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Presurgical evaluation in many epilepsy programmes often includes the intracarotid amobarbital procedure (IAP). Sodium amytal is injected into the internal carotid artery to produce a temporary “pharmacological paralysis” of hemispheric function. Traditionally, the IAP has been employed in patients with refractory temporal lobe epilepsy being considered for anterior temporal lobectomy. In these cases it is used to determine cerebral dominance for language,1 to assess the risk of severe postsurgical amnesia,2 and to predict postsurgical material specific memory changes.3 More recently, the use of the IAP has been extended to compliment EEG localisation and radiological data by lateralising temporal lobe dysfunction.4
The IAP may have a hitherto unrecognised role in patients with refractory frontal lobe epilepsy being considered for frontal lobectomy. Specifically, observation of behavioural function during the period of the ablation may provide useful information about the integrity of the contralateral frontal lobe. This is particularly relevant in those candidates with a history of cerebral trauma in whom damage to the bifrontal lobe is known or suspected. A review of the IAP studies performed on patients with temporal lobe epilepsy in our comprehensive epilepsy programme (1991–8) suggests that the emergence of frontal lobe behavioural features is common in patients in whom the aetiology leads to the suspicion of bifrontal compromise (for example, a history of traumatic head injury). By contrast, these features rarely emerge in cases of non-traumatic aetiology, in which the integrity of frontal lobe systems is presumed. Although it remains an incidental finding in the context of determining the suitability of a candidate for anterior temporal lobectomy, this outcome may have potential implications for the selection of patients for frontal lobectomy.
We report a case of frontal lobe epilepsy secondary to a traumatic head injury. Out of concern for untoward postoperative behavioural change, we employed the IAP in an attempt to predict the risk of a frontal lobe syndrome.
A 39 year old man had a 23 year history of severe refractory epilepsy. The seizures postdated a motor car accident at the age of 12 years when he sustained a head injury with an ill defined period of loss of consciousness. Seizures commenced within months of that injury and, although initially well controlled, became refractory within a few years. The seizure types included staring spells, violent tonic-clonic seizures, and atonic drop attacks. He had complications from his epilepsy including a fractured jaw, two episodes of severe burning due to seizures while showering, multiple episodes of postictal confusion and probable postictal psychosis, a lung abscess secondary to aspiration, and episodes of status epilepticus. Interictal EEG recordings showed bilateral generalised spike and wave discharges at around 2 Hz-2.5 Hz with some mild increase in bilateral slow activity and no convincing evidence of electrographic focalisation. Video EEG monitoring showed apparent generalised seizures without any focal onset on scalp EEG. Brain MRI disclosed a well defined atrophic lesion involving the left frontal pole considered likely to be post-traumatic in origin. Interictal FDG PET and HMPO SPECT disclosed hypoperfusion in the left anterior frontal region commensurate with the abnormality shown on MRI. Although his electroclinical pattern was suggestive of symptomatic generalised epilepsy, because of the left frontal lesion, seizure onset from that region was considered likely.
On neuropsychological examination, his general cognitive function was normal. At a behavioural level, however, he presented as very peurile in manner with a very rigid, inflexible cognitive style. The neuropsychological opinion was of a mild frontal lobe syndrome consistent with the history of traumatic head injury. There was no current evidence of psychiatric disorder. Although having successfully passed his final year of secondary school (together with several courses of advanced education), he had remained unemployed due to his seizures. He was socially isolated and his interpersonal relationships were limited.
He had severe life threatening epilepsy with the surgical option the only remaining avenue of treatment. However, as surgical management would involve resection of the left frontal lobe against a background of traumatic head injury and the possibility of more generalised frontal lobe compromise, a left hemispheric IAP was performed. Sodium amytal (125 mg) was administered via a slow hand injection. Of relevance, no crossflow into the contralateral anterior cerebral artery via the anterior communicating artery was present (as assessed by a separate injection of contrast medium). The injection was accompanied by a dense right hemiplegia and global aphasic arrest. Resolution of language was characterised by a dense perseveration of counting which could not be influenced by the examiner. Despite normal comprehension, he showed severely impaired capacity for motor regulation (go-no go paradigm), together with marked behavioural disinhibition (agitation, swearing, verbosity, childishness). Although seemingly aware of some aspects of his behaviour (apologising for swearing), he seemed unable to modify his responses. The overall impression was of a pronounced frontal lobe syndrome, suggesting that the right frontal lobe had incurred some damage secondary to the documented head trauma and that he must have been reliant on some left frontal contribution.
On the basis of the IAP findings, a selective cortical resection (as opposed to more extensive frontal lobectomy) restricted to the region of damage was advised. Intraoperative electrocorticography showed active focal epileptiform discharges maximal in the inferior frontal lobe in the electrodes closest to the lesion. A cortical resection was performed with frameless stereotaxy guidance excision of the frontal lesion. Histopathology on the resected tissue showed an old post-traumatic cyst involving the cortex and white matter. His postoperative course was unremarkable. When reviewed 3 months after surgery he was seizure free. His performance on neuropsychological evaluation remained commensurate with presurgical status. There were no novel subjective complaints. Mood, behaviour, and temperament remained stable.
Despite its undoubted value in many individual cases of temporal lobe epilepsy, the IAP has remained a controversial assessment instrument.5 Amid this controversy its potential usefulness in other patient groups seems to have been overlooked. A primary criticism of its use in temporal lobe epilepsy has been the question of irrigation and whether the medial temporal lobe is adequately “disabled” during the procedure. This particular limitation is not applicable when used in the patient with frontal lobe epilepsy, as the region of interest is clearly ablated via supply from the carotid arterial system. Caution must, however, be exercised with respect to possible crossflow into the contralateral anterior cerebral artery via the anterior communicating artery. When such crossflow is present, the ability to assess validly the integrity of contralateral frontal lobe function will be confounded by virtue of a pharmacologically induced bilateral frontal lobe syndrome. As with the use in cases of temporal lobe epilepsy, only a restricted form of assessment is possible with the frontal lobe patient during the period of ablation. An assessment focusing on issues of behavioural regulation would seem most useful.
It should be borne in mind that the degree of frontal lobe dysfunction induced by the IAP represents the “worst case scenario” as the entire frontal lobe is included in the ablation. There are likely to be few surgical scenarios in which a comparable extensive resection of tissue is likely to be considered, and results must be interpreted in this context. This limitation not withstanding, the IAP does seem to have a role in separating out those patients in whom more extensive frontal lobe resections could be considered as opposed to those in whom a more conservative approach is warranted.
This case report forms only the basis for a novel hypothesis that clearly requires more rigorous scientific research before its clinical utility can be reliably established. Nonetheless, we think that it is worth drawing the attention of the epileptological community to the potential application of the IAP in the surgical management of extratemporal cases.
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