Involvement of the ventrolateral medulla in parkinsonism with autonomic failure

Eduardo E. Benarroch, Ann M. Schmeichel, Joseph E Parisi

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

Objective: To determine whether patients with PD and autonomic failure (AF), manifested primarily with orthostatic hypotension (OH), have a consistent loss of tyrosine hydroxylase (TH) neurons in the rostral ventrolateral medulla (RVLM), similar to that occurring in patients with multiple system atrophy (MSA) and AF, and to determine whether there is loss of nicotinamide, adenine dinucleotide phosphate (NADPH) diaphorase (NADPH-d) RVLM neurons in both groups of patients. Methods: The numbers of TH and NADPH-d neurons in the RVLM was assessed in brain sections obtained at autopsy from five patients with suspected PD and OH, six patients with MSA, two patients with corticobasal ganglionic degeneration and no AF, and 10 control subjects with no history of neurologic disease. Cell numbers were compared among groups and correlated with their final neuropathologic diagnosis. Results: The number of TH neurons in the RVLM of patients with PD and OH were not significantly different from control subjects, and there were marked individual variations. The TH cell numbers in the RVLM were significantly higher (p < 0.06) in patients with PD than in patients with MSA, despite a similar degree of severity of OH. As a group, patients with PD and OH had reduced numbers of NADPH-d cells in the RVLM compared with control subjects, but again there were marked individual variations. NADPH-d cell numbers were reduced consistently and more markedly in patients with MSA. Conclusion: Unlike the case in patients with MSA, the number of TH neurons in the RVLM is highly variable in patients with PD and is unlikely to contribute significantly to the pathophysiology of OH. As a group, patients with PD have reduced numbers of NADPH-d neurons in the RVLM, but some patients had cell counts similar to control subjects. On the other hand, NADPH-d cell depletion in the RVLM is a consistent finding in MSA and may contribute to cardiorespiratory dysfunction in this disorder.

Original languageEnglish (US)
Pages (from-to)963-968
Number of pages6
JournalNeurology
Volume54
Issue number4
StatePublished - Feb 22 2000

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Parkinsonian Disorders
Multiple System Atrophy
Orthostatic Hypotension
NADP
Tyrosine 3-Monooxygenase
Neurons
Cell Count
Nervous System Diseases
Autopsy

Keywords

  • Multiple system atrophy
  • NADPH-diaphorase
  • PD
  • Tyrosine hydroxylase

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Benarroch, E. E., Schmeichel, A. M., & Parisi, J. E. (2000). Involvement of the ventrolateral medulla in parkinsonism with autonomic failure. Neurology, 54(4), 963-968.

Involvement of the ventrolateral medulla in parkinsonism with autonomic failure. / Benarroch, Eduardo E.; Schmeichel, Ann M.; Parisi, Joseph E.

In: Neurology, Vol. 54, No. 4, 22.02.2000, p. 963-968.

Research output: Contribution to journalArticle

Benarroch, EE, Schmeichel, AM & Parisi, JE 2000, 'Involvement of the ventrolateral medulla in parkinsonism with autonomic failure', Neurology, vol. 54, no. 4, pp. 963-968.
Benarroch EE, Schmeichel AM, Parisi JE. Involvement of the ventrolateral medulla in parkinsonism with autonomic failure. Neurology. 2000 Feb 22;54(4):963-968.
Benarroch, Eduardo E. ; Schmeichel, Ann M. ; Parisi, Joseph E. / Involvement of the ventrolateral medulla in parkinsonism with autonomic failure. In: Neurology. 2000 ; Vol. 54, No. 4. pp. 963-968.
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AB - Objective: To determine whether patients with PD and autonomic failure (AF), manifested primarily with orthostatic hypotension (OH), have a consistent loss of tyrosine hydroxylase (TH) neurons in the rostral ventrolateral medulla (RVLM), similar to that occurring in patients with multiple system atrophy (MSA) and AF, and to determine whether there is loss of nicotinamide, adenine dinucleotide phosphate (NADPH) diaphorase (NADPH-d) RVLM neurons in both groups of patients. Methods: The numbers of TH and NADPH-d neurons in the RVLM was assessed in brain sections obtained at autopsy from five patients with suspected PD and OH, six patients with MSA, two patients with corticobasal ganglionic degeneration and no AF, and 10 control subjects with no history of neurologic disease. Cell numbers were compared among groups and correlated with their final neuropathologic diagnosis. Results: The number of TH neurons in the RVLM of patients with PD and OH were not significantly different from control subjects, and there were marked individual variations. The TH cell numbers in the RVLM were significantly higher (p < 0.06) in patients with PD than in patients with MSA, despite a similar degree of severity of OH. As a group, patients with PD and OH had reduced numbers of NADPH-d cells in the RVLM compared with control subjects, but again there were marked individual variations. NADPH-d cell numbers were reduced consistently and more markedly in patients with MSA. Conclusion: Unlike the case in patients with MSA, the number of TH neurons in the RVLM is highly variable in patients with PD and is unlikely to contribute significantly to the pathophysiology of OH. As a group, patients with PD have reduced numbers of NADPH-d neurons in the RVLM, but some patients had cell counts similar to control subjects. On the other hand, NADPH-d cell depletion in the RVLM is a consistent finding in MSA and may contribute to cardiorespiratory dysfunction in this disorder.

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