Figure 4-3. Schematic illustration of major efferent and afferent connections of the basal ganglia. The green lines indicate neurons with excitatory effects, whereas the red lines indicate inhibitory influences. (See text for details and  Fig. 4-2.) (Reproduced with permission from Kandel ER, Schwartz JH, Jessell TM: Principles of Neural Science, 5th ed. New York: McGraw-Hill, 2013.)
Figure 4-4. A. Schematic diagram of the cortical–basal ganglia–thalamic circuits showing the main neurotransmitter pathways and their effects. Dopaminergic neurons arising in the pars compacta of the substantia nigra have an excitatory influence on the direct pathway (via D1 receptors) and an inhibitory effect on the indirect pathway (via D2 receptors). B. In Parkinson disease, hypokinesia is thought to result from reduced dopamine input from the substantia nigra to the striatum. As a result, decreased inhibition of the globus pallidus interna by the direct pathway, and increased excitation of the globus pallidus interna by the indirect pathway, leads to increased inhibitory drive of the thalamus and therefore decreased excitation of the cortex. C. In Huntington disease, there is degeneration of the striatum. For the direct pathway, there is overall a net inhibition of the globus pallidus interna (due to decreased inhibition from the striatum, increased inhibition from the globus pallidus externa, and decreased excitation from the subthalamic nucleus). For the indirect pathway, there is less inhibition of the globus pallidus externa, leading to more inhibition of the subthalamic nucleus, less excitation of globus pallidus interna. In sum, there is less inhibition of the thalamus, and increased excitation of the cortex, leading to hyperkinetic movements. (continued)
Figure 4-5. A. Characteristic dystonic deformities in a young boy with dystonia musculorum deformans. B. Sporadic instance of severe axial dystonia with onset in adult life. C. Incapacitating postural deformity in a young man with dystonia. (Photos courtesy of Dr. I. S. Cooper and
Dr. Joseph M. Waltz.)
Figure 4-6. Tremor branch diagram.
Figure 4-7. Types of tremor. In each, the lowest trace is an accelerometric recording from the outstretched hand; the upper two traces are surface EMG from the wrist extensor (upper) and flexor (middle) muscle groups. A. A physiologic tremor; there is no evidence of synchronization of EMG activity. B. Essential (familial) tremor; the movements are very regular and EMG bursts occur simultaneously in antagonistic muscle groups. C. Neuropathic tremor; movements are irregular and EMG bursts vary in timing between the two groups. D. Parkinsonian (“rest”) tremor; EMG bursts alternate between antagonistic muscle groups. Calibration is 1 s. (Courtesy of Dr. Robert R. Young.)
Figure 4-8. Dystonic movement disorders. A. Young man with severe spasmodic retrocollis. Note hypertrophy of sternocleidomastoid muscles. B. Meige syndrome of severe blepharospasm and facial-cervical dystonia. C. Characteristic athetoid-dystonic deformities of the hand in a patient with tardive dyskinesia. (Photographs courtesy of Dr. Joseph M. Waltz.)