Online ISSN : 1687-8329

    




Quick Search 
 
Author  
Year    
Title  
Vol:  

 
 
April2013 Vol.50 Issue:      2 Table of Contents
Full Text
PDF


Effect of Verbal Auditory Cues on Cortical Motor Excitability in Parkinson’s disease: Evidence from Motor Evoked Potential

Noha A. Sawy1, Enas M. Shahine1, Ghada A. Achmawi 2

Departments of Physical Medicine, Rheumatology and Rehabilitation1;

Neurology and Psychiatry2; Alexandria University; Egypt



ABSTRACT

Background: Parkinson's disease (PD) patients rely on external cues to guide movements. Objective: To study the effect of verbal auditory cues on cortical motor excitability of PD patients. Methods: The study included 17 PD patients and 15 controls. Motor evoked potentials (MEP) were recorded from abductor pollicis brevis muscle at baseline, following repetitive rhythmic thumb abduction-adduction at preferred speed and with verbal cues. Number of Repetitive movement cycles (RMC), resting motor threshold (RMT), central motor conduction time (CMCT), MEP amplitude ratio and cortical silent period (CSP) duration were measured. Results: At baseline, PD patients had significantly higher MEP amplitude ratio and shorter CSP mean duration than controls. At their preferred speed, PD patients had significantly lower RMC compared to controls (p =0.005) and compared to baseline, they had significantly lower RMT, prolonged CMCT and increased CSP mean duration. With verbal cues, both PD patients and controls could increase significantly RMC (p =0.000, 0.028 respectively). Following verbal cues, none of MEP parameters has changed significantly among patients compared to controls and compared to performance without cues. Conclusion: PD patients have significant cortical hyperexcitability than normal subjects. Performing a repetitive motor task with or without verbal auditory cues may normalize cortical excitability level in PD patients. [Egypt J Neurol Psychiat Neurosurg.  2013; 50(2): 199-204]

 Key Words: Parkinson’s disease, verbal auditory cues, cortical motor excitability, motor evoked potential.

Correspondence to Ghada A. Achmawi, Department of Neurology, Faculty of Medicine, Alexandria University; Egypt.Tel.: +201005786379   e-mail:  dr.ghadaabdelhadi@yahoo.com.





INTRODUCTION

 

Parkinson’s disease (PD) is a neurodegenerative disorder in which the major pathological characteristic is the marked loss of the dopaminergic neurons in substantia nigra pars compacta.1 This leads to a marked deficiency of dopamine content in the striatum thus impending directly onto the motor circuit.2 Normally, the basal ganglia (BG) are involved in movement selection3 which entails the facilitation of intended, desired motor programs and the suppression of competing ones4, the sequencing of a series of movements5, and the production of memorized movements.6

The motor circuit is composed of several subcircuits which project to the output of the BG and has two pathways; direct and indirect. The direct pathway has a facilitatory influence upon the motor cortex, while the indirect pathway exerts an inhibitory effect on the thalamocortical projections.7 Thus, BG serve as an internal non-specific cue to trigger movement.8 In PD, dopaminergic depletion disrupts both the internal balance

of BG and the corticostriatal balance because of the hypoactive direct and overactive indirect pathways with subsequent excessive inhibition of the thalamocortical and brain stem motor nuclei.2 The overall effect is excessive inhibitory influence upon the motor cortex with the cardinal motor features of PD including bradykinesia, akinesia, hypokinesia9, rigidity and tremors at rest. These motor deficits lead to difficulties in initiating and performing complex sequential and repetitive movements.10 One of the specific features of movement deficits in PD is the reliance on external visual and auditory11 cues to guide and correct movements. These externally guided movements utilize the cerebellum-parietal lobe-lateral premotor cortex pathway as a compensatory strategy bypassing the defective BG- supplementary motor area pathway.12 It was assumed that providing verbal cues during performing a repetitive hand movement in PD patients would alter the cortical motor excitability and hence this might reveal one of the mechanisms by which the external cues can improve function.

The aim of this work was to study the effect of verbal auditory cues on cortical motor excitability (CE) of PD patients using transcranial magnetic stimulation (TMS). Study design: case-control cross sectional study.

SUBJECTS AND METHODS

 

Seventeen IPD (idiopathic Parkinson disease) patients were included in this study. Their age range was 30-72 years (52.0±11.6). They were diagnosed according to the UK Parkinson’s disease Society Brain Bank clinical diagnostic criteria of IPD.13 Their disease duration ranged from one to eleven years (4.0±3.0). They were nine men and eight women. Nine patients had more affected right upper limb, while the left one was more affected in eight patients (according to the motor section (part III) of Unified Parkinson's disease rating scale).14 Patients with the following were excluded: PD plus, musculoskeletal disorders of the hand, any associated neuromuscular/neurological disorder, any contra-indications to TMS and medications which may influence cortical excitability. The study was performed after at least 12 hours withdrawal of the antiparkinsonian drugs. The study included 15 age and sex-matched healthy control subjects (eight men and seven women). Their age range was 38- 60 years (48.3±9.1). 

The study was approved by the Local Ethics Committee and was explained to the participants and an informed consent was given by each one. Each patient was subjected to the following: full clinical examination, determination of the clinical motor staging of PD by Hoehn Yahr Motor scale to assess disease severity15 and electrophysiological evaluation. The most affected side of the patients and the dominant side of controls (All were right-handed by self report) were tested according to the following protocol; (1) Standard nerve conduction study for median nerve including F-wave16, (2) Baseline assessment using single pulse TMS and motor evoked potentials (MEP) were recorded from abductor policies brevis (APB) muscle using surface recording electrodes and conventional electromyographic apparatus (Nihon Kohden, Neuropack 2, Japan) according to standard methods.17

Magnetic stimulation was performed using “Magstim 200” equipped with a high power, 9 cm diameter, circular coil capable of generating 2-tesla maximum field intensity (Nova Metrix Inc.) The resting motor threshold (RMT) was determined. Then the stimulus intensity was set at 20% above threshold value. The procedure was performed while the patient was doing mild voluntary contraction of APB muscle. Three reproducible cortical MEPs were elicited and superimposed. MEP was considered absent if a response could not be obtained after 3 successive discharges with maximum output (100% intensity).17

The shortest MEP onset latency which represents the cortical latency (CL) in milliseconds (ms). Then the central motor conduction time (CMCT) was calculated by the following equation: CL – peripheral latency (PL) (PL= minimal F wave latency in ms + M wave latency in ms – 1) ÷ 2.17

MEP maximum peak to peak amplitude in millivolts (mV). Amplitude of MEP was expressed as ratio of M-wave amplitude of the APB muscle. The cortical silent period (CSP) was elicited with an intensity of 120% RMT during maximal tonic voluntary contraction of the APB muscle.18 The level of the contraction was controlled by audio-visual EMG feedback. Four trials were recorded, and the mean CSP duration was calculated. The onset of CSP was measured from the MEP offset to the first return of any volitional EMG activity. Cortical excitability was determined by MEP RMT and amplitude as well as CSP.19

While the participants were sitting in a chair with their tested arm on the armrest, shoulder was positioned at 0˚ flexion, elbow at 90˚ flexion, and forearm is fully supinated, they were asked to do repetitive rhythmic abduction-adduction movements of the thumb of the tested hand at their preferred speed for a period of 30 seconds and the number of cycles was counted and divided by 30 to calculate the movement frequency in Hz.20 

The electrophysiological testing using TMS was immediately performed after the task. The participants were verbally instructed to do the same task “as fast as possible” as an auditory cue (throughout the task) for a period of 10 seconds20 and the number of cycles was counted for each subject and frequency was calculated. The electrophysiological testing using TMS was immediately performed after the task.

 

Statistical Analysis

Data were analyzed using SPSS version 17. Data were summarized using descriptive statistics: mean ± standard deviation (±SD). Change in number of repetitive movement cycles (RMC), MEP variables and CSP duration were calculated by dividing the difference between post-auditory cues value and pre-cues value over pre-cues value. Wilcoxon test was used for intra-group comparisons. Mann-Whitney test was used for comparison between patient and control groups. Correlation between variables was examined by Spearman’s test.  A probability value (p value) ≤ 0.05 was considered statistically significant.

 

RESULTS

 

All the patients and controls completed the study. None of the participants reported any adverse events. Parkinson’s disease severity ranged from 2 to 4 (2.8±0.6).

In repetitive movement cycles (RMC), at their preferred speed, PD patients had significantly slower RMC frequency than controls (0.77±0.21 Hz for patients versus 1.26±0.34 Hz for controls; p =0.005) (Table 1). With auditory cues; PD patients and controls increased significantly frequency of RMC (1.18±0.19 Hz (p=0.000) and 1.61±0.25 (p =0.028) respectively), as seen in Table (1). However, the frequency of RMC was significantly higher in controls (p =0.002). The change in RMC was not significantly different between PD patient and control groups (0.63±0.49 and 0.32±0.27 respectively; p =0.195).

As regards the motor evoked potentials, the baseline assessment revealed that PD patients had significantly higher mean MEP amplitude ratio than controls (0.39 ±0.18 and 0.19±0.02 respectively; p =0.009), as seen in table 1. When PD patients did the task at their preferred speed, RMT lowered and CMCT prolonged significantly (p=0.04 and 0.05 respectively) compared to baseline (Table 2), while controls demonstrated lowered RMT, prolonged CMCT and increased MEP amplitude ratio but did not reach statistical significant level (Table 3). Following auditory cues; patients’ CMCT did not change significantly (p =0.49) as shown in Table (2), while it shortened significantly in controls (p =0.04)as shown table 3. Change in CMCT was significantly larger in control group compared to patients (20.8±16.3 and -6.2±19.0 respectively; p =0.006). Accordingly, auditory cues may not influence significantly central conductivity in PD patients (in contrast to controls). Following auditory cues; RMT and amplitude ratio did not change significantly for either patients or controls (Tables 2 and 3).

            At baseline assessment, Cortical silent period (CSP) mean duration was significantly shorter in patients than controls (p =0.01); table 1. When patients performed repetitive movements at their preferred speed, CSP mean duration lengthened significantly (p =0.01) (Table 2). Performing this task did not affect significantly CSP mean duration in controls (p =0.90); table 3. There was no significant difference between precues CSP duration among PD patients and controls (109.2±20.3 and 116.0±33.9 respectively; p =0.221). Following auditory cues, there was insignificant lengthening of CSP duration among patients compared to precues value (p =0.233). However, this lengthening was significant when compared to baseline value (p =0.04); table 2. Control group showed a significant lengthening of CSP duration following cues compared to precues (p =0.001) (Table 3). Again, there was no significant difference between postcues CSP duration among PD patients and controls (p =0.10) (Table 1).

In PD patients, neither the frequency of RMC with or without verbal auditory cues nor change of RMC frequency correlated with any of MEP variables. In controls, the frequency of RMC without verbal cues correlated positively with baseline CSP mean duration (r = 0.962, p =0.009) while the frequency of RMC with verbal auditory cues correlated negatively with postcues CMCT (r = -0.809, p =0.05).


 

Table 1. Comparison between PD patients and control group regarding MEP parameters, cortical silent period and repetitive movement cycles at baseline, precues and postcues. (Mann–Whitney test).

 

 

PD Patient (17)

Min- max

Mean±SD

Control (15)

Min- max

Mean±SD

Z

p

RMT (%) (baseline)

30-56

39.8±9.2

35-55

43.1±7.5

-1.127

0.260

CMCT (ms) (baseline)

4.2-11.2

7.9±1.5

6.9-9.1

7.7±0.92

-0.455

0.649

Amp ratio (mV) (baseline)

0.07-0.69

0.39±0.18

0.17-0.23

0.19±0.02

-2.59

0.009*

CSP (ms) (baseline)

45.6-135.6

97.5±25.2

51.2-174.0

120.9±34.8

-2.396

0.017*

RMC (Hz) (baseline)

0.43-1.23

0.77±0.21

0.87-1.70

1.26±0.34

-2.805

0.005*

RMT (%) (precues)

29-56

38.5±9.1

35-55

42.1±7.0

-1.164

0.244

CMCT  (ms) (precues)

4.8-12.4

8.3±2.0

7.5-9.6

8.1±0.77

-0.140

0.889

Amp ratio (mV) (precues)

0.09-0.84

0.35±0.20

0.13-0.60

0.27±0.17

-0.947

0.344

CSP (ms) (precues)

59.0-140.3

109.2±20.3

55.0-166.0

116.0±33.9

-1.225

0.221

RMC (Hz) (with cues)

0.80-1.53

1.18±0.196

1.33-2.07

1.61±0.25

-3.132

0.002*

RMT (%) (postcues)

29-56

38.0±8.8

35-50

41.3±5.3

-1.265

0.206

CMCT  (ms) (postcues)

5.0-11.4

8.6±1.6

4.2-8.0

6.5±1.5

-2.346

0.019*

Amp ratio (mV) (postcues)

0.13-0.66

0.38±0.14

0.11-0.70

0.29±0.21

1.617

0.106

CSP (ms) (postcues)

57.7-155.6

115.8±24.5

67.2-166.0

126.7±31.2

-1.605

0.108

Amp amplitude, CMCT central motor conduction time, CSP cortical silent period, RMC repetitive movement cycles, RMT resting motor threshold

*Statistically significant at P>0.05

Table 2. Comparison between baseline, precues and postcues MEP variables in PD patients. (Wilcoxon test).

 

 

PD Patient (17)

Min- max

Mean±SD

(baseline)

PD Patient (17)

Min- max

Mean±SD

(precues)

PD Patient (17)

Min- max

Mean±SD

(postcues)

Z             p1

(baseline) - (precues)

Z              p2

(precues) - (postcues)

RMT

(%)

30-56

39.8± 9.2

29-56

38.5±9.1

29-56

38.0±8.8

-2.025           0.043*

-1.186         0.236

CMCT

(ms)

4.2-11.2

7.9±1.5

4.8-12.4

8.3±2.0

5.0-11.4

8.6±1.6

-1.921          0.055

-0.687          0.492

Amp ratio (mV)

0.07-0.69

0.39±0.18

0.09-0.84

0.35±0.20

0.13-0.66

0.38±0.14

-0.877             0.381

-0.379           0.705

CSP

(ms)

45.6-135.6

97.5±25.2

59.0-140.3

109.2±20.3

57.7-155.6

115.8±24.5

-2.379           0.017*

-1.533         0.125

Amp amplitude, CMCT central motor conduction time, CSP cortical silent period, RMT resting motor threshold

*Statistically significant at P>0.05

 

Table 3. Comparison between baseline, precues and postcues MEP variables in control group. (Wilcoxon test).

 

 

Control (15)

Min- max

Mean± SD

(baseline)

Control (15)

Min- max

Mean±SD

(precues)

Control (15)

Min- max

Mean±SD

(postcues)

Z               p1

(baseline) -  (precues)

Z                p2

(precues) - (postcues)

RMT (%)

35-55

43.1±7.5

35-55

42.1±7.0

35-50

41.3±5.3

-0.816             0.414

-1.000         0.317

CMCT (ms)

6.9-9.1

7.7±0.92

7.5-9.6

8.1±0.77

4.2-8.0

6.5±1.5

-1.054            0.292

-1.992       0.046*

Amp ratio (mV)

0.17-0.23

0.19±0.02

0.13- 0.60

0.27±0.17

0.11-0.70

0.29±0.21

-0.674              0.500

-0.524         0.600

CSP (ms)

51.2-174.0

120.9±34.8

55.0 – 166.0

116.0±33.9

67.2-166.0

126.7±31.2

-0.126              0.900

-3.178       0.001**

Amp amplitude, CMCT central motor conduction time, CSP cortical silent period, RMT resting motor threshold

*Statistically significant at P>0.05 **Statistically significant at P>0.01

 


DISCUSSION

 

This work was carried out to study the effect of verbal cues on CE in PD patients and its impact on the performance of a selected repetitive motor task done by the more affected side.  In the baseline assessment, PD patients had features consistent with increased CE manifested by significant higher MEP amplitude ratio, shorter CSP and lower RMT compared to controls. Increased MEP amplitude in PD may be attributed to an excessive corticospinal output at rest, repetitive firing of motor neurons or increased spinal disinhibition.21 Reduced inhibition of the motor cortex is the most consistent abnormality reported among TMS studies examining CE in PD.22 In PD, CSP shortening was interpreted by deficient GABA transmission with reduction in the facilitatory effect of the transthalamic motor circuit upon the motor cortices secondary to defective dopamine modulation.23 Decreased RMT in PD patients has the same implications as MEP amplitude and signifies increased corticospinal excitability.

As regards the task performance without auditory cues, the reduced movement frequency in PD patients may be related to impaired cortical plasticity which is an important feature in PD. Disturbance of the surround inhibition due to loss of cortical inhibitory mechanisms in PD, leads to recruitment of unspecific motor programs and impairment of focusing on the neuronal elements involved in the intended movement leading to akinesia and bradykinesia.23 Simple repetitive motor task induced a non significant increase of CE in controls and a general tendency to decrease CE in PD patients compared to baseline. The task seemed to normalize the CE of PD patients. In PD it is assumed that the increased cortical inhibition was an attempt by the residual nigrostriatal projections to facilitate movement execution by facilitating transmission by the direct pathway and inhibiting transmission by the indirect pathway.24 Modulation of CE took place in both groups to cope with the task performance through two opposing mechanisms probably because of the difference in the premovement setting of CE of both groups. The main finding of a study performed by Pascual-Leone and colleagues was that the beginning of a change in excitability started quickly, but that it took a longer time to build up the excitability enough to trigger the movement.25 As the frequency is related to the temporal aspect of movement, therefore, the successive delays in movement initiation, execution, and muscle activation can account for the decreased movement frequency in PD. Accordingly, in the current study, the magnitude of the postmovement CE, quantified by MEP and CSP seemed to be independent of the temporal aspect of movement.

In the present study, using verbal cues led to increase movement frequency significantly. It may be plausible to consider the verbal auditory cues employed in this study as one of the attentional cueing strategies mediated by hearing. Attentional strategies may allow movement to be mediated by less automatic and more conscious motor control processes which may be less impaired by BG dysfunction, and thereby improve movement performance in PD.26 The tasks guided by attentional strategies as verbal instructions activates the ipsilateral cerebellum through the cerebello-dentato-thalamocortical circuits to control movements and activate predomi­nantly the preprogrammed strategies.27 However, PD patients showed significantly slower postcues RMC frequency compared to controls. This slowing may be attributed to central causes related to subtle changes in lateral premotor cortex and motor thalamus (both mediating the cued movements).28

In controls, there was tendency to cortical inhibition in response to verbal instruction. In an fMRI study performed by Sadato and colleagues, they stated that a faster movement which is accompanied by more afferent feedback might intensify lateral inhibition, causing a decrease in the activated area of the primary motor cortex.29 Therefore, the resulting excessive inhibition may account for the prolonged CSP duration in controls. In PD patients, there was no significant difference between pre- and post cues CE, suggesting a negligible role of the employed cues in modulating the CE or probably the abnormal presetting of the baseline CE might  operate and cancel the modulating effect of the cues. There was no significant difference of the postcues CE between patients and controls. The postcues CE of both groups had also a similar profile compared to the precues state suggesting that verbal cues had similar underlying mechanisms in modulating CE in both groups. Nevertheless, the lack of significant postcues prolongation of CSP in PD may be attributed to the relatively hyperactive cerebellum in PD patients compared to controls to compensate for the deficit BG with subsequent robust inhibition of the cerebellothalamocortical pathway and hence the decreased intracotrical inhibition.30 The lack of significant correlations between the movement frequency and post movement CE parameters suggests that the latter is not a major determinant of movement speed.

It can be concluded that in quiescent state, cortical hyperexcitability is characteristic for PD patients. On doing a simple repetitive movement at preferred speed, their CE tended to decrease compared to baseline. Moreover, on doing the task as fast as possible using verbal instructions, there was no significant difference between PD patients and controls CE. Therefore, this simple task normalizes CE. It is recommended to study a larger patients sample to validate these results and to assess the time course of CE changes during performing the same experimental setting to allow monitoring of quantitative and qualitative CE changes.

 

[Disclosure: Authors report no conflict of interest]

 

REFERENCES

 

1.        Lukhanina EP, Kapustina MT, Berezetskaya NM, Karaban I. Reduction of the postexcitatory cortical inhibition upon paired-clicka uditory stimulation in patients with Parkinson’s disease. Clin Neurophysiol. 2009; 120: 1852-8.

2.        Obeso JA, Rodriguez-Oroz MC, Benitez-Temino B, Blesa FJ, Guridi J, Marin C, et al. Functional organization of the basal ganglia: therapeutic implications for Parkinson’s disease. Mov Disord. 2008; 23 Suppl 3: S548-59.

3.        Jeuptner M Frith CD, Brooks DJ, Frackowiak RS, Passingham RE .Anatomy of motor learning. II. Subcortical structures and learning by trials and error. J Neurophysiol. 1997; 77: 1325-37.

4.        Groenewegen HJ. The Basal Ganglia and Motor Control. Neural Plast. 2003; 10: 107-20.

5.        Boecker H, Dagher A, Ceballos-Baumann AO, Passingham RE, Samuel M, Friston KJ, et al: Role of the human rostral supplementary motor area and the basal ganglia in motor sequence control: investigations with H2 15O PET. J Neurophysiol. 1998; 79: 1070-80.

6.        Mushiake H, Strick PL. Pallidal neuron activity during sequential arm movements. J Neurophysiol. 1995; 74:2754-8.

7.        Delong MR, Wichmann T. Circuits and circuit disorders of the basal ganglia. Arch Neurol. 2007; 64: 20-4.

8.        Georgiou N, Iansik R, Bradshaw JL, Phillips JG, Mattingley JB, Bradshaw JA. An evaluation of the role of internal cues in the pathogenesis of parkinsonian hypokinesia. Brain. 1993,116 (pt 6): 1575-87.

9.        Berardelli A, Rothwell JC, Thompson PD, Hallett M. Pathophysiology of bradykinesia in Parkinson’s disease. Brain. 2001; 124:2131-46.

10.     Chuma T, Faruque Reza M, Ikoma K, Mano Y. Motor learning of hands with auditory cue in patients with Parkinson’s disease. J Neural Transm. 2006; 113:175-85.

11.     McIntosh GC, Brown SH, Rice RR, Thaut MH. Rhythmic auditory-motor facilitation of gait patterns in patients with Parkinson’s disease. J Neurol Neurosurg Psych. 1997; 62: 22-6.

12.     Cunnington C, Iansek R, Bradshaw J, Phillips JG. Movement-related potentials in Parkinson’s disease. Presence and predictability of temporal and spatial cues. Brain. 1995; 118: 935-50.

13.     Hughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry. 1992; 55:181-4.

14.     Fisher BE, Wu AD, Salem GJ, Song J, Lin CH, Yip J, et al. The effect of exercise training in improving motor performance and corticomotor excitability in people with early parkinson's disease. Arch Phys Med Rehabil. 2008; 89: 1221-9.

15.     Hoehn MM, Yahr MD. Parkinsonism: onset, progression and mortality. Neurology. 1967; 17: 427-42.

16.     Weber R. Motor and sensory conduction and entrapment syndromes. In: Johnson EW, editor. Practical electromyography. 2nd ed. Baltimore: Williams & Wilkins; 1988. pp. 92-186.

17.     Hallett M, Rossini PM, Paulus W, Eisen A. Magnetic stimulation: motor evoked potentials. In: Deuschi G, Eisen A, editors: Recommendations for the practice of clinical neurophysiology: guidelines of the international federation of clinical physiology. Amesterdam: Elsevier; 1999. pp. 171-85.

18.     Ahonen JP, Jehkonen M, Dastidar P, Molnar G, Hakkinen V. Cortical silent period evoked by transcranial magnetic stimulation in ischemic stroke. Electroenceph Clin Neurophysiol. 1998; 109: 224-9.

19.     Säisänen L, Pirinen E, Teitti S, Könönen M, Julkunen P, Määttä S, et al. Factors influencing cortical silent period: Optimized stimulus location, intensity and muscle contraction. J Neurosci Methods. 2008; 169: 231-8.

20.     Del Olmo MF, Bello O, Cudeiro J. Transcranial magnetic stimulation over dorsolateral prefrontal cortex in Parkinson’s disease. Clin Neurophysiol. 2007; 118: 131-9.

21.     Cantallo R, Gianelli M, Bettucci D, Civardi C, De Angelis MS, Mutani R. Parkinson’s disease rigidity. Magnetic motor evoked potentials in a small hand muscle. Neurology. 1991; 41: 1449-56.

22.     Fisher BE, Wu AD, Salem GJ, Song J, Lin CH, Yip J, et al. The effect of exercise training in improving motor performance and corticomotor excitability in people with early Parkinson’s disease. Arch Phys Med Rehabil. 2008; 89: 1221-9.

23.     Lefaucheur JP. Motor cortex dysfunction revealed by cortical excitability studies in Parkinson’s disease: influence of antiparkinsonian treatment and cortical stimulation. Clin Neurophysiol. 2005; 116:244-53.

24.     Obeso JA, LanciegJL. Past, present, and future of the pathophysiological model of the basal ganglia. Front Neuroanat. 2011; 5:2-6.

25.     Pascual-Leone A, Valls-Solé J, Brasil-Neto J, Cohen LG, Hallett M. Akinesia in Parkinson’s disease. I. Shortening of simple reaction time with focal, single-pulse transcranial magnetic stimulation. Neurology. 1994; 44:884-91.

26.     Cunnington R, Iansek R, Bradshaw JL. Movement-related potentials in Parkinson's disease: external cues and attentional strategies. Mov Disord. 1999; 14: 63-8.

27.     Spencer RM, Zelaznik HN, Diedrichsen J, Ivry RB. Disrupted timing of discontinuous but not continuous movements by cerebellar lesions. Science. 2003; 300: 1437-9.

28.     Galvan A, Wichmann T. Pathophysiology of Parkinsonism. Neurophysiol. 2008; 119: 1459-74.

29.     Sadato N, Ibanez V, Campbell G, Deiber MP, Bihan DL, Hallett M. Frequency-Dependent Changes of Regional Cerebral Blood Flow During Finger Movements: Functional MRI Compared to PET. J Cereb Blood Flow Metab. 1997; 17: 670-9.

30.     Yu H, Sternad D, Corcos DM, Vaillancourt DE. Role of hyperactive cerebellum and motor cortex in Parkinson’s disease. Neuroimag. 2007; 35: 222-33.


 

الملخص العربى

 

تأثير المنبهات السمعية على استثارة القشرية  المخية الحركية في مرض  باركنسون ذاتى العلة

 أدلة من الجهد الحركى المستحث

 

المقدمة: يعتمد مرضي مرض  باركنسون ذاتى العلة على الإشارات الخارجية لتوجيه الحركات. الهدف: دراسة  تأثير المنبهات السمعية على استثارة القشرية  المخية الحركية في مرض  باركنسون ذاتى العلة. أشخاص البحث وطرق البحث: اشتملت الدراسة على 17 مريضا باركنسون ذاتى العلة و 15  شخصا كضوابط.  تم تسجيل الجهد الحركى المستحث من عضلة المبعدة القصيرة لإبهام اليد  في الأساس، وبعد تكرار التجربة الإيقاعية ابعاد-التقريب بالسرعة المفضلة ومع تأثير المنبهات السمعية. تم قياس عدد تكرار دورات الحركة، ومقدار المستهل الحركي، وقت التوصيل الحركى المركزي، نسبة السعة وفترة صمت القشرة المخية. النتائج: في الأساس كانت نسبة السعة  فى الجهد الحركى المستحث  لمرضى باركنسون ذاتى العلة أعلى بكثير وأقصر  في فترة صمت القشرة المخية بالمقارنة مع الضوابط. مع تطبيق السرعة المفضلة، كان المرضى أقل بكثير  في عدد تكرار دورات الحركة ابعاد -التقريب مقارنة مع الضوابط  وبالمقارنة مع خط الأساس، كان لديهم أقل بكثير  في مقدار المستهل الحركي وزيادة في وقت التوصيل الحركى المركزي وزيادة  في مقدار المستهل الحركي. مع تأثير المنبهات السمعية، كان هناك زيادة كبيرة  في عدد تكرار دورات الحركة للمرضى والضوابط. بعد تأثير المنبهات السمعية لا يوجد تغير ملحوظ في معلمات استثارة القشرية المخية الحركية بين المرضى مقارنة مع الضوابط بالمقارنة للأداء دون تأثير المنبهات السمعية. الخلاصة: المرضى باركنسون ذاتى العلة عندهم فرط في الاستثارية القشرية  المخية عن الأشخاص الطبيعيين. أداء تكرار دورات الحركة مع أو بدون تأثير المنبهات السمعية قد تتسبب في  تطبيع مستوى استثارة القشرية المخية في مرضي مرض  باركنسون ذاتى العلة.

 



2008 � Copyright The Egyptian Journal of Neurology,
Psychiatry and Neurosurgery. All rights reserved.

Powered By DOT IT