Seizures are thought to arise primarily from the cerebral cortex. However, the propagation and behavioral manifestations of seizures involve a network of both cortical and subcortical structures. The medial thalamus and upper brainstem reticular formation are crucial areas for the maintenance of normal consciousness. Bilateral involvement of these structures may be responsible for loss of consciousness during partial seizures. Therefore, we sought to investigate the role of the medial thalamus and brainstem in seizures. We performed SPECT ictal-interictal difference imaging co-registered with high-resolution MRI scans to localize regions of cerebral blood flow changes in patients undergoing inpatient monitoring for epilepsy. Ictal-interictal SPECT scans from 43 seizures in 40 patients were analyzed. The medial thalami showed SPECT difference imaging changes of >20% in 18 patients. Of patients with medial thalamic changes, the majority (13 of 18) had seizure onset in the temporal lobe, while only 1 had confirmed onset in extratemporal structures, and the remainder were non-localized. In contrast, in the 22 patients without >20% SPECT changes in the medial thalami, 6 had extratemporal onset, 6 had temporal onset, and the remainder were non-localized. In patients with temporal lobe seizures, the side of greater medial thalamic and brainstem reticular formation involvement was strongly related to SPECT injection timing such that there was a sequential pattern of ipsilateral followed by contralateral changes. Brainstem structures showed >20% SPECT changes in 27 of 43 seizures with no clear relation to temporal or extratemporal onset. We conclude that the medial thalamus is preferentially involved in seizures arising from the temporal lobes, possibly reflecting the strong connections between limbic temporal structures and the medial thalamus. Sequential involvement of ipsilateral followed by contralateral structures in the medial thalamus and upper brainstem may explain how seizures produce peri-ictal loss of consciousness despite incomplete involvement of the cerebral cortex.
| Identifer | oai:union.ndltd.org:YALE_med/oai:ymtdl.med.yale.edu:etd-02112003-133913 |
| Date | 11 February 2003 |
| Creators | Norden, Andrew D. |
| Contributors | Hal Blumenfeld |
| Publisher | Yale University |
| Source Sets | Yale Medical student MD Thesis |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://ymtdl.med.yale.edu/theses/available/etd-02112003-133913/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to Yale School of Medicine or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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