Cerebellar Activity, Apneustic Breathing, and the Neural Control of Respiration

Glasser, Richard; Tippett, Joe W.; Davidian, Vartana Jr

doi:10.1038/209810b0

Cited by 22 publications

(10 citation statements)

References 9 publications

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“…Consistent with its role in respiration, the cerebellum may interact with either spinal inspiratory facilitatory reflexes or supraspinal inspiratory inhibitory reflexes to modify the diaphragm and intercostal muscles that control the sniff (Decima and von Euler, 1969). Depression of cerebellar function in the cat by ischemia, topical administration of procaine, or ablation, results in an augmentation of inspiratory activity (Glasser et al, 1966). In addition, electrical stimulation of the anterior lobe of the cerebellum inhibits the inspiratory discharge driven by the medullary respiratory mechanism (Moruzzi, 1940;Decima and von Euler, 1969).…”

Section: Cerebellar Involvement In the Olfactomotor Systemmentioning

confidence: 96%

Olfactory Impairments in Patients with Unilateral Cerebellar Lesions Are Selective to Inputs from the Contralesional Nostril

Mainland¹,

Johnson²,

Khan³

et al. 2005

J. Neurosci.

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Functional imaging studies of olfaction have consistently reported odorant-induced activation of the cerebellum. However, the cerebellar role in olfaction remains unknown. We examined the olfactory and olfactomotor abilities of patients with unilateral cerebellar lesions, comparing performance within subjects across nostrils, as well as between subjects with age-matched and young controls. Regarding olfactory performance, initial testing revealed that patients had a contralesional impairment in olfactory identification but not olfactory detection threshold. However, when tested under conditions that prevented compensatory sniffing strategies, the patients also exhibited a contralesional olfactory detection impairment. Regarding olfactomotor function, a healthy olfactomotor system generates sniffs that are (1) sufficiently vigorous and (2) inversely proportional to odorant concentration in sniff mean airflow velocity, maximum airflow velocity, volume, and duration. Patients' sniffs were lower in overall airflow velocity and volume in comparison with control participants. Furthermore, reduced sniff velocity predicted poorer detection thresholds in patients. Finally, whereas young controls used concentration-dependent sniffs, there was a trend in that direction only for age-matched controls. Patients used sniffs that were concentration invariant. In conclusion, cerebellar lesions impacted olfactory and olfactomotor performance. These findings strongly implicate an olfactocerebellar pathway prominent in odor identification and detection that functionally connects each nostril primarily to the contralateral cerebellum.

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Section: Cerebellar Involvement In the Olfactomotor Systemmentioning

confidence: 96%

Olfactory Impairments in Patients with Unilateral Cerebellar Lesions Are Selective to Inputs from the Contralesional Nostril

Mainland¹,

Johnson²,

Khan³

et al. 2005

J. Neurosci.

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“…35 36 Gasping has been identified as a very powerful autoresuscitative mechanism, one that is unlikely to be influenced by sedatives. [37][38][39] In addition, gasping respirations in the imminently dying patient will not lead to long term survival unless external intervention is also provided, however, the patient, or their surrogate has requested that such external intervention not be used.…”

Section: Agonal Respiration and Sufferingmentioning

confidence: 99%

The agony of agonal respiration: is the last gasp necessary?

Perkin

2002

J Med Ethics

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Gasping respiration in the dying patient is the last respiratory pattern prior to terminal apnoea. The duration of the gasping respiration phase varies; it may be as brief as one or two breaths to a prolonged period of gasping lasting minutes or even hours. Gasping respiration is very abnormal, easy to recognise and distinguish from other respiratory patterns and, in the dying patient who has elected to not be resuscitated, will always result in terminal apnoea.Gasping respiration is also referred to as agonal respiration and the name is appropriate because the gasping breaths appear uncomfortable and raise concern that the patient is suffering and in agony. Enough uncertainty exists about the influence of gasping respiration on patient wellbeing, that it is appropriate to assume that the gasping breaths are burdensome to patients. Therefore, gasping respiration at the end of life should be treated.We propose that there is an ethical basis, in rare circumstances, for the use of neuromuscular blockade to suppress prolonged episodes of agonal respiration in the well-sedated patient in order to allow a peaceful and comfortable death.

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“…In contrast, in group II after AOAA, the biphasic V E response was no longer present, and V E , V T and V T /T I increased above the normoxic values. Since in the older rabbits hypoxia increased the cerebellar GABA concentrations, the sustained response could be due to the GABA-evoked block of inhibitory cerebellar input during hypoxia [37,38]. In a given brain structure, brainstem, cerebrum, and cerebellum, GABA concentrations were similar in rabbits returned to their litters and those studied in the body plethysmograph.…”

Section: Discussionmentioning

confidence: 79%

“…There is no simple explanation of these excitatory effects of AOAA on ventilation. Since in hypoxia-exposed rabbits, AOAA increased cerebellar GABA concentrations, continuous excitatory effects of hypoxia in these animals could be due to the GABA-evoked block of inhibitory cerebellar input [37,46]. The inhibitory cerebellar influence may be stronger in rabbits during their 2nd week of life that immediately after birth because neuronal development of the cerebellum lags behind that of the brainstem in rabbits [47].…”

Section: Effects Of Aoaa On the Ventilatory Response To Hypoxiamentioning

confidence: 99%

Effect of Increased Brain GABA Concentrations on Breathing in Unanesthetized Newborn Rabbits

Monin

Aranda²,

Bansal³

et al. 1999

Neonatology

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Evidence suggests that γ-aminobutyric acid (GABA) is involved in control of breathing and in the hypoxia-related ventilatory depression in newborns. However, this evidence is obtained mainly from studies on anesthetized animals. Because anesthesia may interfere with the GABA system, the objectives of our study were to examine effects of GABA on ventilation (V_E) and ventilatory response to hypoxia and to reveal effects of repeated hypoxia on GABA concentrations in unanesthetized newborns. The study was performed in rabbits in two age groups: 1–3 days old (group I) and 10–14 days old (group II). To increase brain endogenous GABA concentrations, rabbits were injected with an inhibitor of GABA transaminase, aminooxyacetic acid (AOAA; 20 mg/kg i.p.). To prevent postmortem formation of GABA, at the end of experiments the rabbits received an inhibitor of glutamic acid decarboxylase, IP-3-mercaptopropionic acid (100 mg/kg i.p.). Animals were studied in normoxia alone, or they were exposed for 15 min to 8% O₂ before and 10 and 35 min after saline or AOAA. GABA concentrations were measured in brainstem, cerebrum, and cerebellum by means of a capillary electrophoresis. In group I, AOAA had no respiratory effects. In group II, AOAA decreased V_E, tidal volume, and mean inspiratory flow in normoxia and reversed V_E decline during hypoxia 10 min after the injection, GABA concentrations were not age dependent and the highest in the brainstem. Repeated hypoxia increased the cerebellar GABA concentrations and had no effect in group I. These results imply that in unanesthetized rabbits, GABAergic neurotransmission in the respiratory control network becomes functional by the 2nd week of life, but it does not contribute to the biphasic ventilatory response to moderate hypoxia. In contrast, GABA-evoked block of the cerebellar inhibitory input during hypoxia may be responsible for the reversal of the V_E decline in unanesthetized newborns.

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Cerebellar Activity, Apneustic Breathing, and the Neural Control of Respiration

Cited by 22 publications

References 9 publications

Olfactory Impairments in Patients with Unilateral Cerebellar Lesions Are Selective to Inputs from the Contralesional Nostril

Olfactory Impairments in Patients with Unilateral Cerebellar Lesions Are Selective to Inputs from the Contralesional Nostril

The agony of agonal respiration: is the last gasp necessary?

Effect of Increased Brain GABA Concentrations on Breathing in Unanesthetized Newborn Rabbits

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