Smell and taste in idiopathic blepharospasm.

The pathophysiology of blepharospasm is incompletely understood. Current concepts suggest that blepharospasm is a network disorder, involving basal ganglia, thalamus, cortex, and, possibly, the cerebellum. Tracing, imaging, and clinical studies revealed that these structures are also concerned with olfaction and taste. Because of this anatomical overlap, dysfunction of the chemical senses in blepharospasm is expected. Injections of botulinum toxin into the eyelid muscles are the first-line treatment of blepharospasm. Yet, the effects of botulinum toxin on the chemical senses have not been systematically assessed. To contribute to a better understanding of blepharospasm, olfactory and gustatory abilities were assessed in 17 subjects with blepharospasm and 17 age-/sex-matched healthy controls. Sniffin Sticks were used to assess odor threshold, odor discrimination, and odor identification. Results of these three Sniffin Sticks subtests were added to the composite olfactory score. The Taste Strips were applied to assess taste. In an adjacent study, we assessed the sense of smell and taste in eight subjects with blepharospasm before and 4 weeks after botulinum toxin treatment. Subjects with blepharospasm had significantly lower (= worse) scores for odor threshold and for the composite olfactory score than healthy controls, while odor discrimination, odor identification, and the composite taste score were not different between groups. The adjacent study revealed that botulinum toxin did not impact the chemical senses. In this study, subjects with blepharospasm had a lower (= worse) odor threshold than healthy controls. As olfaction is important in daily life, findings justify further research of olfaction in blepharospasm.

Olfaction as a Marker for Dystonia: Background, Current State and Directions.

Dystonia is a heterogeneous group of hyperkinetic movement disorders. The unifying descriptor of dystonia is the motor manifestation, characterized by continuous or intermittent contractions of muscles that cause abnormal movements and postures. Additionally, there are psychiatric, cognitive, and sensory alterations that are possible or putative non-motor manifestations of dystonia. The pathophysiology of dystonia is incompletely understood. A better understanding of dystonia pathophysiology is highly relevant in the amelioration of significant disability associated with motor and non-motor manifestations of dystonia. Recently, diminished olfaction was found to be a potential non-motor manifestation that may worsen the situation of subjects with dystonia. Yet, this finding may also shed light into dystonia pathophysiology and yield novel treatment options. This article aims to provide background information on dystonia and the current understanding of its pathophysiology, including the key structures involved, namely, the basal ganglia, cerebellum, and sensorimotor cortex. Additionally, involvement of these structures in the chemical senses are reviewed to provide an overview on how olfactory (and gustatory) deficits may occur in dystonia. Finally, we describe the present findings on altered chemical senses in dystonia and discuss directions of research on olfactory dysfunction as a marker in dystonia.

Smell and taste in cervical dystonia.

The pathophysiology of cervical dystonia is not completely understood. Current concepts of the pathophysiology propose that it is a network disorder involving the basal ganglia, cerebellum and sensorimotor cortex. These structures are primarily concerned with sensorimotor control but are also involved in non-motor functioning such as the processing of information related to the chemical senses. This overlap lets us hypothesize a link between cervical dystonia and altered sense of smell and taste. To prove this hypothesis and to contribute to the better understanding of cervical dystonia, we assessed olfactory and gustatory functioning in 40 adults with idiopathic cervical dystonia and 40 healthy controls. The Sniffin Sticks were used to assess odor threshold, discrimination and identification. Furthermore, the Taste Strips were applied to assess the combined taste score. Motor and non-motor deficits of cervical dystonia including neuropsychological and psychiatric alterations were assessed as cofactors for regression analyses. We found that cervical dystonia subjects had lower scores than healthy controls for odor threshold (5.8 ± 2.4 versus 8.0 ± 3.2; p = 0.001), odor identification (11.7 ± 2.3 versus 13.1 ± 1.3; p = 0.001) and the combined taste score (9.5 ± 2.2 versus 11.7 ± 2.7; p < 0.001), while no difference was found in odor discrimination (12.0 ± 2.5 versus 12.9 ± 1.8; p = 0.097). Regression analysis suggests that age is the main predictor for olfactory decline in subjects with cervical dystonia. Moreover, performance in the Montreal Cognitive Assessment is a predictor for gustatory decline in cervical dystonia subjects. Findings propose that cervical dystonia is associated with diminished olfactory and gustatory functioning.

Transcallosal inhibition in patients with and without alexithymia.

OBJECTIVE: Previous results indicated a facilitated transcallosal inhibition via the corpus callosum (CC) in alexithymic male students. This study investigates transcallosal inhibition in alexithymic and nonalexithymic psychiatric inpatients. METHOD: Transcallosal inhibition was elicited by means of transcranial magnetic stimulation (TMS) of the primary motor cortex. Seven right-handed male and 12 female psychiatric patients with Toronto Alexithymia Scale (TAS-20) scores of > or = 61 and 12 patients with TAS-20 scores of < 51 were investigated. The transcallosal conduction time (TCT) reflects the TMS-induced inhibitory cortical activity that is mediated via the CC. RESULTS: There was a significant effect of alexithymia on TCT (Wilks lambda = 0.76; F = 4.1; d.f. = 2, 26; p = 0.027) indicating that alexithymic patients had shorter bidirectional TCTs than nonalexithymic patients. The in-between models showed a significant impact of alexithymia on both right to left TCT (F = 4.8; d.f. = 1; p = 0.038) and left to right TCT (F = 5.0; d.f. = 1; p = 0.033). Neither gender nor scores of depression (Montgomery-Asberg Depression Rating Scale) had any significant effects on TCT. CONCLUSION: Our results confirm and extend the previous findings of a facilitated, bidirectional transcallosal inhibition in alexithymia to male and female psychiatric inpatients. Facilitated transcallosal inhibition should be considered as a neurobiological correlate of alexithymia.

Dissociation, hemispheric asymmetry, and dysfunction of hemispheric interaction: a transcranial magnetic stimulation approach.

The authors investigated the hypothesis that dissociation may represent a functional dysconnectivity syndrome using a transcranial magnetic stimulation (TMS) approach. Transcranial magnetic stimulation investigations that included motor thresholds and the transcallosal conduction time (TCT) reflecting the interhemispheric transfer were performed in 74 right-handed students. All subjects completed the Dissociative Experience Scale. The high dissociators had a significantly lower left hemispheric excitability than right hemispheric excitability. They also had a significantly shorter TCT from the left to the right hemisphere than did the low dissociators. These results suggest that the neural basis of dissociation may involve a cortical asymmetry with a left hemispheric superiority or, alternatively, a lack of right hemispheric integration.

Interhemispheric transfer in alexithymia: a transcallosal inhibition study.

OBJECTIVE: This study investigates the hypothesis that alexithymia is associated with an interhemispheric transfer deficit via the corpus callosum (CC). METHOD: The transcallosal inhibition paradigm was used to assess interhemispheric transfer. Transcranial magnetic stimulation (TMS) and peripheral electromyographic recordings were performed in 10 right-handed male and 10 female students with Toronto Alexithymia Scale (TAS-20) scores of > or = 61 and controls (TAS-20 scores of < 61). The transcallosal conduction time (TCT) reflects the TMS-induced inhibitory cortical activity that is mediated via the CC. RESULTS: There was a significant interaction between gender and alexithymia (Wilks lambda = 0.89; F = 3.4; d.f. = 2, 57; p = 0.04) indicating that alexithymic males had shorter bidirectional TCTs than controls and a significantly shorter left to right TCT than controls (p = 0.002). However, the left to right TCT was not significantly different from the right to left TCT in alexithymic males (p = 0.39). Alexithymic females were not different from controls. CONCLUSION: Our results clearly stand in contrast to the hypothesis of a transfer deficit due to a dysfunction of the CC in alexithymia. Facilitated, bidirectional transcallosal inhibition of the contralateral motor activity is associated with alexithymia in males. Facilitated cortical inhibition may be a neurobiological correlate of alexithymia.