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Epilepsy Res.. 2 (1988) 127-131 Elsevier 127 ERS 00186 Short communication lctus emeticus and the insular cortex Miguel E. Fiol13’, 110E. Leppik’33, Ruy Mireles’,* and Robert Maxwell’34 ‘Comprehensive Epilepsy Program, University of Minnesota, ‘Abbott Northwestern Hospital, ‘Department of Neurology, University of Minnesota, 4Department of Neurosurgery, University of Minnesota, Minneapolis, MN (U.S.A.) (Received 1 July 1987; revised received 2 November 1987; accepted 10 November 1987) Key words: Complex partial seizures; Insular cortex; Emesis; Epilepsy surgery A 30-year-old man had a long history of seizures that began with feelings of tightness in his throat and fear, followed by projectile vomiting and head and eye deviation to the left. These episodes were not completely controlled by antiepileptic medications. Video EEG monitoring confirmed his clinical description. Corticography was performed before and after temporal lobectomy and revealed residual spikes in the unresectable tissue of the insula. Three years postoperatively he has had no seizures with vomiting but has occa- sional ‘auras’ of throat tightening and fear. The case suggests that the insula may be a trigger area for emesis but requires anterior-me- sial temporal cortex for completion. INTRODUCTION Much of the functional anatomy of the human brain has been elucidated by studies of persons with epilepsy’. Vomiting is a complex phenome- non which usually arises from topographically dis- tinct areas of the medulla: the lateral reticular for- mation (vomiting center) and the floor of the fourth ventricle (area postrema)‘,9. However, in- volvement of cortical areas may occur as demon- strated by some cases of ictus emeticus2,4.“,11. This paper reports pre- and postoperative find- ings from a patient with intractable partial sei- zures, in which projectile vomiting was prominent. * Dr. Mireles is the recipient of the John Hughings Jackson Clinical Research Fellowship of the Epilepsy Foundation of America. Supported in part by NIH Grant P50-NS16308. Correspondence to: Miguel E. Fiol, M.D., Comprehensive Epilepsy Program. Suite 106, 2701 University Avenue S.E.. Minneapolis, MN 55414, U.S.A. The findings suggest that the insula has a role in triggering vomiting. CASE REPORT A 30-year-old, right-handed, white male was ad- mitted for evaluation and treatment of intractable epilepsy. His seizures began at age 7. Initial at- tacks were described as ‘staring.’ Later they be- came more frequent and began to include projec- tile vomiting. There was no family history of epilepsy, episodic vomiting, migraines or recur- ring abdominal pain. The etiology of his seizures remains unknown. He gave the following description of his seizures: aura of ‘tightness in the throat’ and ‘feeling of fear’ followed by vomiting, head and eye deviation to the left, stiffening of the left arm, and occasional rotation or turning to the left. Sometimes these were followed by unresponsiveness and occa- sionally evolved to generalized tonic-clonic sei- 0920-12111881$03.SO 0 1988 Elsevier Science Publishers B.V. (Biomedical Division)

Ictus emeticus and the insular cortex

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Page 1: Ictus emeticus and the insular cortex

Epilepsy Res.. 2 (1988) 127-131

Elsevier

127

ERS 00186

Short communication

lctus emeticus and the insular cortex

Miguel E. Fiol13’, 110 E. Leppik’33, Ruy Mireles’,* and Robert Maxwell’34

‘Comprehensive Epilepsy Program, University of Minnesota, ‘Abbott Northwestern Hospital,

‘Department of Neurology, University of Minnesota, 4Department of Neurosurgery,

University of Minnesota, Minneapolis, MN (U.S.A.)

(Received 1 July 1987; revised received 2 November 1987; accepted 10 November 1987)

Key words: Complex partial seizures; Insular cortex; Emesis; Epilepsy surgery

A 30-year-old man had a long history of seizures that began with feelings of tightness in his throat and fear, followed by projectile

vomiting and head and eye deviation to the left. These episodes were not completely controlled by antiepileptic medications. Video

EEG monitoring confirmed his clinical description. Corticography was performed before and after temporal lobectomy and revealed

residual spikes in the unresectable tissue of the insula. Three years postoperatively he has had no seizures with vomiting but has occa-

sional ‘auras’ of throat tightening and fear. The case suggests that the insula may be a trigger area for emesis but requires anterior-me-

sial temporal cortex for completion.

INTRODUCTION

Much of the functional anatomy of the human brain has been elucidated by studies of persons with epilepsy’. Vomiting is a complex phenome- non which usually arises from topographically dis- tinct areas of the medulla: the lateral reticular for- mation (vomiting center) and the floor of the fourth ventricle (area postrema)‘,9. However, in- volvement of cortical areas may occur as demon- strated by some cases of ictus emeticus2,4.“,11.

This paper reports pre- and postoperative find- ings from a patient with intractable partial sei- zures, in which projectile vomiting was prominent.

* Dr. Mireles is the recipient of the John Hughings Jackson

Clinical Research Fellowship of the Epilepsy Foundation of

America. Supported in part by NIH Grant P50-NS16308.

Correspondence to: Miguel E. Fiol, M.D., Comprehensive

Epilepsy Program. Suite 106, 2701 University Avenue S.E..

Minneapolis, MN 55414, U.S.A.

The findings suggest that the insula has a role in triggering vomiting.

CASE REPORT

A 30-year-old, right-handed, white male was ad- mitted for evaluation and treatment of intractable epilepsy. His seizures began at age 7. Initial at- tacks were described as ‘staring.’ Later they be- came more frequent and began to include projec- tile vomiting. There was no family history of epilepsy, episodic vomiting, migraines or recur- ring abdominal pain. The etiology of his seizures remains unknown.

He gave the following description of his seizures: aura of ‘tightness in the throat’ and ‘feeling of fear’ followed by vomiting, head and eye deviation to the left, stiffening of the left arm, and occasional rotation or turning to the left. Sometimes these were followed by unresponsiveness and occa- sionally evolved to generalized tonic-clonic sei-

0920-12111881$03.SO 0 1988 Elsevier Science Publishers B.V. (Biomedical Division)

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zures. Occasionally seizures consisted of vomiting only. Their frequency varied from several/day to l/week.

Phenytoin, primidone, valproate and carbama- zepine only partially relieved the attacks. On ad- mission, he was taking 1000 mg of carbamazepine, with a steady-state plasma concentration of 11.2 @g/ml. Physical as well as complete neurological examinations were unremarkable as were labora- tory data and an enhanced and unenhanced CT scan.

Neuropsychologicai studies

The WAIS verbal IQ was 98, performance IQ was 108, and full-scale IQ 103. Wechsler Memory Scale rating was 101. Score on the Porteus Mazes was 111. There was no evidence of an acute or fo- cal language disorder. Subtle left-sided problems in tactile motor coordination were present. Visuo- constructional testing showed mild impairment. There was evidence for a recent memory disorder, non-specific in nature, and mild deficit in acquisi- tion and retention of both verbal and figural mate- rial. Neuropsychological testing indicated mild im- pairment of both mesiotemporal areas, perhaps greater on the right, in the non-dominant hemi- sphere.

Electroencephalographic data (EEG) A number of characteristic interictal and ictal

events were recorded with multiple, 25-channel split-screen video-EEG and radio telemetry recordings utilizing standard surface and sphenoi- da1 electrodes”.

Interictal activity consisted of intermittent spikes recorded from the right sphenoidal and an- terior temporal electrode (F8). Drug activation studies (intravenous pentobarbita13 and diaze- pam) showed symmetrical ‘pentobarbital-induced beta activity’ and there was no significant effect on spike frequency or distribution.

Ten seizures were recorded on video telemetry: the ‘aura’ was stereotyped and consisted of a chok- ing sensation in the throat, fear, shortness of breath, followed by sudden, projectile vomiting during which he did not lose consciousness and was able to seek assistance. This was followed by clonic movements of the left lower face and the

periocular muscle, and head deviation to the left. This was frequently followed by deviation of the torso to the left, generalized body stiffening and. on one occasion, by a generalized tonic-clonic sei- zure. The ictal EEG consisted of rhythmic theta slowing, which started in the right temporal elec- trodes (SP2, F8, T4) during 6 of the 10 attacks. During 2 seizures, diffuse rhythmic slowing was recorded over the right hemisphere, and in the re- maining two, bilateral slow activity without focal onset was observed.

Because his seizures were intractable to antiepi- leptic drugs, a right temporal lobectomy was rec- ommended. Prior to surgery, an intracarotid sodi- um amytal test (WADA) was done. Findings from this test were consistent with left hemisphere dom- inance for speech and language function. Verbal memory appeared to be mediated exclusively through the left temporal region.

A 6 cm en bloc right temporal lobectomy was per- formed. Electrocorticography was obtained using

lctus Emeticus

Pre-resection Electrocorticography

* =SDikes

Fig. 1. Lateral and ventral views of brain showing location of

spikes prior to temporal lobectomy.

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129

lctus Emeticus

Post-resection Electrocorticography

Fig. 2. After right temporal lobectomy, exposed insula and sur-

rounding areas revealed residual spikes. Vomiting stopped, but

simple partial seizure (aura) persisted.

standard Grass electrode recordings from the ex- posed brain. In addition, a 4-electrode-contact- point silastic strip was utilized to record from me- siotemporal and subfrontal areas.

Preresection corticography revealed multiple areas of independent spiking in the frontotempo- ral cortex (Fig. 1).

Postresection corticography (Fig. 2) showed spikes from the anterior and posterior insula as well as from the edge of the sylvian fissure at the foot of the rolandic strip. This spike activity was si- multaneous from these regions (Fig. 3), but ap- peared to originate in the insular cortex. There were no residual spikes at the stump of the hippo- campus or the temporal lobe. No further resection was attempted. Pathological examination of the tissue showed multiple areas of significant satelli- tosis and gliosis.

For over 3 years after surgery he has not had any seizures involving vomiting. However, ‘auras’ of

Fig. 3. Electrocorticographic tracing after right temporal lobectomy reveals spikes mainly in insular cortex (channels 4,5) with some in

surrounding rolandic cortex.

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130

fear and a choking sensation have persisted and occur a few times each month. These no longer progress to projectile vomiting, facial motor sei- zures, head deviation, or generalized tonic-clonic seizures. They do not interfere with any of his ac- tivities.

DISCUSSION

Vomiting as a manifestation of seizures has been reported rarely. Mulder et al.5 in a review of 100 cases of ‘visceral epilepsy’ found only 9 people in whom vomiting was a prominent feature of the sei- zure. Jacome and Fitzgerald* described one such person in whom attacks of vomiting were asso- ciated with generalized epileptiform discharges during seizures and with multifocal interictal ab- normalities.

Vomiting is a highly integrated, complex phe- nomenon that involves contraction of respiratory muscles, diaphragmatic descent, atony of the stomach, inhibition of cardiac sphincter and expul- sion of stomach content. These phenomena origi- nate in 2 functionally different and topographical- ly distinct areas of the medulla: the lateral ret- icular formation (vomiting center) and the floor of the fourth ventricle (area postrema) - chemore- ceptor trigger zone. The former area is responsive to multiple stimuli arising in the gastrointestinal tract, heart, kidneys and uterus and transmitted by the vagus. The chemoreceptor trigger zone is sen- sitive to emetic chemicals and acts on the vomiting center which coordinates the various components of the vomiting act’. The cortex also influences the vomiting center and several areas have been impli- cated.

Transient vomiting has been reported after sur- gical ablation of the inferior and superior frontal as

REFERENCES

1 Berk, E.J., Bockus Gastroenterology, 4th Edn., Saunders, Philadelphia, PA, 1985.

2 Jacome, D.E. and Fitzgerald, R., Ictus emeticus, Neurol- ogy, 32 (1982) 209-121.

3 Lombroso, C.T. and Erba, G.E., Primary and secondary bilateral synchrony in epilepsy, Arch. Neural., 22 (1970) 321-333.

well as of the cingulate gyrus in man’. These pro- cedures were done to relieve severe psychotic be- havior prior to the advent of pharmacotherapy, when psychosurgery was an accepted method of treatment. Intraoperative cortical stimulation of these areas was not obtained to verify whether this observation was due to the ablation or to postoper- ative changes. Penfield and Faulk” reported changes in gastric motility recorded by the electro- gastrograph in 4 of 6 patients during stimulation of the insular cortex. They were able to induce either inhibition or augmentation of gastric motility. Un- pleasant sensations have also been elicited by elec- trical stimulation of this area. In some of these people vomiting was induced. Other areas of the brain which have been associated with changes in gastric tone are the uncus and pes hippocampus”. In addition, animal studies have revealed that many regions of the brain influence GI motility. e.g., orbital cortex, cingulum, amygdala and pre- motor area*. These human and animal studies in- dicate that there are several cortical areas that can influence the vomiting center in the medulla.

In this patient, temporal lobectomy abolished all but the aura of tightness of the throat, which al- most always preceded more fully developed clini- cal seizure including vomiting. This may be related to the postoperative residual spike activity in the region of the insula.

Our case provides some evidence that the insular cortex may act as a trigger to the vomiting center, probably by a pathway involving anterior and me- sial temporal structures.

ACKNOWLEDGEMENT

Dr. Fernando Torres provided the ECoG data.

4 Millichap, J.G., Lombroso, C.T. and Lennox. W.G., Cy- clic vomiting as a form of epilepsy in children, Pediatrics, 1s

(1955) 705-714. 5 Mulder, D.W., Daly, D. and Bailey, A.A.. Visceral

epilepsy, Arch. Intern. Med., 4 (1954) 93. 6 Penfield, W. and Faulk, M.E., The insula: further observa-

tions on its function, Brain, 78 (1955) 445-470.

7 Penfield, W. and Jasper, H.H., Epilepsy and the Functional Anatomy offhe Human Brain, Little, Brown and Company,

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Boston, MA, 1954. electrodes in electrographic study of patients with temporal

8 Perle, T.L., The Neuroanatomic Basis of Clinical Neurol- lobe epilepsy; an evaluation, J. Neurosurg., 18 (1961) ogy, McGraw-Hill, New York, 1961. 151-158.

9 Pool, J.L., The visceral brain of man, J. Neurosurg., 11 11 Van Buren, J.M., Buckman, C.A. and Pritchard, W.L., (1954) 45-63. Autonomic representation in the human orbito-temporal

10 Rovit, R.L., Gloor. P. and Rasmussen, T., Sphenoidal cortex, Neurology, 11 (1961) 214-224.