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COMMENTARY
Year : 2016  |  Volume : 144  |  Issue : 5  |  Page : 650-652

Understanding of skeletal deformities in Parkinson's disease


Department of Neurology, Sanggye Paik Hospital, College of Medicine, Inje University, Seoul, Korea

Date of Submission07-Jul-2016
Date of Web Publication30-Mar-2017

Correspondence Address:
Jong Sam Baik
Department of Neurology, Sanggye Paik Hospital, College of Medicine, Inje University, Seoul
Korea
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijmr.IJMR_1166_16

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How to cite this article:
Baik JS. Understanding of skeletal deformities in Parkinson's disease. Indian J Med Res 2016;144:650-2

How to cite this URL:
Baik JS. Understanding of skeletal deformities in Parkinson's disease. Indian J Med Res [serial online] 2016 [cited 2017 Apr 25];144:650-2. Available from: http://www.ijmr.org.in/text.asp?2016/144/5/650/203448



Abnormal posture and skeletal deformities of limbs, neck and trunk are common in patients with parkinsonism including Parkinson's disease (PD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). These deformities include striatal deformities, camptocormia, Pisa syndrome, antecollis and scoliosis. They interfere with activities of daily living, resulting in postural instability, gait problems, and increased falls [1]. Though some of these deformities are caused by ongoing parkinsonian symptoms or are associated with nigrostriatal dopamine deficiency, especially in scoliosis [2], the exact mechanism is poorly understood. The true incidence or prevalence of these deformities in unknown, especially in Asia including India. The study by Pandey and Kumar [3] in this issue provides some information on striatal and postural deformities in Indian patients with PD. Though this study has a few limitations with a small number of participating patients, it provides important data on Asian patients, especially Indian patients.

There are some interesting results in this study [3] compared to a previous study [1]. First, 48.6 per cent of 70 patients with PD were reported to have either striatal or postural deformities. This rate was higher than the results of 33.5 per cent of 164 PD patients in America in a previous study [1]. Striatal foot was the most common deformity in the present study [3] as well as in other studies [1],[2]. Second, the female to male ratio (2.04:1) in this study [3] was higher than that reported (1:1) in a previous study [1]. Third, although the difference was not significant in the mean age of onset, but PD patients with deformity were older than those without deformity (53.5 vs. 49.5 yr)[3]. This finding was different from that (54.7 vs. 62.5 yr) of a previous study [1]. Finally, patients with scoliosis had a contralateral deformity in relation to initial PD symptoms.

Usually, striatal limb deformities can be seen in patients with advanced PD, although these might also be seen in the early stage of PD and other parkinsonian disorders [4],[5],[6]. Striatal limb is characterized by flexion of the metacarpophalangeal (MCP) joints, flexion of the distal interphalangeal (IP) joints, ulnar hand deviation in the hand, and great toe extension, flexion of the remaining toes and equinovarus foot positioning in the foot [7]. Foot deformities are more frequent in PD patients as part of the disease or as “wearing off” dystonia associated with levodopa therapy than hand deformities. According to a previous study [8], the percentage of striatal foot and hand deformities is up to 10 per cent in untreated patients with advanced PD. Foot deformities can develop in 20-40 per cent of PD patients receiving sustained levodopa treatment [9]. Furthermore, as the earliest signs of striatal hand, MCP flexion and IP extension can be seen, due to contraction of lumbricals and interossei, respectively [10].

Abnormal postures of trunk such as camptocormia, antecollis, Pisa syndrome and scoliosis are common in PD patients. Majority of the patients with camptocormia have a combination of rigidity and dystonia [11]. The main pathophysiological mechanism might be due to increased susceptibility of the paraspinal muscles to injury in the setting of kyphotic postural changes and age-dependent loss of tissue elasticity in PD patients [12]. In the study of Pandey and Kumar [3], camptocormia and antecollis were seen in 20 and 7.14 per cent PD patients, respectively. These were associated with disease severity and longer duration of levodopa therapy. These rates were higher than those reported in previous studies [1],[13]. Pisa syndrome also known as pleurothotonus is defined as marked lateral flexion of the trunk and head to one side with axial rotation of the torso [2]. Because the underlying pathology may be related to cholinergic excess, this syndrome often occurs either as a result of decreased breakdown of acetylcholine or as a result of decreased dopaminergic inhibition of acetylcholine secondary to dopaminergic antagonism or dopaminergic depletion [14]. This syndrome is not usually associated with age, disease duration or the severity of the disease. It was found in about seven per cent of PD patients in the present study [3]. Scoliosis is defined as a lateral curvature of the spine with vertebral rotation that leads to asymmetric deformity of the trunk. It occurs more frequently in PD patients than in the general population. Previous clinical and animal studies have reported that the direction of scoliosis is congruous with the laterality of major signs and symptoms of PD [15],[16]. However, such findings remain controversial. These findings may suggest that scoliosis is closely associated with nigrostriatal dopamine deficiency. Baik et al[17] found 33 per cent of PD patients with scoliosis and the majority of them were women. They also found that patients with scoliosis were significantly older than those without scoliosis. However, there was no significant association between laterality and scoliosis. In addition, the occurrence rate of scoliosis was not different between de novo and levodopa-treated patients [17]. Although genetic, hormonal, biomechanical and neuromuscular factors have been proposed as possible causes of scoliosis in PD, the exact pathophysiology of PD is not yet fully understood [18]. In accordance with frequent dystonia in women with PD [8], scoliosis is known to occur more frequently in women than in men with PD [1],[15],[17] including the present study [3].

Though PD-related dystonia and skeletal deformities are known to have some risk factors, such as young age, female gender and long disease duration, the relationship of age, gender, family history or duration of L-dopa treatment with skeletal deformities in PD is not fully understood. Some skeletal deformities can be improved by botulinum toxin injection, especially in focal deformities such as striatal finger or toes [18]. However, for large muscle group involving deformities such as camptocormia and scoliosis, botulinum toxin injections could be less effective than focal deformities.

Because skeletal deformities can be seen in elderly persons easily, this can be underestimated in PD patients, especially at early stage. Sometimes, one of these deformities such as antecollis in early time can help differentiate the diagnosis between PD and MSA. Otherwise, to prevent permanent contractures, early diagnosis of skeletal deformities, from striatal hand to scoliosis, is important. Hence, if more study results on skeletal deformities in patients with PD are added in future, these will help us understand the clinical features, natural course and pathogenesis of these deformities. Based on these appropriate guidelines, early diagnosis and more accurate treatment will be achieved.



 
   References Top

1.
Ashour R, Jankovic J. Joint and skeletal deformities in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy. Mov Disord 2006; 21 : 1856-63.  Back to cited text no. 1
    
2.
Ashour R, Tintner R, Jankovic J. Striatal deformities of the hand and foot in Parkinson's disease. Lancet Neurol 2005; 4 : 423-31.  Back to cited text no. 2
    
3.
Pandey S, Kumar H. Assessment of striatal & postural deformities in patients with Parkinson's disease. Indian J Med Res 2016; 144 : 682-8.  Back to cited text no. 3
    
4.
Kyriakides T, Hewer RL. Hand contractures in Parkinson's disease. J Neurol Neurosurg Psychiatry 1988; 51 : 1221-3.  Back to cited text no. 4
    
5.
Fahn S, Jankovic J. Practical management of dystonia. Neurol Clin 1984; 2 : 555-69.  Back to cited text no. 5
    
6.
de Yebenes JG, Pernaute RS, Tabernero C. Symptomatic dystonias. In: Watts RL, Koller WC, editors. Movement disorders, neurologic principles and practice. New York: McGraw-Hill; 1997. p. 455-75.  Back to cited text no. 6
    
7.
Quinn NP, Ring H, Honavar M, Marsden CD. Contractures of the extremities in parkinsonian subjects: a report of three cases with a possible association with bromocriptine treatment. Clin Neuropharmacol 1988; 11 : 268-77.  Back to cited text no. 7
    
8.
Jankovic J, Tintner R. Dystonia and parkinsonism. Parkinsonism Relat Disord 2001; 8 : 109-21.  Back to cited text no. 8
    
9.
Poewe WH, Lees AJ. The pharmacology of foot dystonia in parkinsonism. Clin Neuropharmacol 1987; 10 : 47-56.  Back to cited text no. 9
    
10.
Gortvai P. Deformities of the hands and feet in parkinsonism and their reversibility by operation. J Neurol Neurosurg Psychiatry 1963; 26 : 33-6.  Back to cited text no. 10
    
11.
Azher SN, Jankovic J. Camptocormia: pathogenesis, classification, and response to therapy. Neurology 2005; 65 : 355-9.  Back to cited text no. 11
    
12.
Serratrice G, Pouget J, Pellissier JF. Bent spine syndrome. J Neurol Neurosurg Psychiatry 1996; 60 : 51-4.  Back to cited text no. 12
    
13.
Abe K, Uchida Y, Notani M. Camptocormia in Parkinson's disease. Parkinsons Dis 2010; 2010. pii: 267640.  Back to cited text no. 13
    
14.
Villarejo A, Camacho A, García-Ramos R, Moreno T, Penas M, Juntas R, et al. Cholinergic-dopaminergic imbalance in Pisa syndrome. Clin Neuropharmacol 2003; 26 : 119-21.  Back to cited text no. 14
    
15.
Duvoisin RC, Marsden CD. Note on the scoliosis of parkinsonism. J Neurol Neurosurg Psychiatry 1975; 38 : 787-93.  Back to cited text no. 15
    
16.
Lundblad M, Picconi B, Lindgren H, Cenci MA. A model of L-DOPA-induced dyskinesia in 6-hydroxydopamine lesioned mice: relation to motor and cellular parameters of nigrostriatal function. Neurobiol Dis 2004; 16 : 110-23.  Back to cited text no. 16
    
17.
Baik JS, Kim JY, Park JH, Han SW, Park JH, Lee MS. Scoliosis in patients with Parkinson's disease. J Clin Neurol 2009; 5 : 91-4.  Back to cited text no. 17
    
18.
Jankovic J. Botulinum toxin in clinical practice. J Neurol Neurosurg Psychiatry 2004; 75 : 951-7.  Back to cited text no. 18
    




 

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