Bilateral lesions of the fastigial nucleus prevent the recovery of blood pressure following hypotension induced by hemorrhage or administration of endotoxin

Lutherer, L. O.; Lutherer, Berta; Dormer, Kenneth J.; Janssen, Herbert F.; Barnes, Charles D.

doi:10.1016/0006-8993(83)90134-8

Cited by 93 publications

(84 citation statements)

References 10 publications

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“…Cerebellar structures, once associated with motor coordination functions only, are now recognized as playing essential roles in limiting extremes of blood pressure change and modifications in ANS outflow to motor action. 24,35 Other aberrant responses may develop from damage triggered by other means, such as neural injury from inflammatory processes frequently accompanying HF. 36,37 Scattered cerebral infarcts appear in HF patients, 38 likely resulting from emboli; however, these lesions have not been sited in specific autonomic regions or related to specific clinical symptoms.…”

Section: Discussionmentioning

confidence: 99%

Aberrant Central Nervous System Responses to the Valsalva Maneuver in Heart Failure

Woo

Macey

Keens

et al. 2007

Congestive Heart Failure

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Heart failure (HF) is associated with aberrant autonomic nervous system (ANS) activity, with altered responses to blood pressure and breathing challenges that appear to reflect abnormal central nervous system function. The authors used functional magnetic resonance imaging (fMRI) to determine whether the Valsalva maneuver, an ANS challenge, would show abnormal responses in ANS regulatory areas of the brain in HF. Brain fMRI signal changes in 5 HF patients (left ventricular ejection fraction, 0.15±0.08; age, 50±10 years) and 14 controls (age, 47±11 years) were assessed during 3 successive Valsalva maneuvers. The hypothalamus, hippocampus, putamen, amygdala, mid‐cingulate, right insula, and cerebellar cortex showed exaggerated and phase‐shifted fMRI responses in HF; other areas showed inverted signals from those found in controls. Central ANS control areas have altered phase, extent, and direction of responses to Valsalva maneuvers in a small sample of HF patients. These findings suggest that therapeutics that address neuroprotective aspects may be useful interventions for the condition.

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Section: Discussionmentioning

confidence: 99%

Aberrant Central Nervous System Responses to the Valsalva Maneuver in Heart Failure

Woo

Macey

Keens

et al. 2007

Congestive Heart Failure

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“…Cerebellar sites normally participate in mediating respiratory challenges (29) and are frequently recruited during large changes in blood pressure rather than conditions of minor change (30). The ventilatory and blood pressure challenges in other CCHS studies are associated with substantial elevation of blood pressure.…”

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confidence: 99%

“…The cerebellar cortex shows deficits to multiple ventilatory and pressor challenges, including hypercapnia (13), hypoxia (14), expiratory loading (28), and cold pressor challenges (28a). The classic role attributed to cerebellar function has been to mediate extremes of afferent input; the structure normally does not regulate momentary blood pressure changes, for example, but is involved in restorative action to extreme hypo-or hypertension (30). The cerebellum may play similar compensatory roles in hypercapnia and hypoxia, both of which are life-threatening.…”

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confidence: 99%

FMRI Responses to Hyperoxia in Congenital Central Hypoventilation Syndrome

Woo¹,

Macey

et al. 2005

Pediatr Res

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Congenital Central Hypoventilation Syndrome (CCHS) patients show partial retention of peripheral chemoreception despite impaired ventilatory responses to CO 2 and hypoxia. The condition allows examination of central responses to hyperoxia, which minimizes afferent traffic from peripheral chemoreceptors. We used functional magnetic resonance imaging to assess blood oxygen level-dependent signals over the brain during a baseline and subsequent 2-min hyperoxia (100% O 2 ) period in 14 CCHS and 15 control subjects. After partitioning gray matter and correcting for global effects, the images were analyzed using volume-of-interest time trends followed by repeated-measures ANOVA and conventional cluster analyses. Respiratory rates initially (first 20 s) fell in CCHS, but rose in control subjects; CCHS heart rate increased in the first minute, and then decreased in the second minute, as in controls, but with muted rise and extent of decline. Multiple sites within the cerebellum, midbrain, and pons responded similarly to the challenge in both groups. Response patterns differed early in the right amygdala, paralleling initial respiratory pattern deficits, and late in the right insula, concomitant with cardiac rate differences. Signals also differed between groups in the medial and anterior cingulate, hippocampus, head of caudate, and lentiform nuclei, as well as pontine and midbrain structures and regions within the superior temporal and inferior frontal cortical gyri. The findings emphasize that structures that can alter respiratory timing, such as the amygdala, and modulate sympathetic outflow, such as the right insula, are deficient in CCHS. Medullary and pontine areas targeted by PHOX2B expression are also affected. In addition to impaired ventilatory responses to CO 2 and deficient breathing drive during sleep (1), patients with CCHS show inadequate breathing and cardiovascular responses to elevated or lowered levels of O 2 (2-5). The mechanisms involved in altered sensitivity to O 2 in CCHS remain unclear, because some degree of both central and peripheral chemoreception apparently is retained in the syndrome. Respiratory rates increase to hypoxia and decrease to hyperoxia (3,5,6), although both the respiratory and cardiovascular response patterns to challenges are distorted from the normal condition.Determining the neural mechanisms underlying response deficits to differing O 2 levels in CCHS is a significant issue for reasons other than the obvious respiratory implications: CNS responses to hypoxia or hyperoxia recruit the sympathetic nervous system to, among other cardiovascular actions, preferentially alter perfusion of the periphery. CCHS patients show substantial deficits in both sympathetic and parasympathetic components of autonomic nervous system control, which are manifested by such signs as extreme reduction in respiratoryrelated heart rate variability during sleep (7), diminished blood pressure "dipping" during the night (8), syncope to relatively mild provocation (9), a high incidence of cardiac arrhyth...

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“…Cardiovascular control mediated by vestibular nuclei and the cerebellum are important in hazardous situations such as hypovolemic and endotoxin shock (2,3). More than 80% of SIDS victims have shown neuronal apoptosis in vestibular nuclei and nuclei of the tractus solitarii, which are involved in baroand vestibular sympathoreflexes (4).…”

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confidence: 99%

Altered Cardiovascular Control in Preterm Infants with Bronchopulmonary Dysplasia

et al. 2007

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Vestibulo-mediated cardiovascular control in hazardous situations is important. Our hypothesis is that the prerequisite for sudden infant death syndrome (SIDS) is impaired vestibulo-mediated cardiovascular control. Prematurity is a risk factor for SIDS, and postnatal intermittent hypoxia may contribute to this risk. We studied heart rate (HR) and blood pressure (BP) responses in 10 infants with bronchopulmonary dysplasia (BPD) who were born at 27 Ϯ 2.4 (23-30) wk of gestation. Twenty healthy term infants served as controls. Cardiovascular tests were performed under polysomnographic control during slow-wave sleep (SWS) at a corrected age of 12 Ϯ 3.5 (7-19) wk. Control infants showed biphasic HR and BP responses to side motion with an immediate increase followed by a modest decrease and return to baseline. Compared with the controls, half of the BPD infants had altered BP responses (p Ͻ 0.005) without an early increase, followed by a more prominent decrease in BP. BPD infants also presented with a greater variability in BP responses to head-up tilts than did the controls (p Ͻ 0.001). In conclusion, these findings suggest that some BPD infants have impaired vestibular sympathoreflex-mediated cardiovascular control. This dysfunction may become critical in life-threatening situations. V estibular and cerebellar dysfunction has been suggested to be part of the pathophysiology of SIDS (1). Cardiovascular control mediated by vestibular nuclei and the cerebellum are important in hazardous situations such as hypovolemic and endotoxin shock (2,3). More than 80% of SIDS victims have shown neuronal apoptosis in vestibular nuclei and nuclei of the tractus solitarii, which are involved in baroand vestibular sympathoreflexes (4). SIDS victims also present with abnormalities elsewhere in the vestibular sympathoreflex pathway (5-7).During normal daily living, vestibular sympathoreflex dysfunction is not expected to have a profound effect on cardiovascular control because several compensatory circuits are involved in control of HR and BP (8,9). The dysfunction results in greater variability in BP control during postural changes (10). Similarly, increased BP variability has been observed in tilt tests performed in infants who have suffered from apparent life-threatening events (ALTEs) (11,12), further supporting the idea of vestibular dysfunction in SIDS.Most SIDS victims have suffered from hypoxia for at least several hours before the lethal event (13). SIDS victims may also have suffered from hypoxia earlier in life for multiple reasons, including placental insufficiency (14), intrauterine nicotine exposure (15), low or very low birth weight (16,17), hypoxia related to obstructive apnea events (18,19), or unfavorable head position during sleep (20,21). Our hypothesis is that hypoxic episodes cause a dysfunction in vestibulo-mediated cardiovascular control, thus making the infant more liable to die in life-threatening situations. To test the possible effects of hypoxia and test our hypothesis, we previously studied infan...

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Bilateral lesions of the fastigial nucleus prevent the recovery of blood pressure following hypotension induced by hemorrhage or administration of endotoxin

Cited by 93 publications

References 10 publications

Aberrant Central Nervous System Responses to the Valsalva Maneuver in Heart Failure

Aberrant Central Nervous System Responses to the Valsalva Maneuver in Heart Failure

FMRI Responses to Hyperoxia in Congenital Central Hypoventilation Syndrome

Altered Cardiovascular Control in Preterm Infants with Bronchopulmonary Dysplasia

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