Parabrachial nucleus involvement in multiple system atrophy

E. E. Benarroch, A. M. Schmeichel, Phillip Anson Low, Joseph E Parisi

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Multiple system atrophy (MSA) is associated with respiratory dysfunction, including sleep apnea, respiratory dysrhythmia, and laryngeal stridor. Neurons of the parabrachial nucleus (PBN) control respiratory rhythmogenesis and airway resistance. Objectives: The objective of this study is to determine whether there was involvement of putative respiratory regions of the PBN in MSA. Methods: We examined the pons at autopsy in 10 cases with neuropathologically confirmed MSA and 8 age-matched controls. Sections obtained throughout the pons were processed for calcitonin-gene related peptide (CGRP) and Nissl staining to identify the lateral crescent of the lateral PBN (LPB) and the Kölliker-Fuse nucleus (K-F), which are involved in respiratory control. Cell counts were performed using stereology. Results: There was loss of CGRP neurons in the PBN in MSA (total estimated cell counts for the external LPB cluster was 12,584 ± 1146 in controls and 5917 ± 389 in MSA, p < 0.0001); for the external medial PBN (MPB) cluster it was 15,081 ± 1758 in controls and 7842 ± 466 in MSA, p < 0.001. There was also neuronal loss in putative respiratory regions of the PBN, including the lateral crescent of the LPB (13,039 ± 1326 in controls and 4164 ± 872 in MSA, p < 0.0001); and K-F (5120 ± 495 in controls and 999 ± 308 in MSA, p < 0.0001). Conclusions: There is involvement of both CGRP and putative respiratory cell groups in the PBN in MSA. Whereas the clinical implications of CGRP cell loss are still undetermined, involvement of the LPB and K-F may contribute to respiratory dysfunction in this disorder.

Original languageEnglish (US)
Pages (from-to)170-174
Number of pages5
JournalAutonomic Neuroscience: Basic and Clinical
Volume177
Issue number2
DOIs
StatePublished - Oct 2013

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Multiple System Atrophy
Calcitonin Gene-Related Peptide
Pons
Cell Count
Parabrachial Nucleus
Neurons
Pseudogenes
Airway Resistance
Respiratory Sounds
Sleep Apnea Syndromes
Autopsy
Staining and Labeling

Keywords

  • CGRP
  • Lateral parabrachial
  • Medial parabrachial
  • MSA
  • Stridor

ASJC Scopus subject areas

  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Endocrine and Autonomic Systems

Cite this

Parabrachial nucleus involvement in multiple system atrophy. / Benarroch, E. E.; Schmeichel, A. M.; Low, Phillip Anson; Parisi, Joseph E.

In: Autonomic Neuroscience: Basic and Clinical, Vol. 177, No. 2, 10.2013, p. 170-174.

Research output: Contribution to journalArticle

Benarroch, E. E. ; Schmeichel, A. M. ; Low, Phillip Anson ; Parisi, Joseph E. / Parabrachial nucleus involvement in multiple system atrophy. In: Autonomic Neuroscience: Basic and Clinical. 2013 ; Vol. 177, No. 2. pp. 170-174.
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abstract = "Multiple system atrophy (MSA) is associated with respiratory dysfunction, including sleep apnea, respiratory dysrhythmia, and laryngeal stridor. Neurons of the parabrachial nucleus (PBN) control respiratory rhythmogenesis and airway resistance. Objectives: The objective of this study is to determine whether there was involvement of putative respiratory regions of the PBN in MSA. Methods: We examined the pons at autopsy in 10 cases with neuropathologically confirmed MSA and 8 age-matched controls. Sections obtained throughout the pons were processed for calcitonin-gene related peptide (CGRP) and Nissl staining to identify the lateral crescent of the lateral PBN (LPB) and the K{\"o}lliker-Fuse nucleus (K-F), which are involved in respiratory control. Cell counts were performed using stereology. Results: There was loss of CGRP neurons in the PBN in MSA (total estimated cell counts for the external LPB cluster was 12,584 ± 1146 in controls and 5917 ± 389 in MSA, p < 0.0001); for the external medial PBN (MPB) cluster it was 15,081 ± 1758 in controls and 7842 ± 466 in MSA, p < 0.001. There was also neuronal loss in putative respiratory regions of the PBN, including the lateral crescent of the LPB (13,039 ± 1326 in controls and 4164 ± 872 in MSA, p < 0.0001); and K-F (5120 ± 495 in controls and 999 ± 308 in MSA, p < 0.0001). Conclusions: There is involvement of both CGRP and putative respiratory cell groups in the PBN in MSA. Whereas the clinical implications of CGRP cell loss are still undetermined, involvement of the LPB and K-F may contribute to respiratory dysfunction in this disorder.",
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N2 - Multiple system atrophy (MSA) is associated with respiratory dysfunction, including sleep apnea, respiratory dysrhythmia, and laryngeal stridor. Neurons of the parabrachial nucleus (PBN) control respiratory rhythmogenesis and airway resistance. Objectives: The objective of this study is to determine whether there was involvement of putative respiratory regions of the PBN in MSA. Methods: We examined the pons at autopsy in 10 cases with neuropathologically confirmed MSA and 8 age-matched controls. Sections obtained throughout the pons were processed for calcitonin-gene related peptide (CGRP) and Nissl staining to identify the lateral crescent of the lateral PBN (LPB) and the Kölliker-Fuse nucleus (K-F), which are involved in respiratory control. Cell counts were performed using stereology. Results: There was loss of CGRP neurons in the PBN in MSA (total estimated cell counts for the external LPB cluster was 12,584 ± 1146 in controls and 5917 ± 389 in MSA, p < 0.0001); for the external medial PBN (MPB) cluster it was 15,081 ± 1758 in controls and 7842 ± 466 in MSA, p < 0.001. There was also neuronal loss in putative respiratory regions of the PBN, including the lateral crescent of the LPB (13,039 ± 1326 in controls and 4164 ± 872 in MSA, p < 0.0001); and K-F (5120 ± 495 in controls and 999 ± 308 in MSA, p < 0.0001). Conclusions: There is involvement of both CGRP and putative respiratory cell groups in the PBN in MSA. Whereas the clinical implications of CGRP cell loss are still undetermined, involvement of the LPB and K-F may contribute to respiratory dysfunction in this disorder.

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