Journal of veterinary internal medicine · 2013
Sensory nerve conduction and somatosensory evoked potentials of the trigeminal nerve in horses with idiopathic headshaking.
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Aleman M, Williams D C, Brosnan R J, Nieto J E, Pickles K J, Berger J, Lecouteur R A, Holliday T A, Madigan J E
Аннотация
BACKGROUND: Idiopathic headshaking (HSK) in horses is a distressing disorder in which the etiology and pathophysiology are unknown.
HYPOTHESIS: Differences in sensory function of the trigeminal nerve exist between healthy and affected horses.
ANIMALS: Six healthy mature geldings and 6 mature geldings with idiopathic HSK.
METHODS: Prospective study. Sensory nerve action and somatosensory evoked potentials studies were performed. The stimulus site comprised the gingival mucosa dorsal to the maxillary canine. A pair of recording electrodes was placed along the sensory pathway of the trigeminal complex at the infraorbital nerve (R1), maxillary nerve (R2), spinal tract of trigeminal (R3), and somatosensory cortex (R4). Sensory nerve action potential latency (ms), amplitude (μV), duration (ms), area under the curve (μVms), and conduction velocity (m/s) were calculated.
RESULTS: Threshold for activation of the infraorbital branch of the trigeminal nerve was significantly different between 5 affected (≤ 5 mA) and 6 control horses (≥ 10 mA). After initiation of an action potential, there were no differences in all parameters measured and no differences between left and right sides. A horse with seasonal HSK tested during a time of no clinical manifestations showed a threshold for activation similar to control horses.
CONCLUSIONS AND CLINICAL IMPORTANCE: This study confirms involvement of the trigeminal nerve hyperexcitability in the pathophysiology of disease. Further, results might support a functional rather than a structural alteration in the sensory pathway of the trigeminal complex that can be seasonal. The horse could serve as a natural animal model for humans with idiopathic trigeminal neuralgia.
HYPOTHESIS: Differences in sensory function of the trigeminal nerve exist between healthy and affected horses.
ANIMALS: Six healthy mature geldings and 6 mature geldings with idiopathic HSK.
METHODS: Prospective study. Sensory nerve action and somatosensory evoked potentials studies were performed. The stimulus site comprised the gingival mucosa dorsal to the maxillary canine. A pair of recording electrodes was placed along the sensory pathway of the trigeminal complex at the infraorbital nerve (R1), maxillary nerve (R2), spinal tract of trigeminal (R3), and somatosensory cortex (R4). Sensory nerve action potential latency (ms), amplitude (μV), duration (ms), area under the curve (μVms), and conduction velocity (m/s) were calculated.
RESULTS: Threshold for activation of the infraorbital branch of the trigeminal nerve was significantly different between 5 affected (≤ 5 mA) and 6 control horses (≥ 10 mA). After initiation of an action potential, there were no differences in all parameters measured and no differences between left and right sides. A horse with seasonal HSK tested during a time of no clinical manifestations showed a threshold for activation similar to control horses.
CONCLUSIONS AND CLINICAL IMPORTANCE: This study confirms involvement of the trigeminal nerve hyperexcitability in the pathophysiology of disease. Further, results might support a functional rather than a structural alteration in the sensory pathway of the trigeminal complex that can be seasonal. The horse could serve as a natural animal model for humans with idiopathic trigeminal neuralgia.