The Human Brain:
The Structural Basis for Understanding Human Brain Function and Dysfunction

+++ INTERNATIONAL CONFERENCE +++ ROME +++ IRCCS SANTA LUCIA +++ Oct. 5-10, 2002 +++

Home
Greetings
Overview (Calendar)
Objectives
Organization
Speakers
Educational Material
Location
Contact
Sponsors
Announcements
Press Echo
Press Releases
Articles for the Press
Picture Gallery
William W. Blessing
Departments of Physiology and Medicine,
Centre for Neuroscience, Flinders University, Adelaide, SA, Australia
e-mail: w.w.blessing@flinders.edu.au

Presentation:
2002-10-06, 15:00-15:45
Lower brainstem dys-regulation of autonomic function.
My presentation outlines the functional neuroanatomy of lower brainstem neurons regulating cardiovascular and gastrointestinal function, and indicates how neurological disorders, including Parkinson's Disease can affect these structures, resulting in clinical symptomatology. Work in animals has established that discharge of excitatory presympathetic neurons in the rostral ventrolateral medulla oblongata (RVLM) maintains activity in peripheral sympathetic vasomotor and cardiomotor nerves. In animals and in humans, so that it is likely that the fundamental organization of cardiovascular circuitry is similar in humans and other mammals. In animals, approximately 50% of the excitatory presympathetic vasomotor neurons in the RVLM belong to the C1 group of catecholamine-synthesizing neurons present in this medullary region. There is a prominent group of PNMT-containing neurons in the corresponding region of the human medulla corresponding to the RVLM in experimental animals P--NMT-containing neurons in the human ventrolateral medulla presumably at least partially constitute the sympathoexcitatory presympathetic vasomotor neurons responsible for maintaining peripheral sympathetic vasomotor and cardiomotor tone. Loss of RVLM presympathetic vasomotor neurons may contribute to the postural hypotension which sometimes occurs in patients with Parkinson's disease. The lower brainstem contains neural circuitry sufficiently complex to initiate the appropriately coordinated contraction of jaw, facial, largygeal, pharyngeal tongue and cervical muscles, with accompanying inhibition of respiration. Patients with severe forebrain damage can swallow if food or water is placed directly into the mouth, a stimulus which activates primary afferents in trigeminal, facial (nervus intermedius), glossopharygneal and vagal cranial nerves. These afferents synapse in sensory brainstem nuclei, including the principal sensory nucleus of V, the spinal nucleus of V and the nucleus of the solitary tract (Sol). Parasympathetic preganglionic motoneurons regulating gastrointestinal function are located in the dorsal motor nucleus of the vagus (10). This nucleus is one of the earliest brainstem regions to be damaged in Parkinson's Disease. The loss of weight occurring in the later stages of Parkinson's disease may be a manifestation of gastrointestinal dysfunction secondary to damage to 10. Patients with brainstem dysfunction often experience nausea and vomiting, symptoms which rarely occur with pathological processes confined to the forebrain. Indeed, when a patient with a hemispheric neoplasm or intracerebral hemorrhage vomits, there is usually a degree of cerebral swelling which presumably displaces brainstem structures. In contrast, tumors of the posterior fossa commonly cause vomiting early in their course. Similarly, if a patient with focal cerebral ischemia has nausea and vomiting, the ischemic region is nearly always in the lower brainstem, in territory supplied by the vertebrobasilar vessels. Lesions impinging the area postrema (eg an ependymoma of the fourth ventricle. can also cause nausea vomiting. The coordinated autonomic and somatic motor components of the act of vomiting presumably involve projections from Sol to 10 and to the premotor neurons controlling the relevant "swallowing" motoneurons in cranial nerves 5, 7, 9-12.--

 

Top