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Keywords:

  • Ictal vomiting;
  • EEG monitoring;
  • Epilepsy surgery;
  • Lesional epilepsy;
  • Glioma;
  • Medically refractory partial epilepsy;
  • Ictal semiology

Abstract

  1. Top of page
  2. Abstract
  3. METHODS
  4. DISCUSSION
  5. REFERENCES

Summary: Ictal vomiting is considered a localizing sign indicating nondominant lateralization in patients with partial seizures of temporal lobe origin. We report a case of ictal vomiting associated with left temporal seizure activity in a left hemisphere language–dominant patient with a left mesial temporal glioma. Bilateral mesial temporal depth electrodes helped verify seizure lateralization. Surgery consisting of tumor resection and a left anterior temporal lobectomy and amygdalohippocampectomy resulted in freedom from seizures and episodes of vomiting. This case indicates that ictal vomiting can occur as a manifestation of left temporal onset seizures in left hemisphere–dominant patients.

Ictal vomiting is a rare manifestation in partial seizures of temporal lobe origin (1,2). When present, it is considered a localizing sign, having been reported only in association with nondominant lateralization in almost all previous publications (1–5), with one possible exception (6). We report a left hemisphere language–dominant patient with a left temporal lobe tumor who initially had ictal vomiting in association with left temporal seizure activity.

METHODS

  1. Top of page
  2. Abstract
  3. METHODS
  4. DISCUSSION
  5. REFERENCES

We searched the EEG record database at the Mayo Clinic for all patients with ictal vomiting examined in the Epilepsy Monitoring Unit between 1995 and 2001. Patients with vomiting at times other than during a recorded seizure (such as patients with postictal vomiting) were excluded. A total of 11 patients was identified, one of whom manifested ictal vomiting in the setting of left temporal lobe origin seizures, which is reported here. One additional right-hand–dominant patient with diffuse left hemispheric atrophy showed ictal vomiting during left-hemisphere origin seizures, the onset of which could not be localized further. The other nine experienced ictal vomiting in association with nondominant right temporal lobe seizures.

All scalp EEG recordings were performed by using the International 10-20 System for electrode placement. A 32-channel array was used, including four additional inferior temporal electrodes bilaterally, which were selected to improve the detection of temporal electrographic activity. Standard activation methods were used. Magnetic resonance imaging (MRI) was performed with a 1.5-T magnet. Intracranial monitoring was performed by using two eight-contact depth electrodes placed stereotactically into the mesial temporal regions in an anterior–posterior longitudinal orientation via a posterior approach.

Case history

An 18-year-old right-handed woman began having complex partial seizures in 1990 at age 7 years. In 1991, an MRI of the brain revealed a tumor in the left mesial temporal lobe. That year, the tumor was resected, and she became seizure free for 18 months. Her seizures recurred, and in 1994, stereotactic electrocauterization of the left hippocampus, amygdala, and parahippocampal gyrus was performed at another institution without benefit. In 2001, she was seen at the Mayo Clinic for further evaluation and treatment.

Her neurologic examination was normal except for minimal short-term memory difficulties and mild word-finding pauses. MRI of the brain with and without gadolinium enhancement showed evidence of recurrent tumor involving the left mesial temporal lobe (Fig. 1). Interictal scalp EEG showed frequent epileptiform discharges over the left temporal region. Rare activation of right temporal sharp waves was also noted. Intracarotid amobarbital testing confirmed left hemisphere language dominance.

image

Figure 1. Transaxial contrast-enhanced T1-weighted magnetic resonance imaging of the head demonstrates an enhancing lesion in the left anterior mesial temporal lobe (arrow). This proved to be a grade II fibrillary astrocytoma at surgery. Postoperative changes from the patient's previous surgery are also noted.

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Eleven seizures were recorded in a cluster during routine video-scalp EEG monitoring. Each began with a nondescript cephalic aura followed by staring, the development of a fearful facial expression, placement of both hands to the sides of her face, and then gagging and vomiting within a few seconds after onset. Postictal aphasia was present for ≤40 s after some of her seizures, but awareness, responsiveness, and memory were preserved during each of her clinical events. Each sequential seizure within the cluster became progressively briefer and less intense. A clear electrographic seizure discharge could not be identified on scalp EEG during any of her seizures. Because the epileptic nature of this patient's symptoms was not proven with scalp EEG, intracranial monitoring was performed by using bilateral mesial temporal depth electrodes. Electrode positioning was confirmed by co-registering a spiral computed tomography (CT) with her stereotactic MRI (Fig. 2). In addition, scalp EEG recordings were simultaneously acquired by using 16 scalp electrodes placed over the parasagittal and temporal head regions according to the International 10-20 system for electrode placement.

image

Figure 2. Co-registration of spiral computed tomography and magnetic resonance imaging verifies the localization of bilateral mesial temporal depth electrodes.

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Six seizures were recorded in a cluster that showed semiologic features identical to those observed during scalp EEG monitoring. The first two events were more prolonged relative to the subsequent four. During the first two events, electrographic seizure activity was seen originating in the left anterior temporal depth electrode contacts prior to the onset and during ictal vomiting (Fig. 3). No electrographic seizure activity was seen during the subsequent four events, which were of less intensity and shorter duration than the initial two. No electrographic seizure activity was seen in the right depth electrode at the onset of ictal vomiting during any of her seizures.

image

Figure 3. Left mesial temporal seizure discharge recorded during an episode of ictal vomiting as recorded with bilateral mesial temporal depth electrodes. Rhythmic spiking was identified in the left anterior mesial temporal depth electrode (L1–L2) before the onset of ictal vomiting (arrow). Contact 3 was not recording properly in either depth electrode so was removed from the display.

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The patient underwent an anterior left temporal lobectomy with amygdalohippocampectomy and tumor excision. The tumor pathology was consistent with a grade 2 fibrillary astrocytoma. At her 12-month postoperative visit, the patient reported being free of seizures and episodes of vomiting since surgery.

DISCUSSION

  1. Top of page
  2. Abstract
  3. METHODS
  4. DISCUSSION
  5. REFERENCES

Emphasis has been placed on the lateralizing value of ictal vomiting in temporal lobe epilepsy. Nearly all publications to date associate ictal vomiting with nondominant (usually right) hemisphere lateralization (1–5). Fiol (2) described ictal vomiting in a 30-year-old patient with nondominant temporal lobe epilepsy in whom ictal vomiting resolved after an anterior temporal lobectomy. In an extensive semiologic study, Kotagal (7) identified ictal vomiting as a rare manifestation of temporal lobe epilepsy and found this to be associated with right hemisphere lateralization exclusively. In their study of ictal semiology in unitemporal and bitemporal epilepsy, Serles et al. (8) showed ictal vomiting in patients with right unitemporal origin seizures only. Kramer (4) described ictal vomiting in nine patients with right temporal seizures, four of whom were evaluated with subdural electrocorticography. Baumgartner (9) found hyperperfusion involving the nondominant temporal lobe on ictal single-photon emission computed tomography (SPECT) in two patients with ictal vomiting. Indeed, of the 11 cases at our institution reviewed in the preparation of this article, nine showed ictal vomiting in the setting of nondominant right temporal lobe epilepsy.

The lateralizing value of ictal vomiting has recently been challenged. Devinsky (5) reported two patients with ictal vomiting in association with left temporal seizures. However, in one patient, intracranial monitoring demonstrated that vomiting did not occur until the seizure discharge spread to the right temporal lobe. In the other patient, left temporal ictal vomiting was observed, but the patient proved to be right hemisphere dominant for language. Chen (6) presented two patients with ictal vomiting in association with left temporal seizures. Both patients were left hemisphere dominant for language and exhibited retching during left temporal electrographic seizure activity. However, because scalp EEG alone was used, the authors could not completely exclude the possibility of right temporal involvement at the time vomiting commenced.

Our patient had ictal vomiting in the setting of partial seizures related to a low-grade brain tumor in the left temporal lobe. A localized discharge was present involving the left temporal depth electrode at the onset of vomiting in two of her seizures. No right temporal seizure activity was recorded at the onset of ictal vomiting during any of her recorded events. The patient has been free of seizures and other episodes of vomiting for 12 months since surgery. These observations suggest that ictal vomiting can occur in the setting of seizures originating in the dominant, left temporal lobe and is not an exclusive manifestation of nondominant temporal seizure activity. Although it is possible that right temporal seizure activity was present in regions not covered by the intracranial and scalp EEG electrodes used in these recordings at the time of ictal vomiting in this patient, this is unlikely. The patient showed no amnesia for phrases given to her during her seizures, and she remained responsive throughout each one. One would expect an alteration of her sensorium or amnesia if contralateral propagation to the right temporal region had occurred (10). In addition, the scalp EEG consistently failed to show evidence of temporal neocortical seizure activity on the right. Therefore, there was no evidence that nondominant, right temporal seizure activity was present during any of her clinical events. Finally, resection of the left mesial temporal structures and lesion resulted in resolution of the patient's symptoms, which strongly suggests that these structures were the origin of the patient's seizure manifestations.

Electrographic seizure activity could not be identified in four of the patient's episodes of vomiting. This may be due to the position of the mesial depth electrodes in this case relative to the cortical regions correlated with vomiting. Previous investigators have implicated the insula and lateral temporal neocortex as the cortical region associated with vomiting, although this has not been definitively established (2,4,11). Kramer et al. (4), through subdural electrocorticography, showed that ictal vomiting was not seen in mesial temporal onset seizures until propagation to the lateral temporal neocortex occurred. Penfield and Jasper (11) observed that peristaltic activity was associated with electrical stimulation of the insular cortex, suggesting that this region may be associated with the visceromotor function necessary for vomiting. The intracranial electrodes in the present case were limited to the mesial inferior temporal regions and did not include the insula or lateral temporal neocortex. If seizure activity involved either of these structures at the onset of vomiting, the discharge may have remained undetected by the mesial temporal electrodes and temporal scalp array used in this patient. The four seizures in which no electrographic correlate was found occurred at the end of a seizure cluster and were briefer and less intense than those that were associated with recorded seizure activity. It is plausible that the underlying seizure causing these events involved a smaller area of cortex compared with those events that were associated with electrographic seizure activity.

Ictal semiology is a valuable lateralizing tool in the presurgical evaluation of patients with intractable partial epilepsy. A full perspective of the value of ictal semiology requires a realization of the exceptions to the typical localizing significance of individual semiologic signs. Although ictal vomiting usually suggests nondominant lateralization in patients with temporal lobe seizures, this case indicates that it can occur in the setting of left dominant temporal seizure activity as well.

REFERENCES

  1. Top of page
  2. Abstract
  3. METHODS
  4. DISCUSSION
  5. REFERENCES
  • 1
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  • 8
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  • 9
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  • 10
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