The clinical diagnosis of Parkinson disease (PD) is based on the identification of some combination of the cardinal motor signs of bradykinesia, rigidity, tremor, and postural instability, but few attempts have been made to develop explicit diagnostic criteria. We propose a clinical diagnostic classification based on a comprehensive review of the literature regarding the sensitivity and specificity of the characteristic clinical features of PD. Three levels of diagnostic confidence are differentiated: Definite, Probable, and Possible. The diagnoses of Possible and Probable PD are based on clinical criteria alone. Neuropathologic confirmation is required for the diagnosis of Definite PD in patients with the clinical diagnosis of Possible or Probable PD. Criteria for histopathologic confirmation of PD are also presented.

Recent data from several laboratories have shown that spatial-frequency discrimination is not a smooth function of frequency but rather exhibits alternate peaks and troughs. A model for spatial-frequency discrimination analogous to line-element models for color discrimination is presented here and shown to provide a reasonable fit to the available data. This model is based on the predicted responses of six spatial-frequency-tuned mechanisms, whose sensitivity curves have been estimated in previously published masking experiments. In order to fit the data it is necessary to pool responses from units centered under the stimulus as well as from spatially neighboring units. Thus it appears that the visual system utilizes both spatial and spatial-frequency information in discrimination tasks.

We administered local injections of botulinum toxin to 20 patients with torticollis in a blinded, placebo-controlled study. Each patient received four sets of injections: three different doses of botulinum toxin and one placebo. The order of the sessions was random and unknown to the patients. Sixteen of the patients (80%) reported subjective improvement to at least one dose of botulinum toxin; 11 (55%) reported substantial improvement. No objective benefit was documented. Side effects were minor and transient, although dysphagia occurred in four. Some patients reported that the effect waned despite persistent relaxation or even flaccidity of previously overactive muscles, suggesting a change in the pattern of muscle activity after botulinum toxin injections.

We assessed the severity and temporal profile of distant neuromuscular effects from a single dose (280 units) of botulinum neurotoxin injected into neck muscles for torticollis. We performed single-fiber EMG studies on the biceps brachii of six patients to measure jitter (20 pairs) and fiber density on the initial treatment day and then again, at least once more, after 2 to 12 weeks. No patient developed weakness beyond the neck muscles or decrement of the biceps response to repetitive 3-Hz nerve stimulation. Between the baseline and the last follow-up study, the average of mean MCD increased from 29 microseconds to 38 microseconds (31%). Mean fiber density increased concurrently or earlier from 1.35 to 1.79 (33%). There were no electrophysiologic signs of presynaptic blockade, even at 2 and 4 weeks. The effects we observed are compatible with stimulation of terminal sprouting by the neurotoxin, without significant presynaptic inhibition of acetylcholine release. We therefore believe that higher dosages of the neurotoxin may be used if clinically indicated.

Twenty patients with torticollis had electromyographic studies of their neck muscles performed before and after a series of local injections of botulinum toxin. The pattern of muscle activity changed after the injections, and this effect persisted even after head position had returned to baseline. Patients who did not experience any clinical benefit from the injections also demonstrated a change in the pattern of muscle activity. These results suggest that the underlying abnormality in torticollis usually involves a general motor program for head position, rather than the activity of individual neck muscles.