Introduction
Postural deformities are frequent complications in patients with Parkinson’s disease (PwPD) and adversely impact their overall functioning and quality of life (QoL) (Doherty et al. 2011). These deformities include Antecollis (dropped head as a form of extreme anterior flexion of the neck), Camptocormia (anterior flexion of the thoracolumbar spine, marked anterior flexion), and lateral trunk flexion or Pisa Syndrome (PS) (Doherty et al. 2011). The pathophysiology of these disabling postural deformities are not fully understood, but a number of different causes have been proposed (Uzawa et al. 2009; Tinazzi et al. 2016). These causes are emphasized on either central mechanisms (dystonia, rigidity, proprioceptive disintegration), or peripheral mechanisms (myopathy, skeletal and soft tissue changes) (Doherty et al. 2011). Indeed, these mechanisms in addition to ageing may lead to muscle imbalance, weakness, and compensatory posture (Doherty et al. 2011).
Activities of daily living (ADLs) and QoL were deteriorated in PwPD and postural deformities, as a results ambulation and social interactions were restricted as well (Bloem et al. 2001; Cole et al. 2010). Moreover, recently we found that PwPD and PS affect negatively the upper limb function and ADLs (Alwardat et al. 2018). Additionally, previous study reported that low back pain increased result of stooped posture decrease lumber lordosis and forward head pos¬ture (Watanabe et al. 2015). Furthermore, balance is impaired in individuals with chronic low back pain compared to healthy individuals (Berenshteyn et al. 2018).
It has been established that the neuromuscular and musculoskeletal systems are two sides of the same coin, which are important for ergonomic balance and deliberate displacement of the human body (Schwabet al. 2010). Moreover, the relationship between trunk alignments and back function has been recognized previously (Gillen et al. 2007). Postural malalignment is lead to predictable patterns of tissue overload and dysfunction, initiating the cumulative injury cycle (Kendall et al. 2005). Postural deformities and dystonia were developed during the Parkinson disease (PD) can lead to radicular-neuropathic pain through discopathy (Adams et al 2000). In addition, abnormal muscle tone and reduced flexibility of the spine may also cause non-radicular back pain originating from muscle, soft tissues, and skeletal structures. However, not all forms of pain in PwPD show a clear response to dopaminergic medication, and increasing the medication doses will lead to negative side effects (Madeo et al. 2015).
There was a growing body of literature that recognises the importance of the spin alignment and the impact of postural deformity on QoL and ADLs (Doherty et al. 2011; Alwardat et al. 201)]. Moreover, aging is often associated with a increase of postural deformity and risk of fall, as well as the vulnerability of PwPD to develop spinal deformities. So far, very little attention has been paid to the effects of different postural deformity on back function and pain in PwPD. Therefore, the aims of this study is to investigate the effect of different postural deformities include (PS, Camptocormia and Antecollis (C&A)) on back function and pain in PwPD without postural deformities, PwPD and PS, and PwPD and C&A.
Methods
Participants
This observational cross-sectional study was carried out at an outpatient clinic of the Movement Disorders division of Neurology Unit of Policlinico Tor Vergata (Rome, Italy) between May and December 2017. This study include 16 PwPD without any postural deformities (age range 50-69 years, mean 63.73±4.38 SD), 16 PwPD and PS (age range 60-77 years, mean 67.27±4.27 SD) and 16 PwPD and C&A (age range 55-83 years, mean 68.33±7.27). Table 1 summarizes the demographic and clinical characteristics of the participants. All patients underwent neurological evaluation before enrollment. Inclusion criteria were: a medical diagnosis of PD confirmed according to United Kingdom Brain Bank Criteria (Gelb et al. 1999); postural deformities (PS, C&A); walking ability for a short distance (10 meters) without use of assistive device. Exclusion criteria were: severe dyskinesia or “on-off” fluctuations; modified Hoehn & Yahr (mH&Y) stage >3 in “ON” medication phase, cognitive impairment; Mini-Mental status Examination (MMSE) <24, PD medication modification in the 3 months preceding enrollment into the study; need for assistive devices to rise from a chair or bed; other neurological, orthopedic or cardiovascular co-morbidities. Those who had a history of spinal bone fracture or vertebral surgery were also excluded. All patients gave their informed consent to participate in the study. The study was carried out according to the Declaration of Helsinki and was approved by the Local Ethics Committee.
Procedures
Assessments were made in a single session with the patients on their usual drug treatment, during the ON medication phase; all PD patients were on best medical treatment. The diagnostic and neurological evaluations were performed by a specialist in movement disorders. Clinical and demographic variables were recorded: gender, age, weight, height and body mass index (BMI). Patients were assessed using Unified Parkinson's Disease Rating Scale (UPDRS) part II (activities of daily living) and part III (motor performance) (Fahn 1987) and Modified Hoehn and Yahr staging scale (mH & Y) (Hoehn and Yahr 1998); Levodopa equivalent daily dose (LEDD) was calculated using standardized conversion formulas (Tomlinson et al. 2010). MMSE used to eliminate potential cognitive impairment and it’s adjusted for age and educational level (Folstein et al. 1975). Further information were gathered for the PD with different postural deformities patients: PD duration, affected side, postural deformities determined according to the diagnostic criteria published by Doherty and his collogues (Doherty et al. 2011). This study conducted according to STROBE guidelines and reports the required for observational cross sectional studies.
Outcome measure
Oswestry Disability Index (ODI)
ODI is a self-administered questionnaire measuring “back-specific function” on a 10 item scale with six response categories (Monticone et al. 2009). Each item scores from 0 to 5, higher scores being worse, which is transformed into a 0–100 scale. The ten items include pain intensity, personal care, lifting, walking, sitting, standing, sleeping, work, social life and traveling. Patients with scores between 0 to 20 have Minimal Disability, between 21 and 40 have Moderate Disability, between 41–60 have Severe Disability, 61 to 80 are crippled and 81 to 100 are bed-bound or exaggerating their symptoms (Monticone et al. 2009).
Brief Pain Inventory short form (BPI-SF)
BPI-SF used to assess the chronic pain conditions. BPI-SF consist a nine items, the first, optional, item is a screening question about the respondent’s pain on the day. The questionnaire is then composed of pain drawing diagrams, four items about pain intensity (worst pain, least pain, average pain, pain right now), two items on pain relief treatment or medication, and one item on pain interference, with seven sub-items (general activity, mood, walking ability, normal walk, relations with other people, sleep, and enjoyment of life). The BPI gives two main scores: a pain severity (BPI-PS) and pain interference (BPI-PI). The BPI-PS is calculated from the four items about pain intensity. Each item is rated from 0, no pain, to 10, pain as bad as the patient imagine, and contributes with the same weight to the final score, ranging from 0 to 40. The BPI-PI is corresponds to the item on pain interference. The seven sub-items are rated from 0, does not interfere, to 10, completely interferes, and contributes with the same weight to the final score, ranging from 0 to 70 (Cleeland 1994).
Statistical analysis
Differences among the four groups were compared using the Kruskall-Wallis test. We confirmed that the population was not normally distributed by use of the Kolmogorov-Smimov test before running non-parametric tests. A value of p< 0.05 was considered statistically significant. Statistical analyses were performed using the SPSS-22 software package (IBM).
Results
Table 1 shows the clinical and demographical characteristics of the participants. All PD patients were receiving chronic therapy with a dopaminergic drug and showed good motor compensation in appendicular function. All PD groups received the same medication 29 patients took Levodopa and Dopamine Agonist and 19 patients took Levodopa. None had psychiatric disturbances or cognitive impairments. There were no significant differences among the groups in gender, age and biometrical data distribution.
PD group compared with PS and C&A groups showed differences in ODI, BPI-PS, BPI-PI, LEDD and mH&Y staging (P<0.001), but no differences were found in PD duration, UPDRS-II and UPDRS-III in the same groups (Figure 1 & 2). Moreover, PS group compared with C&A group demonstrated no differences in ODI, BPI-PS, BPI-PI, PD duration, LEDD, UPDRS-II, UPDRS-III and mH&Y staging (Figure 1 & 2).
Discussion
One-third of PwPD is develop postural deformities, which lead to back pain, difficulties with walking, breathlessness, unsteadiness leading to falls and impaired ADLs (Ashour et al. 2006; Benatru et al. 2008). Previous study demonstrated a very high prevalence of back pain in PwPD, as well as, PwPD specifically suffer more often from back pain (Broetz et al. 2007). Central and peripheral mechanisms were previously thought to cause postural deformities in PwPD (Doherty et al. 2011). The present study is the first to investigate the effect of different postural deformities on back functioning, disability and pain in PwPD.
The current study found that the ODI scores worse in PS and C&A groups compared with PD group without postural deformity. Moreover, pain severity and interference showed the highest scores in PS and C&A groups compared with PD group. Our result reveled that different postural deformities in PwPD affect both motor and non motor symptoms. Indeed, this result suggested that PS and C&A affect negatively the back functioning, physical performances and aggravated pain levels in PwPD. It seems possible that these results are due to the altered posture, central and peripheral mechanisms in PwPD enhance stress on both spinal discs and soft tissue and bone structures of the spine (Adams et al. 2000; Hallett et al. 2003). These findings expand previous reports of enhanced and control pain in PD patients (Goetz et al. 1986; Ford 1998; Madeo et al. 2015) and provide a rationale for interventions that target the postural abnormalities and the pathological mechanisms in PwPD.
Moreover, we noticed that PD group without postural deformities exhibit lower scores in ODI compared with higher scores in PS and C&A groups. We think that could be an obvious consequence of PD motor disturbances, as previously described in other works (Harrington 1991; Peto et al. 1995; Negrotti et al. 2005; Gebhardt et al. 2008; Proud et al. 2010). ODI scores, UPDRS-II and UPDRS-III were significantly worse in PS and C&A groups. Modified H&Y staging scale showed higher scores in PS and C&A groups’ result of the postural abnormality. Moreover, no significant differences were observed between PD, PS and C&A groups in UPDRS-II, UPDRS-III score and PD duration. A possible explanation for this might be that the back disability, in those patients groups were not related to severe motor dysfunction but it may strongly depend on the lateral trunk deviation, bending of the thoraco-lumbar spine and dropped head.
It is established that the optimal postural alignment, required little or no muscle activity to maintain the balance (Horak and Nashner 1986). Moreover, Panjabi (1992) suggested that stability of the spine depends on three subsystems (Panjabi et al. 1992). The passive system is the spinal column, made up of the vertebrae, disks, facet joints, ligaments, and joint capsules. The active system includes the muscles and tendons that surround and can apply forces to the spinal column. The neurologic or control system monitors the position, loading, and demands on the spine, and directs the active system to provide the required stability and action. In contrast, postural deformities and balance impairments are disabling complications in PwPD (Tinazzi et al. 2016). Additionally, the pathological mechanisms which are responsible for postural deformity in PD demonstrated dystonia, rigidity, impaired proprioception, musculoskeletal changes, loss of postural reflexes and influence of dopaminergic medications (Bloem et al. 2001; Cole et al. 2010; Tinazzi et al. 2016). As a result, these mechanisms may lead to muscles imbalance, weakness, compensatory posture and severe back disability and pain (Doherty et al. 2011).
Based on the current study findings, it’s recommended for the health care providers to pay attention for back function and pain in PwPD, abnormal muscular activation and lack of trunk misalignment awareness. Further studies investigate the consequences of back function and pain in PwPD on, e.g., sleep and the QoL. Our results support the routine evaluation of back function and pain in every patient suffering from PD and postural deformity. Adequate pain medication and a specific physical therapy program may decrease back pain and increase functions and ADLs in these patients.
This study has several limitations, the MMSE is used to test the cognitive function, but we did not use more specific cognitive evaluation batteries. All participants tested and evaluated at "ON" medication phase. Assessment of motor and non motor function at “OFF” medication phase is important because the patients experienced more difficulties in both motor and non motor function than on-medication whereas the symptoms are satisfactory controlled with medication. However, the results are clear in indicating the role of postural deformities in provoking an impairment of back functions and increase pain severity as well as, deteriorating the ADLs and QoL.
Conclusion
Postural deformities such as PS and C&A shows a negative impact on back function, disability in PwPD, as well as pain symptoms in PwPD aggravated and worsens. These findings should be carefully considered when considering the treatment strategy for PwPD with postural deformities. Collectively, we recommended health care providers to consider improving back functions as well as improving the other postural deformities in PwPD.