Quantitative Measurement of Muscle Atrophy and Fat Infiltration of the Supraspinatus Muscle Using Ultrasonography After Arthroscopic Rotator Cuff Repair

OBJECTIVE: To investigate the utility of ultrasonography to objectively examine morphological changes (i.e., muscle atrophy and fatty infiltration) of the supraspinatus muscle. METHODS: Thirty-four patients were prospectively enrolled in this study. The degrees of muscle atrophy and fat infiltration were measured using ultrasonography 3–4 months after arthroscopic supraspinatus tendon repair. Shoulder function (i.e., shoulder active range of motion, visual analogue scale, and constant score) was examined. Using the symmetricity of the muscles in the human body, the degrees of morphological changes of the supraspinatus muscle were quantitatively measured. The associations between the morphological changes of the supraspinatus muscle and shoulder function were identified. RESULTS: There were statistically significant differences in the cross-sectional area (CSA) and echogenicity between the surgery and non-surgery sides (p < 0.001). The CSA ratio, which represents the degree of muscle atrophy, was associated with shoulder forward flexion, external rotation, and constant score; however, the echogenicity ratio, which represents the degree of fat infiltration, was not associated with shoulder function after surgery. CONCLUSION: This study demonstrated that shoulder function could be predicted by evaluating the morphological changes of the supraspinatus muscle using ultrasonography and that objective evaluation is possible through quantitative measurement using the symmetricity of the human body.

Cervical Multifidus Muscle Atrophy in Patients with Unilateral Cervical Radiculopathy

OBJECTIVE: To assess the atrophy of cervical multifidus muscles in patients with unilateral cervical disc herniation or radiculopathy quantitatively and to investigate whether asymmetric muscle atrophy has the relationship with the severity of cervical disc herniation or radiculopathy. METHOD: Twenty-four patients who had cervical disc herniation in magnetic resonance imaging (MRI) were evaluated. The patients were divided into 2 groups; patients with unilateral cervical radiculopathy in electrodiagnosis (RAD) and patients without definite radiculopathy (HIVD). Twenty six controls without disc herniation were also evaluated. Cervical multifidus muscles from C4-5 to C7-T1 levels were detected in T1 axial MRI, and total cross-sectional area (CSA) of multifidus muscle (TMA) and pure muscle CSA (PMA) were measured. RESULTS: The ratios of TMA in involved side to TMA in uninvolved side (ITMA/UTMA) and PMA in involved side to PMA in uninvolved side (IPMA/UPMA) in HIVD and RAD groups was significantly lower than those in control group especially at C7-T1 level (p<0.05). We divided the levels of cervical spine into three parts according to lesions found in MRI or electrodiagnosis; above lesion level, at lesion level and below lesion level. Abnormal cases of IPMA/UPMA were not different among levels in HIVD group, but RAD group showed that most of abnormal cases were below lesion (60%). CONCLUSION: Asymmetric multifidus atrophy was seen in patients with cervical disc herniation and radiculopathy. The ratio of pure muscle CSA between involved and uninvolved sides might be a useful parameter to differentiate patients with unilateral cervical radiculopathy from patients without radiculopathy.

Effect of Stimulation Intensity and Location of Cerebral Infarction on Motor Evoked Potentials in the Rat

OBJECTIVE: To investigate the change of motor evoked potential (MEP) in the cerebral infarction, and observe the effect of stimulation intensity and location of cerebral infarction, using rat model of cerebral ischemia induced by endothelin-1 (ET-1). METHOD: Middle cerebral artery (MCA) infarct, cortical infarct, and internal capsular infarct were induced in Spraugue-Dawley rats, by injecting ET-1 stereotaxically. MEP was recorded in forelimb by transcranial magnetic stimulation at 100%, 120%, and 150% of motor threshold by a small figure-8 coil. The location of cerebral infarction was confirmed histologically by 2,3,5-triphenyltetrazolium chloride (TTC) staining. RESULTS: In MCA infarct, MEP was not recorded at all intensity. In internal capsular infarct, no MEP was recorded at 100% of motor threshold, and amplitude was decreased at 120%. In cortical infarct, MEP was not recorded at 100%, but amplitude was maintained at 120% and 150%. Latency did not change significantly at all intensity. CONCLUSION: Amplitude of MEP decreased after cerebral infarction, but latency did not change. Decrease in amplitude was larger with deeper location of cerebral infarction. Cerebral cortex was stimulated at 100% of motor threshold, subcortical structure was stimulated at 120%, and deeper structure was stimulated at 150%, respectively.