Case 2.

A 65 year old man has been bothered by

shaking of his hands and generalized stiffness of his
body, w/c have become progressively more severe
over the past 4 yrs. On entering the examining
room, he moves slowly and deliberately, shuffling
his feet, his shoulders and trunk are stooped
forward, and his arms are at his sides and not
swinging. His face remains mask-like with no
changes of expression all the time. In both hands, a
resting tremor of the pill-rolling type stops only
when the patient performs a voluntary movement
such as removing his eyeglasses or picking up a
pen. Examination reveals the presence lead-pipe
rigidity manifested by a generalized hypertonicity
with greatly increased resistance to passive
movement. Although the patient moves
infrequently, examination reveals no paralysis or
sensory disturbances in any part of the body.
PARKINSON’S DISEASE/
PARALYSIS AGITANS:

degenerative changes (neuronal

degeneration and depigmentation) in the
substantia nigra (pars compacta) and locus
ceruleus
dopaminergic neurons that project to the
striatum and thus lead to the depletion of
dopamine in the caudate nucleus and putamen
 Striatal projections to the
internal globus pallidus and the
substantia nigra (pars reticulata)
become less active, whereas
projections to the external globus
pallidus become more active
result in loss of inhibition of the
output neurons of the basal
ganglia, and increased inhibition of
 allow the caudate and
putamen to become overly
active and possibly cause
continuous output of
excitatory signals to the
corticospinal motor control
system.
these signals could
certainly excite many or all
of the ms of the body,
leading to rigidity
RIGIDITY ( increased resistance to
passive movement)

when the examiner passively

flexes or extends one the pxn’s
extremities, an increased resistance
occurs that suddenly gives way and
then returns sequentially as the
movement continues, in the manner of
a cogwheel
 TREMOR

different from that of cerebellar

tremor, w/c occurs only when the
person performs intentionally initiated
movements and therefore is called
intention tremor
typically occurs when the pxn is at rest
and consists of 4-6 cps flexion-extension
movt’s of the fingers and wrists, at times in
the form of pill-rolling movement
 AKINESIA

more distressing to the pxn

because to perform even the
simplest movement in severe
parkinsonism, the person must
exert the highest degree of
concentration. Movements are
usually stiff and staccato in
character, instead of smooth.
 AKINESIA

manifested as difficulty in
initiating and performing volitional
movements of the most common
type, including standing, walking,
eating, and writing
OTHER SYMPTOMS:

lines of the face are smooth, the expression is fixed

(“masked face”), and there’s little overt evidence of
spontaneous emotional responses
pxn stands with the head and shoulders stooped
and walks with short, shuffling steps

arms are held at the sides and do not

automatically swing in rhythm with the legs as
they should
 although patients have difficulty in
starting to take their first steps, once
under way, the pace becomes more and
more rapid, and pxn have trouble in
stopping the progress on reaching their
goal. These abnormality of walking is
called “ festinating gait”

muscle stretch (deep tendon)

reflexes usually are normal
TREATMENT:
L-dopa – is converted in the brain into
dopamine, and the dopamine then restores
the normal balance between inhibition and
excitation in the caudate nucleus and
putamen.
-Administration of dopamine itself does
not have the same effect because dopamine
has a chemical structure that will not allow it
to pass through the blood-brain barrier
 L-deprenyl – inhibits monoamine
oxidase, w/c is responsible for
destruction of most of the dopamine after
it has been secreted

surgical lesions were made in the

ventrolateral and ventroanterior nuclei of
the thalamus, which blocked feedback
circuit from the basal ganglia to the
cortex; currently, surgical therapy is
directed at the globus pallidus rather than
the thalamus