Parkinson’s disease

1- Introduction:

– Parkinsonism: akinesia (slowdown in initiating movement) and bradykinesia (the execution of motion); resting tremor and rigidity extrapyramidal plastic. Automatic movements are most affected

– It is the clinical expression of a deficiency in brain dopamine. 9 cases out of 10 of Parkinson’s disease.

– Starts on average between 55 and 65 years.

– It is a degenerative disease characterized by progressive loss of dopaminergic neurons (nigrostriale way). With other disorders (locus coeruleus and nucleus basalis of Meynert), which explains the occurrence during the evolution of signs resistant to dopaminergic therapy. The Lewy bodies is an intraneuronal inclusion characteristic of Parkinson’s disease.

– Etiological factors: environmental (MPTP) genetic (autosomal recessive).

Parkinson's disease

2 Clinic:

– Earthquake: present at rest and disappear during movement; slow (6 Hz); possibly affecting the jaw members but spares the head; unilateral or highly skewed. It is almost pathognomonic. However it is not indicative of the disease in most cases. Some patients never have struck. Tremor is sensitized by stress (mental arithmetic)

– Akinéso-régide Syndrome: writing gene (micrograph); stiffness in the march; walking in small steps; deceptive appearance (stiffness, slow, apathy). Rigidity is sensitized maneuver Froment. Amimie of the face; loss of swinging the arm when walking. Beat time with his foot (gene to alternative movements)

– The following elements will be for the diagnosis of Parkinson’s disease:

* Presence of a resting tremor characteristic

* Asymmetry of Parkinsonian symptomatology

* The normality of the rest of the neurological examination

* The absence of explanatory iatrogenic factors

– Minor signs: naso-palpebral reflex inexhaustible; drooling; sebaceous hypersecretion; sweating.

– The diagnosis is confirmed clinically by obtaining a marked improvement of symptoms during the development of dopaminergic therapy route.

– No diagnostic testing is warranted when these clinical features are obtained except those under 40 years where an MRI and a copper balance sheet are systematic.

3- Differential diagnosis:

– Parkinsonism caused by neuroleptic (Primperan®). Parkinsonism unresponsive to dopaminergic therapy.

– Other degenerative parkinsonian syndromes: low responsiveness to dopaminergic treatment and existence of neurological signs associated with parkinsonism. 4 diseases: multisystem atrophy (Shy-Drager disease); progressive supranuclear palsy; corticobasal degeneration and dementia with Lewis bodies.

– Wilson’s disease: autosomal recessive disease responsible for an accumulation of copper (copper excretion deficit).The onset may be delayed (50). All abnormal movement or parkinsonian syndrome in a patient under 40 requires research of this disease.

– Vascular Parkinsonism

4- Complications:

A- independent complications of dopaminergic treatment:

– Axial signs: trouble postural balance (back drops); gait disturbance: freezing; festination (uncontrollable walk) .Dysarthrie with a maximum silence. Disorders posture with trend triple flexion

– Cognitive Deterioration: evolving towards a dementia condition

B- Complications related to dopaminergic treatment:

– No specific vomiting, orthostatic hypotension

– Dyskinesia (involuntary movement disorder): Type of choreic; ballique; dystonic. Delay = 6 years.

– Fluctuation of efficacy (recurrence of Parkinsonian symptomatology during nycthémère). Phenomenon “on-off” with passage of a normal to severe parkinsonism state. These fluctuations occur 4 years after the onset of the disease.

– Psychiatric complications: hallucinations, delusions

5- Treatment:

– Two classes of drugs are used: L-Dopa and dopamine agonists

– L-dopa is the immediate precursor of dopamine, which crosses the blood-brain barrier (unlike dopamine). The transformation occurs pat SDC (dopa decarboxylase) which is also found outside the CNS (combination with a DDC inhibitor that does not cross the BBB). This treatment is more effective and better tolerated. However, its use in early disease especially in high doses in patients <65 years exposed to early dyskinesia

– The use of dopamine (which are less effective and less tolerated) at the beginning of the disease appears to delay the onset of dyskinesia.

– Amantadine is used for reducing dyskinetic phenomena in advanced forms of the disease.

– The MAO-B inhibitors have a moderate dopaminergic action

– The COMT inhibitors increase the bioavailability and the duration of action of the Dopa.

– To improve tolerance to the therapeutic introduction of a co-prescription domperidone (Motilium) is useful

– In case of fluctuation of efficiency: splitting processing or use of an agonist or strengthening agonist doses or use of sustained release forms or COMT inhibitor

– The occurrence of medium dose dyskinesia justifies the reduction of the dosage point of L Dopa more fractionation on day