Negative motor networks: Electric cortical stimulation and diffusion tensor imaging.

INTRODUCTION: This study investigated the networks of Negative motor areas (NMAs) using electric cortical stimulation and diffusion tensor imaging (DTI). METHODS: Twelve patients with intractable focal epilepsy, in which NMAs were identified by electrical cortical stimulation, were enrolled in this study. Electric stimulation at 50Hz was applied to the electrodes during motor tasks to identify the NMAs. DTI was used to identify the subcortical fibers originating from the NMAs found by electrical stimulation. RESULTS: NMAs were found in lateral frontal areas (premotor area (PM) and precentral gyrus) in all 12 patients, in pre-supplementary motor areas (pre-SMAs) in four patients, and in posterior parietal cortices (PPCs) in four. DTI detected fibers connecting to the ipsilateral PMs, PPCs and temporal regions via U-fibers, superior longitudinal fasciculus (SLF), and arcuate fasciculus (AF) from the lateral frontal NMAs. Pre-SMA-NMAs had connections with ipsilateral PMs and contralateral pre-SMAs via the frontal aslant tract and transcallosal commissural fibers, and PPC-NMAs with ipsilateral PMs via SLF and AF. CONCLUSION: This study found the characteristic cortical network of each NMA, and especially revealed new insight of pre-SMA-NMA and PPC NMA. These NMAs might be associated with different mechanism of negative motor response.

[Colony stimulating factor producing carcinoma of the pancreas--a case report].

Reported is the case of a 71-year-old male patient with a pancreatic carcinoma that showed marked leucocytosis of up to 71300/mm3. Tests revealed that the patient's granulocyte-colony stimulating factor (G-CSF) in serum was 0.65 ng/ml and 0.74 ng/ml in pleural effusion, these values almost triple the values of a normal control (0.20 in serum, 0.25 ng/ml in pleural effusion). These findings have indicated that the tumor itself was responsible for producing the inflated values of the granulocyte-colony stimulating factor. This case of a G-CSF-producing pancreatic carcinoma is discussed, along with a review of the pertinent literature.