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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. and increased inhibition of . whereas projections to the external globus pallidus become more active result in loss of inhibition of the output neurons of the basal ganglia.

leading to rigidity . 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.

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 .

at times in the form of pill-rolling movement . 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. TREMOR different from that of cerebellar tremor.

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

including standing. and writing . eating. walking. AKINESIA manifested as difficulty in initiating and performing volitional movements of the most common type.

shuffling steps arms are held at the sides and do not automatically swing in rhythm with the legs as they should . 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.OTHER SYMPTOMS: lines of the face are smooth.

once under way. the pace becomes more and more rapid. although patients have difficulty in starting to take their first steps. These abnormality of walking is called “ festinating gait” muscle stretch (deep tendon) reflexes usually are normal . and pxn have trouble in stopping the progress on reaching their goal.

and the dopamine then restores the normal balance between inhibition and excitation in the caudate nucleus and putamen.TREATMENT: L-dopa – is converted in the brain into dopamine. -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. surgical therapy is directed at the globus pallidus rather than the thalamus . which blocked feedback circuit from the basal ganglia to the cortex. currently. 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.