Parkinsonism is characterized by varying degrees of: (1) rigidity, (2) bradykinesia, (3) tremor, and (4) postural defects. Dementia, usually appearing late and less severe than the other abnormalities, is also relatively common (approximately 20%) and considered secondary to degeneration of cerebral cortical neurons that can be involved in a more diffuse degenerative process (as in diffuse Lewy body disease). Parkinsonism may also be part of a more prominent dementing process such as Alzheimer's Disease, presumably because the degenerative process also affects the basal ganglia.
Rigidity is plastic in nature and present in all ranges of passive manipulation and active movement. This appears to be due to overactivity in descending motor pathways from the brain stem. The gamma motor system probably is not involved because cutting the dorsal roots does not modify the rigidity. The rigidity has a superimposed cogwheel halting character if tremor is part of the syndrome.
Bradykinesia is actually not a slowness of movement so much as an inability to initiate or carry out movements despite the presence of adequate strength. An illustration of this presumed dyspraxia is seen in the parkinsonian patient who, frozen with bradykinesia, leaps from their wheelchair and runs with full coordination from a burning house and then safe, settles back to an inability to initiate volitional locomotion. The capability for catastrophe motivated, well-learned, and relatively automatic behavior is present, but volitional behavior is defective. Once movement is initiated, it can often be continued with reasonable speed. Bradykinesia and rigidity are additive in hindering movement and are usually present together. Bradykinesia is, however, not dependent on or necessarily proportional to rigidity, and vice versa. There is a small population of patients who have pure bradykinesia without other characteristic parkinsonian deficits. They have been described as having a pure "ignition" syndrome.
Also included by many under bradykinesia is the characteristic depression, or loss, of associated movements, such as arm swinging while walking, and emotional expression --e.g., an immobile face when the patient is happy or sad despite the ability to grimace voluntarily. Facial muscle rigidity can also partly or completely account for the "masked facies."
The tremor of parkinsonism is a rhythmic (four to eight per second) oscillation of opposing muscle groups, which is particularly prominent in the distal portions of the extremities. The upper extremities are affected earlier than the lower extremities. The neck and cranial muscles may also be involved.
Early in parkinsonism the tremor may begin in one extremity, so may rigidity and bradykinesia. In the absence of tremor, the presentation of parkinsonism may be erroneously diagnosed as hemiparesis. The absence of true weakness, the character of rigidity (full range instead of clasp knife) and the decrease in associated movements help to differentiate the two. Generalization to both sides of the body ultimately occurs in most patients with parkinsonism. The tremor has been erroneously considered a tremor at rest, but actually it is a tremor of postural or resting muscle tension. When the patient is completely at rest and relaxed (which is nearly impossible for most patients with Parkinson's disease), the tremor disappears. It is most characteristic that a parkinsonian tremor may be seen with the hands folded in the lap or when walking with the hands hanging by the sides.
The postural (e.g., arm held in position demanding muscle tone) or resting muscle tension tremor of parkinsonism is to be differentiated from the tremor of cerebellar damage, which is not present until the patient directs their limbs into purposeful activity (i.e., intention tremor). The tremor of Parkinson's disease is suppressed by the initiation of voluntary movement. As the disease progresses, however, many patients may begin to develop a coexisting intention tremor, which supports a hypothesis that involvement of the cerebellar system is important in the pathogenesis of parkinsonian tremor. All forms of tremor, and indeed most adventitious movement abnormalities, are increased by anxiety or any other stress that increases muscle tension; they are reduced to varying degrees by relaxation or sedation.
Postural deficits are less well studied and understood. However, it is characteristic for a person with parkinsonism to have difficulty adjusting to postural change. This can be demonstrated by seating the patient on the edge of a tilt table. When the table is tilted, the normal response is to lean uphill, thus preserving one's balance. The parkinsonian patient tilts with the table without adjusting and topples over. If the patient is given a good shove backward, instead of normally catching their balance s/he tends to fall back like a tree. In some patients this retropulsion can be initiated by simply having the patient attempt to look up or back up. Patients with moderately advanced parkinsonism frequently have a flexed (stooped) posture, which may well be a compensation for the postural imbalance that causes retropulsion. Falling is a common problem for parkinsonian patients because of the combination of their rigid/bradykinetic shuffling gait and the postural adjustment deficit. They are unable to make the appropriate kinetic-postural adjustment necessary to prevent them from falling. A bizarre but typically parkinsonian fall occurs when the patient is unable to initiate stepping movement with their feet although s/he has already initiated forward movement of the trunk. To avoid falling on their face, s/he usually drops to the knees.