Pain and calf hypertrophy associated with spontaneous repetitive discharges treated with botulinum toxin

Costa, João; Graça, Pedro; Evangelista, Teresinha; Carvalho, Mamede de

doi:10.1016/j.clinph.2005.07.016

Cited by 26 publications

(16 citation statements)

References 24 publications

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“…It is unlikely that myotonia‐like phenomena will occur in this situation, because myotonia is normally characterized by stronger reduction of gCl (more than 50% of the normal value) (Pusch, 2002). Accordingly, the EMG activity recorded on fluvastatin, atorvastatin and fenofibrate‐treated animals showed signs of altered excitability characterized by brief bursts of AP following normal movement‐induced electrical activity, which were different from those seen during 9‐AC acutely induced myotonia but closer to those recorded in humans during muscle cramping or fasciculation (Costa et al. , 2005; Serrao et al.…”

Section: Discussionmentioning

confidence: 72%

Statins and fenofibrate affect skeletal muscle chloride conductance in rats by differently impairing ClC‐1 channel regulation and expression

Pierno

Camerino

Cippone

et al. 2009

British J Pharmacology

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Background and purpose: Statins and fibrates can produce mild to life-threatening skeletal muscle damage. Resting chloride channel conductance (gCl), carried by the ClC-1 channel, is reduced in muscles of rats chronically treated with fluvastatin, atorvastatin or fenofibrate, along with increased resting cytosolic calcium in statin-treated rats. A high gCl, controlled by the Ca 2+ -dependent protein kinase C (PKC), maintains sarcolemma electrical stability and its reduction alters muscle function. Here, we investigated how statins and fenofibrate impaired gCl. Experimental approach: In rats treated with fluvastatin, atorvastatin or fenofibrate, we examined the involvement of PKC in gCl reduction by the two intracellular microelectrodes technique and ClC-1 mRNA level by quantitative real time-polymerase chain reaction. Direct drug effects were tested by patch clamp analysis on human ClC-1 channels expressed in human embryonic kidney (HEK) 293 cells. Key results: Chelerythrine, a PKC inhibitor, applied in vitro on muscle dissected from atorvastatin-treated rats fully restored gCl, suggesting the involvement of this enzyme in statin action. Chelerythrine partially restored gCl in muscles from fluvastatin-treated rats but not in those from fenofibrate-treated rats, implying additional mechanisms for gCl impairment. Accordingly, a decrease of ClC-1 channel mRNA was found in both fluvastatin-and fenofibrate-treated rat muscles. Fenofibric acid, the in vivo metabolite of fenofibrate, but not fluvastatin, rapidly reduced chloride currents in HEK 293 cells. Conclusions and implications:Our data suggest multiple mechanisms underlie the effect of statins and fenofibrate on ClC-1 channel conductance. While statins promote Ca 2+ -mediated PKC activation, fenofibrate directly inhibits ClC-1 channels and both fluvastatin and fenofibrate impair expression of mRNA for ClC-1.

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Section: Discussionmentioning

confidence: 72%

Statins and fenofibrate affect skeletal muscle chloride conductance in rats by differently impairing ClC‐1 channel regulation and expression

Pierno

Camerino

Cippone

et al. 2009

British J Pharmacology

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“…Commonly, these include old or chronic radiculopathies, peripheral neuropathies, or slowly progressive myopathies. In rare cases of patients with chronic S1 radiculopathies associated with pain and calf hypertrophy, CRDs are seen in the gastrocnemius in ≈50%, raising the possibility that CRDs may contribute to neurogenic hypertrophy in these cases 13. Rarely, CRDs occur in otherwise normal muscles, such as the iliopsoas or biceps.…”

Section: Abnormal Spontaneous Activitymentioning

confidence: 99%

Needle electromyography

2009

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Physiologic assessment of diseases of the motor unit from the anterior horn cells to the muscles relies on a combination of needle electromyography (EMG) and nerve conduction studies (NCS). Both require a unique combination of knowledge of peripheral nervous system anatomy, physiology, pathophysiology, diseases, techniques, and electricity is necessary. Successful, high-quality, reproducible EMG depends on the skills of a clinician in patient interaction during the physical insertion and movement of the needle while recording the electrical signals. These must be combined with the skill of analyzing electric signals recorded from muscle by auditory pattern recognition and semiquantitation.1052 This monograph reviews the techniques of needle EMG and waveform analysis and describes the types of EMG waveforms recorded during needle EMG.

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“…While the pathophysiology of neurogenic muscle hypertrophy is unclear, there have been anecdotal reports on the use of a variety of therapeutic options. These include surgical decompression of the affected nerve root, 8 injection of botulinum toxin 13 into affected muscles and steroids particularly, in those who demonstrated focal myositis 14 . The effect of steroids is postulated to act via suppression of ectopic nerve impulse generation 15 and modulation of the membrane excitability in different portions of the spinal motor neurones.…”

Section: Discussionmentioning

confidence: 99%

An unusual cause of calf hypertrophy: severe lumbar canal stenosis with S1 nerve root radiculopathy

Ong¹,

Jones

Steuer³

2007

APLAR Journal of Rheumatology

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We report an unusual case of calf hypertrophy in a 62-year-old woman who developed progressive enlargement of the left calf in association with chronic lower back pain. Magnetic resonance imaging (MRI) of the affected calf confirmed enlargement of the soleus muscle. MRI of the lumbar spine showed multilevel degenerative changes. Electromyography revealed neurogenic features consistent with S1 radiculopathy. Our case illustrates that muscular hypertrophy may follow chronic denervation as a consequence of spinal neural compressive disease. The various mechanisms postulated for this distinct condition and therapeutic strategies are outlined.

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Pain and calf hypertrophy associated with spontaneous repetitive discharges treated with botulinum toxin

Cited by 26 publications

References 24 publications

Statins and fenofibrate affect skeletal muscle chloride conductance in rats by differently impairing ClC‐1 channel regulation and expression

Statins and fenofibrate affect skeletal muscle chloride conductance in rats by differently impairing ClC‐1 channel regulation and expression

Needle electromyography

An unusual cause of calf hypertrophy: severe lumbar canal stenosis with S1 nerve root radiculopathy

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