Abstract
Essential tremor (ET) is one of the most common neurological disorders that often affects people in the prime of their lives, leading to a significant reduction in their quality of life, gradually making them unable to independently perform the simplest activities. Here we show that current ET pharmacotherapy often does not sufficiently alleviate disease symptoms and is completely ineffective in more than 30% of patients. At present, deep brain stimulation of the motor thalamus is the most effective ET treatment. However, like any brain surgery, it can cause many undesirable side effects; thus, it is only performed in patients with an advanced disease who are not responsive to drugs. Therefore, it seems extremely important to look for new strategies for treating ET. The purpose of this review is to summarize the current knowledge on the pathomechanism of ET based on studies in animal models of the disease, as well as to present and discuss the results of research available to date on various substances affecting dopamine (mainly D3) or adenosine A1 receptors, which, due to their ability to modulate harmaline-induced tremor, may provide the basis for the development of new potential therapies for ET in the future.
Highlights
Tremor is an involuntary, rhythmic, and oscillating movement produced by alternating or synchronous contractions of antagonistic muscles in different parts of the body
Tremor can be classified according to the circumstances and conditions under which they occur: (1) resting tremor occurs in the resting state of the limb, which does not have to counteract the force of gravity; (2) action tremor, which can appear when the patient voluntarily holds a part of the body in a selected position, against the force of gravity; (3) kinetic tremor, which appears at the time of performing a specific voluntary movement; and (4) isometric tremor, which appears during the isometric contraction of the muscles against constant resistance, e.g., squeezing a selected object in the hand [1,3]
Data that support such a hypothesis were provided, among others, by studies of coherence between signals recorded simultaneously from electrodes located on the surface of the skull and EMG signals from a selected muscle, which revealed a network of areas consisting of the contralateral primary motor cortex, premotor cortex, thalamus, ipsilateral cerebellum, and brainstem that are consistent with muscle activity during episodes of tremor [62]
Summary
Rhythmic, and oscillating movement produced by alternating or synchronous contractions of antagonistic muscles in different parts of the body. They may occur as a consequence of motor dysfunction secondary to tremor, which, through a negative impact on the performance of the basic functions of everyday life, leads to a decrease in the patient’s independence, lower self-esteem, and social isolation, and to the development of depression or anxiety. They may be due to the patient’s pharmacotherapy (a side effect of medications) or as a result of neurodegeneration in various parts of the nervous system, assuming that ET is a neurodegenerative disease [11]. The results of studies by Louis et al [12] indicated that in patients who self-reported depression compared to those taking antidepressants, the incidence of ET was much higher, suggesting that depression may be the primary symptom of the disease development and may constitute a kind of pre-motor marker or risk factor for ET
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