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Physiologic evidence indicates that a balanced functional architecture, one excitatory and the other inhibitory, is operative within the individual circuits The direct striatomedial pallidonigral pathway is activated by glutaminergic projections from the sensorimotor cortex and by dopaminergic nigral (pars compacta) striatal projections Activation of this direct pathway inhibits the medial pallidum, which, in turn, disinhibits the ventrolateral and ventroanterior nuclei of the thalamus As a consequence, thalamocortical drive is enhanced and cortically initiated movements are facilitated The indirect circuit arises from putaminal neurons that contain gamma-aminobutyric acid (GABA) and smaller amounts of enkephalin These striatal projections have an inhibitory effect on the lateral pallidum, which, in turn, disinhibits the subthalamic nucleus through GABA release, providing excessive subthalamic drive to the medial pallidum and substantia nigra pars reticulata The net effect is thalamic inhibition that reduces thalamocortical input to the precentral motor elds and impedes voluntary movement These complex, and in part still theoretical anatomic and physiologic relationships have been summarized in numerous schematic diagrams similar to Fig 4-4 and those in Lang and Lozano and in Standaert and Young (see References) Restated, enhanced conduction through the indirect pathway leads to hypokinesia (by increasing pallidothalamic inhibition), whereas enhanced conduction through the direct pathway results in hyperkinesia (by reducing pallidothalamic inhibition) The direct pathway is perceived by Marsden and Obeso as facilitating cortically initiated movements and the indirect pathway as suppressing potentially con icting and unwanted motor patterns In Parkinson disease, for example, loss of dopaminergic input from the substantia nigra diminishes activity in the direct pathway and increases activity in the indirect pathway; the net effect is to increase inhibition of the thalamic nuclei and to reduce excitation of the cortical motor system Further insight into Parkinson disease has come from the discovery that it can be faithfully reproduced in humans and primates by the toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) This toxin was discovered accidentally in drug addicts who self-administered an analogue of meperidine The toxin binds with high af nity to monoamine oxidase (MAO), an extraneural enzyme that transforms it to a toxic metabolite pyridinium The latter is bound by melanin in the dopaminergic nigral neurons in.

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We executed the first step and the report is inserted into the migration wizard to be processed As indicated by the Change button, in the first step, we could have gone into the WAD template and made a change to the template before the migration process if we wanted to adjust the description or some other parameters within the WAD template Once we are through with Step 1, we can then execute Step 2 In this step, we identify whether we would like the system to generate the XML and all the other components of the WAD template, such as the graphics, different style sheets, and XHTML conversion These options for both Step 1 and 2 are shown in the following illustration

suf cient quantities to destroy the cells, probably by interfering with mitochondrial function In monkeys made parkinsonian by the administration of MPTP, electrophysiologic studies have shown increased activity in the medial globus pallidus and decreased activity in the lateral globus pallidus, as predicted from the previously described models This comes about because of the differential loss of activity of dopaminergic striatal neurons that project to each of these parts of the pallidum The end result is increased inhibition of thalamocortical neurons It is, however, dif cult to explain why medial pallidal lesions do not regularly cause parkinsonism, as pointed out by Bhatia and Marsden Perhaps it is because the subtle imbalance between the medial and lateral pallidal circuits that exists in Parkinson disease is not reproduced This subtlety may also explain why crude lesions such as infarcts, hemorrhages, and tumors rarely produce the complete parkinsonian syndrome of tremor, bradykinesia, and rigidity without paralysis or re ex changes Indeed, striking improvements in parkinsonian symptoms are obtained by placing lesions in the medial pallidum (pallidotomy), as discussed on page 924 However, there are de ciencies in all current models, particularly as they relate to Parkinson disease and its treatment For example, the abatement of drug-induced dyskinesias by a lesion in the subthalamic nucleus is an anomaly, and the effects of thalamic lesions are not easily explained (see Chap 39) It is likely that the static model of inhibitory and excitatory pathways and the parsing of a direct and an indirect pathway, as useful as it is as a mnemonic, does not account for the dynamic activities of the basal ganglia In particular, the activity of the neurons in these systems oscillate and in uence the frequency of oscillations in other parts of the system, as well as bringing individual cells closer to ring It has also been pointed out that currently conceived models do not account for the tremor of Parkinson disease Furthermore, the various subtypes of dopamine receptors act in both excitatory and inhibitory ways under different circumstances depending on their location The complexity of basal ganglionic interactions can hardly be explained in these simpli ed models, but they remain reasonable prototypes for understanding abnormal hyperkinetic and hypokinetic movements In more conventional but not yet antiquated physiologic terms, Denny-Brown and Yanagisawa, who studied the effects of ablation of individual extrapyramidal structures in monkeys, concluded that the basal ganglia function as a kind of clearinghouse where, during an intended or projected movement, one set of activities is facilitated and all other unnecessary ones are suppressed They used the analogy of the basal ganglia as a brake or switch, the tonic inhibitory ( brake ) action of the basal ganglia preventing target structures from generating unwanted motor activity and the switch function referring to the capacity of the basal ganglia to select which of many available motor programs will be active at any given time Still other theories focus on the role of the basal ganglia in the initiation, sequencing, and modulation of motor activity ( motor programming ) Also, it appears that the basal ganglia participate in the constant priming of the motor system, enabling the rapid execution of motor acts without premeditation eg, hitting a baseball In most ways, these conceptualizations restate the same notions of balance and selectivity imparted to all motor actions by the basal ganglia The manner in which excessive or depleted activity of various components of the basal ganglia gives rise to hypokinetic and hyperkinetic movement disorders is discussed further on, under Symptoms of Basal Ganglia Disease.

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