Abstract
Recent clinical data indicate that internal cueing mechanisms required for the triggering of movement sequences are impaired in Parkinson's disease (PD). Nevertheless, most PD subjects produce maximal syllable repetition rates similar to those observed in healthy control individuals during oral diadochokinesis tasks. There is some evidence that tremor oscillations may pace repetitive movements in Parkinsonians giving rise to hastening phenomena. Conceivably, the performance of PD patients in syllable repetition tasks thus reflects a specific timing deficit, i.e., articulatory hastening. It is the aim of the present study to investigate the contribution of speech hastening to oral diadochokinesis in the presence of internal anti external cues. By means of an optoelectric movement analysis system, the displacements of the lips during repetitions of the syllable /pa/ were recorded in two akinetic-rigid PD individuals. Subjects were asked to synchronize labial diadochokinesis to sequences of periodic acoustic stimuli (2.5-6 Hz). One of the PD patients showed speech hastening, i.e., he produced repetitions of 8 to 9 Hz whenever stimulus frequencies exceeded 4 Hz. The other Parkinsonian adequately matched the stimulus frequencies required. However, she achieved a higher diadochokinesis rate in the matching task than under the instruction to repeat 'as fast as possible.' Thus, the presence of an external cue improved performance. In conclusion, our data indicate two deficits of the temporal control of repetitive articulatory gestures in PD: speech hastening and impaired self-paced sequencing. These two pathomechanisms may allow to reconcile the controversial findings on oral diadochokinesis in PD reported so far.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 312-319 |
| Number of pages | 8 |
| Journal | Brain and Language |
| Volume | 56 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 1 1997 |
Bibliographical note
Funding Information:Recent clinical data indicate that internal cueing mechanisms required for the triggering of movement sequences are impaired in Parkinson’s disease (PD). Nevertheless, most PD subjects produce maximal syllable repetition rates similar to those observed in healthy control individuals during oral diadochokinesis tasks. There is some evidence that tremor oscillations may pace repetitive movements in Parkinso-nians giving rise to hastening phenomena. Conceivably, the performance of PD patients in syllable repetition tasks thus reflects a specific timing deficit, i.e., articulatory hastening. It is the aim of the present study to investigate the contribution of speech hastening to oral diadochokinesis in the presence of internal and external cues. By means of an optoelectric movement analysis system, the displacements of the lips during repetitions of the syllable /pa/ were recorded in two akinetic-rigid PD individuals. Subjects were asked to synchronize labial diadochokinesis to sequences of periodic acoustic stimuli (2.5–6 Hz). One of the PD patients showed speech hastening, i.e., he produced repetitions of 8 to 9 Hz whenever stimulus frequencies exceeded 4 Hz. The other Parkinsonian adequately matched the stimulus frequencies required. However, she achieved a higher diadochokinesis rate in the matching task than under the instruction to repeat ‘‘as fast as possible.’’ Thus, the presence of an external cue improved performance. In conclusion, our data indicate two deficits of the temporal control of repetitive articulatory gestures in PD: speech hastening and impaired self-paced sequencing. These two pathomechanisms may allow to reconcile the controversial findings on oral diadochokinesis in PD reported so far. 1997 Academic Press This study was supported by grants of the BMFT (01 KL9001 O) and the DFG (SFB 307, A3). The authors thank Prof. Dr. Johannes Dichgans and Dr. Sybille Spieker, Department of Neurology, University of Tübingen, for critical discussion and helpful comments. Address correspondence and reprint requests to Hermann Ackermann, M.D., M.A., Department of Neurology, University of Tübingen, Hoppe-Seyler-Str. 3, D-72076 Tübingen, Germany. 312