Asynchrony in Peritumoral Resting-State Blood Oxygen Level-Dependent fMRI Predicts Meningioma Grade and Invasion.

BACKGROUND AND PURPOSE: Meningioma grade is determined by histologic analysis, with detectable brain invasion resulting in a diagnosis of grade II or III tumor. However, tissue undersampling is a common problem, and invasive parts of the tumor can be missed, resulting in the incorrect assignment of a lower grade. Radiographic biomarkers may be able to improve the diagnosis of grade and identify targets for biopsy. Prior work in patients with gliomas has shown that the resting-state blood oxygen level-dependent fMRI signal within these tumors is not synchronous with normal brain. We hypothesized that blood oxygen level-dependent asynchrony, a functional marker of vascular dysregulation, could predict meningioma grade. MATERIALS AND METHODS: We identified 25 patients with grade I and 11 patients with grade II or III meningiomas. Blood oxygen level-dependent time-series were extracted from the tumor and the radiographically normal control hemisphere and were included as predictors in a multiple linear regression to generate a blood oxygen level-dependent asynchrony map, in which negative values signify synchronous and positive values signify asynchronous activity relative to healthy brain. Masks of blood oxygen level-dependent asynchrony were created for each patient, and the fraction of the mask that extended beyond the contrast-enhancing tumor was computed. RESULTS: The spatial extent of blood oxygen level-dependent asynchrony was greater in high (grades II and III) than in low (I) grade tumors (P < 0.001) and could discriminate grade with high accuracy (area under the curve = 0.88). CONCLUSIONS: Blood oxygen level-dependent asynchrony radiographically discriminates meningioma grade and may provide targets for biopsy collection to aid in histologic diagnosis.

[Effect of metformin on mitochondrial pathway of apoptosis and oxidative stress in cell model of nonalcoholic fatty liver disease].

Objective: To investigate the effects of metformin on mitochondrial pathway of apoptosis and oxidative stress in cell model of nonalcoholic fatty liver disease. Methods: An in vitro cell model of nonalcoholic fatty liver disease was established using 0.6 mmol/L oleic acid to induce lipid accumulation in HepG2 cells. HepG2 cells were divided into control (Con) group, oleic acid (OA) group, and metformin-low (1mmol/L) and high (10mmol/L) dose group. Oil Red O stain was used to detect intracellular lipid droplet distribution. The levels of alanine aminotransferase and aspartate aminotransferase in the culture supernatant were detected by assay kits. DCFH-DA method was used to detect the reactive oxygen species of HepG2 cells. Double staining flow cytometry was used to detect the apoptosis rate of HepG2 cells. Western blot was used to detect caspase-3, B-lymphocyte lymphoma-related protein, B-cell lymphoma 2, and cytochrome c protein. One-way analysis of variance was used to compare the data between groups. Results: Oleic acid-induced HepG2 cells were significantly increased with lipid droplets. Low and high-dose metformin had reduced intracellular lipid droplets accumulation. The effect of metformin in the high-dose group was more significant than that in the low-dose group. Aspartate aminotransferase and alanine aminotransferase in HepG2 cells of OA group were significantly increased, which were (43.41 ± 7.11) U/L and (29.56 ± 4.11) U/L, respectively. The intracellular aspartate aminotransferase and alanine aminotransferase were decreased significantly after the treatment with low and high-dose metformin, which were (32.44 ± 4.08)U/L, (19.31 ± 3.03) U/L, (26.00 ± 3.11) U/L and (15.11 ± 4.11) U/L, respectively and the differences were statistically significant (P < 0.05). DCFH-DA test results showed that the fluorescence intensity of reactive oxygen species in the oleic acid group was 41.21% ± 4.23%, while the fluorescence intensity of reactive oxygen species in the low and high-dose metformin groups were reduced to 27.44% ± 3.91%, and 17.55% ± 5.11%, respectively and the differences between the groups were statistically significant (P < 0.05). The results of flow cytometry analysis showed that the cell apoptosis rate of the OA group was significantly higher than that of the Con group (12.12% ± 0.72% vs. 3.04% ± 0.57%, P < 0.05).The apoptosis rate of HepG2 cells was significantly reduced after metformin treatment at low and high doses (8.71% ± 0.71%, 5.71% ± 0.61%, P < 0.05). Western blot results showed that compared with the Con group, the expressions of B-lymphocyte lymphoma-related protein, cytochrome c, and caspase-3 were increased in the OA group, while the B-cell lymphoma 2 were decreased (P < 0.05). The expression of B-lymphocyte lymphoma-related protein, cytochrome c, and caspase-3 protein in HepG2 cells was decreased after treatment with low and high-dose metformin, while B-cell lymphoma 2 was increased (P < 0.05). Conclusion: Metformin can effectively alleviate steatosis and improve the HepG2 function in cell model of nonalcoholic fatty liver disease. The mechanism of metformin may be related to the reduction of oxidative stress injury, the regulation of protein expression related to mitochondrial apoptosis pathway and the inhibition of cell apoptosis.

The lumbar multifidus muscle in polysegmentally innervated.

We conducted a prospective case study to determine whether the lumbar multifidus muscle is polysegmentally innervated. A 49-year-old man with chronic mechanical low back pain underwent bilateral percutaneous radiofrequency neurotomy of the medial branches of the L3 dorsal rami. Electromyography (EMG) examination was performed in the L2-5 multifidi both prior to and 3 weeks after the procedure. Positive sharp waves and fibrillations appeared in the L3-L5 multifidi after the neurotomy. This study provides electrophysiological evidence in the human lumbar spine that the medial branch of the lumbar root innervates the multifidus muscle at multiple levels, i.e., the lumbar multifidus muscle is polysegmentally innervated. As a result, electromyography of the multifidus cannot identify a specific level of lumbar radiculopathy.

Sensory nerve conduction velocity is inversely related to axonal length.

It was found that the axonal length was inversely related to motor conduction velocity (CV). However, it is not clear that sensory CV is inversely related to axonal length. The nerve lengths of the median sensory fascicles from the C6 and C7 intervertebral foramen to the digital branches of the thumb and middle finger were compared in ten cadavers. Sixty healthy subjects (24 men, 36 women; mean age 35, range 24-54 years) had median sensory CV testing. The median sensory nerve action potentials were obtained antidromically in the thumb and middle finger with wrist and elbow. The CVs across the forearm for the thumb and the middle finger fascicles were then calculated. It was found that the nerve length of C7 was longer than C6 with a difference of 3.6 +/- 0.6 cm. The mean forearm CV for the median sensory axons innervating the middle finger (60.0 +/- 3.9 m/s) was slower than the CV for the median sensory axons innervating the thumb (61.4 +/- 4.1 m/s,p = 0.0012). These results demonstrate that sensory CV is slowed by 3.9 m/s per 10 cm of axon length. This study confirms that the inverse relation of CV and axonal length reported in motor axons also applies to the sensory nerves.

Thoracodorsal nerve conduction study.

There is no nerve conduction study for the thoracodorsal nerve in the literature. A conduction study for this nerve is described. Thirty healthy adults (16 males) with a mean age of 41.5 +/- 10.6 (range, 22-63) years were studied. The thoracodorsal nerve was stimulated at axilla and Erb's point with recording over the latissimus dorsi. The latency was 1.9 +/- 0.4 (range, 1.2-2.7) ms and 3.6 +/- 0.4 (range, 2.8-4.5) ms for the axillary and Erb's stimulations, respectively. The amplitude of the compound muscle action potential was 4.1 +/- 1.8 mv on the right and 3.9 +/- 1.4 mv on the left. The compound muscle action potential ratio was 0.8 +/- 0.12 (range, 0.55-0.99). This study may be useful to evaluate the integrity of the thoracodorsal nerve and to assist in the diagnosis and prognosis of brachial plexus injury.

Correlation of EMG, CMAP and SNAP amplitude decrease in mononeuropathies with axonal loss.

We retrospectively reviewed electrodiagnostic studies from 1983 to 1994 and found 48 patients who met our criteria for mononeuropathy with axonal loss (40 ulnar, 4 peroneal, 4 radial). Appropriate diagnostic criteria required bilateral studies with a normal contralateral, sensory nerve action potential (SNAP) amplitude decrease of > 50% compared to contralateral, and/or distal compound muscle action potential (CMAP) amplitude decrease of > 40% compared to contralateral, and/or presence of denervation potentials; and sufficient electrodiagnostic investigation to rule out peripheral polyneuropathy. We conclude that in the electrodiagnosis of mononeuropathy with axonal loss: 1) a significant quantitative correlation between CMAP and SNAP amplitude percentage decrease does not exist (r = 0.274, p = 0.06), 2) SNAP amplitude percentage decrease [75.3 +/- 31.8%] is greater than CMAP amplitude percentage decrease [43.9 +/- 31.3%] (paired t-test, p = 0.0001), and 3) CMAP amplitude decrease is positively correlated with the presence of denervation potentials (Xtrend2 = 6.22, p = 0.013).

Electromyographic motor Tinel's sign in ulnar mononeuropathies at the elbow.

A novel test for localizing ulnar mononeuropathies (UM), the electromyographic (EMG) motor Tinel's sign, has been developed. While recording with a monopolar needle from the abductor digiti minimi, the ulnar nerve is lightly rolled at multiple sites across the elbow, and the test is considered positive if a burst of EMG activity is observed simultaneously with nerve compression. To determine the use of the EMG Tinel's sign, we evaluated 70 control nerves and 50 clinically suspected UMs. The EMG Tinel's sign had a 78% sensitivity and a 79% specificity for suspected UM at the elbow. The clinical Tinel's sign was present in 68% of suspected UM cases, and the combined sensitivity of the EMG and clinical Tinel's sign was 96%. Using nerve conduction study (NCS) values derived from the control nerves, 62% of UM nerves had abnormal NCS/EMG findings, and 28% of UM nerves had NCS/EMG abnormalities that could be localized to the elbow. The development of motor axon mechanosensitivity at the site of nerve injury is a new finding, not previously observed in electrophysiologic studies of animal nerve injury models or reported in the electrodiagnostic literature.

An EMG case report of lead neuropathy 19 years after a shotgun injury.

The clinical picture of lead neuropathy was classically described as a painless progressive motor neuropathy with axonal loss. The literature review fails to demonstrate a consensus on the site of axonal loss. This is an EMG report of a patient who developed a late lead neuropathy after a shotgun injury. A 69-year-old Filipino, healthy, male nondrinker sustained a shotgun injury to his left elbow. Nineteen years later he developed abdominal pain, followed by generalized weakness, distal greater than proximal in the extremities, and impaired pin-prick, proprioception, and two-point discrimination. He became nonambulatory and totally dependent in daily activities. He was lost to follow-up for 2 years until January 1993 when he presented with a blood lead level of 84 micrograms/dL. EMG examination revealed a sensorimotor peripheral polyneuropathy with severe axonal loss. This case demonstrates that axonal loss is the predominant feature in lead neuropathy and the location of pathology is in the peripheral nerves.

Temperature correction factors derived from normal subjects may be invalid in demyelinating neuropathies.

This study investigates the temperature effect on motor nerve conduction velocity (MNCV) in patients with neuropathic processes. Fourteen subjects, ages 18-77 yr old, with a diagnosis of uremic polyneuropathies (UPN, n = 5), diabetic polyneuropathies (DPN, n = 6) or carpal tunnel syndrome (CTS, n = 3) and ten normal controls were studied. After limb cooling in a cold water bath for 30 min, skin temperatures were sequentially obtained from the volar midwrist. Motor conduction velocities were obtained at 2-3 degrees increments between 22 and 33 degrees C. Results indicated a large individual variability; 0.1 to 1.8 in the median and 0.8 to 2.0 m/s/degrees C in the ulnar nerve when all three groups are considered together. There was a significant difference between the correction factors for control v DPN and control v CTS. A significant difference was also present for UPN v DPN and UPN v CTS (p < 0.05). There was a positive correlation (r = 0.746, p = 0.0001) between the baseline conduction velocities and the size of the correction factors in all the subjects. The effect of temperature on MNCV appears to be inversely correlated with the severity of conduction slowing or demyelination. These findings suggest that the use of a correction factor may be invalid when studying a demyelinated nerve, and that the extremity should be warmed to a specific temperature before an electrodiagnostic study.