Parkinsonism is a syndrome associated with damage to the basal ganglia and their connections and is manifested by akinesia, rigidity, rest tremor, instability when changing posture (postural instability).
The disease develops due to many causes affecting the subcortical ganglia: primary insufficiency of the enzymatic structures of the caudatonigral complex, intoxications, including drugs (neuroleptics, reserpine, dopegyt), encephalitis, traumatic brain injury, brain tumors.
Currently, the majority of cases occur in the idiopathic form (Parkinson’s disease) and drug-induced parkinsonism. There is a decrease in the content of catecholamines in the caudate nucleus and substantia nigra of the midbrain, leading to dysfunction of the extrapyramidal system.
The clinical picture includes a triad of symptoms: akinesia, rigidity, and muscle tremor. This is accompanied by a violation of gait, autonomic disorders, pain. The idiopathic form of the disease usually occurs after 50 years and begins either with hand trembling, or with partial or general stiffness. Gradually, tremor and akinesia become generalized, muscle rigidity appears with a gradual increase in tone in the limb with repeated passive movements and jerky hypertension (cog wheel phenomenon). The posture and gait change: the patient stoops more and more, walks in small steps, friendly hand movements disappear when walking (acheirokinesis). The facial expressions of the sick are impoverished; blinking is reduced, the face becomes mask-like.
Paradoxical kinesias are characteristic: the patient, unable to walk independently, easily runs up the stairs, can dance, ski. Some patients have propulsion: slow movement is suddenly replaced by a fast run, which the patient is unable to overcome until he falls or encounters an obstacle.
There is greasiness of the skin of the face, hypersalivation. Urination is not often disturbed. To a certain extent, the mental life of the sick also becomes impoverished, dementia gradually develops. Muscle strength is normal, reflex and sensory spheres do not suffer. The disease, as a rule, progresses, but the rate of increase in movement disorders is very different. In severe cases or in the late stage of the disease, the patient is almost completely immobilized and cannot get out of bed even with outside help.
The differential diagnosis with senile tremor is based on the absence of subsequent muscle rigidity. Essential tremor occurs at a younger age. Tremor in thyrotoxicosis and delirium tremens is combined with the characteristic signs of these diseases. Pyramidal spasticity is most pronounced at the beginning of passive movements (jackknife symptom).
With drug-induced parkinsonism caused by taking antipsychotics, dopegyt, the dosage of the products used is reduced, they are prescribed only in conjunction with correctors (cyclodol and its analogues). With manganese parkinsonism, which is very rare at the present time, a change in work, the appointment of complexones are shown.
In all cases of parkinsonism, the leading place is occupied by replacement therapy (L-DOPA). Since L-DOPA undergoes extensive decarboxylation in the systemic circulation, only products in which L-DOPA is combined with decarboxylase inhibitors are currently used, which makes it possible to significantly reduce the dose of L-DOPA. Such drugs are madopar-125 and nakom. Gradually increasing the dose, prescribe (depending on the effect) 4-6-8 capsules of Madopar 125 or 3-6 tablets of Nakom. Drugs are taken only at the end of a meal; among the side effects – not often vomiting, dyskinesia. Along with L-DOPA, central anticholinergics (cyclodol and its analogues) are prescribed, as well as midantan, parlodel or amitriptyline.
In addition to drug therapy, massage and physiotherapy exercises are shown; sick people should be constantly encouraged to do what they can, bearing in mind that “the bed is the enemy of parkinsonism.” In some cases, mainly in young patients, in the absence of the effect of drug treatment, stereotaxic intervention on the subcortical ganglia is indicated.
In cases of drug-induced parkinsonism, the withdrawal of the drug that causes the disease sometimes leads to the complete elimination of all symptoms. The idiopathic form, as well as atherosclerotic and postencephalitic parkinsonism, progress steadily if L-DOPA replacement therapy is ineffective. After 7-8 years, the effect of L-DOPA and its analogues “wears out”, the effect of taking replacement products stops, and then it is found that the disease has advanced far during the treatment. Hence the desire to prescribe madopar and nakom only when the disease creates already insurmountable difficulties for the young sick person for self-service and work.
In elderly patients, these agents should be included from the time of diagnosis.
Articles from the forum on the topic ” Parkinsonism “
Juvenile parkinsonism, who faced personally, I would like to talk.
It was at 13 or 14 years old.
Juvenile parkinsonism is a special hereditary form of primary parkinsonism, studied in detail only in the last 10-15 years [Narabayashi H. et al., 1986; Takahashi H. et al., 1994; Ishikawa, Tsuji S., 1996; Tassin J. et al., 1998]. The disease is ubiquitous and somewhat more common in women. The mode of inheritance in most descriptions is autosomal recessive, and therefore many cases of juvenile parkinsonism in small families are sporadic.
The debut of symptoms most often falls on the 2nd-4th decade of life, less often at an earlier age. The clinical picture of juvenile parkinsonism has a number of features compared to classical Parkinson’s disease. The main ones are: the absence (even with a long-term course of the disease) of dementia and other mental disorders and, conversely, the frequent combination of parkinsonism with increased tendon reflexes and other pyramidal symptoms. The course of the disease is slowly progressive (over decades), the prognosis is relatively favorable.
This gene was isolated in 1998: it contains 12 exons and encodes a new parkin protein, consisting of 465 amino acids [Kilada T. et al, 1998]. In the neuron, parkin is localized in the Golgi complex and cytosol; The immunohistochemical method showed that in patients with juvenile parkinsonism, parkin is absent in all parts of the brain [Shimura et al., 1999]. The exact function of parkin in the cell has not yet been established.