Massive Brain Stem Necrosis in the Human Neonate: Presentation of Three Cases With Review of the Literature

Leech, Richard W.; Brumback, Roger A.

doi:10.1177/088307388800300405

Cited by 23 publications

(8 citation statements)

References 9 publications

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“…This traditional model was supported by other authors (Stella 1938, St John et al 1971, von Euler et al 1976, Caille et al 1981, Ling et al 1994, Morrison et al 1994) and the function of the pneumotaxic center, which is believed to be located in the medial parabrachial and Kölliker-Fuse nuclei in pontine tegmentum, has been confirmed (Foutz et al 1988, Feldman et al 1992, Ling et al 1994. In asphyxiated children with brainstem involvement, the tegmentum areas are often more vulnerable (Myers 1975, Leech et al 1988, Roland et al 1988, and this might Case Report 565 explain the presence of apneusis in our subjects. Neuroradiological imaging showed severe atrophies of their pontine tegmenti, which indicates lesions in the pneumotaxic centers.…”

Section: Discussionsupporting

confidence: 58%

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Apneustic breathing in children with brainstem damage due to hypoxic–ischemic encephalopathy

Saito¹,

Hashimoto²,

Iwata³

et al. 1999

Develop Med Child Neuro

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To confirm the presence of apneusis in patients with hypoxic–ischemic encephalopathy and to clarify which factors influence their respiratory patterns, polygraphic studies were performed on two patients. Apneusis was clinically suspected in both patients who had severe brainstem damage. In one subject, inputs of vagal afferents from the gastrointestinal tract and the urinary bladder often resulted in extreme tachypnea instead of apneusis. Lung inflation facilitated expiration during inspiratory arrest. Expiration preceded a periodic inhibition of rigospastic discharge in the right biceps muscle. In the other subject, prolonged inspiratory pauses with cyanosis occurred with or without preceding epileptic seizure. Both phenytoin dose reduction and treatment with tandospirone, a serotonin‐1A agonist, were effective in improving the respiratory distress in this subject.

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Section: Discussionsupporting

confidence: 58%

“…Brain-stem involvement, especially injury to the tegmentum area, is well recognized in neonates with hypoxic or hypotensive brain damage (Leech and Brumback 1988, Roland et al 1988, Friede 1989, Natsume et al 1995. The infants with birth asphyxia in these studies had respiratory failure and often died during infancy.…”

mentioning

confidence: 99%

Apneustic breathing in children with brainstem damage due to hypoxic–ischemic encephalopathy

Saito¹,

Hashimoto²,

Iwata³

et al. 1999

Develop Med Child Neuro

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“…The neuropathology of the asphyxiated term infant has been characterized extensively 9, 36–47. Clinical details are generally indicative of severe perinatal hypoxic–ischemic insults, often with overt intrapartum sentinel events.…”

Section: Neonatal Hypoxic–ischemic Encephalopathy: Animal Models and mentioning

confidence: 99%

Neonatal encephalopathy: An inadequate term for hypoxic–ischemic encephalopathy

Volpe

2012

Annals of Neurology

289

251

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This Point of View article addresses neonatal encephalopathy (NE) presumably caused by hypoxia-ischemia and the terminology currently in wide use for this disorder. The nonspecific term NE is commonly utilized for those infants with the clinical and imaging characteristics of neonatal hypoxic-ischemic encephalopathy (HIE). Multiple magnetic resonance imaging studies of term infants with the clinical setting of presumed hypoxia-ischemia near the time of delivery have delineated a topography of lesions highly correlated with that defined by human neuropathology and by animal models, including primate models, of hypoxia-ischemia. These imaging findings, coupled with clinical features consistent with perinatal hypoxic-ischemic insult(s), warrant the specific designation of neonatal HIE.

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“…Neuronal losses occur in forebrain and brainstem regions after HI (Leech & Brumback, 1988; Marin‐Padilla, 1999; Thompson et al. , 2007; Buller et al.…”

Section: Introductionmentioning

confidence: 99%

Disruption of raphé serotonergic neural projections to the cortex: a potential pathway contributing to remote loss of brainstem neurons following neonatal hypoxic–ischemic brain injury

Reinebrant

Wixey

Buller

2012

Eur J of Neuroscience

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Neuronal injury is a key feature of neonatal hypoxic-ischemic (HI) brain injury. However, the mechanisms underpinning neuronal losses, such as in the brainstem, are poorly understood. One possibility is that disrupted neural connections between the cortex and brainstem may compromise the survival of neuronal cell bodies in the brainstem. We investigated whether brainstem raphé serotonergic neurons that project to the cortex are lost after HI. We also tested if neuroinflammation has a role in disrupting brainstem raphé projections. Postnatal day 3 (P3) rats underwent unilateral carotid artery ligation followed by hypoxia (6% oxygen for 30 min). A retrograde tracer, choleratoxin b, was deposited in the motor cortex on P38. On P45 we found that retrogradely labelled neurons in the dorsal raphé dorsal, ventrolateral, interfascicular, caudal and ventral nuclei were lost after P3 HI. All retrogradely labelled neurons in the raphé nuclei were serotonergic. Numbers of retrogradely labelled neurons were also reduced in the ventromedial thalamus and basolateral amygdala. Minocycline treatment (45 mg/kg 2 h post-HI, 22.5 mg/kg daily P4-P9) attenuated losses of retrogradely labelled neurons in the dorsal raphé ventrolateral, interfascicular and ventral raphé nuclei, and the ventromedial thalamus. These results indicate that raphé neurons projecting to the cortex constitute a population of serotonergic neurons that are lost after P3 HI. Furthermore, neuroinflammation has a role in the disruption of raphé and thalamic neural projections. Future studies investigating the cellular mechanisms of axonal degeneration may reveal new targets for interventions to prevent neuronal losses after neonatal HI.

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Massive Brain Stem Necrosis in the Human Neonate: Presentation of Three Cases With Review of the Literature

Cited by 23 publications

References 9 publications

Apneustic breathing in children with brainstem damage due to hypoxic–ischemic encephalopathy

Apneustic breathing in children with brainstem damage due to hypoxic–ischemic encephalopathy

Neonatal encephalopathy: An inadequate term for hypoxic–ischemic encephalopathy

Disruption of raphé serotonergic neural projections to the cortex: a potential pathway contributing to remote loss of brainstem neurons following neonatal hypoxic–ischemic brain injury

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