Overactive - Pathophysiology

Pathophysiology

The causes of the majority of the above hyperkinetic movements can be traced to improper modulation of the basal ganglia by the subthalamic nucleus. In many cases, the excitatory output of the subthalamic nucleus is reduced, leading to a reduced inhibitory outflow of the basal ganglia. Without the normal restraining influence of the basal ganglia, upper motor neurons of the circuit tend to become more readily activated by inappropriate signals, resulting in the characteristic abnormal movements.

There are two pathways involving basal ganglia-thalamocortical circuitry, both of which originate in the neostriatum. The direct pathway projects to the internal globus pallidus (GPi) and to the substantia nigra pars reticulata (SNr). These projections are inhibitory and have been found to utilize both GABA and substance P. The indirect pathway, which projects to the globus pallidus external (GPe), is also inhibitory and uses GABA and enkephalin. The GPe projects to the subthalamic nucleus (STN), which then projects back to the GPi and GPe via excitatory, glutaminergic pathways. Excitation of the direct pathway leads to disinhibition of the GABAergic neurons of the GPi/SNr, ultimately resulting in activation of thalamic neurons and excitation of cortical neurons. In contrast, activation of the indirect pathway stimulates the inhibitory striatal GABA/enkephalin projection, resulting in suppression of GABAerigc neuronal activity. This, in turn, causes disinhibition of the STN excitatory outputs, thus triggering the GPi/SNr inhibitory projections to the thalamus and decreased activation of cortical neurons. While deregulation of either of these pathways can disturb motor output, hyperkinesia is thought to result from overactivity of the direct pathway and decreased activity from the indirect pathway.

Hyperkinesia occurs when dopamine receptors, and norepinephrine receptors to a lesser extent, within the cortex and the brainstem are more sensitive to dopamine or when the dopaminergic receptors/neurons are hyperactive. Hyperkinesia can be caused by a large number of different diseases including metabolic disorders, endocrine disorders, heritable disorders, vascular disorders, or traumatic disorders. Other causes include toxins within the brain, autoimmune disease, and infections, which include meningitis.

Since the basal ganglia often have many connections with the frontal lobe of the brain, hyperkinesia can be associated with neurobehavioral or neuropsychiatric disorders such as mood changes, psychosis, anxiety, disinhibition, cognitive impairments, and inappropriate behavior.

In children, primary dystonia is usually inherited genetically. Secondary dystonia, however, is most commonly caused by dyskinetic cerebral palsy, due to hypoxic or ischemic injury to the basal ganglia, brainstem, cerebellum, and thalamus during the prenatal or infantile stages of development. Chorea and ballism can be caused by damage to the subthalamic nucleus. Chorea can be secondary to hyperthyroidism. Athetosis can be secondary to sensory loss in the distal limbs; this is called pseudoathetosis in adults but is not yet proven in children.

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