Fasciculation-myokymic activity and prolonged nerve conduction block. A physiopathological relationship in radiation-induced brachial plexopathy

Esteban, Ángel; Traba, A.

doi:10.1016/0168-5597(93)90111-2

Cited by 28 publications

(10 citation statements)

References 34 publications

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“…Radiation-induced plexopathy is usually associated with total doses greater than or equal to 5000 cGy, but can be seen with lower doses as well. Clinical diagnosis can be supported by electrodiagnostic testing which may demonstrate segmental slowing on nerve conduction studies, fasciculations and myokymic discharges on electromyography (EMG) which are specific for the condition but present in only about 60% of patients 36 . CT or MRI may show diffuse loss of tissue planes and occasionally fibrosis which can be confused with tumor if sufficiently bulky, but PET imaging characteristically shows hypometabolism.…”

Section: Peripheral Nervous System Complicationsmentioning

confidence: 99%

Cancer-treatment-induced neurotoxicity—focus on newer treatments

2015

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Neurotoxicity from traditional chemotherapy and radiotherapy is widely recognized. The adverse effects of newer therapeutics such as biological and immunotherapeutic agents are less familiar and they are also associated with significant neurotoxicity in the central and peripheral nervous systems. This review addresses the main toxicities of cancer treatment by symptom with a focus on the newer therapeutics. Recognition of these patterns of toxicity is important as drug discontinuation or dose adjustment may prevent further neurologic injury. Also, knowledge of these toxicities helps to differentiate treatment-related symptoms from progression of cancer or its involvement of the nervous system.

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Section: Peripheral Nervous System Complicationsmentioning

confidence: 99%

Cancer-treatment-induced neurotoxicity—focus on newer treatments

2015

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“…Focal demyelination in peripheral motor or sensory axons can lead to increased axonal excitability and ectopic firing, and fasciculations may develop after peripheral compressive nerve injury or traumatic motor root lesions 37. Sometimes focal fasciculations follow radiation injury to cervical plexus38 or to the spinal cord as part of a slowly progressive LMN syndrome 39. Fasciculations are prominent in chronic lower motor neuron disorders such as postpolio syndrome,40 spinal muscular atrophy, especially bulbo-facial fasciculation in Kennedy’s disease 41.…”

Section: Clinical Correlates Of Fasciculationmentioning

confidence: 99%

Fasciculation in amyotrophic lateral sclerosis: origin and pathophysiological relevance

Carvalho

Kiernan

Swash

2017

J Neurol Neurosurg Psychiatry

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This review considers the origin and significance of fasciculations in neurological practice, with an emphasis on fasciculations in amyotrophic lateral sclerosis (ALS), and in benign fasciculation syndromes. Fasciculation represents a brief spontaneous contraction that affects a small number of muscle fibres, causing a flicker of movement under the skin. While an understanding of the role of fasciculation in ALS remains incomplete, fasciculations derive from ectopic activity generated in the motor system. A proximal origin seems likely to contribute to the generation of fasciculation in the early stages of ALS, while distal sites of origin become more prominent later in the disease, associated with distal motor axonal sprouting as part of the reinnervation response that develops secondary to loss of motor neurons. Fasciculations are distinct from the recurrent trains of axonal firing described in neuromyotonia. Fasciculation without weakness, muscle atrophy or increased tendon reflexes suggests a benign fasciculation syndrome, even when of sudden onset. Regardless of origin, fasciculations often present as the initial abnormality in ALS, an early harbinger of dysfunction and aberrant firing of motor neurons.

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“…Chronic conduction block with clinical motor unit hyperactivity in the affected muscles has been previously described and a causal relationship hypothesized. 8,22,23 Roth and Magistris 22 reported 14 patients with various types of demyelinating neuropathies characterized electrophysiologically by prolonged conduction block of 3 months to 9 years duration who all demonstrated excess motor unit activity in involved muscles, characterized by fasciculations, grouped fasciculations, and myokymic discharges. This excess motor unit activity was more prominent in the presence of severe or complete conduction block, as was observed in our patient.…”

Section: Discussionmentioning

confidence: 99%

Conduction block and continuous motor unit activity in chronic acquired demyelinating polyneuropathy

Meriggioli

Sanders

1999

Muscle Nerve

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The term continuous motor unit activity (CMUA) may be used to refer to the involuntary, sustained activity of motor units caused by hyperactivity of peripheral motor nerves CMUA has been reported in association with acquired neuropathies such as chronic inflammatory demyelinating polyneuropathy. The precise mechanism responsible for the excess muscle activity is not defined, but the activity is believed to originate in the peripheral nerves, perhaps at sites of focal demyelination. We describe a case of an acquired, demyelinating neuropathy associated with distal motor conduction block in which CMUA was observed in muscles innervated by blocked axons. Despite the prolonged disease duration of nearly 40 years, marked clinical and electrophysiological improvement as well as resolution of the CMUA were observed following immunosuppressive therapy. A relationship between the chronic motor conduction block and the excess muscle activity is postulated. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 532–537, 1999.

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Fasciculation-myokymic activity and prolonged nerve conduction block. A physiopathological relationship in radiation-induced brachial plexopathy

Cited by 28 publications

References 34 publications

Cancer-treatment-induced neurotoxicity—focus on newer treatments

Cancer-treatment-induced neurotoxicity—focus on newer treatments

Fasciculation in amyotrophic lateral sclerosis: origin and pathophysiological relevance

Conduction block and continuous motor unit activity in chronic acquired demyelinating polyneuropathy

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