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13-i clinical features of parkinson's disease - Coggle Diagram
13-i
clinical features of parkinson's disease
Parkinson’s disease has both
hypokinetic and hyperkinetic features.
Its cardinal features are a triad of
akinesia, rigidity and tremor;
of which
akinesia - hypokinetic feature
rigidity - hyperkinetic feature
tremors - hyperkinetic feature
Akinesia or hypokinesia.
The patient is unable to
initiate the voluntary movements
(akinesia)
or
the voluntary movements are decreased (hypokinesia).
causes
Akinesia is not due to any paralysis or decrease in muscle power;
the sensory system is also normal.
Difficulty in initiating voluntary movements is because of:
hypertonictiy
of the muscles.
Manifestations of
akinesia or hypokinesia include:
Delayed motor initiative,
as evidenced by prolonged reaction time.
Slow performance of voluntary movements (bradykinesia).
Mask-like facial expression due to decrease in movements of facial
muscles.
Absence of normal associated movements, e.g. swinging of arms
during walking.
Shuffling or festinant type gait, in which patient is bent forward and
walks quickly with short steps as if trying to catch up centre of
gravity or preventing himself from falling.
Retropulsion, i.e. when a walking patient is suddenly pulled
backwards, he begins to walk backwards and is unable to stop.
Rigidity
Refers to increase in tone of the muscles.
Cause
Characteristic features
It occurs due to increased tone in both the protagonists and antagonist muscles.
Mainly large proximal group of muscles of limbs, e.g. biceps and knee flexors are affected.
Usually, there occurs uniform resistance to flexion giving a feeling as
if lead pipe is being bent (lead-pipe rigidity).
Sometimes, there is a series of catches during passive motion of the limbs (cogwheel rigidity).
Due to rigidity, posture becomes that of flexion attitude in which: back is flexed, arms are abducted and flexed and the knees are bent.
In advanced cases, the rigidity may increase to such an extent that a
statue-like appearance is produced with complete absence of movements.
Rigidity differs from spasticity seen in lesions of pyramidal tracts.
Neural mechanism.
The striatum (caudate nucleus and putamen) is under the influence of both excitatory (cholinergic) fibres and inhibitory (dopaminergic) fibres.
Under normal circumstances, there exists a balance between the
excitatory and inhibitory influences.
In patients with Parkinson’s disease,
lack of dopaminergic activity due to
degeneration of neurons in the substantia nigra shifts the balance
towards excitatory cholinergic fibres.
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An increased discharge of γ-efferents supplying the muscle spindle causes rigidity.
This fact is confirmed by the observation that local injection of 1% procaine solution into the affected muscles decreases rigidity by
abolishing the γ-discharge.
Tremors
Tremors (i.e. involuntary, rhythmic and oscillatory movements of the distal parts of limbs and head) seen in Parkinson’s disease have following
characteristics:
The tremors are present at rest, but disappear during activity.
It is hallmark of Parkinson’s disease and so popularly known as resting
(static) tremors.
Frequency of tremors ranges from 4 to 6 times/s. It is frequently seen as frill-rolling movements of the hand, i.e. rhythmic contraction of thumb over first two fingers.
Tremors are suppressed during sleep and exaggerated by stress anxiety and excitement.
The tremors are observed as rhythmic movements of pronation and supination in fingers, hands, lips or tongue.