For those of us with dystonia:

Klin Neurophysiol 2004; 35
DOI: 10.1055/s-2004-832129
Sensorimotor Integration in Basal Ganglia Disorders: New Findings on Impaired Kinaesthesia in Focal Dystonia and Parkinson's Disease
N Putzki1, P Stude2, K Graf3, M Maschke4

The term „movement disorders“ is often used to subsume conditions resulting from basal ganglia pathology and refers to the predominating motor symptoms. However, clinically unapparent sensory deficits were also found in these disorders.

Recent neurophysiological, neuroimaging and animal studies have revealed that sensory processing is impaired in Huntington's disease, Parkinson's disease and focal dystonia.

This raised the interesting question to what extent impaired sensorimotor integration contributes to the clinical symptoms in these disorders. We analyzed kinaesthesia, the conscious perception of limb position, in a passive movement task (repeated extension and flexion of the index finger between 0.2° and 4° in 45 trials of random order) and compared results of patients with idiopathic focal dystonia (blepharospasm n=3, torticollis n=6) and patients with idiopathic PD (n=8) to an age-matched group of healthy controls (n=5).

Patients and controls were without cognitive decline and did not show sensory deficits in routine clinical examination. PD patients detected the correct direction of a 0.2° displacement of the index finger in only 59% of the trials compared to 82% in healthy controls. Patients with focal dystonia also revealed a kinaesthetic deficit given that they responded correctly in only 76% of trials in the same task.

The overall differences for detecting the correct direction of index finger movements between patient groups and controls were statistically significant (β2, p=0.001 for PD group, p=0.002 for dystonia group). Calculated thresholds for 75% correct responses were 0.3° in PD patients, 0.2° in dystonia patients and 0.1° in control subjects.

Additionally, we analyzed the ability to judge the extent of a passive movement of the index finger by asking the patients to compare two consecutive passive movements.

PD patients appeared to be more impaired than dystonia patients and both groups were different from the control group. Our findings in PD patients confirm results of previous studies that revealed kinaesthetic deficits in PD.

Furthermore, the results of the present study suggest that a kinaesthetic impairment is also prevalent in focal dystonia. Together with previous findings the present results indicate that a deficit in processing multimodal sensory information might contribute to motor deficits in distinct basal ganglia disorders. Our results show the potential role of the basal ganglia as a sensory analyzer.