15.1. Introduction
Clinical anatomical correlations as well as functional studies with PET, SPECT, functional MRI and magnetoencephalography reveal that distributed networks form the anatomical basis of behavioral neurology. In essence, a lesion in varied areas of the brain may destroy a functional network which may cause a specific deficit. However, it is still clinically useful to assign major functions to specific anatomical areas of the brain with the understanding that this one area may be only one link in a distributed network.
Diaschisis of Von Monakow is another concept that must be borne in mind when performing pathological, anatomical and clinical correlation. This concept suggests that the anatomical connections of a distributed network have metabolic and neurotransmitter concomitants, which may cause a neurological deficit at a distance from the injury. Discharge from one area of the brain if severe and persistent may damage either its homologous area or another part of the distributed network by:
- Glutamate-NMDA excitotoxicity mechanism
- Induction of apoptosis from intracellular calcium dysregulation
- Neural plasticity induced by immediate early response genes
Many anatomical pathological clinical correlates have withstood the test of time, but basic mechanisms have changed.
Most external sensory information reaches the cortex through the thalamus. Autonomic and properties of the homeostatic condition of the body are projected from the brain stem and hypothalamus through the medial thalamic nuclei to the limbic cortex. These areas consist of medial temporal and insular cortices, orbital cortex and the cingulate gyrus.
Specific areas of the reticular formation activate specific areas of the cortex.
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