Multifocal or generalized tonic dystonia of complex regional pain syndrome: A distinct clinical entity associated with HLA-DR13

Hilten, Jacobus J. van; Beek, W. J. T. Van De; Roep, Bart O.

doi:10.1002/1531-8249(200007)48:1<113::aid-ana18>3.0.co;2-9

Cited by 100 publications

(21 citation statements)

References 15 publications

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“…Collectively, these findings indicate that in patients with a younger onset of CRPS, genetic factors may play a role in the onset or chronicity of the syndrome. A genetic predisposition is also suggested by associations that were found with different human leukocyte antigen (HLA) class I and II factors (de Rooij et al 2009c; Kemler et al 1999; van Hilten et al 2000; Vaneker et al 2002). Interestingly, HLA class I molecules have been implicated in non-immune roles including neuroplasticity (Corriveau et al 1998; Goddard et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Spreading of complex regional pain syndrome: not a random process

et al. 2011

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Complex regional pain syndrome (CRPS) generally remains restricted to one limb but occasionally may spread to other limbs. Knowledge of the spreading pattern of CRPS may lead to hypotheses about underlying mechanisms but to date little is known about this process. The objective is to study patterns of spread of CRPS from a first to a second limb and the factors associated with this process. One hundred and eighty-five CRPS patients were retrospectively evaluated. Cox’s proportional hazards model was used to evaluate factors that influenced spread of CRPS symptoms. Eighty-nine patients exhibited CRPS in multiple limbs. In 72 patients spread from a first to a second limb occurred showing a contralateral pattern in 49%, ipsilateral pattern in 30% and diagonal pattern in 14%. A trauma preceded the onset in the second limb in 37, 44 and 91%, respectively. The hazard of spread of CRPS increased with the number of limbs affected. Compared to patients with CRPS in one limb, patients with CRPS in multiple limbs were on average 7 years younger and more often had movement disorders. In patients with CRPS in multiple limbs, spontaneous spread of symptoms generally follows a contralateral or ipsilateral pattern whereas diagonal spread is rare and generally preceded by a new trauma. Spread is associated with a younger age at onset and a more severely affected phenotype. We argue that processes in the spinal cord as well as supraspinal changes are responsible for spontaneous spread in CRPS.

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Section: Discussionmentioning

confidence: 99%

Spreading of complex regional pain syndrome: not a random process

et al. 2011

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“…Fixed dystonic postures start in the injured limb and commonly spread 4. Pain is a prominent feature and there is a considerable overlap of fixed dystonia with chronic regional pain syndrome (CRPS), when it may also be termed causalgia‐dystonia or tonic dystonia of CRPS 5, 6. There is continued controversy as to whether isolated fixed dystonia is of psychogenic origin, either caused by unconscious mechanisms (conversion disorder) or purposefully feigned (malingering/factitious disorder) 7–10.…”

Section: Introductionmentioning

confidence: 99%

Mental rotation of body parts and sensory temporal discrimination in fixed dystonia

et al. 2010

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Fixed dystonia is an uncommon but severely disabling condition typically affecting young women following a minor peripheral injury. There is no evidence of any structural lesions of the central nervous system nor any clear peripheral nerve or root damage. Electrophysiological techniques such as short intracortical inhibition, cortical silent period and a plasticity inducing protocol have revealed similarities but also differences compared to classical mobile dystonia. To further explore the pathophysiology of fixed dystonia we compared mental rotation of body parts and sensory temporal discrimination in 11 patients with fixed dystonia, 11 patients with classical mobile dystonia and 10 healthy controls. In the mental rotation task subjects were presented with realistic photos of left or right hands, feet and the head of a young women with a black patch covering the left or the right eye in six different orientations. Subjects had to verbally report the laterality of the presented stimuli. To assess sensory temporal discrimination subjects were asked to discriminate whether pairs of visual, tactile (electrical), or visuo-tactile stimuli were simultaneous or sequential (temporal discrimination threshold) and in the latter case which stimulus preceded the other (temporal order judgement). In accordance with previous studies patients with mobile dystonia were abnormal in mental rotation and temporal discrimination, whereas patients with fixed dystonia were only impaired in mental rotation. Possible explanations for this deficit may include the influence of the abnormal body posture itself, a shared predisposing pathophysiology for mobile and fixed dystonia, or a body image disturbance. These findings add information to the developing pathophysiological picture of fixed dystonia.

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“…The peripheral mechanisms discussed include immune cell mediated inflammatory processes (Alexan- der et al, 2005;Calder et al, 1998;Huygen et al, 2002;Huygen et al, 2004;Ludwig and Baron, 2004), autoimmune inflammatory processes (Blaes et al, 2004;Goebel et al, 2002;Goebel et al, 2005;Kemler et al, 1999;van Hilten et al, 2000), neurogenic inflammation Graif et al, 1998;Ludwig and Baron, 2004;Oyen et al, 1993;Weber et al, 2001) and tissue hypoxia (Birklein et al, 2000b;Heerschap et al, 1993;Koban et al, 2003). The peripheral mechanisms discussed include immune cell mediated inflammatory processes (Alexan- der et al, 2005;Calder et al, 1998;Huygen et al, 2002;Huygen et al, 2004;Ludwig and Baron, 2004), autoimmune inflammatory processes (Blaes et al, 2004;Goebel et al, 2002;Goebel et al, 2005;Kemler et al, 1999;van Hilten et al, 2000), neurogenic inflammation Graif et al, 1998;Ludwig and Baron, 2004;Oyen et al, 1993;Weber et al, 2001) and tissue hypoxia (Birklein et al, 2000b;Heerschap et al, 1993;Koban et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Behavioral and sensory changes after direct ischemia‐reperfusion injury in rats

Ludwig

Gorodetskaya

Schattschneider

et al. 2007

European Journal of Pain

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Complex regional pain syndromes (CRPS) are disabling pain syndromes that can develop after trauma or minor tissue injury affecting a limb. Characteristics of CRPS are sensory signs and symptoms, autonomic abnormalities, trophic changes and an impaired motor function. Pathophysiological mechanisms for the development of CRPS are still a matter of investigation. Based on clinical data and investigations of CRPS patients it is hypothesized that tissue hypoxia and inflammation are important for the development of CRPS. The aim of the current study was therefore to examine if direct ischemia-reperfusion injury can induce behavior in rats with symptoms present in patients with CRPS. After baseline behavior measurements the femoral artery of Wistar rats was ligated for 3h with consecutive reperfusion. Sham-operated rats underwent the same preparation except ligation of the artery. Subsequent behavioral testing (observations of spontaneous pain behavior, paw withdrawal to mechanical, noxious mechanical, cold and heat stimuli) was performed up to two months after surgery. Both in rats that underwent ischemia and in sham-operated rats no obvious changes of hindpaw tissue were observed after ischemia-reperfusion injury (trophic changes, edema, differences in skin color or temperature). In behavioral tests only minor changes were observed, these being not different between postischemic rats and sham-operated rats. Using Wistar rats, our data do not support the idea that an ischemia-reperfusion injury can play a major role in the development of CRPS.

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Multifocal or generalized tonic dystonia of complex regional pain syndrome: A distinct clinical entity associated with HLA-DR13

Cited by 100 publications

References 15 publications

Spreading of complex regional pain syndrome: not a random process

Spreading of complex regional pain syndrome: not a random process

Mental rotation of body parts and sensory temporal discrimination in fixed dystonia

Behavioral and sensory changes after direct ischemia‐reperfusion injury in rats

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