Trans-Synaptic Degeneration of Peripheral Motor Axons from Metastatic Brain Tumors: Electrophysiological Findings in Two Cases
0
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Denervation potentials obtained during electromyography (EMG) are usually considered as evidence of axonal degeneration in the peripheral nervous system (PNS). However, they may also appear when only central nervous system (CNS) lesions exist. Here, we present trans-synaptic degeneration from CNS lesions in 2 cases with electrophysiologic findings of motor axon degeneration caused not by PNS lesions, but by metastatic tumors involving the corresponding primary motor cortexes. When cancer patients show denervation potentials in needle EMG results, physicians usually consider PNS-related etiologies first, such as drug-induced generalized peripheral polyneuropathy or metastatic lesions (e.g., Pancoast tumor). However, metastatic brain tumors in the motor cortex could cause the same denervation potentials as PNS lesions, such as cervical polyradiculopathies or plexopathies. When PNS-type abnormalities are revealed on EMG in cancer patients, further screening to evaluate CNS lesions involving the corresponding corticospinal tracts should be included to ensure a timely and proper intervention.
Abstract
Denervation potentials obtained during electromyography (EMG) are usually considered as evidence of axonal degeneration in the peripheral nervous system (PNS). However, they may also appear when only central nervous system (CNS) lesions exist. Here, we present trans-synaptic degeneration from CNS lesions in 2 cases with electrophysiologic findings of motor axon degeneration caused not by PNS lesions, but by metastatic tumors involving the corresponding primary motor cortexes. When cancer patients show denervation potentials in needle EMG results, physicians usually consider PNS-related etiologies first, such as drug-induced generalized peripheral polyneuropathy or metastatic lesions (e.g., Pancoast tumor). However, metastatic brain tumors in the motor cortex could cause the same denervation potentials as PNS lesions, such as cervical polyradiculopathies or plexopathies. When PNS-type abnormalities are revealed on EMG in cancer patients, further screening to evaluate CNS lesions involving the corresponding corticospinal tracts should be included to ensure a timely and proper intervention.
참고문헌 (10)
- Arasaki K, "Reduction in the motor unit number estimate(MUNE)after cerebral infarction", J Neurol Sci, 250, pp.27~32 (2006)
- Benecke R, "Denervation activity in the EMG of patients with upper motor neuron lesions : time course, local distribution and pathogenetic aspects", J Neurol, 230, pp.143~151 (1983)
- Giglio P, "Neurologic complications of cancer and its treatment", Curr Oncol Rep, 12, pp.50~59 (2010)
- Van Eijk JJ, "Neuralgic amyotrophy : an update on diagnosis, pathophysiology, and treatment", Muscle Nerve, 53, pp.337~350 (2016)
- Zhang J, "Secondary neurodegeneration in remote regions after focal cerebral infarction: a new target for stroke management?", Stroke, 43, pp.1700~1705 (2012)
- Terao S, "Upper motor neuron lesions in stroke patients do not induce anterograde transneuronal degeneration in spinal anterior horn cells", Stroke, 28, pp.2553~2556 (1997)
- Dang G, "Dynamic secondary degeneration in the spinal cord and ventral root after a focal cerebral infarction among hypertensive rats", Sci Rep, 6, pp.22655~ (2016)
- Van De Meent H, "Severe degeneration of peripheral motor axons after spinal cord injury: a European multicenter study in 345 patients", Neurorehabil Neural Repair, 24, pp.657~665 (2010)
- Saksena S, "The corpus callosum wallerian degeneration in the unilateral brain tumors : evaluation with diffusion tensor imaging(DTI)", J Clin Diagn Res, 7, pp.320~325 (2013)
- Sawlani V, "MRI demonstration of Wallerian degeneration in various intracranial lesions and its clinical implications", J Neurol Sci, 146, pp.103~108 (1997)
