Vol.64

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.63

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.62

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.61

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.60

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.59

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.58

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.57

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.56

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.55

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.54

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.53

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.52

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.51

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.50

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.49

• No.1
• No.2/3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.48

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

• Vol.47 to 1
  (Members Only)

• HOME
• Vol.59 No.9
• CLINICA NEUROL, 59: 592−595, 2019
• Vol.59 No.9 contents

Brief Clinical Note

Continuous hyperCKemia without calf muscle hypertrophy associated with S1 radiculopathy

Takashi Nakamura, M.D.¹⁾, Tatsuya Ueno, M.D., Ph.D.¹⁾, Akira Arai, M.D., Ph.D.¹⁾, Chieko Suzuki, M.D., Ph.D.¹⁾³⁾, Ichizo Nishino, M.D., Ph.D.²⁾ and Masahiko Tomiyama, M.D., Ph.D.¹⁾³⁾

¹⁾Department of Neurology, Aomori Prefectural Central Hospital
²⁾Department of Neuromuscular Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry
³⁾Present address: Department of Neurology, Hirosaki University Graduate School of Medicine

A 72-year-old man presented with continuous hyperCKemia and intermittent claudication. He exhibited no calf muscle hypertrophy at that time or afterward. Other than an increased creatine kinase (CK) level (1,525 U/l), none of the laboratory tests was abnormal, including that for myositis-related autoantibodies. Electromyography showed neurogenic changes in the left gastrocnemius. Lumbar magnetic resonance imaging revealed spinal canal stenosis (L3/4, L4/5), left L4 radiculopathy, and bilateral S1 radiculopathy. T₂-weighted and short tau inversion recovery images showed high signal intensity in the bilateral biceps femoris and gastrocnemius. Histopathological evaluation of a specimen obtained from the right gastrocnemius muscle revealed neurogenic changes. The patient was diagnosed with S1 radiculopathy caused by lumbar spinal canal stenosis with hyperCKemia. Although S1 radiculopathy with hyperCKemia is usually associated with calf muscle hypertrophy, we should consider S1 radiculopathy in patients with intermittent claudication and hyperCKemia even in the absence of calf muscle hypertrophy.
Full Text of this Article in Japanese PDF (1220K)

(CLINICA NEUROL, 59: 592−595, 2019)
key words: S1 radiculopathy, lumbar spinal canal stenosis, muscle hypertrophy, hyperCKemia, muscle MRI

(Received: 12-Feb-19)