What are the Clinical Features of Parkinson’s Disease

Clinically, Parkinson’s disease is characterized by the triad of a rigidity and tremor (A-R-T). Of these, akinesia, is a hypo-kinetic features while rigidity and tremors are hyperkinetic features.

Akinesia includes the following features:

(i) Delayed motor initiative, as evident prolonged reaction time,

(ii) Slow performance of voluntary movement (bradykinesia), measured by movement times (i.e., the time n to perform a simple stereotyped movement),

(iii) Difficulty reaching target with a single continuous movement (hypokinesia), movement must stop and resume to touch the intended objective.

(iv) Rapid fatigue with repetitive movement,

(v) Inability to execute simultaneous actions, e.g., the patient can salute when seated not when walking,

(vi) Inability to execute sequential actions.

(vii) Defective kinetic automatism, i.e., the loss of associated movements like reduced facial expression and hand gestures speech, arm swinging during gait, etc. The patient possesses face appearance with no emotional response,

(viii) Patient walks with short, quick steps and experiences difficulty in taking initial steps and in terminating the movements. The possible cause akinesia is because of the dysfunction of the caudate loop, which hampers the smooth transition from one motor program to another difficult.

The rigidity takes place due to increased muscle tone of both agonist and antagonist muscles. During passive flexion or extension of a limb, the muscular resistance increases and decreases alternately as if it is overcoming a series of catches (cog-wheel rigidity). Sometimes, there may be a more uniform resistance to passive flexion (lead-pipe rigidity). Rigidity probably results from withdrawal of facilitation of inverse-stretch (Golgi tendon) reflex. In Parkinson’s disease, the increased inhibitory output from the globus pallidus reduces the descending facilitatory influences on the inhibitory interneuron in the Golgi tendon reflex pathway.

Since the Golgi tendon reflex is inhibitory to muscle tone, reduction of supraspinal facilitatory inputs to the reflex results in increase in muscle tone. The resulting rigidity is different from spasticity, which results from excessive facilitation of the stretch reflex.

Tremor at rest is a prominent sign in Parkinson’s disease. The frequency of tremors range from 3-6 Hz. The tremor activity usually suppressed during voluntary movements and sleep, and is exaggerated by stress and anxiety.

The tremor occurs with regular frequency, when the subject is at rest. It is characterized by pill-rolling movement of the hand. The tremor disappears during movement and is increased in emotion. The tremor seems to occur due to a pacemaker activity in the nucleus ventralis intermedius of the thalamus. Thalamic neurons have an intrinsic autorhythmicity and it is possible that this automaticity gets unmasked by the increases in the inhibitory input from the globus pallidus.

The thalamic pacemaker activity induces oscillations in the long-loop reflex pathways. Long-loop reflex pathways originate from muscle spindle. The reflex path runs through the thalamus up to the cortex and then loops back to extrafusal muscle fibers along the corticospinal tract.