Oromandibular dystonia, mental distress and oro-facial dysfunction-A follow-up 8-10 years after start of treatment with botulinum toxin.

BACKGROUND: Oromandibular dystonia (OMD) with involuntary jaw and tongue movements may be misdiagnosed as temporomandibular disorders (TMD) and because of the complex muscle activity and involvement of several small muscles, OMD is also considered difficult to treat. OBJECTIVES: The aim was to evaluate OMD in patients 8-10 years after start of treatment with botulinum toxin (BoNT) by self-reported and standardised global scales and questionnaires. METHODS: Of 21 previously reported patients with OMD, 14 responded to a mail health questionnaire to describe the disease course and treatment effect as well as the overall impact of OMD by a visual analogue scale (VAS), the Patient Health Questionnaire (PHQ) for depression and anxiety, and the Jaw Functional Limitation Scale (JFLS). The results were analysed with non-parametric statistical analysis (Wilcoxon matched-pairs test and Spearman's rank-order correlations). RESULTS: The OMD was still present in 13 patients. In nine patients, the BoNT treatment had continued as monotherapy or combined with oral medication. VAS for OMD was significantly reduced (P < 0.04) over the years, and most patients felt improvement from the treatment. However, the patients had still some functional limitations, typically regarding jaw mobility and communication, and both JFLS and mental distress (PHQ) were significantly correlated with the OMD VAS (rS 0.77 and 0.74). CONCLUSION: The results showed marked reduction of the experienced OMD with treatment and over time, and also stressed similarities between OMD and TMD. Both dentists and neurologists should be aware of this overlap and reduce misdiagnosis by applying an interdisciplinary approach.

Interdisciplinary recognizing and managing of drug-induced tardive oromandibular dystonia: two case reports.

Tardive dystonia is a risk factor in medical antipsychotic treatment. It often begins with repetitive involuntary jaw and tongue movements resulting in impaired chewing and detrimental effect on the dentition. The orofacial dysfunction may go unrecognized in a neurological setting. The diagnosis may be difficult so we suggest interdisciplinary collaboration.

Sensorimotor gating deficits in multiple system atrophy: comparison with Parkinson's disease and idiopathic REM sleep behavior disorder.

BACKGROUND: Prepulse inhibition (PPI) of the auditory blink reflex is a measure of sensorimotor gating, which reflects an organism's ability to filter out irrelevant sensory information. PPI has never been studied in patients with multiple system atrophy (MSA), although sensorimotor deficits are frequently associated with synucleinopathies. We investigated whether alterations in PPI were more pronounced in MSA compared with Parkinson's disease (PD), idiopathic rapid eye movement sleep behavior disorder (iRBD) and healthy controls. METHODS: 10 patients with MSA, 12 patients with iRBD, 40 patients with PD, and 20 healthy controls completed the study. A passive acoustic prepulse inhibition paradigm was applied with prepulses 5 dB and 15 dB above background noise at 30-, 60-, 120- and 300-ms intervals. RESULTS: Non-parametric analyses showed that MSA patients had significantly lower prepulse inhibition, as measured with max-amplitude, than PD patients and iRBD patients on the 60 ms-85 dB and 120 ms-85 dB inter-stimulus intervals. The same relation was found when using area under the curve. No differences were found between groups for the 30 ms-85 dB and 300 ms-85 dB. Furthermore, blink reflex characteristics such as habituation did not differ between patients and controls. CONCLUSIONS: The present study showed that sensorimotor gating, as measured with PPI, is markedly reduced in MSA. This may be due to the pronounced severity of striatal and brainstem dysfunction, as well as the degeneration of other structures related to the PPI modulating pathways in MSA. PPI may be a non-invasive neurophysiological measure that can aid in the differential diagnosis between PD and MSA.