Basal Ganglia Notes
BASAL GANGLIA
Recent advances in the knowledge of basal ganglia functional anatomy and physiology make it possible to hypothesize how specific neural mechanisms relate to manifestations of TS. Recent studies have shown a model of selection and suppression of competing behaviours by the basal ganglia circuits and on dopamine modulation of these circuits to provide the basis for basal ganglia dysfunction in TS.
The basal ganglion consists of the striatum, subthalamic nucleus, globus pallidus and substantia nigra and consists of several interconnected nuclei in the forebrain, midbrain and diencephalon. Evidence suggests that the dysfunction of the basal ganglia or their connection with frontocortical circuits has a fundamental importance in the pathophysiology of TS.
BASAL GANGLIA CIRCUITRY
The striatum and the subthalamic nucleus are the primary input structures of the basal ganglia, receiving excitatory input from the cerebral cortex. The globus pallidus and the substantia nigra are the primary output structures, sending inhibitory output signals to the thalamus and brainstem. Therefore increased Basal Ganglia output results in an increase inhibition of thalamocortcical and brainstem targets, which are responsible for pre motor control. In addition to the striatum receiving cortical input it also receives input from dopamine containing neurons in the substantia nigra.
The output from the subthallamic nucleus is excitatory, the output from the striatum is inhibitory. The basal ganglia motor output has multilevels of organisation, the body below the neck is represented by the globus pallidus, whereas the head and eyes are represented in the substantia nigra, with this means that there are separate outputs to different motor cortex areas.
MOTOR PATTERN: DAMAGE
If striatal neurons become abnormally active, abnormal inhibition of a group of basal ganglia output neurons occurs, an unwanted competing motor neuron pattern can be triggered, resulting in a tic – monkey
Recent advances in the knowledge of basal ganglia functional anatomy and physiology make it possible to hypothesize how specific neural mechanisms relate to manifestations of TS. Recent studies have shown a model of selection and suppression of competing behaviours by the basal ganglia circuits and on dopamine modulation of these circuits to provide the basis for basal ganglia dysfunction in TS.
The basal ganglion consists of the striatum, subthalamic nucleus, globus pallidus and substantia nigra and consists of several interconnected nuclei in the forebrain, midbrain and diencephalon. Evidence suggests that the dysfunction of the basal ganglia or their connection with frontocortical circuits has a fundamental importance in the pathophysiology of TS.
BASAL GANGLIA CIRCUITRY
The striatum and the subthalamic nucleus are the primary input structures of the basal ganglia, receiving excitatory input from the cerebral cortex. The globus pallidus and the substantia nigra are the primary output structures, sending inhibitory output signals to the thalamus and brainstem. Therefore increased Basal Ganglia output results in an increase inhibition of thalamocortcical and brainstem targets, which are responsible for pre motor control. In addition to the striatum receiving cortical input it also receives input from dopamine containing neurons in the substantia nigra.
The output from the subthallamic nucleus is excitatory, the output from the striatum is inhibitory. The basal ganglia motor output has multilevels of organisation, the body below the neck is represented by the globus pallidus, whereas the head and eyes are represented in the substantia nigra, with this means that there are separate outputs to different motor cortex areas.
MOTOR PATTERN: DAMAGE
If striatal neurons become abnormally active, abnormal inhibition of a group of basal ganglia output neurons occurs, an unwanted competing motor neuron pattern can be triggered, resulting in a tic – monkey