Investigation of spinal pathology in notalgia paresthetica

Şavk, Öner; Şavk, Ekin

doi:10.1016/j.jaad.2005.01.138

Cited by 88 publications

(59 citation statements)

References 17 publications

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“…Other investigators have noted radiographic findings of degenerative vertebral changes or herniated discs in areas that corresponded to the dermatomal distribution of the patients' symptoms. 3,4 In our experience, many patients present with NP caused by muscular stiffness in the upper back after exercises at the gym or after sporting activities. We therefore propose a dual classification of NP.…”

Section: Discussionmentioning

confidence: 99%

Notalgia paraesthetica: A pilot study of treatment with simple exercises and stretches

2015

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Notalgia paraesthetica is a distressing condition for which current treatments are either poorly effective or have unacceptable adverse effects. The aim of this pilot study was to evaluate the effectiveness of a programme of simple exercises and stretches for this condition. In total, 12 patients participated in a trial of simple exercises and stretches over 12 weeks, designed to relieve the sensory neuropathy caused by paraspinal muscle entrapment. Of the 12 patients 11 achieved satisfactory amelioration of their symptoms with no adverse effects. Our pilot study was unblinded and consisted of small patient numbers. Further research to evaluate this approach is warranted.

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Section: Discussionmentioning

confidence: 99%

Notalgia paraesthetica: A pilot study of treatment with simple exercises and stretches

2015

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“…Increasing evidence suggests disorders of the spine, particularly those leading to impingement of dorsal spinal nerves, may be responsible. 26 Notalgia paresthetica was reported in a young patient with transient long thoracic nerve palsy secondary to neuralgic amyotrophy where marked scapular winging was suggested to cause dysfunction of dorsal spinal nerves. 27 Notalgia paresthetica associated with CNXI lesions has not been reported to our knowledge but we would suggest the same mechanism was responsible in our case.…”

Section: Discussionmentioning

confidence: 99%

TMS Neuro-Cardiovascular Coupling in Vascular Compression Cranial Neuropathy

Kirton

Gunraj

Chen

2009

Can. j. neurol. sci.

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Vascular compression probably underlies many cranial mononeuropathies 1 but is controversial 2,3 and lacks a definitive diagnostic investigation. Imaging may identify cerebrovascular abnormalities associated with cranial mononeuropathies. 4,5 However, diagnosis of potential neurovascular compression (NVC) syndromes such as trigeminal neuralgia or hemifacial spasm is usually clinical, lacking proof of the underlying mechanism. Resulting uncertainty creates difficulty in decision making for microvascular decompression surgery and limits studies of pathophysiology.Only a single case of progressive CNXI palsy with evidence of vascular compression has been reported. 6 The intimate anatomical relationship between the posterior inferior cerebellar ABSTRACT: Background: Neurovascular compression (NVC) may cause cranial mononeuropathy but lacks a definitive diagnostic investigation. We hypothesized that the arterial pressure wave (APW) would interact at the neurovascular interface in NVC to inhibit transmission of transcranial magnetic stimulation (TMS) stimuli to affected muscles. Methods: We report a novel neurophysiological method coupling cardiovascular physiology with TMS. The electrocardiogram (ECG) and arterial pressure wave (APW) were coupled to triggering of cortical TMS in a patient with NVC-induced spinal accessory (CNXI) mononeuropathy. Outcome measures included motor evoked potential (MEP) amplitudes and firing probabilities of normal and affected trapezieus (TPZ). Values at intervals in proximity to the APW (40/80/120/160ms) were compared to baseline (800ms) using ANOVA and student t-test. Results: Electrocardiogram triggered TMS of CNXI pathways with 100% reliability. MEP amplitudes were decreased in proximity to the APW, particularly at 120ms (0.21±0.04 mV versus 0.39±0.10mV, p=0.003). TPZ firing probabilities were similarly inhibited (43.8% versus 88.2%, p=0.009). No effect of APW proximity was observed on the unaffected side (p=0.868). Procedures were well tolerated. Conclusions: Vascular compression causes CNXI mononeuropathy. Transcranial magnetic stimulation-cardiovascular coupling may evaluate neurovascular junction interactions and non-invasively diagnose NVC.RÉSUMÉ: Couplage neuro-cardiovasculaire par SMT dans la neuropathie crânienne due à une compression vasculaire. Contexte : Une compression neuro-vasculaire (CNV) peut causer une mononeuropathie crânienne, mais les moyens d'en établir le diagnostic sont mal définis. Nous avons émis l'hypothèse que l'onde de pression artérielle (OPA) interagit au niveau de l'interface neuro-vasculaire dans la CNV pour inhiber la transmission de stimuli aux muscles atteints lors de la stimulation magnétique transcrânienne (SMT). Méthodes : Nous rapportons une nouvelle méthode neurophysiologique de couplage de la physiologie cardiovasculaire avec la SMT. L'électrocardiogramme (ECG) et l'onde de pression artérielle (OPA) ont été couplés à l'activation de la SMT chez un patient atteint de mononeuropathie du nerf spinal (NCXI) provoquée par une CNV. Nous avons mesuré...

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“…[2] Hastalık, vakaların önemli bir kısmında servikal radyografik değişiklikler ile ilişkili bulunmuştur. [3] 55 yaşında bayan hasta kliniğimize yaklaşık olarak 1 yıldır var olan sırtta kaşıntı, duyusal değişiklikler ve boyunda ağrı yakınmaları ile başvurdu. Hastanın dermatolojik muayenesinde; sol skapula altında lokalize, sınırları belirsiz, yaklaşık olarak 7x7 cm büyüklüğünde hiperpigmente alan ve yer yer ekskoriasyon mevcuttu (Şekil 1).…”

Section: Pain a Riunclassified