Camptocormia in a Patient with Parkinson Disease and a Myopathy with Nemaline Rods

Özer, Feriha; Ozturk, Oya; Meral, Hasan; Serdaroğlu, Pıraye; Yayla, Vildan

doi:10.1097/phm.0b013e31802b8bde

Cited by 22 publications

(17 citation statements)

References 21 publications

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“…Camptocormia is enhanced during standing and walking [17] and relieved in recumbent or supine position [18,19,20]. In quite a number of cases, camptocormia is associated with lower back pain [1,3,7,21,22,23,24] but in others it is painless [19].…”

Section: Clinical Presentationmentioning

confidence: 99%

“…PNS conditions associated with camptocormia include primary myopathies, such as myotonic dystrophy type 1 [16,21] and type 2 [39], dysferlinopathy [24], nemaline myopathy [20], axial myopathy [7,40,41], or mitochondrial myopathy (table 1) [42]. Secondary myopathies with camptocormia include hypothyroid myopathy [43], dermatomyositis, polymyositis [43,44], focal or segmental myositis [33,45,46], inclusion body myositis [3], or myasthenia gravis (table 1) [47].…”

Section: Etiologymentioning

confidence: 99%

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Presentation, Etiology, Diagnosis, and Management of Camptocormia

Finsterer

Strobl

2010

Eur Neurol

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Camptocormia (bent spine syndrome, cyphose hystérique) is an abnormality characterized by severe forward flexion of the thoracolumbar spine which typically increases during walking or standing and completely disappears in supine position. Camptocormia can be due to central nervous system diseases, such as Parkinson’s disease, dystonia, multisystem atrophy, or Alzheimer’s disease, due to peripheral nervous system diseases, such as primary myopathy, secondary myopathy, motor neuron disease, myasthenia, or chronic inflammatory demyelinating polyneuropathy, due to side effects of drug treatment, due to disc herniation, arthritis or spinal trauma, or due to paraneoplasia. Only rarely may camptocormia be attributable to psychiatric disease. The diagnosis is based on clinical findings, imaging of the cerebrum or spine, needle electromyography, or muscle biopsy. Treatment options are limited and frequently futile and rely on conservative measures, such as psychotherapy, physiotherapy, use of orthoses, drugs, injection of botulinum toxin, withdrawal of causative drugs, electroconvulsive therapy, or invasive measures, such as surgical correction or deep brain stimulation. The outcome is generally fair. Some patients profit from therapy whereas others do not respond to treatment and become progressively immobile.

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Section: Clinical Presentationmentioning

confidence: 99%

Section: Etiologymentioning

confidence: 99%

Presentation, Etiology, Diagnosis, and Management of Camptocormia

Finsterer

Strobl

2010

Eur Neurol

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“…Furthermore, none of the patients were reported to have generalized muscle weakness. 3,10,13 It is therefore possible that secondary myopathic changes from prolonged stooped posture in parkinsonian patients can account for such pathological findings. A diagnosis of LGMD 2B is unlikely in our patient for several reasons.…”

Section: Discussionmentioning

confidence: 99%

Camptocormia as a presentation of generalized inflammatory myopathy

et al. 2009

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Camptocormia is an abnormal truncal flexion posture that occurs while walking or standing. It is usually caused by various hypokinetic movement disorders such as Parkinson disease and multiple system atrophy. Myopathy or motor neuron disease can also be infrequent causes of camptocormia. Paraspinous muscle biopsy usually reveals focal myositis, regardless of the etiology of camptocormia. We describe the first case of generalized inflammatory myopathy with prominent camptocormia and proximal muscle weakness. Muscle biopsy of the quadriceps confirmed the diagnosis of polymyositis, and the posture showed modest improvement in response to steroid treatment.

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“…15,25,30 Gydnia et al 15 have studied 19 consecutive muscle biopsies obtained in patients with PD and either camptocormia or droppedhead syndrome (anterocollis), finding abnormal muscle biopsies in all patients. Although MRI images were not abnormal in all patients, MR imaging generally showed fatty degeneration of the paravertebral musculature or neck extensor musculature in many of them.…”

Section: Myopathy Associated Postural Deformity In Pdmentioning

confidence: 99%

Spinal deformity and Parkinson disease: a treatment algorithm

Upadhyaya¹,

Starr²,

Mummaneni³

2010

FOC

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Object The authors review the literature on the treatment of spinal deformity in patients with Parkinson disease (PD) and formulate a treatment algorithm. Methods The authors provide representative cases of patients with PD and spinal deformity who underwent deep brain stimulation (DBS) or spinal surgery. Results In patients with PD and spinal deformity who undergo spinal surgery there is a high rate of acute and delayed complications. Patients who undergo DBS, while having significantly fewer complications, often do not regain sagittal balance. Conclusions Cases involving PD and camptocormia have a high rate of complications when spinal surgery is performed. The authors prefer to offer spinal surgery only to patients with coexisting spinal stenosis causing radiculopathy or myelopathy. Patients with PD and camptocormia without spinal stenosis may be considered for DBS, but the results are mixed.

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Camptocormia in a Patient with Parkinson Disease and a Myopathy with Nemaline Rods

Cited by 22 publications

References 21 publications

Presentation, Etiology, Diagnosis, and Management of Camptocormia

Presentation, Etiology, Diagnosis, and Management of Camptocormia

Camptocormia as a presentation of generalized inflammatory myopathy

Spinal deformity and Parkinson disease: a treatment algorithm

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