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An Approach to Pupillary Disorders
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Sarosh M. Katrak, Azad M. Irani
The sympathetic nerve supply to the eye contains pupillary dilator fibers as well as vasomotor, sudomotor and vasodilator fibers to the face. Hence, in Horner syndrome (HS) there are pupillary as well as non-pupillary signs. The pupillary signs are anisocoria and ipsilateral miosis. Normally during deep sleep, there is miosis and when the subject is suddenly woken up – startle response – there is a reflex dilatation of the pupil in the first 5 seconds because of a sudden increase in sympathetic tone [4]. In HS, this startle response is also lost or there is delayed dilatation beyond 5 seconds (dilatation lag). The non-pupillary signs are ipsilateral subtle ptosis, due to weakness of the Muller's muscle, conjunctival congestion due to paresis of the vasomotor and anhidrosis through involvement of the sudomotor fibers. The latter will involve the full face in a preganglionic lesion. As the postganglionic sympathetic fibers “piggyback” with the nasociliary branch of the ophthalmic division of the trigeminal nerve within the orbit, a postganglionic lesion will produce anhidrosis only in the supraorbital area [1, 5]. Thus anhidrosis of only the supraorbital area of the face is an important pointer to a postganglionic lesion and is commonly associated with ICA dissection.
Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
The auditory startle response is a normal brainstem reflex characterized by closure of the eyes; flexion of the neck, trunk, arms; and variable lower limb manifestations. The response in healthy individuals normally habituates quickly on repetitive stimulation. In pathological startle syndromes, the response is exaggerated and does not habituate.
The effects of epilepsy and its treatments on affect and emotion
Published in Howard J. Rosen, Robert W. Levenson, Neurocase, 2020
John D. Hixson, Heidi E. Kirsch
In addition to basic fear conditioning, there is substantial evidence that the basic acoustic startle reflex is also deranged following ATL (Buchanan, Tranel, & Adolphs, 2004; Funayama, Grillon, Davis, & Phelps, 2001; Kettle, Andrewes, & Allen, 2006). In general, negatively valenced emotional stimuli are expected to result in a potentiated startle response, while positive stimuli create an overall attenuation (Buchanan et al., 2004). Using slightly different experimental methods, several studies have shown convincing evidence of an impaired startle response to negative stimuli in patients after ATL (Buchanan et al., 2004; Funayama et al., 2001; Kettle et al., 2006; Weike et al., 2005). While some groups found equal levels of impairment regardless of the side of surgery (Buchanan et al., 2004; Kettle et al., 2006), others suggest that right-sided surgery patients display failed startle responses to emotional imagery only (Funayama et al., 2001) while patients with left-sided lobectomies may exhibit impaired responses when there is a linguistic component to the affective stimulus. Although the effect of laterality has not been sorted out, these studies agree in their conclusion: an intact amygdala is critical to the basic startle reflex.
Variation in trauma-related behavioral effects using a preclinical rat model of three predator exposure stress
Published in Stress, 2022
Emily Scott, Matthew May, Gabriella Silva, Rachel Taylor, Nicole Fenlon, Emily Lowery-Gionta, Liana Matson
There were no group differences in SR behavior, though SR decreased from baseline at 24-h post-PE. The lack of significant startle response in the current study may be due to a numbing effect immediately after PE, which may be supported by the observation that SR decreased from baseline to 24-h in PE subjects. As prior pre-clinical and clinical literature identifies increased SR as a reliable effect of stress exposure, it is curious that this was not observed following PE in the current study. The lack of increased SR observations may be related to the fact that increased SR has generally been observed after exposure to more chronic traumatic stress in both animal models (Khan & Liberzon, 2004) and humans with PTSD (Holstein et al., 2010). Therefore, enhanced startle may not be an acute effect of traumatic stress, and thus is not able to be measured at the acute timepoints used in the current study.
Agmatine-attenuated cognitive and social deficits in subchronic MK-801 model of schizophrenia in rats
Published in Psychiatry and Clinical Psychopharmacology, 2018
Gokhan Unal, Alpay Ates, Feyza Aricioglu
The test procedure of PPI has been described in the previous literature [8]. Before the testing day, rats were put into the chambers and exposed to the background noise for 5 minutes and five startle stimuli for adaptation to apparatus and testing of startle function, respectively. On the test day, rats were placed in the chambers and exposed to 70 dB background noise for 5 minutes. Then, rats were exposed to three trial blocks. Block 1 consisted of five presentations of 40 ms 120 dB pulse trials. Block 2 was 40 pseudo-random trials (average inter-trial intervals of 15 s) which consisted of eight presentations of each prepulse + pulse trials (74, 78, 86 dB 20 ms duration and 100 ms before 40 ms 120 dB pulse), eight presentations of 120 dB pulse-alone, and eight presentations of no stimulus trials. Block 3 had five presentations of pulse trials. Startle response was defined as the average of 100 readings (1 ms interval) of the acoustic startle stimulus. Only Block 2 was taken into account for percent prepulse inhibition. The percent prepulse inhibition of startle response was calculated for each rat as per following formula: %PPI= 100 – (PP + P)/(P) × 100. “PP + P” and “P” means the startle response after the presentation of prepulse + pulse stimulus and pulse-alone stimulus, respectively. Average PPI was calculated by the following formula: Average PPI = [PPI (74 dB) + PPI (78 dB) + PPI (86 dB)]/3. Startle response to pulse-alone trials and basal activity in no stimulus trials were also measured in this study.
A-582941, cholinergic alpha 7 nicotinic receptor agonist, improved cognitive and negative symptoms of the sub-chronic MK-801 model of schizophrenia in rats
Published in Psychiatry and Clinical Psychopharmacology, 2018
The test procedure of PPI has been described in previous literature [20]. Briefly, before the testing day, rats were put in the chambers and exposed to a background noise for 5 min and five startle stimuli for adaptation to apparatus and for testing of hearing and startle function. On the test day, rats were placed in the chambers and exposed 70 dB of background noises for 5 min. After the acclimation period, rats were exposed to three trial blocks. Block 1 consisted of five presentations of 40 ms 120 dB pulse-alone trials. Block 2 had 50 pseudo-random trials (average intertrial intervals of 15s) which consisted of 10 presentations of each prepulse + pulse trials (74, 78, and 86 dB of 20 ms duration and 100 ms before 40 ms 120 dB pulse), 10 presentations of 120 dB pulse-alone and 10 presentations of no stimulus. Block 3 had five presentations of pulse-alone trials. Startle response was defined as the average of 100 readings collected every 1 ms beginning at the onset of the acoustic startle stimulus. Only Block 2 was taken into account for per cent prepulse inhibition. Per cent prepulse inhibition of startle response was calculated for each rat as per the following formula: