The Management of Orthostatic Hypotension in Parkinson’s Disease
Identifieur interne : 000413 ( Ncbi/Merge ); précédent : 000412; suivant : 000414The Management of Orthostatic Hypotension in Parkinson’s Disease
Auteurs : Álvaro Sánchez [Espagne] ; Julián Benito [Espagne] ; Juan G [Espagne]Source :
- Frontiers in Neurology ; 2013.
Abstract
Orthostatic hypotension (OH) is a common and disabling symptom affecting Parkinson’s disease (PD) patients. We present the effect of the different therapies commonly used to manage PD on this clinical manifestation. For this purpose, we describe the relationship between OH and the current treatments employed in PD, such as L-DOPA, dopaminergic agonists, and continuous dopaminergic stimulation therapies. Additionally, we review the therapeutic measures that could be used to ameliorate OH. There are different approaches to deal with this manifestation, including pharmacological and non-pharmacological treatments, although none of them is specifically aimed for treating OH in PD.
Url:
DOI: 10.3389/fneur.2013.00064
PubMed: 23772219
PubMed Central: 3677136
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A" first="Álvaro" last="Sánchez">Álvaro Sánchez</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Neurology, University Hospital “12 de Octubre,”</institution><addr-line>Madrid</addr-line>,<country>Spain</country></nlm:aff><country xml:lang="fr">Espagne</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Department of Medicine, Faculty of Medicine, Complutense University</institution>,<addr-line>Madrid</addr-line>,<country>Spain</country></nlm:aff><country xml:lang="fr">Espagne</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas</institution>,<addr-line>Madrid</addr-line>,<country>Spain</country></nlm:aff><country xml:lang="fr">Espagne</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Instituto de Salud Carlos III</institution>,<addr-line>Madrid</addr-line>,<country>Spain</country></nlm:aff><country xml:lang="fr">Espagne</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Benito Le N, Julian" sort="Benito Le N, Julian" uniqKey="Benito Le N J" first="Julián" last="Benito">Julián Benito</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Neurology, University Hospital “12 de Octubre,”</institution><addr-line>Madrid</addr-line>,<country>Spain</country></nlm:aff><country xml:lang="fr">Espagne</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Department of Medicine, Faculty of Medicine, Complutense 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strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Neurology</title><idno type="e-ISSN">1664-2295</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Orthostatic hypotension (OH) is a common and disabling symptom affecting Parkinson’s disease (PD) patients. We present the effect of the different therapies commonly used to manage PD on this clinical manifestation. For this purpose, we describe the relationship between OH and the current treatments employed in PD, such as L-DOPA, dopaminergic agonists, and continuous dopaminergic stimulation therapies. Additionally, we review the therapeutic measures that could be used to ameliorate OH. There are different approaches to deal with this manifestation, including pharmacological and non-pharmacological treatments, although none of them is specifically aimed for treating OH in PD.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Abassi, Z A" uniqKey="Abassi Z">Z. A. Abassi</name></author><author><name sortKey="Binah, O" uniqKey="Binah O">O. Binah</name></author><author><name sortKey="Youdim, M B" uniqKey="Youdim M">M. B. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Neurol</journal-id><journal-id journal-id-type="iso-abbrev">Front Neurol</journal-id><journal-id journal-id-type="publisher-id">Front. Neurol.</journal-id><journal-title-group><journal-title>Frontiers in Neurology</journal-title></journal-title-group><issn pub-type="epub">1664-2295</issn><publisher><publisher-name>Frontiers Media S.A.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23772219</article-id><article-id pub-id-type="pmc">3677136</article-id><article-id pub-id-type="doi">10.3389/fneur.2013.00064</article-id><article-categories><subj-group subj-group-type="heading"><subject>Neuroscience</subject><subj-group><subject>Review Article</subject></subj-group></subj-group></article-categories><title-group><article-title>The Management of Orthostatic Hypotension in Parkinson’s Disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Sánchez-Ferro</surname><given-names>Álvaro</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="aff" rid="aff3"><sup>3</sup></xref><xref ref-type="aff" rid="aff4"><sup>4</sup></xref></contrib><contrib contrib-type="author"><name><surname>Benito-León</surname><given-names>Julián</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="aff" rid="aff3"><sup>3</sup></xref><xref ref-type="corresp" rid="cor1">*</xref></contrib><contrib contrib-type="author"><name><surname>Gómez-Esteban</surname><given-names>Juan Carlos</given-names></name><xref ref-type="aff" rid="aff5"><sup>5</sup></xref></contrib></contrib-group><aff id="aff1"><sup>1</sup><institution>Department of Neurology, University Hospital “12 de Octubre,”</institution><addr-line>Madrid</addr-line>,<country>Spain</country></aff><aff id="aff2"><sup>2</sup><institution>Department of Medicine, Faculty of Medicine, Complutense University</institution>,<addr-line>Madrid</addr-line>,<country>Spain</country></aff><aff id="aff3"><sup>3</sup><institution>Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas</institution>,<addr-line>Madrid</addr-line>,<country>Spain</country></aff><aff id="aff4"><sup>4</sup><institution>Instituto de Salud Carlos III</institution>,<addr-line>Madrid</addr-line>,<country>Spain</country></aff><aff id="aff5"><sup>5</sup><institution>Department of Neurology, Cruces Hospital, University of the Basque Country</institution>,<addr-line>Bilbao</addr-line>,<country>Spain</country></aff><author-notes><fn fn-type="edited-by"><p>Edited by: Santiago Perez-Lloret, Toulouse University, France</p></fn><fn fn-type="edited-by"><p>Reviewed by: Miguel Coelho, University of Lisbon, Portugal; Paola Sandroni, Mayo Foundation, USA; Malco Damian Rossi, Raul Carrea Institute for Neurological Research, Argentina</p></fn><corresp content-type="corresp" id="cor1">*Correspondence: Julián Benito-León, Department of Neurology, University Hospital “12 de Octubre,” Avda. de la Constitución 73, Portal 3, 7° Izquierda, Coslada, Madrid E-28821, Spain e-mail: <email>jbenitol@meditex.es</email></corresp><fn fn-type="other" id="fn002"><p>This article was submitted to Frontiers in Movement Disorders, a specialty of Frontiers in Neurology.</p></fn></author-notes><pub-date pub-type="epreprint"><day>08</day><month>4</month><year>2013</year></pub-date><pub-date pub-type="epub"><day>10</day><month>6</month><year>2013</year></pub-date><pub-date pub-type="collection"><year>2013</year></pub-date><volume>4</volume><elocation-id>64</elocation-id><history><date date-type="received"><day>21</day><month>3</month><year>2013</year></date><date date-type="accepted"><day>19</day><month>5</month><year>2013</year></date></history><permissions><copyright-statement>Copyright © 2013 Sánchez-Ferro, Benito-León and Gómez-Esteban.</copyright-statement><copyright-year>2013</copyright-year><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/3.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.</license-p></license></permissions><abstract><p>Orthostatic hypotension (OH) is a common and disabling symptom affecting Parkinson’s disease (PD) patients. We present the effect of the different therapies commonly used to manage PD on this clinical manifestation. For this purpose, we describe the relationship between OH and the current treatments employed in PD, such as L-DOPA, dopaminergic agonists, and continuous dopaminergic stimulation therapies. Additionally, we review the therapeutic measures that could be used to ameliorate OH. There are different approaches to deal with this manifestation, including pharmacological and non-pharmacological treatments, although none of them is specifically aimed for treating OH in PD.</p></abstract><kwd-group><kwd>treatment</kwd><kwd>orthostatic hypotension</kwd><kwd>dopamine agonists</kwd><kwd>L-DOPA</kwd><kwd>continuous dopaminergic stimulation</kwd><kwd>Parkinson’s disease</kwd></kwd-group><counts><fig-count count="0"></fig-count><table-count count="3"></table-count><equation-count count="0"></equation-count><ref-count count="149"></ref-count><page-count count="11"></page-count><word-count count="10204"></word-count></counts></article-meta></front><body><sec id="S1"><title>Introduction</title><p>After the first comprehensive description of the cardinal features of Parkinson’s disease (PD) (Parkinson, <xref ref-type="bibr" rid="B104">2002</xref>) many non-motor features have been recognized (Hughes et al., <xref ref-type="bibr" rid="B53">1992</xref>). One of the most disabling is orthostatic hypotension (OH), which is defined by a sustained reduction of systolic blood pressure (SBP) of at least 20 mmHg or diastolic blood pressure (DBP) of 10 mmHg within 3 min of standing or head-up tilt to at least 60 on a tilt table (Kaufmann, <xref ref-type="bibr" rid="B59">1996</xref>; Freeman et al., <xref ref-type="bibr" rid="B37">2011</xref>).</p><p>The presumed pathophysiology of OH is related to the impairment of sympathetic vasomotor neurons due to the neurodegenerative process of PD (Senard et al., <xref ref-type="bibr" rid="B123">2001</xref>; Metzler et al., <xref ref-type="bibr" rid="B86">2012</xref>).</p><p>Growing attention has been paid to this non-motor feature of the disease; especially since dopaminergic drugs were introduced [<sc>l</sc>-DOPA and dopamine agonists (DA)] (Barbeau et al., <xref ref-type="bibr" rid="B7">1969</xref>; Calne et al., <xref ref-type="bibr" rid="B18">1970</xref>; McDowell and Lee, <xref ref-type="bibr" rid="B85">1970</xref>; Duby et al., <xref ref-type="bibr" rid="B30">1972</xref>).</p><p>Even in those cross-sectional initial descriptions, the frequency of this symptom has been highlighted, affecting more than 30% of the PD patients (Barbeau, <xref ref-type="bibr" rid="B6">1969</xref>). A similar pooled estimated prevalence has recently been reported in a systematic review (Velseboer et al., <xref ref-type="bibr" rid="B145">2011</xref>). Other inferences have showed higher frequencies [41% (Kaufmann and Goldstein, <xref ref-type="bibr" rid="B61">2007</xref>) and 47% in a community-based study (Allcock et al., <xref ref-type="bibr" rid="B3">2004</xref>)].</p><p>Additionally, its consequences are important as it may imply an increased mortality and comorbidity (mainly owing to falls and concomitant vascular disorders) (Fedorowski et al., <xref ref-type="bibr" rid="B33">2010</xref>; Maule et al., <xref ref-type="bibr" rid="B84">2012</xref>).</p><p>In the current article, our aim is to review all the therapeutic options available to treat this frequent and incapacitating symptom, focusing on those aspects less studied. We begin describing the influence that common drugs and advanced therapies used in PD may exert on it. Thereafter, we detail non-pharmacological approaches that could be employed to ameliorate this symptom. We end summarizing the existing pharmacological options to treat it.</p></sec><sec id="S2"><title>The Effect of the Anti-Parkinsonian Therapies on Orthostatic Hypotension</title><p>One of the initial steps required when assessing a patient who is going to receive any anti-parkinsonian medication/treatment or who needs a dose adjustment is to anticipate the potential effect on his blood pressure, as it is one of the commonly related factors to the appearance of OH (Perez-Lloret et al., <xref ref-type="bibr" rid="B109">2012</xref>).</p><p>Several actions could help to improve the detection of this complication, either by the physician or the subject. It seems reasonable to instruct the patient about OH symptoms (lightheadedness or dizziness after standing, fatigue, and others), although many cases go unnoticed (Arbogast et al., <xref ref-type="bibr" rid="B4">2009</xref>). An initial pressor response assessment (blood pressure after standing) could be valuable to have a simple measurement to monitor future changes, as this measurement is one of the easiest ways to appraise OH in various healthcare settings.</p><p>Many caveats should be considered prior to establishing the real influence of PD medications on OH. First, there are different diagnostic criteria for defining OH. Additionally, much evidence is based on cross-sectional analyses and other confounding effects, as disease duration or previous autonomous nervous system damage (Awerbuch and Sandyk, <xref ref-type="bibr" rid="B5">1992</xref>; Muller et al., <xref ref-type="bibr" rid="B91">2011</xref>), have not always been considered.</p><p>We present the current evidence to estimate the potential role of current PD treatments on OH. The influence of other drugs, such as antidepressants, diuretics, and antihypertensives, is not reviewed here. Nevertheless, they should be considered when dealing with this complication and decreasing the dose or stopping the responsible medication might be advisable.</p><sec id="S2-1"><title>L-DOPA</title><p>Orthostatic hypotension has been documented as a potential side effect of <sc>l</sc>-DOPA therapy since its early use on PD (Barbeau, <xref ref-type="bibr" rid="B6">1969</xref>). Multiple evidence (Barbeau, <xref ref-type="bibr" rid="B6">1969</xref>; Calne et al., <xref ref-type="bibr" rid="B18">1970</xref>; Keenan, <xref ref-type="bibr" rid="B62">1970</xref>; McDowell and Lee, <xref ref-type="bibr" rid="B85">1970</xref>; Goldberg and Whitsett, <xref ref-type="bibr" rid="B42">1971</xref>; Hoehn, <xref ref-type="bibr" rid="B46">1975</xref>; Camerlingo et al., <xref ref-type="bibr" rid="B19">1990</xref>; Senard et al., <xref ref-type="bibr" rid="B124">1997</xref>; Bouhaddi et al., <xref ref-type="bibr" rid="B14">2004</xref>) has supported this relationship with ranges of decline oscillating from 4.6–20 mmHg in SBP to 2.1–5.0 mmHg in DBP. Other studies failed to show any clear direct relationship (Sachs et al., <xref ref-type="bibr" rid="B119">1985</xref>; Goetz et al., <xref ref-type="bibr" rid="B41">1986</xref>; Haapaniemi et al., <xref ref-type="bibr" rid="B45">2000</xref>; Perez-Lloret et al., <xref ref-type="bibr" rid="B109">2012</xref>).</p><p>The size of the effect in the studies where a decrease on blood pressure was measured is summarized in Table <xref ref-type="table" rid="T1">1</xref>. Methodologically limited earlier studies (small sample, not randomized, without blinding) suggested the role of fludrocortisone (0.05–0.2 mg/q.d.) and etilefrine (5 mg/t.i.d.) for treating <sc>l</sc>-DOPA-associated OH (Miller et al., <xref ref-type="bibr" rid="B87">1973</xref>; Hoehn, <xref ref-type="bibr" rid="B46">1975</xref>).</p><table-wrap id="T1" position="float"><label>Table 1</label><caption><p><bold><italic>Lowering effect</italic> of PD treatments on blood pressure</bold>.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1"></th><th align="left" rowspan="1" colspan="1">Reference</th><th align="left" rowspan="1" colspan="1">SBP change</th><th align="left" rowspan="1" colspan="1">DBP change</th><th align="left" rowspan="1" colspan="1">Sample size</th></tr></thead><tbody><tr><td align="left" rowspan="1" colspan="1"><bold><sc>l</sc>-DOPA</bold></td><td align="left" rowspan="1" colspan="1">Bouhaddi et al. (<xref ref-type="bibr" rid="B14">2004</xref>)</td><td align="left" rowspan="1" colspan="1">8.1</td><td align="left" rowspan="1" colspan="1">5.0</td><td align="left" rowspan="1" colspan="1">18</td></tr><tr><td align="left" rowspan="1" colspan="1"></td><td align="left" rowspan="1" colspan="1">Camerlingo et al. (<xref ref-type="bibr" rid="B19">1990</xref>)</td><td align="left" rowspan="1" colspan="1">9.2<sup>1</sup></td><td align="left" rowspan="1" colspan="1">2.1<sup>1</sup></td><td align="left" rowspan="1" colspan="1">12</td></tr><tr><td align="left" rowspan="1" colspan="1"></td><td align="left" rowspan="1" colspan="1">Barbeau et al. (<xref ref-type="bibr" rid="B7">1969</xref>)</td><td align="left" rowspan="1" colspan="1">>20<sup>2</sup></td><td align="left" rowspan="1" colspan="1">Na</td><td align="left" rowspan="1" colspan="1">86</td></tr><tr><td align="left" rowspan="1" colspan="1"></td><td align="left" rowspan="1" colspan="1">Calne et al. (<xref ref-type="bibr" rid="B18">1970</xref>)</td><td align="left" rowspan="1" colspan="1">8.7</td><td align="left" rowspan="1" colspan="1">4.4</td><td align="left" rowspan="1" colspan="1">20</td></tr><tr><td align="left" rowspan="1" colspan="1"><bold>Dopamine agonists (excluding apomorphine)</bold></td><td align="left" rowspan="1" colspan="1">Haapaniemi et al. (<xref ref-type="bibr" rid="B45">2000</xref>)</td><td align="left" rowspan="1" colspan="1">16.1<sup>3</sup></td><td align="left" rowspan="1" colspan="1">2.8<sup>3</sup></td><td align="left" rowspan="1" colspan="1">17</td></tr><tr><td align="left" rowspan="1" colspan="1"><bold>Monoamine Oxidase inhibitors</bold></td><td align="left" rowspan="1" colspan="1">Churchyard et al. (<xref ref-type="bibr" rid="B24">1999</xref>)</td><td align="left" rowspan="1" colspan="1">19<sup>4</sup></td><td align="left" rowspan="1" colspan="1">5<sup>4</sup></td><td align="left" rowspan="1" colspan="1">20</td></tr><tr><td align="left" rowspan="1" colspan="1"></td><td align="left" rowspan="1" colspan="1">Haapaniemi et al. (<xref ref-type="bibr" rid="B45">2000</xref>)</td><td align="left" rowspan="1" colspan="1">12.5<sup>3</sup></td><td align="left" rowspan="1" colspan="1">5.2<sup>3</sup></td><td align="left" rowspan="1" colspan="1">17</td></tr><tr><td align="left" rowspan="1" colspan="1"><bold>CDS therapies</bold></td></tr><tr><td align="left" rowspan="1" colspan="1">DBS</td><td align="left" rowspan="1" colspan="1">Stemper et al. (<xref ref-type="bibr" rid="B130">2006</xref>)</td><td align="left" rowspan="1" colspan="1">17.7<sup>5</sup></td><td align="left" rowspan="1" colspan="1">−2<sup>5</sup></td><td align="left" rowspan="1" colspan="1">14</td></tr><tr><td align="left" rowspan="1" colspan="1">Apo</td><td align="left" rowspan="1" colspan="1">Pahwa et al. (<xref ref-type="bibr" rid="B103">2007b</xref>)</td><td align="left" rowspan="1" colspan="1">8.7<sup>6</sup></td><td align="left" rowspan="1" colspan="1">Not reported</td><td align="left" rowspan="1" colspan="1">56</td></tr><tr><td align="left" rowspan="1" colspan="1">CDLI</td><td align="left" rowspan="1" colspan="1">Pursiainen et al. (<xref ref-type="bibr" rid="B114">2012</xref>)</td><td align="left" rowspan="1" colspan="1">23.2</td><td align="left" rowspan="1" colspan="1">9.1</td><td align="left" rowspan="1" colspan="1">9</td></tr></tbody></table><table-wrap-foot><p><italic>CDS, continuous dopaminergic stimulation; DBS, deep brain stimulation; CDLI, continuous duodenal <sc>l</sc>-DOPA infusion; Apo, apomorphine pump; BP, blood pressure; SBP, systolic blood pressure; DBP, diastolic blood pressure; *values after tilting in mmHg (positive figures indicate a decrease); <sup>1</sup>BP 3 min after tilting and 2 year after starting <sc>l</sc>-DOPA therapy; <sup>2</sup>mean decrease after <sc>l</sc>-DOPA therapy; <sup>3</sup>the blood-pressure reported is immediately after tilting; <sup>4</sup>the blood-pressure reported is 2 min after tilting; <sup>5</sup>blood-pressure reported after tilting with stimulation on; <sup>6</sup>20 min after apomorphine injection on standing</italic>.</p></table-wrap-foot></table-wrap></sec><sec id="S2-2"><title>Dopamine agonists</title><p>Likewise with <sc>l</sc>-DOPA, DA use has been commonly reported to produce OH in PD (Guttman, <xref ref-type="bibr" rid="B44">1997</xref>; Senard et al., <xref ref-type="bibr" rid="B124">1997</xref>; Lieberman et al., <xref ref-type="bibr" rid="B73">1998</xref>; Korczyn et al., <xref ref-type="bibr" rid="B65">1999</xref>; Pinter et al., <xref ref-type="bibr" rid="B111">1999</xref>; Kujawa et al., <xref ref-type="bibr" rid="B66">2000</xref>; Brunt et al., <xref ref-type="bibr" rid="B17">2002</xref>; Boehringer Ingelheim Pharmaceuticals, <xref ref-type="bibr" rid="B11">2003</xref>; GlaxoSmithKline, <xref ref-type="bibr" rid="B39">2003a</xref>,<xref ref-type="bibr" rid="B40">b</xref>; UCB, Inc, <xref ref-type="bibr" rid="B143">2003</xref>; Poewe et al., <xref ref-type="bibr" rid="B113">2007</xref>), although not always symptomatic (Kujawa et al., <xref ref-type="bibr" rid="B66">2000</xref>); however, in some studies this relationship was not shown (Hubble et al., <xref ref-type="bibr" rid="B52">1995</xref>; Perez-Lloret et al., <xref ref-type="bibr" rid="B109">2012</xref>).</p><p>The figures of patients treated with DA having OH are similar to that reported for <sc>l</sc>-DOPA (Stowe et al., <xref ref-type="bibr" rid="B132">2008</xref>). With active standing, 34% of the DA resulted in OH (Kujawa et al., <xref ref-type="bibr" rid="B66">2000</xref>); nonetheless, OH symptomatic cases listed in clinical trials ranged from 4.6 to 44.0% of the participants (Guttman, <xref ref-type="bibr" rid="B44">1997</xref>; Lieberman et al., <xref ref-type="bibr" rid="B73">1998</xref>; Pinter et al., <xref ref-type="bibr" rid="B111">1999</xref>; Brunt et al., <xref ref-type="bibr" rid="B17">2002</xref>; Boehringer Ingelheim Pharmaceuticals, <xref ref-type="bibr" rid="B11">2003</xref>; GlaxoSmithKline, <xref ref-type="bibr" rid="B39">2003a</xref>,<xref ref-type="bibr" rid="B40">b</xref>; UCB, Inc, <xref ref-type="bibr" rid="B143">2003</xref>). The mean decrease of blood pressure was 16.1 mmHg in the SBP and 2.8 mmHg in the DBP (see Table <xref ref-type="table" rid="T1">1</xref>) (Haapaniemi et al., <xref ref-type="bibr" rid="B45">2000</xref>).</p><p>There is not an established causal relationship with a specific agonist, as OH has been reported in users of ergotic and non-ergotic compounds (Guttman, <xref ref-type="bibr" rid="B44">1997</xref>; Korczyn et al., <xref ref-type="bibr" rid="B65">1999</xref>; Haapaniemi et al., <xref ref-type="bibr" rid="B45">2000</xref>; Kujawa et al., <xref ref-type="bibr" rid="B66">2000</xref>; Korchounov et al., <xref ref-type="bibr" rid="B64">2004</xref>; Stowe et al., <xref ref-type="bibr" rid="B132">2008</xref>), and in all the current pharmaceutical preparations (conventional, extended release, and patch prescription) (Boehringer Ingelheim Pharmaceuticals, <xref ref-type="bibr" rid="B11">2003</xref>; GlaxoSmithKline, <xref ref-type="bibr" rid="B39">2003a</xref>,<xref ref-type="bibr" rid="B40">b</xref>; UCB, Inc, <xref ref-type="bibr" rid="B143">2003</xref>; Poewe et al., <xref ref-type="bibr" rid="B113">2007</xref>). There is no direct comparison between all DA and many clinical trials have not reported this adverse event (Giladi et al., <xref ref-type="bibr" rid="B38">2007</xref>; Pahwa et al., <xref ref-type="bibr" rid="B102">2007a</xref>; Stocchi et al., <xref ref-type="bibr" rid="B131">2008</xref>; Stowe et al., <xref ref-type="bibr" rid="B132">2008</xref>; Poewe et al., <xref ref-type="bibr" rid="B112">2011</xref>; Schapira et al., <xref ref-type="bibr" rid="B120">2011</xref>), so no clear conclusions can be drawn on this issue. Additionally, studies that evaluated different agonists yielded heterogeneous results. In a research involving bromocriptine, ropinirole, selegiline, <sc>l</sc>-DOPA, and amantadine, an increased frequency of OH was observed when therapies were combined (<sc>l</sc>-DOPA plus another DA) and with all the DA (a slightly greater increase was found with bromocriptine compared with ropinirole) (Korchounov et al., <xref ref-type="bibr" rid="B64">2004</xref>). In meta-analytic data addressing the profile of adverse events of DA found no differences between them compared with <sc>l</sc>-DOPA (Etminan et al., <xref ref-type="bibr" rid="B32">2003</xref>) and only in another meta-analytic study, an increased risk of OH was suggested for cabergoline (Kulisevsky and Pagonabarraga, <xref ref-type="bibr" rid="B67">2010</xref>). In summary, no clear conclusions can be drawn concerning the risk of OH with a specific DA.</p></sec><sec id="S2-3"><title>Monoamine oxidase inhibitors</title><p>Drugs that inhibit MAO-B selectively, as rasagiline and selegiline, have been also recognized as a potential factor for inducing OH (Churchyard et al., <xref ref-type="bibr" rid="B23">1997</xref>, <xref ref-type="bibr" rid="B24">1999</xref>; Turkka et al., <xref ref-type="bibr" rid="B139">1997</xref>; Haapaniemi et al., <xref ref-type="bibr" rid="B45">2000</xref>; Bhattacharya et al., <xref ref-type="bibr" rid="B10">2003</xref>; Abassi et al., <xref ref-type="bibr" rid="B1">2004</xref>; Rascol et al., <xref ref-type="bibr" rid="B116">2005</xref>; Olanow et al., <xref ref-type="bibr" rid="B98">2009</xref>; Tolosa and Stern, <xref ref-type="bibr" rid="B138">2012</xref>). There have been several studies evaluating the effect of selegiline (Churchyard et al., <xref ref-type="bibr" rid="B23">1997</xref>, <xref ref-type="bibr" rid="B24">1999</xref>; Turkka et al., <xref ref-type="bibr" rid="B139">1997</xref>; Bhattacharya et al., <xref ref-type="bibr" rid="B10">2003</xref>; Korchounov et al., <xref ref-type="bibr" rid="B64">2004</xref>). The percentage of affected individuals ranged from 30% (Churchyard et al., <xref ref-type="bibr" rid="B24">1999</xref>) to 50% (Bhattacharya et al., <xref ref-type="bibr" rid="B10">2003</xref>) and the mean decrease oscillated between 10.4 and 19 mmHg (Churchyard et al., <xref ref-type="bibr" rid="B24">1999</xref>; Bhattacharya et al., <xref ref-type="bibr" rid="B10">2003</xref>) for SBP and five to even an increase of 2 mmHg for DBP (Churchyard et al., <xref ref-type="bibr" rid="B24">1999</xref>; Bhattacharya et al., <xref ref-type="bibr" rid="B10">2003</xref>) (Table <xref ref-type="table" rid="T1">1</xref>). As with the previously reviewed treatments, the hypotensive effect observed with selegiline was not greater than the one occurring with other drugs such as <sc>l</sc>-DOPA (Bhattacharya et al., <xref ref-type="bibr" rid="B10">2003</xref>) or DA (Haapaniemi et al., <xref ref-type="bibr" rid="B45">2000</xref>) except in one study (Korchounov et al., <xref ref-type="bibr" rid="B64">2004</xref>). There was an initial concern about an increased mortality associated to selegiline, also suggesting a role of its autonomic adverse effects on it, but this has been recently discarded (Lees, <xref ref-type="bibr" rid="B71">1995</xref>; Ives et al., <xref ref-type="bibr" rid="B55">2004</xref>; Turnbull et al., <xref ref-type="bibr" rid="B140">2005</xref>). In addition to OH, hypertensive crises have been reported with selegiline (Rose et al., <xref ref-type="bibr" rid="B118">2000</xref>; Ito et al., <xref ref-type="bibr" rid="B54">2001</xref>).</p><p>Rasagiline is a more recent IMAO-B widely used in the clinical practice for its potential neuroprotective effect (Abassi et al., <xref ref-type="bibr" rid="B1">2004</xref>; Parkinson Study Group, <xref ref-type="bibr" rid="B105">2004</xref>, <xref ref-type="bibr" rid="B106">2005</xref>; Rascol et al., <xref ref-type="bibr" rid="B116">2005</xref>, <xref ref-type="bibr" rid="B117">2011</xref>; Olanow et al., <xref ref-type="bibr" rid="B98">2009</xref>; Tolosa and Stern, <xref ref-type="bibr" rid="B138">2012</xref>). The percentage of individuals with symptomatic OH was comprised of between 1.5 and 6.5% (Olanow et al., <xref ref-type="bibr" rid="B98">2009</xref>; Tolosa and Stern, <xref ref-type="bibr" rid="B138">2012</xref>). Some of the clinical trials involving rasagiline did not make any comment about the percentage of subjects with OH and the mean decrease on blood pressure was not reported (Parkinson Study Group, <xref ref-type="bibr" rid="B106">2005</xref>).</p></sec><sec id="S2-4"><title>Other common prescribed agents (L-DOPA metabolism inhibitors, anticholinergics, amantadine, acetylcholinesterase inhibitors)</title><p>There are descriptions of OH occurring with other medications such as amantadine (Korchounov et al., <xref ref-type="bibr" rid="B64">2004</xref>; Perez-Lloret et al., <xref ref-type="bibr" rid="B109">2012</xref>), and acetylcholinesterase inhibitors (in PD dementia) (Novartis Pharmaceuticals, <xref ref-type="bibr" rid="B94">2003b</xref>). The evidence with anticholinergics is less clear, not increasing OH frequency (Martin et al., <xref ref-type="bibr" rid="B80">1974</xref>), but affecting cardiovascular reflexes (Korchounov et al., <xref ref-type="bibr" rid="B64">2004</xref>). The COMT inhibitors entacapone (Lyytinen et al., <xref ref-type="bibr" rid="B79">2001</xref>; Novartis Pharmaceuticals, <xref ref-type="bibr" rid="B93">2003a</xref>; Olanow et al., <xref ref-type="bibr" rid="B97">2004</xref>) and tolcapone (Tolcapone Study Group, <xref ref-type="bibr" rid="B137">1999</xref>; Koller et al., <xref ref-type="bibr" rid="B63">2001</xref>), as well as DOPA-decarboxylase inhibitors, showed no clear influence on OH (Leibowitz and Lieberman, <xref ref-type="bibr" rid="B72">1975</xref>; Rappelli et al., <xref ref-type="bibr" rid="B115">1978</xref>), except in one study where entacapone showed a protective effect (Perez-Lloret et al., <xref ref-type="bibr" rid="B109">2012</xref>).</p></sec><sec id="S2-5"><title>Is there a dose-dependent effect or an influence of therapies combinations on OH? When does OH occur in treated subjects?</title><p>It seems plausible, based on different observational approaches, that higher doses of dopaminergic medications (Senard et al., <xref ref-type="bibr" rid="B124">1997</xref>; Allcock et al., <xref ref-type="bibr" rid="B2">2006</xref>; Chitsaz et al., <xref ref-type="bibr" rid="B22">2007</xref>) and combined therapies (Korchounov et al., <xref ref-type="bibr" rid="B64">2004</xref>) could also increase the chances of manifesting OH. Also some works have suggested that the main effect of medications could be at the beginning of the therapy developing some tolerance thereafter (Pathak and Senard, <xref ref-type="bibr" rid="B107">2004</xref>).</p><p>Based on all these evidence, the possibility of OH should be especially considered, when starting/adding a new drug or increasing its dose as the probability of symptoms could increase.</p></sec><sec id="S2-6"><title>Continuous dopaminergic stimulation therapies</title><sec id="S2-6-1"><title>Deep brain stimulation</title><p>Cross-sectional studies have suggested a positive effect of subthalamic Deep Brain Stimulation (DBS) on autonomous responses of PD subjects (Stemper et al., <xref ref-type="bibr" rid="B130">2006</xref>; Ludwig et al., <xref ref-type="bibr" rid="B78">2007</xref>). In one of this analysis, including 14 patients, there was a mean general decrease on blood pressure in <italic>on</italic> and <italic>off</italic> stimulation status (Table <xref ref-type="table" rid="T1">1</xref>), but the baroreflex responses were preserved only when the stimulation was <italic>on</italic>, suggesting, therefore, a positive influence of the DBS in BP mediated by its influence on central autonomous nervous system pathways (Stemper et al., <xref ref-type="bibr" rid="B130">2006</xref>). In another study comparing subthalamic DBS with a pharmacotherapy-only group, no positive correlation was found between the <italic>on-stimulation</italic> state and the decrease in blood pressure; but this occurred in the only medicated group. Based on this finding it was suggested that subthalamic DBS did not affect cardiovascular autonomous responses (Ludwig et al., <xref ref-type="bibr" rid="B78">2007</xref>). Noteworthy, in a previous longitudinal study, the initial differences of blood pressure were not found after 1 year’s follow-up, with a similar mean blood-pressure decrease for the subthalamic DBS and the only medicated groups (Holmberg et al., <xref ref-type="bibr" rid="B51">2005</xref>). Additionally, two other studies could not find differences in the cardiovascular responses of the treated subjects (Lipp et al., <xref ref-type="bibr" rid="B74">2005</xref>; Erola et al., <xref ref-type="bibr" rid="B31">2006</xref>).</p><p>In summary, subthalamic DBS could exert a neutral/positive influence at the beginning of the therapy because of its direct effects on central pathways, controlling autonomous responses (Benedetti et al., <xref ref-type="bibr" rid="B8">2004</xref>), or the accompanying decrease in medication to subthalamic stimulation (Borgohain et al., <xref ref-type="bibr" rid="B13">2012</xref>). This effect seems to vanish with time (Holmberg et al., <xref ref-type="bibr" rid="B51">2005</xref>). In addition, medial electrode placement in the subthalamus can produce hypertensive crisis (authors experience; unpublished data). As with the common prescribed drugs, further studies will help to clarify the effect of DBS on this disabling symptom.</p></sec><sec id="S2-6-2"><title>Apomorphine pump/apomorphine injections</title><p>Orthostatic hypotension has been reported since the early use of apomorphine (Duby et al., <xref ref-type="bibr" rid="B30">1972</xref>; Corsini et al., <xref ref-type="bibr" rid="B25">1979</xref>). In these initial descriptions, it was suggested that the peripheral DA domperidone, could diminish this complication (Corsini et al., <xref ref-type="bibr" rid="B25">1979</xref>) recommending to pretreat patients 72 h before its administration. A recent report with another peripheral blocker, commercialized in the US, did not show this protective effect and only younger age influenced the development of OH in apomorphine users (Ondo et al., <xref ref-type="bibr" rid="B100">2012</xref>).</p><p>The frequency of OH after apomorphine treatment is heterogeneous across the studies. The variability could be influenced, as with the other treatments, by the definitions used (manometric vs. symptomatic), pressure cutoffs, and subsets of patients evaluated. The figures oscillated between 1.9% (Tyne et al., <xref ref-type="bibr" rid="B142">2004</xref>) and more than 80% of the subjects affected (Duby et al., <xref ref-type="bibr" rid="B30">1972</xref>). In more recent reports, using current diagnostic criteria, a maximum of 17.6% of the subjects receiving 4 mg of apomorphine had OH vs. 14.3% of the orally treated ones (no equivalent levodopa doses reported). No clear differences between the two groups were found (Pahwa et al., <xref ref-type="bibr" rid="B103">2007b</xref>). The main decrease in blood pressure was observed 20–40 min after the injection (Table <xref ref-type="table" rid="T1">1</xref>).</p></sec><sec id="S2-6-3"><title>Continuous duodenal L-DOPA infusions</title><p>There are different evidences connecting continuous duodenal <sc>l</sc>-DOPA infusions (CDLI) to OH (Pursiainen et al., <xref ref-type="bibr" rid="B114">2012</xref>; Fernandez et al., <xref ref-type="bibr" rid="B34">2013</xref>). In a recent clinical trial interim analysis (NCT00335153), 8.3% of the subjects had OH as an adverse event related to this therapy (Fernandez et al., <xref ref-type="bibr" rid="B34">2013</xref>). In a longitudinal study involving nine CDLI cases an initial decrease of blood pressure after the therapy instauration was observed (Table <xref ref-type="table" rid="T1">1</xref>), but after 2 months the figures rose again, suggesting a compensatory mechanism (Pursiainen et al., <xref ref-type="bibr" rid="B114">2012</xref>).</p></sec></sec><sec id="S2-7"><title>Conclusions about the effect of PD therapies on OH</title><p>Many of the common prescribed treatments used for PD could increase the frequency of OH. It seems advisable to monitor blood pressure and this side effect when starting any “<italic>conventional medication</italic>” or advanced PD therapy and when a dose adjustment is required. If symptoms occur adjunctive therapies should be initiated (see non-pharmacological and pharmacological treatments sections).</p><p>Other outcomes, like supine nocturnal hypertension (nocturnal BP means>120/70 mmHg) (Perez-Lloret et al., <xref ref-type="bibr" rid="B110">2008</xref>), should be addressed, as patients taking higher doses of dopaminergic treatment had less decreases in SBP and DBP at night (Berganzo et al., <xref ref-type="bibr" rid="B9">2013</xref>).</p><p>Further studies are needed to clarify the adjusted effect of the medication/treatments compared with the one produced by the neurodegenerative process itself.</p><p>This will help to draw more specific conclusions for subsets of subjects/treatments and anticipate the risk of OH, granting a more individualized approach when treating PD patients.</p></sec></sec><sec id="S3"><title>Therapeutic Measures</title><sec id="S3-8"><title>General considerations</title><p>The common practice nowadays is to manage only the symptomatic cases, as no current therapy has yet evidenced a protective action on the autonomic nervous system impairment and the role of asymptomatic OH is still not defined (Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>).</p><p>It should be stressed that there are not specifically designed therapies for OH in PD subjects. This is linked to the methodological concerns limiting most of the studies presented and making the current evidence insufficient to define clear guidelines for the management of OH in PD. Nevertheless, there are different therapies that might be helpful (Lahrmann et al., <xref ref-type="bibr" rid="B68">2006</xref>; Figueroa et al., <xref ref-type="bibr" rid="B35">2010</xref>; Zesiewicz et al., <xref ref-type="bibr" rid="B149">2010</xref>; Seppi et al., <xref ref-type="bibr" rid="B125">2011</xref>), which we will review after this section.</p><p>An additional important feature to consider is that situations of orthostatic stress (early hours of the morning, meals, physical activity among others) may trigger OH that otherwise may go unnoticed (Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>). Supine hypertension, an interrelated aspect of OH defined as BP means>120/70 mmHg (Perez-Lloret et al., <xref ref-type="bibr" rid="B110">2008</xref>), should be also monitored (Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>; Berganzo et al., <xref ref-type="bibr" rid="B9">2013</xref>) as treatments used to increase blood pressure, could lead to a worsening of this manifestation. Some authors suggest that supine blood pressure should never exceed 180/110 mmHg (Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>). In the case of hypertensive patients, short half-life drugs are preferable and evening administration.</p><p>Initially, it is also agreed to start with non-pharmacological measures (Lahrmann et al., <xref ref-type="bibr" rid="B68">2006</xref>), because of the lower likelihood of adverse outcomes, the possibility of using them in moments of orthostatic stress (Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>) and for their simplicity (Seppi et al., <xref ref-type="bibr" rid="B125">2011</xref>).</p></sec><sec id="S3-9"><title>Non-pharmacological measures</title><p>In Table <xref ref-type="table" rid="T2">2</xref> there is a description of the main employed strategies.</p><table-wrap id="T2" position="float"><label>Table 2</label><caption><p><bold>Non-pharmacological therapies</bold>.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1">Measure</th><th align="left" rowspan="1" colspan="1">Increase on blood pressure (mmHg)</th><th align="left" rowspan="1" colspan="1">% Compliance<sup>1</sup></th><th align="left" rowspan="1" colspan="1">Comment</th></tr></thead><tbody><tr><td align="left" rowspan="1" colspan="1">Fluid (water) intake</td><td align="left" rowspan="1" colspan="1">15–25</td><td align="left" rowspan="1" colspan="1">88</td><td align="left" rowspan="1" colspan="1">Recommended daily intake 2–2.5 l</td></tr><tr><td align="left" rowspan="1" colspan="1">Salt Intake</td><td align="left" rowspan="1" colspan="1">10–15</td><td align="left" rowspan="1" colspan="1">82</td><td align="left" rowspan="1" colspan="1">150–200 Na+ mmol/day (Salt: 9–12 g/day)</td></tr><tr><td align="left" rowspan="1" colspan="1">Meal frequency</td><td align="left" rowspan="1" colspan="1">Unknown</td><td align="left" rowspan="1" colspan="1">82</td><td align="left" rowspan="1" colspan="1">Multiple smaller meals containing less carbohydrates</td></tr><tr><td align="left" rowspan="1" colspan="1">Alcohol consumption</td><td align="left" rowspan="1" colspan="1">Unknown</td><td align="left" rowspan="1" colspan="1">59</td><td align="left" rowspan="1" colspan="1">Avoid its consume throughout the day</td></tr><tr><td align="left" rowspan="1" colspan="1">Night time head-up tilt</td><td align="left" rowspan="1" colspan="1">2–11</td><td align="left" rowspan="1" colspan="1">76</td><td align="left" rowspan="1" colspan="1">Elevated head of the bed (10–15 cm or 12°)</td></tr><tr><td align="left" rowspan="1" colspan="1">Stockings/abdominal bandages</td><td align="left" rowspan="1" colspan="1">12–26</td><td align="left" rowspan="1" colspan="1">59</td><td align="left" rowspan="1" colspan="1">Abdominal bandage more effective than stockings alone and may favor compliance</td></tr><tr><td align="left" rowspan="1" colspan="1">Physical countermanouvers<sup>2</sup></td><td align="left" rowspan="1" colspan="1">10–15</td><td align="left" rowspan="1" colspan="1">Unknown</td><td align="left" rowspan="1" colspan="1">Leg crossing, squatting, bending-forward, and tiptoeing</td></tr></tbody></table><table-wrap-foot><p><italic><sup>1</sup>Based on Schoffer et al. (<xref ref-type="bibr" rid="B121">2007</xref>); <sup>2</sup>leg crossing, thigh contraction, or squatting</italic>.</p></table-wrap-foot></table-wrap><sec id="S3-9-4"><title>Water and salt</title><p>Standing-up implies that 500–700 ml of blood will pool in lower extremities and abdomen (Diedrich and Biaggioni, <xref ref-type="bibr" rid="B29">2004</xref>). This is one of the reasons for trying to increase plasma volume to counter this effect. Many studies have evaluated the influence of drinking water on blood pressure (Jordan et al., <xref ref-type="bibr" rid="B57">1999a</xref>; Senard et al., <xref ref-type="bibr" rid="B122">1999</xref>; Shannon et al., <xref ref-type="bibr" rid="B126">2002</xref>; Mathias and Young, <xref ref-type="bibr" rid="B83">2004</xref>; Waters et al., <xref ref-type="bibr" rid="B146">2005</xref>; Deguchi et al., <xref ref-type="bibr" rid="B26">2007</xref>; Schoffer et al., <xref ref-type="bibr" rid="B121">2007</xref>). A positive effect has been found in autonomic disorders, including multiple system atrophy or pure autonomic failure (Jordan et al., <xref ref-type="bibr" rid="B57">1999a</xref>; Shannon et al., <xref ref-type="bibr" rid="B126">2002</xref>; Mathias and Young, <xref ref-type="bibr" rid="B83">2004</xref>; Waters et al., <xref ref-type="bibr" rid="B146">2005</xref>; Deguchi et al., <xref ref-type="bibr" rid="B26">2007</xref>). In PD subjects, no difference in BP has been clearly evidenced, but the sample of evaluated individuals was small (Senard et al., <xref ref-type="bibr" rid="B122">1999</xref>; Schoffer et al., <xref ref-type="bibr" rid="B121">2007</xref>). In non-PD-related autonomic failure, blood-pressure augmented once drinking 350–500 ml of water shortly after the ingestion (20–35 min) with a mean increase ranging between 23 and 31 mmHg for SBP and 15–25 in DBP (Shannon et al., <xref ref-type="bibr" rid="B126">2002</xref>; Mathias and Young, <xref ref-type="bibr" rid="B83">2004</xref>; Deguchi et al., <xref ref-type="bibr" rid="B26">2007</xref>). This increase is even comparable to the one obtained with some of the commonly prescribed medications for OH (Ten Harkel et al., <xref ref-type="bibr" rid="B135">1994</xref>) but lasted shortly (1 h) (Jordan et al., <xref ref-type="bibr" rid="B57">1999a</xref>). It has been recommended to apply this strategy in the morning period, where blood pressure is even lower (Omboni et al., <xref ref-type="bibr" rid="B99">2001</xref>; Wieling et al., <xref ref-type="bibr" rid="B147">2002</xref>). The adverse outcomes are said to be mild (Schoffer et al., <xref ref-type="bibr" rid="B121">2007</xref>), i.e., urinary incontinence. No follow-up data for the long-term effect have been presented (Mathias and Young, <xref ref-type="bibr" rid="B83">2004</xref>).</p><p>Salt ingestion could also increase plasma volume (Wieling et al., <xref ref-type="bibr" rid="B147">2002</xref>; Waters et al., <xref ref-type="bibr" rid="B146">2005</xref>). One of the reasons to supplement it, is that subjects with autonomic failure are unable to reduce renal sodium excretion during salt restrictions, which could potentially lead to an increase in the blood-pressure drop upon standing (Wieling et al., <xref ref-type="bibr" rid="B147">2002</xref>). The daily dietary average intake of sodium is 150 mmol (Hollenberg, <xref ref-type="bibr" rid="B50">2006</xref>). An increase on blood pressure of 10–15 mmHg could be achieved with a high-salt containing diet (150–200 mmol/day of sodium or 9–12 g/day of common salt), combined with other measures (Wieling et al., <xref ref-type="bibr" rid="B147">2002</xref>). It is necessary to check urine sodium (range between 170 and 260 mmol/day) (Wieling et al., <xref ref-type="bibr" rid="B147">2002</xref>), as well as blood pressure (Hollenberg, <xref ref-type="bibr" rid="B50">2006</xref>), to monitor the positive effects and prevent any deleterious outcomes, as high-salt intake could increase cardiovascular mortality (with urine sodium levels above 300 mmol/day) (O’Donnell et al., <xref ref-type="bibr" rid="B96">2011</xref>). One study including PD cases failed to show this positive influence (Schoffer et al., <xref ref-type="bibr" rid="B121">2007</xref>) after common salt supplements of 10–20 g/day (170–350 mmol/day of sodium). Another aspect yet to be determined is the salt-sensitivity of PD subjects affected by OH, as it is known that is not the same in all individuals (Hollenberg, <xref ref-type="bibr" rid="B50">2006</xref>); further analyses are needed to clarify salt influence on OH in PD.</p></sec><sec id="S3-9-5"><title>Physical countermaneuvers</title><p>Several drills aimed to promote venous return and maintain cardiac output have been proposed for different autonomic disorders (Ten Harkel et al., <xref ref-type="bibr" rid="B134">1992</xref>, <xref ref-type="bibr" rid="B135">1994</xref>; Wieling et al., <xref ref-type="bibr" rid="B148">1993</xref>; Bouvette et al., <xref ref-type="bibr" rid="B15">1996</xref>; Tutaj et al., <xref ref-type="bibr" rid="B141">2006</xref>). They include tiptoeing, leg crossing, bending-forward, and squatting (Ten Harkel et al., <xref ref-type="bibr" rid="B134">1992</xref>, <xref ref-type="bibr" rid="B135">1994</xref>; Wieling et al., <xref ref-type="bibr" rid="B148">1993</xref>; Bouvette et al., <xref ref-type="bibr" rid="B15">1996</xref>; Tutaj et al., <xref ref-type="bibr" rid="B141">2006</xref>). The range of increase in blood-pressure fluctuated between 10 and 15 mmHg (Wieling et al., <xref ref-type="bibr" rid="B148">1993</xref>). The importance of these maneuvers is still controversial (Ten Harkel et al., <xref ref-type="bibr" rid="B135">1994</xref>; Bouvette et al., <xref ref-type="bibr" rid="B15">1996</xref>; Tutaj et al., <xref ref-type="bibr" rid="B141">2006</xref>).</p></sec><sec id="S3-9-6"><title>Stockings and abdominal bands</title><p>Besides the previous active maneuvers, there have been trials to raise the peripheral vascular pressure passively based on studies evaluating antigravity suits (Denq et al., <xref ref-type="bibr" rid="B27">1997</xref>). This was aimed to oppose the mentioned blood pooling upon standing, exerting pressure on different capacitance beds such as the lower extremities and abdomen (Denq et al., <xref ref-type="bibr" rid="B27">1997</xref>). An abdominal band has shown to be more effective and maybe with a better compliance, than the usual recommended stockings (Schoffer et al., <xref ref-type="bibr" rid="B121">2007</xref>). This band could increase the blood pressure as much as 12 mmHg (Denq et al., <xref ref-type="bibr" rid="B27">1997</xref>; Tanaka et al., <xref ref-type="bibr" rid="B133">1997</xref>). In a study including PD patients 30 mmHg pressure stockings failed to show any beneficial effect on OH subjects (Schoffer et al., <xref ref-type="bibr" rid="B121">2007</xref>).</p></sec><sec id="S3-9-7"><title>Head-of-bed elevation</title><p>There is a physiological drop in blood pressure in the morning, which has been related with night recumbence, although other factors have not been ruled out (Omboni et al., <xref ref-type="bibr" rid="B99">2001</xref>). In patients with PD and autonomic failure, nocturnal hypertension leads to natriuresis and polyuria, which, in turn, may cause severe OH in the morning hours. Raising the head of the bed (10–15 cm or 12°) decreased the nocturnal blood-pressure levels and the release of atrial natriuretic peptide, reducing nocturia, and OH in the early hours of the morning, especially when combined with other measures (Ten Harkel et al., <xref ref-type="bibr" rid="B134">1992</xref>; van Lieshout et al., <xref ref-type="bibr" rid="B144">2000</xref>). The main increase in BP in non-PD cases ranged from 2 to 11 mmHg and symptomatic relief has also been reported (Ten Harkel et al., <xref ref-type="bibr" rid="B134">1992</xref>).</p></sec><sec id="S3-9-8"><title>Other proposed measures</title><p>Other proposed strategies are based on evidences of different factors, which influence blood pressure in autonomic failure (Lahrmann et al., <xref ref-type="bibr" rid="B68">2006</xref>; Freeman, <xref ref-type="bibr" rid="B36">2008</xref>; Gupta and Nair, <xref ref-type="bibr" rid="B43">2008</xref>; Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>; Mostile and Jankovic, <xref ref-type="bibr" rid="B90">2009</xref>). Frequent meals with fewer carbohydrates could diminish the postprandial hypotension component (Thomaides et al., <xref ref-type="bibr" rid="B136">1993</xref>). It has been suggested that food could lower blood pressure in autonomic failure through vasodilatation (Thomaides et al., <xref ref-type="bibr" rid="B136">1993</xref>; Chaudhuri et al., <xref ref-type="bibr" rid="B20">1997</xref>) and insulin secretion (Nozaki et al., <xref ref-type="bibr" rid="B95">1993</xref>). Avoiding alcohol during the day has been suggested (Chaudhuri et al., <xref ref-type="bibr" rid="B21">1995</xref>; Narkiewicz et al., <xref ref-type="bibr" rid="B92">2000</xref>). Averting rapid postural changes and warm temperatures and an adequate physical activity have been recommended (Lahrmann et al., <xref ref-type="bibr" rid="B68">2006</xref>; Freeman, <xref ref-type="bibr" rid="B36">2008</xref>; Gupta and Nair, <xref ref-type="bibr" rid="B43">2008</xref>; Mostile and Jankovic, <xref ref-type="bibr" rid="B90">2009</xref>). None of them have shown a favorable influence, when evaluated in PD individuals suffering from OH (Schoffer et al., <xref ref-type="bibr" rid="B121">2007</xref>).</p></sec></sec><sec id="S3-10"><title>Pharmacological measures</title><p>When non-pharmacological therapies are not satisfactory, pharmacological should be considered. Supine hypertension should be always monitored, as some of the pharmacological therapies may worsen it. Additionally, the long-term prognostic implications of OH are not known, so the aim of the therapy focuses on ameliorating the symptoms. The main drugs used to treat OH, not limited to PD, are summarized in Table <xref ref-type="table" rid="T3">3</xref>. We describe the most important ones.</p><table-wrap id="T3" position="float"><label>Table 3</label><caption><p><bold>Pharmacological therapies</bold>.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1">Drug</th><th align="left" rowspan="1" colspan="1">Dose</th><th align="left" rowspan="1" colspan="1">Posology</th><th align="left" rowspan="1" colspan="1">Increase on SBP/DBP (mmHg)<sup>1</sup></th><th align="left" rowspan="1" colspan="1">Adverse effects</th><th align="left" rowspan="1" colspan="1">Comment</th></tr></thead><tbody><tr><td align="left" rowspan="1" colspan="1">Pyridostigmine</td><td align="left" rowspan="1" colspan="1">30–60 mg</td><td align="left" rowspan="1" colspan="1">b.i.d./t.i.d.</td><td align="left" rowspan="1" colspan="1">Unknown/6.8</td><td align="left" rowspan="1" colspan="1">Abdominal colic, nausea, sialorrhea</td><td align="left" rowspan="1" colspan="1">No supine hypertension</td></tr><tr><td align="left" rowspan="1" colspan="1">Fludrocortisone</td><td align="left" rowspan="1" colspan="1">0.1–0.2 mg/day</td><td align="left" rowspan="1" colspan="1">q.d.</td><td align="left" rowspan="1" colspan="1">9–42/0–16</td><td align="left" rowspan="1" colspan="1">Hypokaliemia, edema, congestive heart failure, supine hypertension</td><td align="left" rowspan="1" colspan="1">Effect may appear after 1–2 weeks of treatment. Titer slowly</td></tr><tr><td align="left" rowspan="1" colspan="1">Midodrine</td><td align="left" rowspan="1" colspan="1">2.5–10 mg</td><td align="left" rowspan="1" colspan="1">b.i.d./t.i.d.</td><td align="left" rowspan="1" colspan="1">20–22/11–15</td><td align="left" rowspan="1" colspan="1">Paresthesia, pruritus, piloerection, supine hypertension</td><td align="left" rowspan="1" colspan="1">Tested in a randomized clinical trial</td></tr><tr><td align="left" rowspan="1" colspan="1">L-DOPS</td><td align="left" rowspan="1" colspan="1">200–400 mg</td><td align="left" rowspan="1" colspan="1">q.d/b.i.d.</td><td align="left" rowspan="1" colspan="1">23–28/9–12</td><td align="left" rowspan="1" colspan="1">Dizziness, tiredness, visual disturbance, supine hypertension, malignant neuroleptic syndrome</td><td align="left" rowspan="1" colspan="1">High doses of DOPA-decarboxylase inhibitors could abolish its effect</td></tr><tr><td align="left" rowspan="1" colspan="1">Octreotide</td><td align="left" rowspan="1" colspan="1">50–100 μg</td><td align="left" rowspan="1" colspan="1">q.d.</td><td align="left" rowspan="1" colspan="1">No differences</td><td align="left" rowspan="1" colspan="1">Injection-related, abdominal colic, tiredness, headache</td><td align="left" rowspan="1" colspan="1">Useful for postprandial hypotension</td></tr><tr><td align="left" rowspan="1" colspan="1">Yohimbine</td><td align="left" rowspan="1" colspan="1">5 mg</td><td align="left" rowspan="1" colspan="1">q.d</td><td align="left" rowspan="1" colspan="1">18–33/11–16</td><td align="left" rowspan="1" colspan="1">Nausea, tremor, confusion, nervousness</td><td align="left" rowspan="1" colspan="1">May be useful in postprandial orthostatic hypotension</td></tr><tr><td align="left" rowspan="1" colspan="1">Erythropoietin</td><td align="left" rowspan="1" colspan="1">25–75 UI/kg</td><td align="left" rowspan="1" colspan="1">3 times/week</td><td align="left" rowspan="1" colspan="1">16–19/16–17</td><td align="left" rowspan="1" colspan="1">Supine hypertension</td><td align="left" rowspan="1" colspan="1">Only if concomitant anemia is present</td></tr></tbody></table><table-wrap-foot><p><italic>SBP, systolic blood pressure; DBP, diastolic blood pressure; <sup>1</sup>values are rounded</italic>.</p></table-wrap-foot></table-wrap><sec id="S3-10-9"><title>Fludrocortisone</title><p>Several studies have evaluated the effects of fludrocortisone on OH based on its volume expanding (by means of enhancing renal sodium reabsorption) and α-adrenoreceptor sensitizing activities (Hoehn, <xref ref-type="bibr" rid="B46">1975</xref>; Ten Harkel et al., <xref ref-type="bibr" rid="B134">1992</xref>; Schoffer et al., <xref ref-type="bibr" rid="B121">2007</xref>). The common prescribed dosages range between 0.1 and 0.2 mg/day (Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>). Supine hypertension could worsen under this treatment and other adverse outcomes like hypokalemia and peripheral edema should be considered (Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>). The combining action with other non-pharmacological measures like salt ingestion and head-up tilt has proved to be more effective on increasing blood pressure (Ten Harkel et al., <xref ref-type="bibr" rid="B134">1992</xref>).</p></sec><sec id="S3-10-10"><title>Pyridostigmine</title><p>Pyridostigmine acts mainly improving ganglionic cholinergic transmissions through cholinesterase inhibition. It favors normal physiologic responses upon standing, without worsening supine hypertension (Singer et al., <xref ref-type="bibr" rid="B129">2006</xref>; Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>). The pressor effect was modest (a 6.4 mmHg increase in DBP) (Singer et al., <xref ref-type="bibr" rid="B129">2006</xref>), so it is recommended for initial treatment or mild cases (Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>). Doses are started at 30 mg b.i.d. or t.i.d. and could be increased to 60 mg b.i.d. or t.i.d (Singer et al., <xref ref-type="bibr" rid="B129">2006</xref>). Adverse outcomes include diarrhea and nausea, among other cholinergic symptoms (Singer et al., <xref ref-type="bibr" rid="B129">2006</xref>; Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>).</p></sec><sec id="S3-10-11"><title>Midodrine</title><p>This drug is a α1-agonist with a short duration effect (2–4 h). Its main action is to augment vascular resistance and therefore blood pressure. In addition to the anti-OH effect, it can also enhance supine hypertension, so close monitoring of recumbent blood pressure and avoiding evening administration are required (Jankovic et al., <xref ref-type="bibr" rid="B56">1993</xref>; Low and Singer, <xref ref-type="bibr" rid="B77">2008</xref>). Doses range between 2.5 and 10 mg b.i.d or t.i.d (Jankovic et al., <xref ref-type="bibr" rid="B56">1993</xref>; Low et al., <xref ref-type="bibr" rid="B76">1997</xref>). Along with hypertension, other common adverse events are piloerection, paresthesia, and itching (characteristically in the scalp) (Jankovic et al., <xref ref-type="bibr" rid="B56">1993</xref>; Low et al., <xref ref-type="bibr" rid="B76">1997</xref>).</p></sec><sec id="S3-10-12"><title>L-DOPS</title><p><sc>l</sc>-Threo-dihydroxyphenylserine or droxidopa is a pro-drug converted by DOPA decarboxylase into norepinephrine. Doses between 100 and 900 mg have been used in PD and other autonomic disorders, improving the drop in blood pressure in OH significantly (Kaufmann, <xref ref-type="bibr" rid="B60">2008</xref>; Mathias, <xref ref-type="bibr" rid="B81">2008</xref>). Side effects were mild, but supine hypertension should be monitored (Kaufmann, <xref ref-type="bibr" rid="B60">2008</xref>). Noteworthy, DOPA-decarboxylase inhibitors used in high doses (200 mg) could block this therapeutic effect (Kaufmann, <xref ref-type="bibr" rid="B60">2008</xref>), but the current combinations employed with <sc>l</sc>-DOPA (25–50 mg of inhibitor) do not produce this interference (Kaufmann, <xref ref-type="bibr" rid="B60">2008</xref>). Recently, promising results suggesting a positive influence on symptoms and OH related outcomes (falls and fall related injuries) have been presented by Isaacson et al. (2013), American Academy of Neurology, San Diego, CA, USA.</p></sec><sec id="S3-10-13"><title>Other drugs</title><p>Many other medicaments have been attempted to correct the effects of OH. The evidence in which they are based is weak, mostly because of the small samples sizes and the designs used. We describe some, but this is not intended to be an exhaustive review of them.</p><p>Octreotide has been used mainly to correct postprandial hypotension linked to OH (Hoeldtke and Israel, <xref ref-type="bibr" rid="B48">1989</xref>), as it could counter the release of vasoactive peptides secreted with food/alcohol ingestion (Bordet et al., <xref ref-type="bibr" rid="B12">1995</xref>; Chaudhuri et al., <xref ref-type="bibr" rid="B21">1995</xref>; Hoeldtke et al., <xref ref-type="bibr" rid="B47">1998</xref>). Its combination with midodrine was more effective than when it was given alone (Hoeldtke and Israel, <xref ref-type="bibr" rid="B48">1989</xref>). The doses range from 50 to 100 μg/kg (subcutaneous injection). In some studies, no clear change of blood pressure could be evidenced, but symptomatic relief was reported (Bordet et al., <xref ref-type="bibr" rid="B12">1995</xref>).</p><p>Yohimbine is an alpha-2 adrenergic receptor antagonist, which enhances the residual sympathetic tone (Onrot et al., <xref ref-type="bibr" rid="B101">1987</xref>; Shibao et al., <xref ref-type="bibr" rid="B128">2010</xref>). Some reports, including PD cases, have suggested a positive role and even better results on raising blood pressure than pyridostigmine (Shibao et al., <xref ref-type="bibr" rid="B128">2010</xref>).</p><p>Erythropoietin has been useful in correcting a drop in blood pressure in patients with concomitant anemia and autonomic failure (Hoeldtke and Streeten, <xref ref-type="bibr" rid="B49">1993</xref>; Perera et al., <xref ref-type="bibr" rid="B108">1995</xref>).</p><p>Desmopressin studies have suggested a positive influence on orthostatic tolerance (Mathias et al., <xref ref-type="bibr" rid="B82">1986</xref>; Larina et al., <xref ref-type="bibr" rid="B70">2009</xref>). Desmopressin reduced nocturnal polyuria, raised supine blood pressure, and reduced the postural fall, especially in the morning, when patients were often at their worst (Mathias et al., <xref ref-type="bibr" rid="B82">1986</xref>; Larina et al., <xref ref-type="bibr" rid="B70">2009</xref>).</p><p>Caffeine has been studied alone or in combination with ergotamine to treat OH and postprandial hypotension in subjects with PD and other conditions causing autonomic failure (Lipsitz et al., <xref ref-type="bibr" rid="B75">1994</xref>; Dewey et al., <xref ref-type="bibr" rid="B28">1998</xref>).</p><p>Domperidone (30 mg t.i.d), a dopaminergic antagonist, has also shown beneficial effects on OH (Montastruc et al., <xref ref-type="bibr" rid="B88">1985</xref>; Lang, <xref ref-type="bibr" rid="B69">2001</xref>; Schoffer et al., <xref ref-type="bibr" rid="B121">2007</xref>). It has also been recommended to treat autonomic symptoms related to apomorphine (see above).</p><p>Ephedrine is an indirect sympathomimetic agent that has also been used in OH (Brooks et al., <xref ref-type="bibr" rid="B16">1989</xref>), but due to its central nervous system actions, midodrine, that does not cross the blood-brain barrier, may be preferred. Supine hypertension is also related to its use (Brooks et al., <xref ref-type="bibr" rid="B16">1989</xref>).</p><p>Etilefrine (5–10 mg) was used in 15 PD patients to increase blood pressure upon standing (mean increase of 4.3%) reporting only headaches as adverse outcomes (Miller et al., <xref ref-type="bibr" rid="B87">1973</xref>).</p><p>Fluoxetine (20 mg) was used in a pilot study including 14 PD patients, reducing the drop in blood pressure in 11 mmHg and improving orthostatic symptoms (Montastruc et al., <xref ref-type="bibr" rid="B89">1998</xref>).</p><p>For treating supine hypertension, it has been recommended to use nitroglycerine patches (0.025–0.2 mg/h) (Jordan et al., <xref ref-type="bibr" rid="B58">1999b</xref>), or clonidine (0.1 mg) (Shibao et al., <xref ref-type="bibr" rid="B127">2006</xref>), but further studies are needed to measure the impact of this drugs on PD cases.</p></sec></sec></sec><sec id="S4"><title>Overall Summary</title><p>Orthostatic hypotension is a common and challenging symptom affecting PD patients. The neurodegenerative process is responsible for damaging the autonomous nervous system, but anti-parkinsonian treatments could enhance the symptoms derived from it. Current therapeutical strategies include non-pharmacological and pharmacological measures aimed to favor baropressor responses or to increase blood volume. There is insufficient evidence to recommend any specific treatment for the PD-related autonomic failure. Therefore, it should be individualized for the individual patient. 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