We reasoned that the patient, who had had epileptogenesis from an early age, fell ill when her mother began to interfere with her life and overprotect her. The stress resulting from this situation was the likely trigger and modulator of her epileptic seizures. Because of her illness, she had little connection with society and her relationship with her mother had deteriorated greatly. As a child, she was considered to be "a good girl" and her mother gave more attention to her elder sister. When she fell ill, she might have had ambivalent feelings of joy over the mother's concern and rebellion against her mother's interference, and she may have then somaticized her ambivalence. As her mother often ignored her since childhood, she had fallen into an escape behavior pattern and retreated into illness when faced with stressors. As a behavioral pattern for avoiding problems, she was gradually conditioned to exhibit vomiting when she was overly stressed, and she then developed repeated episodes of vomiting. In addition, the uncontrolled vomiting from her epilepsy that occurred in the absence of stress increased her feelings of helplessness. If the vomiting were solely a psychological symptom, she might have more easily controlled and understood it. Such feelings of lack of control became an additional trigger for her epilepsy: A vicious cycle was formed. When the vomiting began, the epilepsy may have been at the core. However, after about 10 years, the vomiting had become part of a vicious cycle, and her epilepsy was poorly controlled by medication alone. Integrated treatments that involved nurturing her immature personality mentally and socially and supporting the growth of all family members who were in the vicious cycle were needed. After the diagnosis of TLE and use of medication, the patient's EEG results improved but vomiting still occurred in the presence of stress. All symptoms resolved when she became independent through our support, though the spike and wave complexes remained with drowsiness.
The improvement of symptoms was thought to be due to the patient's emotional stabilization and physical improvement, involving sleep, nutrition and physical activity, which may have stabilized the limbic system. The end result was that the epileptic threshold was raised and it was possible to control the patient's symptoms without medication.
Since components of the limbic system mediate emotional experiences, and memory and behavioral responses, patients with epileptic disturbances in these structures might be particularly vulnerable to the triggering of seizures by certain stimuli that evoke emotional responses . Recently, Eggers proposed a circuit of stress (or circuit of emotion), which runs from the hippocampus to the amygdala, dorsal raphe nucleus, entorthinal cortex, and then back to the hippocampus . Eggers also noted that the central pathophysiology of both chronic stress and TLE (the most common cause of intractable adult epilepsy) is cell loss in the dentate, and psychological stress is a frequent trigger for TLE . Intense emotional reactions , "tension and anxiety", and "unhappiness/depression"  are reported to be seizure inducing factors, while "relaxation" and "happiness" are associated with decreased seizure frequency . Williams et al. reported that approximately 70% of patients whose seizures appeared to be precipitated at times by emotional stress and were not controlled by anticonvulsant medication demonstrated substantial improvement in seizure control after psychiatric treatment, while 32% had their anticonvulsant medication dose reduced and 16% discontinued medication altogether . Psychological therapies are helpful for the management of poorly controlled epilepsy [15, 16]. A relationship between EEG and stress was reported in a 1959 study which found that psychological stress was associated with EEG abnormalities . All of the aforementioned studies are consistent with our hypothesis in this case report.
This case was not typical TLE, because the main symptom was persistent vomiting, and the vomiting continued for several days. This made the diagnosis more difficult. Another difficulty in this patient was performing an EEG in the presence of severe vomiting, which also delayed the diagnosis.
Gastrointestinal symptoms that continue for several hours have been noted previously in patients with TLE. Yukselen  reported a case of psychomotor epilepsy, with a partial seizure, after a traffic accident in an adult whose symptoms were abdominal pain lasting for several hours followed by nausea and vomiting. Peppercorn  reported a case of abdominal epilepsy with temporal region EEG abnormality, in which the symptoms were nausea sustained for several hours and severe dizziness. Cases of abdominal pain in patients with epilepsy (abdominal epilepsy; a form of TLE) have also been reported [19–21]. To the best of our knowledge, there has not been an adult case report of persistent vomiting that continued for several days without alteration of consciousness. There have been reports of two pediatric cases with symptoms in common with our case [22, 7]. The case that most closely resembled ours was a child with migraine headaches and paroxysmal vascular abnormality in the temporal regions. Repeated vomiting episodes lasting for 2 to 10 days occurred without seizures. Ictal EEGs showed delta activity in the front-temporal areas, and SPECT showed decreased tracer uptake in both temporal regions during the attack-free period . Another pediatric case was a child with epilepsy who had recurrent episodes of severe vomiting lasting for a day and sometimes associated with unusual behavior suggestive of fright. EEG during presentation of symptoms showed slow and sharp waves origination from the left front-temporal regions . Our case and both of these pediatric cases had common foci of abnormal EEG in the temporal lobes.
This case would have fulfilled the criteria of CVS if the diagnosis of epilepsy had not been made. Although the etiology is not clearly known, there may be specific subgroups of CVS that have different etiologies, such as migraine, metabolic, neuroendocrine, and gastrointestinal mechanisms . In other reports of adult CVS cases, most patients did not have an EEG examination . Therefore, it is possible that EEG abnormalities may be present among CVS cases.