The location and function of respiratory fibres in the second cervical spinal cord segment: respiratory dysfunction syndrome after cervical cordotomy.

Lahuerta, Juan José; Buxton, P. H.; Lipton, S; Bowsher, David

doi:10.1136/jnnp.55.12.1142

Cited by 33 publications

(13 citation statements)

References 20 publications

(1 reference statement)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The term “Ondine’s curse” was first used by Severinhaus and Mitchell87 to describe patients who had minimal motor loss and retained the ability to breathe voluntarily after they underwent high bilateral spinothalamic tract cordotomies but became apneic during sleep and had poor ventilatory responsiveness to inhaled carbon dioxide. Unilateral lesions are less likely to have hypoventilation, and damage to C2 fibers is implicated in these cases 88. Brainstem infarctions and ischemia can result in central hypoventilation syndromes 89–91.…”

Section: Other Acquired Alveolar Hypoventilation Disordersmentioning

confidence: 99%

Central Alveolar Hypoventilation Syndromes

Muzumdar

Arens

2008

Sleep Medicine Clinics

View full text Add to dashboard Cite

KeywordsCentral alveolar hypoventilation; Congenital central hypoventilation syndromeThe ventilatory control system is tightly regulated. Three elements known to regulate this system include (1) sensors, such as peripheral and central chemoreceptors, and mechanoreceptors; (2) central controllers that receive input and integrate the response from the above sensors; and (3) effectors, including the muscles of respiration, that respond to the commands of the central controllers.Thus, alveolar ventilation is regulated most of the time involuntarily by the respiratory centers located beneath the ventral surfaces of the pons and medulla, that receive afferent input from the sensors and control ventilation automatically (chemically) via the respiratory muscles. This chemical control regulates breathing during non-rapid eye movement (NREM) sleep. Voluntary control by cortical centers can also occur, particularly during wakefulness and during rapid eye movement (REM) sleep.Central alveolar hypoventilation disorders denote conditions resulting from underlying neurologic disorders affecting the sensors, the central controller, or the integration of the signals. Such disorders can lead to insufficient ventilation and an increase in PaCO 2 (hypercarbia), as well as a decrease in PaO 2 (hypoxemia). The condition may be congenital or acquired, and affected children may be at risk from the neonatal period. Central alveolar hypoventilation may be present during sleep alone or in more severe cases during sleep and wakefulness.It is important to make an early diagnosis of central hypoventilation to prevent the deleterious effects of hypercapnia, acidosis, and hypoxemia on cardiovascular and neurocognitive function. This review discusses the current knowledge on central alveolar hypoventilation syndromes, particularly in children, with special emphasis describing the recent knowledge about congenital central hypoventilation syndrome (CCHS) and rapid-onset obesity, hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD). CONGENITAL ALVEOLAR HYPOVENTILATION DISORDERS Congenital Central Hypoventilation SyndromeCCHS or congenital central alveolar hypoventilation syndrome has also been referred to as Ondine's curse and has been recognized in the literature for more than 30 years.1 Ondine's curse (also known as Undine) was referenced to the story of a water sprite from European lore who cursed her unfaithful lover to lose all automatic functions and therefore stop breathing * Corresponding author: rarens@montefiore.org (R. Arens). NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript when he fell asleep. This rather apt description of the plight of subjects with CCHS has now become a part of medical mythology, but does not accurately reproduce the fable of Ondine. 2 The identification of associated features including Hirschsprung's disease, which is considered a neurocristopathy or developmental anomaly of the neural crest,3 neural crest tumors, and autonomic nervous system (...

show abstract

Section: Other Acquired Alveolar Hypoventilation Disordersmentioning

confidence: 99%

Central Alveolar Hypoventilation Syndromes

Muzumdar

Arens

2008

Sleep Medicine Clinics

View full text Add to dashboard Cite

show abstract

“…Acquired central hypoventilation, leading to loss of automatic respiration with preserved voluntary breathing (Ondine’s curse), occurs with medullary lesions, usually ischaemic infarctions,1 Chiari malformation,2 brainstem glioma3 or cervical spinal damage 4. Although central hypoventilation related to anti-Hu associated paraneoplastic encephalomyelitis has been reported,5 6 the frequency of this complication among these patients is not known.…”

mentioning

confidence: 99%

Central hypoventilation as the presenting symptom in Hu associated paraneoplastic encephalomyelitis

Gómez-Choco

Zarranz

Sáiz

et al. 2007

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

“…Clinical evidence strongly suggests that bulbospinal fibers project separately from the relevant corticospinal fibers. For instance, patients with brain stem lesions (Plum and Leight 1981) or very high cervical cord lesions (Davis and Plum 1972;Lahuerta et al 1992) can breathe voluntarily, but lack automatic breathing when drowsy or asleep. Corticospinal pathways bypass the brain stem respiratory centers and provide direct cortical control to the spinal respiratory motoneurons during voluntary breathing (Corfield et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Voluntary Breathing Influences Corticospinal Excitability of Nonrespiratory Finger Muscles

Rymer

2011

Journal of Neurophysiology

View full text Add to dashboard Cite

Li S, Rymer WZ. Voluntary breathing influences corticospinal excitability of nonrespiratory finger muscles. J Neurophysiol 105: 512-521, 2011. First published December 15, 2010 doi:10.1152/jn.00946.2010. The present study aimed to investigate neurophysiologic mechanisms mediating the newly discovered phenomenon of respiratory-motor interactions and to explore its potential clinical application for motor recovery. First, young and healthy subjects were instructed to breathe normally (NORM); to exhale (OUT) or inhale (IN) as fast as possible in a self-paced manner; or to voluntarily hold breath (HOLD). In experiment 1 (n ϭ 14), transcranial magnetic stimulation (TMS) was applied during 10% maximal voluntary contraction (MVC) finger flexion force production or at rest. The motor-evoked potentials (MEPs) were recorded from flexor digitorum superficialis (FDS), extensor digitorum communis (EDC), and abductor digiti minimi (ADM) muscles. Similarly, in experiment 2 (n ϭ 11), electrical stimulation (ES) was applied to FDS or EDC during the described four breathing conditions while subjects maintained 10%MVC of finger flexion or extension and at rest. In the exploratory clinical experiments (experiment 3), four patients with chronic neurological disorders (three strokes, one traumatic brain injury) received a 30-min session of breathing-controlled ES to the impaired EDC. In experiment 1, the EDC MEP magnitudes increased significantly during IN and OUT at both 10%MVC and rest; the FDS MEPs were enhanced only at 10%MVC, whereas the ADM MEP increased only during OUT, compared with NORM for both at rest and 10%MVC. No difference was found between NORM and HOLD for all three muscles. In experiment 2, when FDS was stimulated, force response was enhanced during both IN and OUT, but only at 10%MVC. When EDC was stimulated, force response increased at both 10%MVC and rest, only during IN, but not OUT. The averaged response latency was 83 ms for the finger extensors and 79 ms for the finger flexors. After a 30-min intervention of ES to EDC triggered by forced inspiration in experiment 3, we observed a significant reduction in finger flexor spasticity. The spasticity reduction lasted for Ն4 wk in all four patients. TMS and ES data, collectively, support the phenomenon that there is an overall respiration-related enhancement on the motor system, with a strong inspiration-finger extension coupling during voluntary breathing. As such, breathing-controlled electrical stimulation (i.e., stimulation to finger extensors delivered during the voluntary inspiratory phase) could be applied for enhancing finger extension strength and finger flexor spasticity reduction in poststroke patients.

show abstract

The location and function of respiratory fibres in the second cervical spinal cord segment: respiratory dysfunction syndrome after cervical cordotomy.

Cited by 33 publications

References 20 publications

Central Alveolar Hypoventilation Syndromes

Central Alveolar Hypoventilation Syndromes

Central hypoventilation as the presenting symptom in Hu associated paraneoplastic encephalomyelitis

Voluntary Breathing Influences Corticospinal Excitability of Nonrespiratory Finger Muscles

Contact Info

Product

Resources

About