The issue of the functional state of the thyroid gland in parkinsonism deserves special attention . Clinicians have long drawn attention to some common features in the manifestations of hyperthyroidism and the tremulous form of parkinsonism, hypothyroidism, and akinetic-rigid forms of parkinsonism.
Studying the functional state of the thyroid gland in patients with parkinsonism using the radioactive isotope 131I often reveals a decrease in its functional activity. In the work of S.I. Savenko, Yu. G. Prasol and I.N. Marega, a relationship was found between a decrease in thyroid function and the severity of the course of parkinsonism.
The pathological picture of parkinsonism is described , in which significant morphological changes in the sympathetic cervical ganglia are combined with damage to the thyroid gland.
It has been suggested that Parkinson’s syndrome may be genetically associated with thyrotoxicosis. However, this assumption contradicts the rarity of the combination of these diseases.
The hypothesis about the role of encephalitis in the origin of both syndromes is not shared by all researchers, because signs of thyrotoxicosis can be observed with Parkinson’s syndrome of nonencephalitic etiology. Often clinically, Parkinsonism and thyrotoxicosis can be in a complex relationship. Sometimes thyrotoxicosis enhances the manifestation of parkinsonism, but it can also mask the manifestations of parkinsonism, which depends on the form of the latter.
Most often, symptoms of parkinsonism prevail in the clinical picture of the disease. Therapeutic suppression of thyroid function in patients with this combined syndrome often leads to a marked decrease in the severity of parkinsonian symptoms. Often there is an exacerbation of the manifestations of one disease with the addition of another.
Catecholamines and thyroid hormones have common precursors in the form of amino acids – phenylalanine and tyrosine. Phenylalanine deficiency can lead to a lack of synthesis of both catecholamines and thyroid hormones.
Apparently, the relationship between thyroid hormones and catecholamines , as well as between the state of the thyroid gland and parkinsonism, is more complex. The development of parkinsonism syndrome as a complication of thyroidectomy is described.
In our previous studies , facts were obtained that testify to the pathogenetic heterogeneity of Parkinson’s syndrome, which is based on the uneven functional state of some parts of the activating systems of the brain, which, as you know, have adrenergic mediation. Based on these data, it can already be a priori assumed that antithyroid therapy (conservative or surgical) can reduce the symptoms of parkinsonism in only a part of patients with tremulous forms of parkinsonism (or rather, in the presence of a high level of motor-activation shifts).
In patients with akinetic manifestations, suppression of thyroid function can only exacerbate the severity of parkinsonism. In such cases, thyroidectomy can apparently reveal subclinical or beginning parkinsonism. Further observations are needed to finally resolve this issue.