Brief Considerations Of Pathology

Given the many critical functions of the pons and medulla oblongata, pathology in these hindbrain derivatives can have a wide variety of effects. Specific or diverse symptoms may result, depending on whether the pathology is focal, involving a particular nucleus or pathway, or more widespread. In either case, the pathological manifestations can be devastating and potentially life-threatening since so many areas of the pons and medulla participate in vital processes. Thus, contusions, tumors, and vascular lesions are often fatal. Several well-known pathological syndromes can be distinguished on the basis of particular combinations of symptoms, as these relate directly to the location of the lesion and the level at which fiber tracts decussate. For example, medial lesions typically present symptoms such as contralateral hemiparesis (corticospinal tract) and loss of proprioception (medial lemniscus). In contrast, lateral lesions typically present symptoms such as ipsilateral loss of facial cutaneous sensation (trigeminal sensory nucleus and tract), contralateral loss of pain and temperature sensation (spinothalamic tract), and Horner syndrome (ipsilateral descending autonomic fibers). In addition, each type of lesion will potentially affect the function of specific cranial nerves.

The different medial and lateral pontine and medullary syndromes lie within the basic diagnostic repertoire of the practicing neurologist. Hindbrain pathology reulting from genetic disorders is a less common class of diagnosis but almost certainly occurs more frequently than is currently recognized. Mutations in transcription factor genes have been established as the cause of a few pathological syndromes, such as Waardenberg's syndrome, that involve developmental defects in the cranial neural crest (cristopa-thies). Similar mutations in genes patterning the hindbrain neural tube could lead to catastrophic consequences if they disrupt major elements of the pattern, but they could also lead to more focal defects compromising the function of specific networks, with more subtle symptoms as a result. For example, nonlethal mutation of the Krox-20 gene in the mouse, which disrupts rhombomeric patterning, perturbs the development of respiratory networks and leads to varying degrees of apnea. There are probably a large number of idiopathic conditions affecting the hind-brain that have a genetic basis, and it is not unreasonable to expect that as genetic analysis of hindbrain patterning progresses new syndromes will be classified for which mutation of identified patterning genes is the underlying cause.



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