Bradykinesia is a requirement to make the diagnosis of PD using the United Kingdom Parkinson Disease Society Brain Research Center (UKPDSBRC) criteria (7). Bradykinesia is best characterized as slowness of movement (8), and its presence is the best clinical correlate of nigrostriatal degeneration in PD (9). In Parkinson disease (PD), bradykinesia typically manifests as slowness in initiating movements with a progressive reduction in the speed and amplitude of the repetitive movements. Early fatiguing and arrests in movement are also components of the bradykinesia in PD (5). Psychogenic parkinsonism (PP) patients also have significant difficulty performing rapid repetitive movements. Unlike PD patients, PP patients typically demonstrate extreme effort, with sighing, grimacing, or using whole-body movements in order to perform a simple motor task (5). PP patients do not typically demonstrate fatigue or decrement in movement amplitude when performing rapid repetitive movements (5). A patient who manifests very slow, pained-appearing repetitive tasks
for the examiner (such as finger taps) while easily performing other casual activities requiring similar finger dexterity and movements (easily opening and closing a purse) is demonstrating psychogenic bradykinesia, not the true bradykinesia of PD (5,10). In our experience, axial bradykinesia, hypomimia, and decreased blink rate are common in PD and rare in PP.

In addition to bradykinesia, PD patients also frequently suffer from slowed cognitive processing associated with impairment of concentration and apathy, or bradyphrenia (11, 12, 13). Patients with PP may also suffer from depression, which can cause psychomotor retardation (14), a condition which may be difficult to distinguish from the bradyphrenia of PD. In one study comparing PD patients and depressed patients, it appeared that both cognitive and motor slowing contributed to slowing of responses in both (13). The authors suggested that bradyphrenia in PD and psychomotor retardation in depression are closely related, and impairment of mesocorticolimbic dopaminergic systems may be involved in both conditions (13). Separating bradyphrenia from psychomotor retardation may even be difficult in a “pure” population of PD patients given that approximately half of them also suffer depressive symptoms (15).

PD tremor is classically a gradual-onset, 4 to 6 Hz rest tremor of consistent frequency, usually with transient dampening upon assuming a new posture (5,16,17). The amplitude may vary depending upon the activity and the emotional state of the patient. Tremor was present in 12 of 14 PP patients in the series by Lang et al. (5), with sudden onset in 10 of the 14 patients. Tremor of the arm or hand is most typical in PP and rest tremor of the chin or leg/foot would be highly unusual in PP. PP tremor is typical of other psychogenic tremors in that the amplitude and frequency of the tremor vary widely in an individual patient (5,18,19). Unlike what is typical of PD tremor, PP tremor is distractible in the affected limb by having the patient perform complex motor tasks in the contralateral limb or serial arithmetic (5). Patients with PP typically demonstrate entrainment, where the limb with psychogenic tremor will assume the frequency of a contralateral repetitive movement, unlike PD where the tremor itself often entrains the rate of repetitive movements (5). PP tremors also frequently persist with action or sustained postures, unlike PD tremors in most patients. When the examiner directs attention to the tremor of PP patients, the tremor usually worsens. The tremor may even spread from one contiguous body part to another, or even to contralateral limbs when the primarily affected joints are immobilized, especially with suggestion.

Cogwheel rigidity is a cardinal finding in PD and other forms of organic parkinsonism; however, this does not typically occur in PP (5). Rigidity in PP typically has a feature of voluntary resistance or difficulty relaxing and was only present in six of the 14 patients with PP in the series of Lang et al. (5). Performing synkinetic movements of a contralateral limb appears to help reduce the rigidity characteristically found in PP (presumably through distraction)—exactly the opposite of what occurs in PD (5). Visible cogwheeling during voluntary movement about a joint as an isolated symptom/sign is more typical of anxiety and not of PD.

A shuffling gait with freezing and turning en bloc is typical in moderate to advanced PD; however, this is not typically seen in PP. Gait freezing in PD may have unusual relieving factors including improvement with visual/auditory cues leading to confusion with PP. Gait is frequently bizarre in PP, as is typical of PMDs. Only one patient in the Lang et al. (5) series was noted to have a shuffling gait, while four patients had unusual or bizarre gaits.

Postural stability is typically impaired in moderate to advanced PD, but not in early disease. Unlike PD patients, those with PP typically demonstrate postural instability regardless of the duration of symptoms. The PP patients in our practice typically have unusual or even bizarre gaits, and many have abnormal pull tests. PP patients with abnormal pull tests frequently demonstrate retropulsion or back arching and flailing of the arms without falling. Other PP patients will fall backwards into the examiner’s arms “like a log,” not attempting to take steps backward to avoid falling.

Patients may complain of a myriad of problems in addition to the motor features characteristic of PP. Impaired concentration and memory, alterations in speech or language function, functional or “give-way” weakness, nonanatomical sensory loss, and selective disabilities are typical. In our experience, some PP patients also demonstrate distractible, bizarre dysarthrias or stuttering. PP patients also commonly report pain in varied distributions (5), frequently chronic and unrelated to the development of PP, however, occasionally coincident with PP onset. Pain can also be a feature of the nonmotor fluctuations in PD (20,21), usually occurring in the “off” state and responding to levodopa or dopamine agonists. Pain,
regardless of cause, does not usually respond to levodopa or dopamine agonists in patients with PP. Some PP patients complain of unusual, unexplained visual disturbances (such as bilateral tunnel vision) in addition to their PP motor symptoms.