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An unusual case of electromyographic recorded myokymic potentials: A case report
727
CLINICAL NOTE
An Unusual Case of Electromyographic Recorded Myokymic Potentials: A Case Report Angela M. D’Alessandro, MD, Gregory J. Mulford, MD ABSTRACT. D’Alessandro AM, Mulford GJ. An unusual case of electromyographic recorded myokymic potentials: a case report. Arch Phys Med Rehabil 2002;83:727-9. Abnormal spontaneous potentials, specifically myokymia, can occur from various causes. We present the case of a 64-year-old woman with a 12-month history of left leg weakness and difficulty descending stairs. The patients’ medical history was significant for breast carcinoma (no node involvement), hypercholesterolemia, and vitamin B12 deficiency. She previously had a modified radical mastectomy and received chemotherapy (5-flurouracil, methotrexate, Cytoxan [cyclophosphamide]), but received no radiation. She took simvastatin for hypercholesterolemia and received vitamin B12 injections for her B12 deficiency. She initially noticed her symptoms when she began taking simvastatin, and they were exacerbated when her dose was increased from 10 to 20mg/d. Electrodiagnostic studies were performed twice at a 6-month interval. Nerve conduction studies were normal, but the initial needle electromyography showed significant myokymic discharges in bilateral iliopsoas, adductor magnus, and left deltoid muscles. The second electromyograph had similar findings, except for the absence of myokymic discharges in the left deltoid muscle. The possible origins of these myokymic discharges are discussed. Key Words: Case report; Myokymia; Rehabilitation; Simvastatin; Vitamin B12 deficiency. © 2002 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation BNORMAL SPONTANEOUS discharges observed on needle electromyography examination that arise from neuA ral generators include fasciculations, continuous muscle fiber activity, cramps, tetany, tremor, and myokymia.1 Myokymia is a clinical phenomenon that has been described as a persistent rippling movement of the skin. Myokymic discharges, seen as electrophysiologic potentials during needle electromyography, have a characteristic pattern of normal motor unit action potentials, a regular rhythm, and persistent firing with occasional abrupt cessation. Myokymic discharges represent groups of motor units. Their sound has been compared with the sputtering of a motorboat engine. Myokymic potentials are not affected by voluntary movement, and there may be 2 to 10
From the New York Presbyterian Hospital, New York, NY (D’Alessandro); and Department of Rehabilitation Medicine, Rehabilitation Institute of Morristown Memorial Hospital, Morristown, NJ (Mulford). Accepted in revised form May 3, 2001. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors(s) or upon any organization with which the author(s) is/are associated. Reprint requests to Gregory J. Mulford, MD, Dept of Rehabilitation Medicine, Rehabilitation Institute of Morristown Memorial Hospital, 95 Mt Kemble Ave, Thebaud Bldg, 4th Fl, Morristown, NJ 07962-1978. 0003-9993/02/8305-6622$35.00/0 doi:10.1053/apmr.2002.32199
discharges in a single burst that can fire at 20 to 150Hz.2 These discharges differ from complex repetitive discharges in several ways. Myokymic discharges do not usually start and stop abruptly nor do they display a regular pattern of spikes from 1 group to the next. The myokymic discharge has been theorized to originate from anywhere along the motoneuron from the cell body to the terminal axon.1 Myokymic discharges can occur secondary to a variety of etiologies, and are classified as focal, segmental, or generalized.1 Focal myokymia observed only in the face may be seen in multiple sclerosis, brainstem neoplasm, polyradiculopathy, Bell’s palsy, or a normal variant. Segmental myokymia has been reported in radiculopathies or syringomyelia, whereas generalized myokymia has been noted in uremia, thyrotoxicosis, timber rattlesnake envenomation, GuillainBarre´ syndrome, and chronic inflammatory polyradiculoneuropathy. Myokymic discharges in the irradiated extremity have been associated with radiation plexopathy.3 The etiologies that cause myokymic discharges change the axon membrane microenvironment. Changing levels of calcium in the microenvironment of the axon can change the firing pattern of the myokymic discharge.4 Our case involved an individual with subjective weakness, stiffness, and documented myokymic discharges in whom many of the potential origins had been ruled out. The most likely origins of her electromyographically recorded myokymic discharges included vitamin B12 deficiency or a side effect of simvastatin use. CASE DESCRIPTION A 64-year-old woman with a chief complaint of a 12-month history of left leg weakness, difficulty descending stairs, and some difficulty initiating walking when getting up from a chair was referred for electrodiagnostic consultation. She also complained of a sensation of the left leg nearly buckling while walking. She denied any falls, had no swallowing or visual changes, and denied any muscle cramps. Her medical history was significant for breast carcinoma, hypercholesterolemia, vitamin B12 deficiency, a 40-pack per year history of smoking, and water retention. She had a modified radical mastectomy in October 1993, with no node involvement. Her course of chemotherapy included 5-flurouracil, methotrexate, and Cytoxan (cyclophosphamide) followed by tamoxifen. Tamoxifen was eventually discontinued without any noticeable impact on her symptoms. She did not receive any radiation. Around the time her symptoms began, her vitamin B12 level was low at 180pg/mL (normal range, ⬎200pg/mL). Her red blood cell indices remained high pre- and postintramuscular replacement of vitamin B12. After replacement, her mean corpuscular volume was 109.1fL (normal range, 80 –100fL), and her mean corpuscular hemoglobin was 38.1pg (normal range, 27–33pg). The vitamin B12 level rose to 285pg/mL with intramuscular replacement without any noticeable improvement in her symptoms. At presentation, her medications were simvastatin, furosemide, and intramuscular injections of vitamin B12. The patient had been on lovastatin for 6 years and was changed to atorvastatin calcium for 4 months and then to simvastatin, which she had been taking for the 12 months before her Arch Phys Med Rehabil Vol 83, May 2002
728
UNUSUAL CAUSES FOR MYOKYMIA ON ELECTROMYOGRAPHY, D’Alessandro Table 1: Initial Electrodiagnostic Data Site
Motor nerve Right peroneal
Right posterior tibial
Sensory nerve Right sural
EDB Ankle Fibular head Abductor hallicus Ankle Knee Lateral malleolus calf
Distal Latency (ms)
Amplitude (mV)
Velocity (m/s)
4.22 9.69
16.41 15.64
48.5
5.47 12.81
13.67 11.51
49.0
2.56
37.94
42.9
Abbreviation: EDB, extensor digitorum brevis.
presentation to our laboratory. The timing of the simvastatin use appears to coincide with a noticeable increase in the patient’s symptoms. Increasing the simvastatin dose from 10 to 20mg per day resulted in a subjective worsening of her symptoms. A detailed review of systems was otherwise unremarkable. Several diagnostic studies had been performed before her electrodiagnostic consultation. Magnetic resonance imaging (MRI) of the brain with and without gadolinium revealed no abnormalities. MRI of the spine without contrast revealed small left L2–3 and L4 –5 foraminal disk herniations not associated with any definite nerve root compression. MRI of the left knee was significant for probable meniscal degeneration of the posterior horn of the medial meniscus but no definite meniscal tear. Physical examination showed no focal deficits of strength or sensation, and reflexes were normal. Cranial nerve function was intact. On visual inspection, there was no obvious muscle atrophy, fasciculations, clinical myotonia, or myokymia. Her cerebellar examination was normal, and she had no deviations in gait. Examination of her pulses showed a diminished femoral pulse, dorsalis pedis pulse, and tibial pulse on the left when compared with the right. There were no trophic skin changes on the left lower extremity. Electrodiagnostic testing was performed initially and 6 months later. Nerve conduction studies were normal (table 1). Needle electromyography showed significant myokymic discharges in bilateral iliopsoas, adductor magnus, and left deltoid muscles on the first evaluation. Six months later, after intramuscular vitamin B12 replacement and no change in her simvastatin use, the electromyography was repeated. She continued to experience left leg weakness, occasional stiffness, and difficulty climbing stairs. Once again, myokymic discharges were found in bilateral iliopsoas and adductor magnus muscles, but no abnormal spontaneous activity was observed in the left deltoid. On electromyography, her motor unit morphology and amplitude were normal, with biphasic and triphasic motor units of 2 to 4mV in amplitude. The recruitment pattern was normal with submaximal effort, and interference was incomplete on maximal effort in muscles that had evidence of myokymic discharge. Her myokymic discharges on needle electromyography may have been a normal variant, or may have been related to a specific cause. The most likely origin was a vitamin B12 deficiency, although simvastatin use may have contributed to her symptoms and the pathology. DISCUSSION A comprehensive review of the literature on electrodiagnostic findings and either simvastatin use or vitamin B12 deficiency indicates that vitamin B12 deficiency can affect both the upper Arch Phys Med Rehabil Vol 83, May 2002
and lower motoneurons. The neurologic manifestations of vitamin B12 deficiency include encephalopathy, subacute combined degeneration, myelopathy, optic neuropathy, and peripheral neuropathy.5 One study6 of 38 patients with vitamin B12 deficiency after gastric surgery identified decreased amplitude of the sensory potentials of the median nerve at the wrist in 13 patients (34%) but no abnormal spontaneous activity or myokymic discharge on electromyography.6 In another report,7 3 patients with vitamin B12 deficiency had abnormal nerve conduction studies, with electrophysiologic findings showing slowing of motor nerve conduction velocities, delayed F-wave latencies, and small or absent sural sensory potentials. Normalization of tibial and peroneal F-wave responses has been reported after hydroxycobalamin replacement for 11 months.5 In another report,8 a 35-year-old man with vitamin B12 deficiency had electrophysiologic studies that showed a prominent proximal conduction block in the tibial and median nerves and abundant fibrillation activity; after 5 months of vitamin B12 replacement, the conduction block disappeared in both the upper and lower limbs. In our case, the electrophysiologic studies continued to show myokymic discharges at 6-month follow-up, even after more than 6 months of vitamin replenishment. Because of this lack of improvement in symptoms or electrophysiologic findings after 6 months of vitamin B12 replacement, we sought other explanations for her persistent symptoms. According to the patient’s history, the timing of her increase in symptoms closely corresponded to her simvastatin use. Simvastatin is an inhibitor of 3-hydroxy-3methylglutaryl-coenzyme A (HMG-CoA) reductase, which is the enzyme that converts HMG-CoA to mevalonate, an early step in the synthesis of cholesterol. A known side effect of simvastatin use is myopathy with elevated creatine kinase (CK) and muscle weakness. Our patient’s CK level was normal, but this level was obtained 18 months after she began simvastatin use and symptom onset, and the CK could have normalized by that time. Patients have experienced muscle pain without CK elevation while taking HMG-CoA reductase inhibitors.9 A study10 in which myopathy was induced in rabbits by administering HMG-CoA reductase inhibitors showed the development of myotonic potentials. The rabbits were divided into 3 groups: group 1 received simvastatin (50mg 䡠 kg1 䡠 d1 for 4wk), group 2 received pravastatin (100mg 䡠 kg1 䡠 d1 for 4wk), and group 3 received pravastatin (200mg 䡠 kg1 䡠 d1 for 3wk plus 300mg 䡠 kg1 䡠 d1 for 3wk). The rabbits receiving simvastatin all showed myotonic discharges on electromyography. Their serum CK levels peaked in the second or third weeks, but returned to normal by the fourth week in the simvastatin group.10 The only electrophysiologic abnormality displayed on needle electromyography study in our case was myokymia,
UNUSUAL CAUSES FOR MYOKYMIA ON ELECTROMYOGRAPHY, D’Alessandro
which supports vitamin B12 deficiency as the primary origin. Because it is possible that the simvastatin use may play a contributory role in the worsening of her symptoms, it was recommended that she discontinue her simvastatin and closely monitor her symptoms and cholesterol profile. CONCLUSIONS This case describes a patient who presented with a complaint of lower-extremity weakness, with myokymia present on needle electromyography examination. Many of the usual causes of myokymic discharges, including radiation plexopathy, chronic nerve compression, rattlesnake venom, multiple sclerosis, brainstem neoplasm, polyradiculopathy, and Bell’s palsy were ruled out clinically. After careful review of her history and electrodiagnostic findings, we concluded that the 2 most likely factors contributing to her symptoms were vitamin B12 deficiency causing electrophysiologic myokymia, along with simvastatin-associated myopathy that further exacerbated her subjective weakness. References 1. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley & Belfus; 1995. p 234-6.
729
2. Daube JA, Kelly JJ, Martin RA. Facial myokymia with polyradiculoneuropathy. Neurology 1979;29:662-9. 3. Albers JW, Allen AA II, Bastron JD, Daube JR. Limb myokymia. Muscle Nerve 1981;4:494-504. 4. Gutmann L. AAEM Minimonograph #37: facial and limb myokymia. Muscle Nerve 1991;14:1043-9. 5. Wu T, Nai-Shin C. Recovery patterns of motor and somatosensory evoked potentials following treatment of vitamin B12 deficiency. J Formosa Med Assoc 1996;95:157-61. 6. Roos D. Electrophysiological findings in gastrectomized patients with low serum B12. Acta Neurol Scand 1977;56:247-55. 7. Carvalho MA, Schwartz MS. Abnormalities in motor conduction in vitamin B12 deficiency. Electromyogr Clin Neurophysiol 1996; 36:275-8. 8. Al-Shubaili AF, Farah SA, Hussein JM. Axonal and demyelinating neuropathy with reversible proximal conduction block, an unusual feature of vitamin B12 deficiency. Muscle Nerve 1998; 21:1341-3. 9. Sinzinger H, Schmid P, O’Grady J. Two different types of exercise-induced muscle pain without myopathy and CK-elevation during HMG-Co-enzyme-A-reductase inhibitor treatment. Atherosclerosis 1999;143:459-60. 10. Nakahara K, Kuriyama M, Sonoda Y. Myopathy induced by HMG-CoA reductase inhibitors in rabbits: a pathological, electrophysiological, and biochemical study. Toxicol Appl Pharmacol 1998;152:99-106.
Arch Phys Med Rehabil Vol 83, May 2002
CLINICAL NOTE
An Unusual Case of Electromyographic Recorded Myokymic Potentials: A Case Report Angela M. D’Alessandro, MD, Gregory J. Mulford, MD ABSTRACT. D’Alessandro AM, Mulford GJ. An unusual case of electromyographic recorded myokymic potentials: a case report. Arch Phys Med Rehabil 2002;83:727-9. Abnormal spontaneous potentials, specifically myokymia, can occur from various causes. We present the case of a 64-year-old woman with a 12-month history of left leg weakness and difficulty descending stairs. The patients’ medical history was significant for breast carcinoma (no node involvement), hypercholesterolemia, and vitamin B12 deficiency. She previously had a modified radical mastectomy and received chemotherapy (5-flurouracil, methotrexate, Cytoxan [cyclophosphamide]), but received no radiation. She took simvastatin for hypercholesterolemia and received vitamin B12 injections for her B12 deficiency. She initially noticed her symptoms when she began taking simvastatin, and they were exacerbated when her dose was increased from 10 to 20mg/d. Electrodiagnostic studies were performed twice at a 6-month interval. Nerve conduction studies were normal, but the initial needle electromyography showed significant myokymic discharges in bilateral iliopsoas, adductor magnus, and left deltoid muscles. The second electromyograph had similar findings, except for the absence of myokymic discharges in the left deltoid muscle. The possible origins of these myokymic discharges are discussed. Key Words: Case report; Myokymia; Rehabilitation; Simvastatin; Vitamin B12 deficiency. © 2002 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation BNORMAL SPONTANEOUS discharges observed on needle electromyography examination that arise from neuA ral generators include fasciculations, continuous muscle fiber activity, cramps, tetany, tremor, and myokymia.1 Myokymia is a clinical phenomenon that has been described as a persistent rippling movement of the skin. Myokymic discharges, seen as electrophysiologic potentials during needle electromyography, have a characteristic pattern of normal motor unit action potentials, a regular rhythm, and persistent firing with occasional abrupt cessation. Myokymic discharges represent groups of motor units. Their sound has been compared with the sputtering of a motorboat engine. Myokymic potentials are not affected by voluntary movement, and there may be 2 to 10
From the New York Presbyterian Hospital, New York, NY (D’Alessandro); and Department of Rehabilitation Medicine, Rehabilitation Institute of Morristown Memorial Hospital, Morristown, NJ (Mulford). Accepted in revised form May 3, 2001. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors(s) or upon any organization with which the author(s) is/are associated. Reprint requests to Gregory J. Mulford, MD, Dept of Rehabilitation Medicine, Rehabilitation Institute of Morristown Memorial Hospital, 95 Mt Kemble Ave, Thebaud Bldg, 4th Fl, Morristown, NJ 07962-1978. 0003-9993/02/8305-6622$35.00/0 doi:10.1053/apmr.2002.32199
discharges in a single burst that can fire at 20 to 150Hz.2 These discharges differ from complex repetitive discharges in several ways. Myokymic discharges do not usually start and stop abruptly nor do they display a regular pattern of spikes from 1 group to the next. The myokymic discharge has been theorized to originate from anywhere along the motoneuron from the cell body to the terminal axon.1 Myokymic discharges can occur secondary to a variety of etiologies, and are classified as focal, segmental, or generalized.1 Focal myokymia observed only in the face may be seen in multiple sclerosis, brainstem neoplasm, polyradiculopathy, Bell’s palsy, or a normal variant. Segmental myokymia has been reported in radiculopathies or syringomyelia, whereas generalized myokymia has been noted in uremia, thyrotoxicosis, timber rattlesnake envenomation, GuillainBarre´ syndrome, and chronic inflammatory polyradiculoneuropathy. Myokymic discharges in the irradiated extremity have been associated with radiation plexopathy.3 The etiologies that cause myokymic discharges change the axon membrane microenvironment. Changing levels of calcium in the microenvironment of the axon can change the firing pattern of the myokymic discharge.4 Our case involved an individual with subjective weakness, stiffness, and documented myokymic discharges in whom many of the potential origins had been ruled out. The most likely origins of her electromyographically recorded myokymic discharges included vitamin B12 deficiency or a side effect of simvastatin use. CASE DESCRIPTION A 64-year-old woman with a chief complaint of a 12-month history of left leg weakness, difficulty descending stairs, and some difficulty initiating walking when getting up from a chair was referred for electrodiagnostic consultation. She also complained of a sensation of the left leg nearly buckling while walking. She denied any falls, had no swallowing or visual changes, and denied any muscle cramps. Her medical history was significant for breast carcinoma, hypercholesterolemia, vitamin B12 deficiency, a 40-pack per year history of smoking, and water retention. She had a modified radical mastectomy in October 1993, with no node involvement. Her course of chemotherapy included 5-flurouracil, methotrexate, and Cytoxan (cyclophosphamide) followed by tamoxifen. Tamoxifen was eventually discontinued without any noticeable impact on her symptoms. She did not receive any radiation. Around the time her symptoms began, her vitamin B12 level was low at 180pg/mL (normal range, ⬎200pg/mL). Her red blood cell indices remained high pre- and postintramuscular replacement of vitamin B12. After replacement, her mean corpuscular volume was 109.1fL (normal range, 80 –100fL), and her mean corpuscular hemoglobin was 38.1pg (normal range, 27–33pg). The vitamin B12 level rose to 285pg/mL with intramuscular replacement without any noticeable improvement in her symptoms. At presentation, her medications were simvastatin, furosemide, and intramuscular injections of vitamin B12. The patient had been on lovastatin for 6 years and was changed to atorvastatin calcium for 4 months and then to simvastatin, which she had been taking for the 12 months before her Arch Phys Med Rehabil Vol 83, May 2002
728
UNUSUAL CAUSES FOR MYOKYMIA ON ELECTROMYOGRAPHY, D’Alessandro Table 1: Initial Electrodiagnostic Data Site
Motor nerve Right peroneal
Right posterior tibial
Sensory nerve Right sural
EDB Ankle Fibular head Abductor hallicus Ankle Knee Lateral malleolus calf
Distal Latency (ms)
Amplitude (mV)
Velocity (m/s)
4.22 9.69
16.41 15.64
48.5
5.47 12.81
13.67 11.51
49.0
2.56
37.94
42.9
Abbreviation: EDB, extensor digitorum brevis.
presentation to our laboratory. The timing of the simvastatin use appears to coincide with a noticeable increase in the patient’s symptoms. Increasing the simvastatin dose from 10 to 20mg per day resulted in a subjective worsening of her symptoms. A detailed review of systems was otherwise unremarkable. Several diagnostic studies had been performed before her electrodiagnostic consultation. Magnetic resonance imaging (MRI) of the brain with and without gadolinium revealed no abnormalities. MRI of the spine without contrast revealed small left L2–3 and L4 –5 foraminal disk herniations not associated with any definite nerve root compression. MRI of the left knee was significant for probable meniscal degeneration of the posterior horn of the medial meniscus but no definite meniscal tear. Physical examination showed no focal deficits of strength or sensation, and reflexes were normal. Cranial nerve function was intact. On visual inspection, there was no obvious muscle atrophy, fasciculations, clinical myotonia, or myokymia. Her cerebellar examination was normal, and she had no deviations in gait. Examination of her pulses showed a diminished femoral pulse, dorsalis pedis pulse, and tibial pulse on the left when compared with the right. There were no trophic skin changes on the left lower extremity. Electrodiagnostic testing was performed initially and 6 months later. Nerve conduction studies were normal (table 1). Needle electromyography showed significant myokymic discharges in bilateral iliopsoas, adductor magnus, and left deltoid muscles on the first evaluation. Six months later, after intramuscular vitamin B12 replacement and no change in her simvastatin use, the electromyography was repeated. She continued to experience left leg weakness, occasional stiffness, and difficulty climbing stairs. Once again, myokymic discharges were found in bilateral iliopsoas and adductor magnus muscles, but no abnormal spontaneous activity was observed in the left deltoid. On electromyography, her motor unit morphology and amplitude were normal, with biphasic and triphasic motor units of 2 to 4mV in amplitude. The recruitment pattern was normal with submaximal effort, and interference was incomplete on maximal effort in muscles that had evidence of myokymic discharge. Her myokymic discharges on needle electromyography may have been a normal variant, or may have been related to a specific cause. The most likely origin was a vitamin B12 deficiency, although simvastatin use may have contributed to her symptoms and the pathology. DISCUSSION A comprehensive review of the literature on electrodiagnostic findings and either simvastatin use or vitamin B12 deficiency indicates that vitamin B12 deficiency can affect both the upper Arch Phys Med Rehabil Vol 83, May 2002
and lower motoneurons. The neurologic manifestations of vitamin B12 deficiency include encephalopathy, subacute combined degeneration, myelopathy, optic neuropathy, and peripheral neuropathy.5 One study6 of 38 patients with vitamin B12 deficiency after gastric surgery identified decreased amplitude of the sensory potentials of the median nerve at the wrist in 13 patients (34%) but no abnormal spontaneous activity or myokymic discharge on electromyography.6 In another report,7 3 patients with vitamin B12 deficiency had abnormal nerve conduction studies, with electrophysiologic findings showing slowing of motor nerve conduction velocities, delayed F-wave latencies, and small or absent sural sensory potentials. Normalization of tibial and peroneal F-wave responses has been reported after hydroxycobalamin replacement for 11 months.5 In another report,8 a 35-year-old man with vitamin B12 deficiency had electrophysiologic studies that showed a prominent proximal conduction block in the tibial and median nerves and abundant fibrillation activity; after 5 months of vitamin B12 replacement, the conduction block disappeared in both the upper and lower limbs. In our case, the electrophysiologic studies continued to show myokymic discharges at 6-month follow-up, even after more than 6 months of vitamin replenishment. Because of this lack of improvement in symptoms or electrophysiologic findings after 6 months of vitamin B12 replacement, we sought other explanations for her persistent symptoms. According to the patient’s history, the timing of her increase in symptoms closely corresponded to her simvastatin use. Simvastatin is an inhibitor of 3-hydroxy-3methylglutaryl-coenzyme A (HMG-CoA) reductase, which is the enzyme that converts HMG-CoA to mevalonate, an early step in the synthesis of cholesterol. A known side effect of simvastatin use is myopathy with elevated creatine kinase (CK) and muscle weakness. Our patient’s CK level was normal, but this level was obtained 18 months after she began simvastatin use and symptom onset, and the CK could have normalized by that time. Patients have experienced muscle pain without CK elevation while taking HMG-CoA reductase inhibitors.9 A study10 in which myopathy was induced in rabbits by administering HMG-CoA reductase inhibitors showed the development of myotonic potentials. The rabbits were divided into 3 groups: group 1 received simvastatin (50mg 䡠 kg1 䡠 d1 for 4wk), group 2 received pravastatin (100mg 䡠 kg1 䡠 d1 for 4wk), and group 3 received pravastatin (200mg 䡠 kg1 䡠 d1 for 3wk plus 300mg 䡠 kg1 䡠 d1 for 3wk). The rabbits receiving simvastatin all showed myotonic discharges on electromyography. Their serum CK levels peaked in the second or third weeks, but returned to normal by the fourth week in the simvastatin group.10 The only electrophysiologic abnormality displayed on needle electromyography study in our case was myokymia,
UNUSUAL CAUSES FOR MYOKYMIA ON ELECTROMYOGRAPHY, D’Alessandro
which supports vitamin B12 deficiency as the primary origin. Because it is possible that the simvastatin use may play a contributory role in the worsening of her symptoms, it was recommended that she discontinue her simvastatin and closely monitor her symptoms and cholesterol profile. CONCLUSIONS This case describes a patient who presented with a complaint of lower-extremity weakness, with myokymia present on needle electromyography examination. Many of the usual causes of myokymic discharges, including radiation plexopathy, chronic nerve compression, rattlesnake venom, multiple sclerosis, brainstem neoplasm, polyradiculopathy, and Bell’s palsy were ruled out clinically. After careful review of her history and electrodiagnostic findings, we concluded that the 2 most likely factors contributing to her symptoms were vitamin B12 deficiency causing electrophysiologic myokymia, along with simvastatin-associated myopathy that further exacerbated her subjective weakness. References 1. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley & Belfus; 1995. p 234-6.
729
2. Daube JA, Kelly JJ, Martin RA. Facial myokymia with polyradiculoneuropathy. Neurology 1979;29:662-9. 3. Albers JW, Allen AA II, Bastron JD, Daube JR. Limb myokymia. Muscle Nerve 1981;4:494-504. 4. Gutmann L. AAEM Minimonograph #37: facial and limb myokymia. Muscle Nerve 1991;14:1043-9. 5. Wu T, Nai-Shin C. Recovery patterns of motor and somatosensory evoked potentials following treatment of vitamin B12 deficiency. J Formosa Med Assoc 1996;95:157-61. 6. Roos D. Electrophysiological findings in gastrectomized patients with low serum B12. Acta Neurol Scand 1977;56:247-55. 7. Carvalho MA, Schwartz MS. Abnormalities in motor conduction in vitamin B12 deficiency. Electromyogr Clin Neurophysiol 1996; 36:275-8. 8. Al-Shubaili AF, Farah SA, Hussein JM. Axonal and demyelinating neuropathy with reversible proximal conduction block, an unusual feature of vitamin B12 deficiency. Muscle Nerve 1998; 21:1341-3. 9. Sinzinger H, Schmid P, O’Grady J. Two different types of exercise-induced muscle pain without myopathy and CK-elevation during HMG-Co-enzyme-A-reductase inhibitor treatment. Atherosclerosis 1999;143:459-60. 10. Nakahara K, Kuriyama M, Sonoda Y. Myopathy induced by HMG-CoA reductase inhibitors in rabbits: a pathological, electrophysiological, and biochemical study. Toxicol Appl Pharmacol 1998;152:99-106.
Arch Phys Med Rehabil Vol 83, May 2002