Secondary parkinsonism is a clinical term that combines all cases of the appearance of parkinsonism syndrome caused by the influence of various factors affecting the central nervous system or the presence of a primary disease. Unlike Parkinson’s disease, secondary Parkinsonism has a more acute onset, is characterized by the initial symmetry of Parkinsonian manifestations and the presence of other symptoms of central nervous system damage. It is diagnosed on the basis of anamnestic and clinical data, taking into account the results of MRI of the brain. Treatment is aimed at relieving the main etiological factor and blocking the pathogenetic mechanisms of the development of parkinsonism.
G21 Secondary parkinsonism
Secondary parkinsonism is a generalizing clinical concept that includes all cases of symptoms of Parkinson’s disease associated with damage to the neurons of the basal nuclei of the brain under the influence of various exogenous and endogenous factors. Unlike Parkinsonism of a secondary nature, idiopathic Parkinson’s disease occurs independently, without connection with any brain-damaging factor. Secondary Parkinsonism is about 30%, in other cases, Parkinson’s disease is diagnosed. In accordance with the etiology, medicinal, post-traumatic, toxic, posthypoxic, postinfectious, vascular parkinsonism are distinguished. The most common is drug-induced parkinsonism. Most of its cases are due to malignant neuroleptic syndrome, which develops with prolonged or inadequate intake of neuroleptics. The issue of differentiation of Parkinson’s disease and secondary Parkinsonism is of fundamental importance for practitioners in the field of neurology, since approaches to their therapy differ significantly.
Parkinsonian manifestations may occur due to severe TBI (bruising and compression of the brain) or frequent mild TBI (concussions of the brain). The causes of post-infectious parkinsonism are encephalitis and common infections (measles, HIV, mumps, herpes, etc.). Various poisoning (heavy metals, carbon monoxide, prussic acid, methanol), in case of failure to timely detoxification, can cause toxic parkinsonism. The occurrence of Parkinsonism syndrome is possible with manganese intoxication, which is observed in drug addiction with the use of synthetic drugs (synthetic heroin, ecstasy). Pharmaceutical preparations, when taking which there is a risk of developing secondary Parkinsonism, include antipsychotics (neuroleptics, some antidepressants), anticonvulsants, sympatholytics, antiemetics (metoclopramide).
The etiofactors of vascular parkinsonism are extensive ischemic stroke, multiple lacunar infarcts of the brain, chronic cerebral ischemia in atherosclerosis. Parkinsonism can be observed after hypoxia, regardless of its genesis, including in patients who survived after resuscitation. The following can provoke the development of secondary parkinsonism: hydrocephalus, repeated episodes of hypoglycemia, intracerebral tumors. Parkinsonism syndrome can be observed in various degenerative diseases of the central nervous system: Wilson’s disease, dementia with Lewy bodies, progressive supranuclear paralysis, corticobasal degeneration, multiple sclerosis, etc. In relation to such cases, the term “parkinsonism plus” is used.
The main clinical manifestations of Parkinsonism are bradykinesia, muscle rigidity and postural tremor. Bradykinesia is a decrease in the number and speed of movements; patients become slow, gestures gradually disappear, facial expressions become impoverished, walking ceases to be accompanied by accompanying hand movements. Muscle rigidity is a constant tension of the muscles, which is first detected when trying passive movements in the limb, and then becomes noticeable by the limbs constantly bent at the elbows and knees. Postural tremor is usually expressed in the hands and head, a small tremor of which occurs at rest and disappears during motor acts. Over time, these symptoms lead to significant immobility of the patient, accompanied by postural disorders (impaired coordination of movements, the ability to hold a certain pose); characteristic personality changes occur, mnestic disorders are added.
A distinctive feature of the secondary Parkinsonism clinic is the faster development of symptoms during the manifestation of the disease and their accelerated progression in the future. The symmetry of manifestations is typical, while in Parkinson’s disease, symptoms appear initially on one side and acquire a bilateral character only after some time. With the secondary nature of parkinsonism, its manifestations are combined with other symptoms of cerebral lesion: pyramidal syndrome, cerebellar ataxia, early intellectual disabilities, etc. In the anamnesis of patients, as a rule, there is an indication of the effect of one or another etiofactor that preceded the appearance of parkinsonian syndrome (TBI, stroke, taking neuroleptics, encephalitis, etc.). In the treatment, there is little effectiveness of dopaminergic agents, and the elimination of the etiofactor sometimes contributes to a significant regression of parkinsonian manifestations.
Various etiological variants of parkinsonism are characterized by their own characteristics of the clinic. Thus, Parkinsonism after encephalitis is characterized by strong rigidity, the presence of pronounced vegetative manifestations and oculogyric crises; tremor is often absent. In posthypoxic parkinsonism, tremor, on the contrary, is pronounced. Vascular parkinsonism is accompanied by cognitive disorders, early formation of postural disorders; tremor is expressed slightly. Secondary parkinsonism in hydrocephalus is characterized by the dominance of the Hakim triad — dementia, ataxia, urinary incontinence, with corticobasal degeneration, it is combined with cortical symptoms — apraxia, a disorder of complex types of sensitivity, the syndrome of “alien” limbs, with dementia with Levi’s corpuscles, along with parkinsonism, cognitive disorders and mental disorders are observed — psychoses, hallucinatory syndrome.
An essential diagnostic value in the presence of a parkinsonism symptom complex is the identification of signs of its secondary nature: the existence of an etiofactor in the anamnesis, rapid manifestation, the presence of other neurological symptoms in the status. If psychopathological manifestations appear, a psychiatrist’s consultation is necessary. An ophthalmologist’s examination makes it possible to determine the presence of changes in the fundus characteristic of hydrocephalus or pigmentation pathognomonic for Wilson’s disease along the periphery of the iris (Kaiser-Fleischer ring).
Identification of the probable causes of secondary Parkinsonism syndrome is carried out using MRI of the brain, which is more informative in comparison with CT imaging of degenerative foci and differentiation of intracerebral volume formations. In hydrocephalus, MRI detects dilated ventricles of the brain, in post—stroke conditions – heart attack zones, etc. However, the detection of such changes in itself does not indicate the secondary nature of Parkinsonism. It is necessary to interpret the results of tomography only by correlating them with clinical data, since it is impossible to exclude the presence of a combination of Parkinson’s disease with a number of other cerebral diseases or, for example, the existence of secondary non-vascular Parkinsonism against the background of vascular disorders.
The basis of therapy consists of drugs used to treat Parkinson’s disease. These include dopamine receptor agonists (piribedil, pramipexole, bromocriptine), levadopa pharmaceuticals, selective irreversible MAO inhibitors (moclobemide, pirlindol, befol). Treatment starts with monotherapy. The drug of choice, as a rule, is pronoran. Unlike Parkinson’s disease in secondary Parkinsonism, levadopa shows poor effectiveness.
In parallel with antiparkinsonian treatment, therapy is carried out aimed at the cause of damage to the basal nuclei. With toxic parkinsonism, detoxification is carried out, with posthypoxic — oxygenotherapy and neurometabolic treatment, with vascular — vascular therapy (vinpocetine, nicergoline, pentoxifylline). Medicinal parkinsonism is an indication for the cancellation or replacement of the drug that caused its occurrence. In post-traumatic and post-infectious parkinsonism, courses of neurometabolic therapy (piracetam, pyritinol, vitamins g. B, lipoic acid) are indicated. aimed at slowing down degenerative processes occurring in neurons. The main treatment is supplemented with massage to reduce rigidity and exercise therapy for the longest possible preservation of the patient’s motor activity.