Spinal hyperexcitability and bladder hyperreflexia during reversible frontal cortical inactivation induced by low-frequency electrical stimulation in the cat.
Spinal hyperexcitability and hyperreflexia gradually develop in the majority of stroke patients. These pathologies develop as a result of reduced cortical modulation of spinal reflexes, mediated largely indirectly via relays in the brainstem and other subcortical structures. Cortical control of spinal reflexes is markedly different in small animals, such as rodents, while in some larger species, such as cats, it is more comparable to that in humans. In this study, we developed a novel model of stroke in the cat, with controllable and reversible inhibition of cortical neuronal activity appearing approximately 1h after initiation of low-frequency electrical stimulation in the frontal cerebral cortex, evidenced by a large increase in the alpha frequency band (7-14 Hz) of the frontal electrocorticographic signal. Hyperreflexia of the urinary bladder developed 3h or more after induction of reversible cortical inactivation with optimized stimulation parameters (frequency of 1-2 Hz, amplitude of 10 mA, applied for 30 min). The bladder hyperreflexia persisted for at least 8h, and disappeared within 24h. At the S2 level of the spinal cord, where neural circuits mediating micturition and other pelvic reflexes reside, we have recorded an increase in neuronal activity correlated with the development of hyperreflexia. The low-frequency stimulation-induced reversible cortical inactivation model of stroke is highly reproducible and allows evaluation of spinal hyperexcitability and hyperreflexia using within-animal comparisons across experimental conditions, which can be of great value in examination of mechanisms of spinal hyperreflexia following stroke or brain trauma, and for developing more effective treatments for these conditions.
Pikov
Victor
V
Neural Engineering Program, Huntington Medical Research Institutes, Pasadena, CA 91105, USA. pikov@hotmail.com
McCreery
Douglas B
DB
D000818:Animals; D020211:Autonomic Dysreflexia / Q000209:etiology / Q000503:physiopathology; D002415:Cats; D004195:Disease Models, Animal; D004525:Efferent Pathways / Q000503:physiopathology; D004558:Electric Stimulation / Q000009:adverse effects / Q000379:methods; D004569:Electroencephalography; D005071:Evoked Potentials / Q000502:physiology; D005625:Frontal Lobe / Q000033:anatomy & histology / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology; D015203:Reproducibility of Results; D013116:Spinal Cord / Q000033:anatomy & histology / Q000503:physiopathology*; D020521:Stroke / Q000150:complications / Q000503:physiopathology*; D001743:Urinary Bladder / Q000294:innervation / Q000503:physiopathology; D001750:Urinary Bladder, Neurogenic / Q000209:etiology / Q000503:physiopathology*; D014554:Urination / Q000502:physiology