technetium-tc-99m-exametazime has been researched along with Neuralgia* in 2 studies
2 other study(ies) available for technetium-tc-99m-exametazime and Neuralgia
| Article | Year |
|---|---|
Concurrent activation of the somatosensory forebrain and deactivation of periaqueductal gray associated with diabetes-induced neuropathic pain.
We combined behavioral testing with brain imaging using (99m)Tc-HMPAO (Amersham Health) to identify CNS structures reflecting alterations in pain perception in the streptozotocin (STZ) model of type I diabetes. We induced diabetic hyperglycemia (blood glucose >300 mg/dl) by injecting male Sprague-Dawley rats with STZ (45 mg/kg i.p.). Four weeks after STZ-diabetic rats exhibited behaviors indicative of neuropathic pain (hypersensitivity thermal stimuli) and this hypersensitivity persisted for up to 6 weeks. Imaging data in STZ-diabetic rats revealed significant increases in the activation of brain regions involved in pain processing after 6 weeks duration of diabetes. These regions included secondary somatosensory cortex, ventrobasal thalamic nuclei and the basolateral amygdala. In contrast, the activation in habenular nuclei and the midbrain periaqueductal gray were markedly decreased in STZ rats. These data suggest that pain in diabetic neuropathy may be due in part to hyperactivity in somatosensory structures coupled with a concurrent deactivation of structures mediating antinociception. Topics: Amygdala; Animals; Behavior, Animal; Brain; Cerebrovascular Circulation; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Habenula; Hyperglycemia; Male; Neuralgia; Periaqueductal Gray; Prosencephalon; Radiopharmaceuticals; Rats; Rats, Sprague-Dawley; Reaction Time; Somatosensory Cortex; Technetium Tc 99m Exametazime; Thalamic Nuclei | 2007 |
The role of cortex in central pain syndromes: preliminary results of a long-term technetium-99 hexamethylpropyleneamineoxime single photon emission computed tomography study.
The role of the somatosensory cortex in central pain syndromes is widely questioned. Two recent position emission tomography studies detected a strong activation of the parietal and cingular cortices after brief nociceptive stimuli. On the other hand, a recent single photon emission computed tomography study found no cortical activation in five patients affected by central poststroke pain and algodystrophia. In this study, we present the single photon emission computed tomography findings in five patients suffering from central pain syndromes. Two of these, one with facial postrhizotomy anesthesia dolorosa and the other with central poststroke pain, showed a decrease of blood flow in the parietal lobe, further decreasing after stimulation by nonpainful maneuvers. Our results suggest that somatosensory cortical areas might be involved in the generation of anomalous pain states in some cases of central pain syndromes. Topics: Adult; Aged; Aged, 80 and over; Brain Damage, Chronic; Cerebral Cortex; Female; Humans; Male; Middle Aged; Neural Inhibition; Neuralgia; Organotechnetium Compounds; Oximes; Pain Measurement; Somatosensory Cortex; Technetium Tc 99m Exametazime; Tomography, Emission-Computed, Single-Photon | 1993 |