Blink reflexes are usually considered the most representative and consistent response of the auditory startle reaction (ASR), and they are often the only response evaluated in human psychophysiological studies. However, auditory stimuli also induce an auditory blink reflex (ABR), the physiological characteristics and brainstem circuitry of which may be different from those of the ASR. This study aimed to investigate whether there were differences between the orbicularis oculi (OOc) responses elicited with the ABR (OOcABR) and those elicited with the ASR (OOcASR) regarding their behavior to prepulse modulation. For comparison, we also examined the OOc responses to supraorbital nerve stimulation (OOcEBR). Electromyographic responses were simultaneously recorded from the OOc, masseter (MAS) and sternocleidomastoid (SCM) muscles. ABRs were considered when auditory stimuli induced responses limited to the OOc, and ASRs were considered when responses were induced in all muscles recorded from. Prepulse stimuli were either a weak electrical stimulation at the third finger (somatosensory prepulse) or a weak acoustic tone (auditory prepulse) that preceded the response-eliciting stimuli by intervals ranging from 0 to 200 ms. Prepulse effects differed according to prepulse modality, but the OOcABR and the OOcASR were always modulated in the same way. In both responses, somatosensory prepulses induced facilitation from 20 to 50 ms, followed by inhibition beyond 75 ms, and auditory prepulses induced no facilitation but a significant inhibition beyond 30 ms. In the OOcEBR, both somatosensory and acoustic prepulses induced facilitation of R1 and inhibition of R2 beyond 30 ms. Our results suggest that the OOcABR and the OOcASR exhibit the same physiological behavior regarding prepulse modulation. It is hypothesized that prepulse facilitation is due to direct impingement of subthreshold excitatory inputs onto the facial motoneurons while prepulse inhibition results from the engagement of a presynaptic inhibitory circuit in the brainstem.

We report nine patients who developed dystonia following head trauma. The most frequent form was hemidystonia only (six patients). One patient presented with hemidystonia plus torticollis, one with bilateral hemidystonia and one with torticollis only. Seven patients sustained a severe head injury, and two had a mild head injury. At the time of injury, six were younger than 10 years, two were adolescents, and the patient with torticollis only was an adult. Except in the patient with torticollis only, the onset of dystonia varied considerably from months to years. All patients with hemidystonia had posthemiplegic dystonia of delayed onset. Seven out of 8 patients with hemidystonia had lesions involving the contralateral caudate or putamen, as demonstrated by CT and MR. The patient with hemidystonia plus torticollis had no lesion to the basal ganglia, but a contralateral pontomesencephalic lesion. Response to medical treatment was generally poor. Functional stereotactic operations were performed in seven patients. A variety of factors may be responsible for the vascular or nonvascular posttraumatic basal ganglia lesions, which may lead to dystonia. The pathophysiology seems to be more complex than thought previously. We believe that dystonia following head injury is not as rare as is assumed. Awareness of its characteristics and optimized diagnostic procedures will lead to wider recognition of this entity.

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We investigated cognitive and behavioral changes after unilateral posteroventral pallidotomy, and their relationship with lesion size and location as identified in magnetic resonance image quantitative analysis. Fifteen consecutive patients with Parkinson's disease were assessed neuropsychologically before and after unilateral posteroventral pallidotomy (five right and 10 left). Immediate postsurgery evaluation (1 week) demonstrated significant worsening of memory, motor learning, motor speed, and verbal fluency. In the 3‐month follow up, learning, memory, and speed returned to the presurgical level, but verbal fluency remained below the baseline. Significant improvements were observed in visuospatial functions and obsessive‐compulsive behavior. Lesional volume did not correlate with neuropsychologic changes. Left lesions produced more impairment in verbal fluency than right‐sided lesions. Regression analysis identified two lesional areas in the pallidum mediale internum. These regions accounted for 68% of the variance in the visuospatial changes.