Neurogenic Regulation
Considerable evidence has shown that the cerebral vasculature
is extensively innervated.[63]
The density of innervation
declines with vessel size, and the greatest neurogenic influence appears to be exerted
on larger cerebral arteries.[64]
This innervation
includes cholinergic (parasympathetic[65]
and nonparasympathetic),
[66]
[67]
[68]
adrenergic (sympathetic[69]
and nonsympathetic),
[70]
serotonergic,[71]
[72]
and VIPergic[73]
systems of extra- and intra-axial origin. It is certain that in animals there is
an extracranial sympathetic influence through the superior cervical ganglion[69]
[74]
[75]
[76]
[77]
and parasympathetic innervation through the
sphenopalatine ganglion.[65]
The intra-axial pathways
are less well defined, although there is considerable evidence of innervation arising
from several nuclei in animals, including the locus ceruleus,[70]
the fastigial nucleus,[68]
the dorsal raphe nucleus,
[72]
and the basal magnocellular nucleus of Meynert.
[66]
[67]
Evidence
of the functional significance of neurogenic influences has been derived from studies
of CBF autoregulation[74]
[76]
[78]
[79]
[80]
and ischemic injury.[81]
[82]
Hemorrhagic shock, a state with high sympathetic tone, results in a lower CBF at
a given MAP than occurs when hypotension is produced with sympatholytic drugs, presumably
because during shock, a sympathetically mediated vasoconstrictive effect shifts the
lower end of the "autoregulatory" plateau ( Fig.
21-5
) to the right. It is not clear what the relative contributions of
humoral and neural mechanisms are to this phenomenon; however, a neurogenic component
is certainly operative in some species because sympathetic denervation increases
CBF during hemorrhagic shock.[74]
[78]
[83]
Activation of cerebral sympathetic innervation
also shifts the upper limit of autoregulation to the right and offers some protection
against hypertensive breakthrough of the BBB.[79]
[80]
Experimental interventions that alter these
neurogenic control pathways influence outcomes after standardized ischemic insults,
[81]
[82]
presumably
through influences on vascular tone and therefore CBF. The nature and influence
of such pathways in humans are not known, and at present, there are no clinical interventions
designed to manipulate these pathways that are relevant to neurosurgical patients.
[84]
 |
