Cortical Neuron Loss in Post-Traumatic Higher Brain Dysfunction Using 123I-Iomazenil SPECT
In patients with higher brain dysfunction (HBD) after mild traumatic brain injury (MTBI), diagnostic imaging of cortical neuron loss in the frontal lobes was studied using SPECT with 123I-iomazenil (IMZ), as a radioligand for central benzodiazepine recept
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Abstract In patients with higher brain dysfunction (HBD) after mild traumatic brain injury (MTBI), diagnostic imaging of cortical neuron loss in the frontal lobes was studied using SPECT with 123I-iomazenil (IMZ), as a radioligand for central benzodiazepine receptor (BZR). Statistical imaging analysis using three-dimensional stereotactic surface projections (3D-SSP) for 123I-IMZ SPECT was performed in 17 patients. In all patients with HBD defined by neuropsychological tests, cortical neuron loss was indicated in the bilateral medial frontal lobes in 14 patients (83 %). A comparison between the group of 17 patients and the normal database demonstrated common areas of cortical neuron loss in the bilateral medial frontal lobes involving the medial frontal gyrus (MFG) and the anterior cingulate gyrus (ACG). In an assessment of cortical neuron loss in the frontal medial cortex using the stereotactic extraction estimation (SEE) method (level 3), significant cortical neuron loss was observed within bilateral MFG in 9 patients and unilateral MFG in 4, and bilateral ACG in 12 and unilateral ACG in 3. Fourteen patients showed significant cortical neuron loss in bilateral MFG or ACG. In patients with MTBI, HBD seemed to correlate with selective cortical neuron loss within the bilateral MFG or ACG where the responsible lesion could be. 3D-SSP and SEE level 3 analysis for 123I-IMZ SPECT could be valuable for diagnostic imaging of HBD after MTBI. Keywords Post-traumatic higher brain dysfunction • Cortical neuron loss • I-iomazenil (IMZ) SPECT • 3D stereotactic surface projections • Stereotactic extraction estimation
J. Nakagawara (*), K. Kamiyama, M. Takahashi, and H. Nakamura Department of Neurosurgery, Nakamura Memorial Hospital, South-1, West-14, Chuo-ku, Sapporo 060-8570, Japan e-mail: [email protected]; [email protected]; [email protected]; [email protected]
Introduction It is still unknown that post-traumatic higher brain dysfunction (HBD) [1] could be induced by mild traumatic brain injury (MTBI) associated with no or mild unconsciousness (Japan Coma Scale [JCS] 1–3) at the time of brain injury [2]. Structural neuroimaging such as CT or MRI could be insufficient for obtaining significant findings concerning HBD. However, the recent development of diffusion tensor imaging could show diffuse axonal injury (DAI) in white matter such as the corpus callosum or internal capsule in patients with MTBI [3], defined as unconsciousness within 0–20 min and mild Glasgow Coma Scale (GCS) score (13–15) [4]. Traumatic injury of the corpus callosum could be assumed to be the main cause of post-traumatic HBD; the presence of unconsciousness at the time of brain injury might not be a necessary factor in certifying the diagnosis of posttraumatic HBD. We then investigated a focal lesion using 123I-iomazenil (IMZ) SPECT, which provides an indicator of cortical neuron damage in patients with post-traumatic HBD after MTBI and consists of cognitive impairment such as memory, attention, performance, and social behavio
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