Objective. The aim of this study was to identify patients with Parkinson's disease who showed loss or decrease of nocturnal blood pressure fall (nondipper patients) as a marker of autonomic dysfunction. Presence or absence of orthostatic hypotension was considered to investigate whether alterations in circadian blood pressure pattern are associated with posture-related dysregulation of blood pressure. Methods. 40 patients with Parkinson's disease underwent 24-hour blood pressure monitoring. 21 patients were diagnosed with arterial hypertension and received anti-hypertensive drugs. Nondipper patients were defined as having nocturnal decrease of mean systolic and diastolic blood pressure less than 10%. Presence or absence of orthostatic hypotension was determined by Schellong's test. Results. We identified 35 nondipper patients (88%). Nondipping was detected in 20 patients with orthostatic hypotension (95%) and in 15 patients without orthostatic hypotension (79%). 18 patients with hypertensive and 22 patients with normal blood pressure values were detected. Conclusions. In conclusion 24-hour blood pressure monitoring showed a high prevalence of nondipping in 40 patients with Parkinson's disease with and without orthostatic hypotension independent of coexisting arterial hypertension and antihypertensive treatment. 24-hour blood pressure monitoring may be useful to identify non-dipping as a marker of autonomic dysfunction in patients with Parkinson's disease. 1. Introduction Parkinson’s disease is a multisystem degeneration [1]. Beside motor symptoms, and psychiatric symptoms autonomic dysfunction is a common finding in Parkinson’s disease [2]. Neuropathological studies showed the presence of Lewy bodies in central and peripheral structures involved in autonomic regulation [3–6]. Involvement of the autonomic nervous system (ANS) occurs in the early stages of the disease [2]. Cardiovascular dysautonomia, especially orthostatic hypotension, is frequently reported in Parkinson’s disease [7]. Involvement of peripheral components of the ANS can be demonstrated by MIBG scintigraphy. MIBG scintigraphy shows reduced cardiac uptake of MIBG (meta-[123I]iodobenzylguanidine) representing loss of postganglionic myocardial sympathetic nerve fibers in patients with Parkinson’s disease and autonomic failure [8]. However these findings are also seen in the early stages of the disease independent of symptoms of cardiovascular dysautonomia [9]. Further effects of autonomic cardiovascular dysfunction are demonstrated in earlier studies such as baroreceptor reflex dysfunction,
References
[1]
D. J. Moore, A. B. West, V. L. Dawson, and T. M. Dawson, “Molecular pathophysiology of Parkinson's disease,” Annual Review of Neuroscience, vol. 28, pp. 57–87, 2005.
[2]
H. Braak, E. Ghebremedhin, U. Rüb, H. Bratzke, and K. Del Tredici, “Stages in the development of Parkinson's disease-related pathology,” Cell and Tissue Research, vol. 318, no. 1, pp. 121–134, 2004.
[3]
A. H. Rajput and B. Rozdilsky, “Dysautonomia in Parkinsonism: a clinicopathological study,” Journal of Neurology Neurosurgery and Psychiatry, vol. 39, no. 11, pp. 1092–1100, 1976.
[4]
E. Ohama and F. Ikuta, “Parkinson's disease: distribution of lewy bodies and monoamine neuron system,” Acta Neuropathologica, vol. 34, no. 4, pp. 311–319, 1976.
[5]
J. W. Langston and L. S. Forno, “The hypothalamus in Parkinson disease,” Annals of Neurology, vol. 3, no. 2, pp. 129–133, 1978.
[6]
S. Hunter, “The rostral mesencephalon in Parkinson's disease and Alzheimer's disease,” Acta Neuropathologica, vol. 68, no. 1, pp. 53–58, 1985.
[7]
M. Gross, R. Bannister, and R. Godwin-Austen, “Orthostatic hypotension in Parkinson's disease,” The Lancet, vol. 1, no. 7743, pp. 174–176, 1972.
[8]
W. H. Jost, K. Del Tredici, C. Landvogt, and S. Braune, “Importance of 123I-metaiodobenzylguanidin (MIBG) scintigraphy / SPECT for diagnosis and differential diagnostics of Parkinson syndromes,” Neurodegenerative Disorders, vol. 7, pp. 341–347, 2010.
[9]
C. A. Haensch, H. Lerch, J. J?rg, and S. Isenmann, “Cardiac denervation occurs independent of orthostatic hypotension and impaired heart rate variability in Parkinson's disease,” Parkinsonism and Related Disorders, vol. 15, no. 2, pp. 134–137, 2009.
[10]
A. Pathak and J. M. Senard, “Blood pressure disorders during Parkinson's disease: epidemiology, pathophysiology and management,” Expert Review of Neurotherapeutics, vol. 6, no. 8, pp. 1173–1180, 2006.
[11]
C. A. Haensch and J. J?rg, “Beat-to-beat blood pressure analysis after premature ventricular contraction indicates sensitive baroreceptor dysfunction in Parkinson's disease,” Movement Disorders, vol. 21, no. 4, pp. 486–491, 2006.
[12]
C. Friedrich, H. Rüdiger, C. Schmidt et al., “Baroreflex sensitivity and power spectral analysis in different extrapyramidal syndromes,” Journal of Neural Transmission, vol. 115, no. 11, pp. 1527–1536, 2008.
[13]
A. Ahsan Ejaz, I. S. Sekhon, and S. Munjal, “Characteristic findings on 24-h ambulatory blood pressure monitoring in a series of patients with Parkinson's disease,” European Journal of Internal Medicine, vol. 17, no. 6, pp. 417–420, 2006.
[14]
M. Plaschke, P. Trenkwalder, H. Dahlheim, C. Lechner, and C. Trenkwalder, “Twenty-four-hour blood pressure profile and blood pressure responses to head-up tilt tests in Parkinson's disease and multiple system atrophy,” Journal of Hypertension, vol. 16, no. 10, pp. 1433–1441, 1998.
[15]
C. Schmidt, D. Berg, Herting et al., “Loss of nocturnal blood pressure fall in various extrapyramidal syndromes,” Movement Disorders, vol. 24, no. 14, pp. 2136–2142, 2009.
[16]
J. M. Senard, B. Chamontin, A. Rascol, and J. L. Montastruc, “Ambulatory blood pressure in patients with Parkinson's disease without and with orthostatic hypotension,” Clinical Autonomic Research, vol. 2, no. 2, pp. 99–104, 1992.
[17]
T. G. Pickering, “Strategies for the evaluation and treatment of hypertension and some implications of blood pressure variability,” Circulation, vol. 76, no. 1, pp. I77–I82, 1987.
[18]
M. J. Horan, “Role of ambulatory blood pressure recording in the diagnosis, prognosis, and management of hypertension,” Clinical and Experimental Hypertension, vol. 7, no. 2-3, pp. 205–216, 1985.
[19]
W. R. G. Gibb and A. J. Lees, “The relevance of the Lewy body to the pathogenesis of idiopathic Parkinson's disease,” Journal of Neurology Neurosurgery and Psychiatry, vol. 51, no. 6, pp. 745–752, 1988.
[20]
I. J. Schatz, R. Bannister, R. L. Freeman et al., “Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy,” Neurology, vol. 46, no. 5, p. 1470, 1996.
[21]
B. L. Walter, “Cardiovascular autonomic dysfunction in patients with movement disorders,” Cleveland Clinic Journal of Medicine, vol. 75, pp. S54–S58, 2008.
[22]
D. P. Veerman, B. P. M. Imholz, W. Wieling, K. H. Wesseling, and G. A. Van Montfrans, “Circadian profile of systemic hemodynamics,” Hypertension, vol. 26, no. 1, pp. 55–59, 1995.
[23]
I. Biaggioni, R. M. Robertson, and D. Robertson, “Manipulation of norepinephrine metabolism with yohimbine in the treatment of autonomic failure,” Journal of Clinical Pharmacology, vol. 34, no. 5, pp. 418–423, 1994.
[24]
J. M. Senard, P. Valet, G. Durrieu et al., “Adrenergic supersensitivity in Parkinsonians with orthostatic hypotension,” European Journal of Clinical Investigation, vol. 20, no. 6, pp. 613–619, 1990.
[25]
R. Bannister and C. J. Mathias, “Managment of postural hypotension,” in Autonomic Failure: A Textbook of Clinical Disorders of the Autonomic Nervous System, R. Bannister and C. J. Mathias, Eds., pp. 622–645, Oxford University Press, Oxford, UK, 3rd edition, 1992.
[26]
G. Cornélissen, F. Halberg, K. Otsuka, R. B. Singh, and C. H. Chen, “Chronobiology predicts actual and proxy outcomes when dipping fails,” Hypertension, vol. 49, no. 1, pp. 237–239, 2007.