 % years of age. From then until age 17 she had more than 20 such episodes, 19 of which resulted i n admission to hospital. Nausea a a s birtually always the first symptom. Headache was noted in only one episode, lasting for a day before onset of vomiting. The patient never complained of abdominal pain or visual disturbances during the episodes. Dizziness and vertigo did precede several episodes, but a neurologist interpreted these symptoms as secondary to ear infections. Each episode typically lasted between four and seven days, during which time her behaviour and affect markedly changed. She would become agitated, withdrawn and uncommunicative for days, not responding to questions and appearing ‘nearly autistic’. Regressive behaviours included drooling, biting herself and others, picking at herself, incontinence and masturbation. She was often unco-operative and aggressive, even combative. Because she was receiving psychiatric treatment for emotional problems, the cyclic vomiting was regarded as psychosomatic and selfserving, and her unco-operative behaviour was viewed as an extension of her attention-seeking and jealous anger. Neurological evaluations were normal, as were two standard EEGs done during different episodes. A brain scan and skull X-rays at age six, when the episodes were most frequent, showed no evidence of abnormality. She had been born three weeks prematurely, but showed no developmental delays or gross problems other than multiple ear infections, for which tubes were placed at age four. She had no gross CNS abnormality on standard neurological examination, but psychological testing revealed gross and fine motor clumsiness, visualmotor integration difficulties, and a certain literalness in her thinking.
The family history included migraines on the maternal side, and the father described himself as having had frequent episodes of childhood vomiting, which sometimes lasted for two days.
W LCI
0 W
m
Testing The patient was first referred for an evaluation to include QEEG and evoked potentials at age nine, following admission to hospital for her twelfth episode of cyclic vomiting. Laboratory tests showed her WBC, H b , electrolytes, including serum ammonia, PCOz and pH, to be within the normal range. The C T scan was normal. In the wake of numerous tests (on days one and two) that had all proved negative, she was referred for QEEG to determine whether there was any other physiological basir for the episode; i.e. whether the vomiting episodes had an organic basis or, as had been suggested, were psychosomatic. Testing was done during the episode (on day three) and again nine weeks later. Six years later a second evaluation was completed during the patient’s eighteenth episode (on day four) and at follow-up five weeks later. Again, laboratory studies were unremarkable, except for a slighty elevated WBC ( 1 4 . 4 ~109/L, with 89 per cent segmented neutrophils on admission, which subsided to normal by day four. Hb was stable. Repeated pH and PCOZ remained normal. Serum electrolytes were normal on admission. There was a mild drop of serum potassium to 3.3mmol/L on day two, which responded to IV fluid correction and returned to normal by day four. Otherwise repeated electrolytes, including serum ammonia, remained within the normal range. During the two vomiting episodes she was taking no medication that would affect the QEEG and evoked potentials. The neurometric assessment battery (John er al. 1977, 1980, 1983; Ahn er a/. 1980; Prichep er a/. 1983) uses a computer-controlled data acquisition system to record artifact-free quantitative EEG and evoked potential data. Electrodes are placed according to the standardized 10-20 system. Eight bipolar EEG derivations are computed from monopolar recordings for central, temporal, parieto-occipital and fronto-temporal regions referenced to linked ears. The EEG data are divided into a frequency spectrum consisting of four bands: delta (1.5-3.5Hz), theta (3.5-7.5Hz), alpha (7.5-12.5Hz) and beta (12.5-25Hz). The relative (percent) power is calculated for each frequency in each region, and the data are compared statistically with standardized normative data based on derived age-regression equations (John et a/. 1980, 1983). Using these age-regression equations, z-transformations express the degree to which the values obtained from an individual patient depart from values expected in normally functioning individuals of the same age. Hemispheric differences are computed, using coherence and amplitude asymmetry measures. Visual and auditory evoked potentials form part of the neurometric battery, but the present paper will be limited to presentation and discussion of the QEEG results only. QEEG data were recorded while the patient was resting, awake but with eyes closed, seated in a semidarkened room. The EEG was sampled at a rate of 100Hz, and 60 seconds of artifact-free data were
h 2
3
‘h
B
81
TABLE 1 Z Scores during and after vomiting episodes
Episode 1
2
During Delta Alpha
Brain region Central left Central right Temporal left Temporal right Parieto-occipital Parieto-occipital Fronto-temporal Fronto-temporal Central left Central right Temporal left Temporal right Parieto-occipital Parieto-occipital Fronto-temporal Fronto-temporal
left right left right
2.4* 1.6 1.7 2.6** 4.0t 2.9** - 1.2 -0.6
- 1-7 - 1.7 -2.7** - 3.47 -4.0t -2.9** -2.0* -2.0*
left right left right
2.3* 2.2* 4.lt 4.lt 3.9t 2.8** 2.4* 1.7
-2.5' -3.57 -3.87 -5.4t -6.lt -4.9t - 2.3* -2.7**
After Delta Alpha 0.1
0.8 0.5
0.8 0.5
0.7 -0.4 0.2
0.2 -0.4 -0.2 -0.6 -0.4 -0.9 0.8 0.5
-1.3
1.4
-1.5
1.0
0.3 -0.1 0.7 0.3 -2.5* -2.6**
-0.7 -2.2* -2.3* -2.1* 0.7 2.4*
Positive numbers indicate an excess, negative numbers a deficit of relative power within a specific frequency band. *p
