Anatomical Balance between various interacting neuronal systems such as locomotion which includes initiation and maintenance of rhythmic stepping, balance, and ability to adapt to the environment. Deficit appears to be localized in the putamen and globus pallidus resulting in a reduction in the muscle force produced at the initiation of the movement. Initiation of a movement starts by inducing stepping through reticulospinal and vestibulospinal projection in ventromedial descending brainstem pathways. The bulbospinal pathways are modulated with the support of and swing of the gait cycle, and this modulation is accomplished through the connections with the cerebral vermis. Diseases that affect the vestibular system such as gait disorders often impair the initiation of a movement. Most of the patients with<unk> 's syndrome suffer from hypokinetic gait disorder defined as slowness of movement due to the dysfunction of the circuitry controlled by the basal ganglia, frontal lobe and brainstem. Patients are limited to a wide-based or variable stance and truncal imbalance. Another region involved in the psychogenic tremor is the temporoparital junction depicted by a hypo-activation in patients that were functional imaging recorded during an episode of functional tremor or when the same patients were voluntarily mimicking their tremor. This region is thought to be a comparator region, comparing actual with predicted sensory feedback. This experiment suggests that the hypoactivity might represent a failure to match the actual and predicted sensory feedback, resulting in an inhibition of the movement. In addition, another functional imaging study in psychogenic movement disorder noted abnormally strong amygdala–supplementary motor area connectivity when patients were presented with emotionally stimuli and abnormally weak supplementary motor area–prefrontal cortex connectivity in a reaction time task. Scientists thus speculated that the hypoactivity may be due to the lack of an appropriate prediction outcome signal of the conversion tremor. Thus, without the predicted outcome signal, there would be no comparison between the predicted versus the actual sensory outcome of the conversion movement and hence the temporoparietal junction hypoactivity and the sensation that the movement is not under one’s control enabling the initiation of it. Pathophysiology Psychogenic disorder has been linked with basal ganglia dysfunction and dopamine deficiency observed by a decrease in neuronal density in substantia nigra in elderly patients. On an in-vivo study, the absence of dopamine in the cultures perturbed the dynamics of the subthalamic nucleus (STN) and the GABAergic neurons of the globus pallidus(GP). It is believed that the activation of the indirect pathway (striatum-GP-STN-output nuclei) increases the firing rate of GP-STN neurons resulting in an excessive inhibition of basal ganglia targets. In psychogenic disorder, the activity in the indirect pathway (inhibits movement, thoughts) predominates over that on the direct pathway (increases movement, thoughts, feelings), giving rise to an increase in the globus pallidus interior (GPi) inhibitory output, which results in decrease motor activity. Specifically, it begins on the cerebral cortex sending projections to neurons in striatum. These neurons will inhibit the external segment of the Globus Pallidus (GPe), which normally inhibits the subthalamic nucleus (STN). However, the GPe is inhibited and no longer inhibit the STN and the STN will excite the GPi which finally inhibits the thalamus and prevents from exciting to the cerebral cortex and command the spinal cord for initiation of a movement. In addition, scientists have found that the degree of slowness of movement is characterized by the decrease of F-fluorodpa uptake in the striatum and nucleus accumbens complex.
Blocq's disease
Tornwaldt's disease
Cruveilhier–Baumgarten disease
Majocchi's disease
Mondor's disease
Milroy's disease
Gorham's disease
Kimura's disease