A characteristic of Parkinson's disease is the high number of symptoms, both motor and non-motor, responsible for significant disability and serious repercussions on the quality of life of individuals affected by the disease.
The motor symptoms typical of Parkinson's disease will be described in more detail below .
- Akinesia : it is common to describe one of the main symptoms of Parkinson's disease with the difficulty in automatically performing elementary and complex movements. It has also been shown that the execution of repetitive movements is altered in amplitude, rhythm and speed. The akinesia, therefore, is characterized by a high difficulty of movement, so much so that individuals affected by Parkinson's disease with extreme difficulty succeed in performing automatic movements, such as touching their faces, crossing their arms or crossing their legs. In addition, the normal pendulum movements of the arms, which usually follow the pace, are reduced during walking, the expressiveness of the face is lacking, the gesticulation associated with conversation is reduced and the automatic act of swallowing also decreases, consequently causing accumulation of saliva in the mouth, a phenomenon commonly called sialorrhea.
- Bradykinesia : represents the most characteristic symptom of Parkinson's disease and consists of a long period of latency between the command and the beginning of the movement. The result is a reduction in the speed of execution of motor gestures compared to normal conditions. Individuals suffering from Parkinson's disease are able to activate the agonist muscle correctly and also manage the antagonist to allow them to move in the right direction; they are therefore able to control the muscles correctly, even if in a much slower manner than healthy individuals. Therefore, a correct motor program is performed in the wrong way.
Deepening: the premotor area of the cortex is responsible for the inputs of the striatum-pallid complex. It is important to emphasize that the premotor area of the cortex should be able to guarantee the execution of the movement when the motor behavior is still not well established. Following learning, the basal ganglia allow the motor program to be performed automatically but scrupulously. In the event that damage occurs at the level of the basal ganglia, here come into action the cortical mechanisms. However, the latter are less flexible and less accurate for the execution of motor programs. The result is a loss of automatic movement.
- Stiffness : the muscles are continuously tense, even when the individual with Parkinson's disease appears relaxed. This form of hypertonia is not selective for some muscle groups, but manifests itself with a certain prevalence at the level of the flexor muscles of the trunk and limbs. In addition, it also affects the small facial muscles, tongue and larynx. It is not uncommon for Parkinson's disease patients to experience pain during the night due to the hardness and increased consistency of the muscles. After a movement, the part of the body that has moved is able to maintain the new position, and to assume awkward postures. A form of rigidity typical of Parkinson's disease was discovered in 1901, called the cogwheel phenomenon and characterized by the passive mobilization of an extremity (for example the flexion of the hand on the forearm) followed by a rhythmically interrupted resistance.
Deepening: the physiopathology responsible for the symptom of rigidity has not yet been understood. One of the hypotheses holds that among the main causes there is an excessive and uncontrollable supraspinal activity towards the motor neurons, which then translates into the non-ability on the part of individuals affected by Parkinson's disease to relax the muscular masses. It is important to emphasize that rigidity should be seen as a positive symptom that derives from the activity of other central nervous system structures that would normally be inhibited by the basal ganglia.
- Tremor : this symptom is also quite representative of Parkinson's disease. It is an involuntary, fairly regular rhythmic oscillation of a part of the body around a fixed point, on a single plane. This tremor can be physiological, always present, and can manifest itself imperceptibly even during certain phases of sleep. Furthermore, it can also be pathological, present only during the waking phase and only in some muscle groups, such as the distal part of the limbs, the head, the tongue, the jaw and sometimes the trunk. During the movement, in the individual affected by Parkinson's, the tremor disappears or decreases clearly, but then reappears as soon as the limb goes to take the so-called rest position. In this case, the tremor does not significantly interfere with the individual's normal activities. It has been observed that generally the tremor appears homolaterally, hitting more a hand and fingers with a phenomenon known as " pill-rolling tremor ", a movement that resembles that of counting coins. In practice, it consists of a flexion-extension of the fingers in combination with the abdo-abduction of the thumb. After several months or even years, this symptom also manifests itself in the other hand. However, generally in half of the patients the tremor manifests itself as an initial symptom of Alzheimer's disease, despite the fact that due to anxiety and stress the frequency with which it manifests itself tends to increase.
Deepening: two theories have been developed, which would seem to be opposite to each other, to try to explain how resting tremor is born in Parkinson's disease. In the first hypothesis it was based on the fact that, while some cells are activated by muscle contraction or thanks to afferent signals coming from such muscular activity, some cells are rhythmically active before the tremor. They represent the pacemaker of the tremor itself and, from the studies conducted by Ohye, it would be located in the middle ventral nucleus, which receives cerebellar and spino-thalamic projections. Subsequently the pyramidal bundles transmit the thalamic rhythmic activities to the spinal motor neurons. The selective destruction of this structure inhibits resting tremor without affecting stiffness.
In the second theory, however, it has been shown that resting tremor, which manifests itself as a reflex response to the activation of peripheral receptors, can be generated by voluntary movements. In this case, a neuronal circuit that includes the neuromuscular spindles, the thalamus, the motor cortex and ending up through the pyramidal bundles on the motor neurons, could include the tremor pacemaker. Finally, it is typical of individuals affected by Parkinson's disease, to feel an "internal" tremor, invisible to the outside, but felt by the patient himself.
