Effects of sex and age on strength-duration properties.

OBJECTIVE: To evaluate the possible effects of sex and age on strength-duration time constant (SDTC). METHODS: The SDTC of 126 healthy volunteers was measured following stimulation of right median nerve at the wrist. Variations in values were evaluated according to sex and age. RESULTS: The SDTC was 438.6+/-114.5 micros in women and 396.2+/-90.3 in men (P=.023). In men, as age increased, so did SDTC. However, this was not true in women. Comparing the values of women and men, aged below 40, demonstrated a difference in excitability, confined to younger patients. CONCLUSIONS: As SDTC depends on the biophysical properties of the axonal membrane and can provide some information about Na(+) channel function, these data raise the possibility of a difference in Na(+) channel function between men and women and a difference in the conductance with age. SIGNIFICANCE: The age- and sex-related differences shown in this study suggest a possible biochemical or hormonal influence on axonal excitability.     

Effects of botulinum toxin on strength-duration properties

Axonal excitability studies have been used in several diseases to investigate the underlying pathophysiology. The threshold tracking technique was developed to measure noninvasively several indices of axonal excitability, such as strength-duration properties. This study investigated the possible effects of botulinum toxin on strength-duration time constant (SDTC) in patients with the symptoms and signs of botulism. The clinical and electrophysiological findings of 13 patients who were admitted to the authors' clinic with botulism signs and symptoms were evaluated in a 5-day period after exposure to the toxin prospectively. After routine diagnostic electroneuromyographic examinations and electromyogram with repetitive nerve stimulation at 20-50 Hz, SDTC was studied. The results were compared with 13 age- and sex-matched healthy volunteers. The SDTCs were 381 +/- 60 micros and 471 +/- 84 micros in patients and controls, respectively. There was a statistical difference between the two groups (p = .003, Mann Whitney U test). These findings suggest a possible effect of botulinum toxin, known to be effective at neuromuscular junction, on Na(+)/K(+) pump activity, and Na(+) or K(+) conductance.     

The effect of hyperventilation on downbeat nystagmus in cerebellar disorders.

Hyperventilation can affect nystagmus in patients with vestibular disorders. However, the effects on nystagmus in patients with cerebellar disease have not been systematically studied. Using the magnetic field search coil technique, we studied the effects of hyperventilation on nystagmus in a series of cerebellar patients. In four of eight patients, hyperventilation produced an increase in the slow-phase velocity of downbeat nystagmus. We speculate that this effect may be mediated through metabolic effects on cerebellar calcium channels.     

F-wave-duration in diabetic polyneuropathy

The diagnostic sensitivity of F-wave duration (F_dur) in diabetic polyneuropathy was analyzed. Some patients had abnormal F_dur values with normal minimum F latencies (F_min). The incidence of abnormality for tibial and peroneal F_dur was somewhat more common than for F_min in cases of suspected mild or early phase polyneuropathy. F_dur may provide additional diagnostic information in certain cases, particularly those in which there is mild polyneuropathy. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21: 246–249, 1998     

The effect of skin temperature on vibratory sensitivity in polyneuropathy.

In normal subjects, a rise in skin temperature causes a decrease in vibratory perception thresholds. In this study, vibratory thresholds on the foot were measured before and after local warming of the skin in patients with diabetic or uraemic neuropathy. On warming, the thresholds increased in nine of 11 diabetic patients while they decreased in 10 of 13 uraemic patients. In two-thirds of the patients, the response was outside the range of normal short term variation.     

人神经生长因子对DPN大鼠坐骨神经CGT的作用

目的　观察人神经生长因子 ( h NGF)对早期糖尿病多发性神经病 ( DPN)大鼠坐骨神经中半乳糖神经酰胺转移酶 m RNA( CGTm RNA)表达的影响。方法　用链脲佐菌素 ( STZ)一次性腹腔注射诱导糖尿病大鼠模型 ,在 DPN 4周 (造模后 4周 )腹腔注射 h NGF( 90 U .kg- 1 .d- 1 ) ,共 4周。用 RT- PCR和免疫组化方法观察坐骨神经CGTm RNA,NGFm RNA和蛋白表达。结果　 DPN 8周大鼠坐骨神经 CGTm RNA升高 ,NGFm RNA和蛋白表达减少。用 h NGF治疗的 DPN大鼠 CGTm RNA明显降低 ,NGFm RNA和蛋白表达增加。结论　 h NGF治疗能纠正早期DPN大鼠坐骨神经 CGTm RNA异常     

The standardization of hyperventilation on EEG recording in childhood. I. The quantity of hyperventilation activation

In thirty-seven children free of neurological symptoms, we attempted the standardization of hyperventilation on EEG. We also attempted to determine the quantity of hyperventilation activation necessary to produce equivalent degrees of EEG slowing at different ages. The respiratory rate (RR), total expiratory volume/min (VE), O2 consumption volume/min (VO2), expiratory CO2 volume/min (VCO2), tcpO2 and tcpCO2 were monitored before, during and after hyperventilation. The optimal conditions for adequate activation were found to be: a respiratory rate of 30/min, a 3-fold elevation of VE and a duration of 4 minutes. With this activation, the degree of EEG slowing was found to be nearly inversely proportional to the age (in the age range of 6 years to 17 years old). Therefore, this activation may be adequate and useful for evaluating the EEG development in childhood. As to the relationship between the appearance of EEG slowing and changes in respiratory factors, the pCO2 decrease and the cerebral blood flow decrease, which may be evoked by the pCO2 decrease, are the most fundamental factors that produce EEG slowing during hyperventilation. The difference in the response on hyperventilation between children and adults may be due to age-related CNS sensitivity to CO2 and/or cerebral vascular CO2 responsiveness.     

Gallbladder hypomotility in diabetic polyneuropathy

This study was performed to evaluate the gallbladder motility in long-standing diabetes mellitus. The gallbladder function of diabetic patients was measured by means of quantitative hepatobiliary scintigraphy, and the severity of the associated autonomic and sensory polyneuropathy was determined. The presence of a marked gallbladder hypomotility was established, and a positive correlation was observed between the severity of the autonomic disturbance and the contractile disorder. This study underlines the important role of the neuropathy in the development of gallbladder hypomotility accompanying long-term diabetes mellitus.     

The extracellular matrix of peripheral nerve in diabetic polyneuropathy

The pattern of collagenisation in peripheral nerve in diabetic polyneuropathy was examined in nerve biopsy specimens from patients with diabetic polyneuropathy in comparison with organ donor control nerves and disease controls (other neuropathies). There was increased endoneurial collagenisation both in the diabetic polyneuropathy cases and the disease controls, this predominantly involving types I and III. Type II collagen was not detected in organ donor control nerves or in the diabetic and the disease control nerves. There was a relative increase in type VI collagen in the endoneurium in the diabetic nerves immediately surrounding groups of Schwann cells. This was not a feature in the other neuropathies. The quantity of types IV, V and VI collagen was increased around the endoneurial microvessels in the diabetic patients and, to a lesser extent, in those with hereditary motor and sensory neuropathy (HMSN). Increased deposition of types IV and V collagen was observed in the perineurium in the diabetic nerves, the latter being most evident in the innermost lamellae where the amount of laminin was possibly also increased. The diameter of the general endoneurial collagen fibrils was greater in the diabetic nerves, although this was not more than in a disease control (HMSN). The collagen fibrils that were present within the basal laminal tubes that had surrounded degenerated myelinated fibres in the diabetic nerves, and those within the onion bulbs of the HMSN cases, were of the normal endoneurial calibre. The expression of laminin by Büngner bands in diabetic neuropathy did not differ from that in disease control nerves, nor were any differences detected for fibronectin. Whether the changes observed are important for the impaired regenerative capacity in diabetic neuropathy requires further investigation. Received: 11 August 1997 / Revised, accepted 16 August 1999     

Muscle fiber conduction abnormalities in early diabetic polyneuropathy.

OBJECTIVE: Diabetic polyneuropathy (PNP) has been proposed to be a primary disorder of sensory nerves. At an early stage motor nerve conduction velocity (MNCV) and muscle strength remain preserved due to compensatory mechanisms (axonal sprouting, reinnervation). We evaluated the use of invasive muscle fiber conduction velocity (MFCV) measurements as a method to detect muscle fiber denervation atrophy, as an early sign of motor axonal loss in diabetes mellitus (DM). METHODS: Twelve selected male patients (8 type 1, 4 type 2; mean age 35.8 years, SD 10.6), without any sign of micro- or macroangiopathy, were studied by systematic clinical and neurophysiological testing including MFCV estimation. RESULTS: Hand-held dynamometry was normal in all subjects. There were no signs of recent denervation by concentric needle EMG in any of the patients. Sensory nerve conduction velocity (SNCV) was abnormal in 6 subjects, MFCV in 6 subjects (5 had also low SNCV). The ratio of fastest/slowest muscle fibers in MFCV was correlated to SNCV of sural nerve (-.59, p < .05), but not to MNCV. CONCLUSIONS: Half of the clinically asymptomatic DM subjects showed sensory involvement together with MFCV abnormalities, despite normal needle EMG and force. SIGNIFICANCE: MFCV estimation offers a sensitive method in detecting early signs of motor axonal dysfunction in DM.     

Conduction slowing in diabetic distal polyneuropathy

The pathophysiologic significance of motor conduction slowing observed in diabetic distal symmetrical polyneuropathy (DSP) remains controversial. We have used multiple linear regression analysis of compound muscle action potential (CMAP) amplitude vs. motor conduction velocity (CV) and distal latency (DL) in 57 patients with diabetic DSP and 34 patients with amyotrophic lateral sclerosis (ALS) to determine whether motor conduction slowing in diabetic DSP is due mainly to loss of large axons as in ALS or whether there is an additional demyelinative component. We found amplitude-dependent slowing of CV and DL in both diabetic DSP and ALS in the upper and lower extremities, consistent with a loss of large myelinated fibers. However, in diabetic DSP, there was also significant amplitude-independent slowing in intermediate but not distal nerve segments, supportive of an additional demyelinative component. CMAP amplitude vs. CV and DL regression analyses using ALS as a control group for relatively pure axon loss may provide pathophysiologic information about motor nerves in other neuropathic disorders.     

Increased endoneurial albumin in diabetic polyneuropathy

Albumin was measured in the endoneurium of fascicular biopsies of sural nerves and in plasma from diabetic patients with polyneuropathy by solid phase radioimmunoassay, and normalized to total endoneurial and plasma protein, respectively, to obtain an index of the blood-nerve barrier (BNB-Index). Fifteen diabetic patients with polyneuropathy had a mean BNB-Index of 29.7 +/- 12.6% SD, 3.8 times higher than control values (7.8 +/- 2.0% SD, n = 4). These data suggest that the blood-nerve barrier of endoneurial capillaries is impaired in patients with diabetic polyneuropathy.     

Paranodal structure in diabetic sensory polyneuropathy

Observations have been made on the structure of the paranodal region at nodes of Ranvier in the sural nerve of patients with diabetic sensory polyneuropathy. The structure of the paranodes was examined with particular attention to the definition and assessment of axoglial dysjunction, which has been claimed to be a characteristic feature of both human and experimental diabetic neuropathy and which has been related to paranodal swelling. In the present series of cases it was not possible to confirm that axoglial dysjunction is a distinctive feature of diabetic polyneuropathy in fibres not undergoing active demyelination or wallerian-type degeneration, neither was excessive paranodal enlargement found. Received: 11 March 1996 / Revised, accepted: 10 June 1996     

Single-fiber electromyography in diabetic peripheral polyneuropathy

In this study we examined the value of single-fiber electromyography (SFEMG) in assessing the degree of reinnervation in diabetic patients with clinical neuropathy. Relationships between reinnervation and the degree of metabolic control, and/or duration of diabetes were examined. Thirty-six insulin-dependent diabetics and 54 non-insulin-dependent diabetics underwent SFEMG examination of the tibialis anterior muscle, as well as conventional nerve conduction studies of the upper and lower limbs. All patients examined exhibited some abnormality of SFEMG even in the presence of normal nerve conduction studies found in 18% of patients. In diabetic patients, the jitter in the tibialis anterior muscle correlated positively with glycosylated hemoglobin; whereas lower limb nerve conduction studies did not correlate with this measure of diabetic control. These data suggest that SFEMG is a sensitive measure of nerve function and reinnervation and that it may reflect the dynamic changes in metabolic status in diabetic patients. © 1996 John Wiley & Sons, Inc.     

Sensory testing versus nerve conduction velocity in diabetic polyneuropathy.

We sought to evaluate the utility of quantitative sensory testing (QST) and nerve conduction velocity (NCV) studies as measures of distal symmetric polyneuropathy (DSP). We studied 36 diabetic patients divided into four clinical categories of increasing severity. QST included thermal testing and vibration thresholds. NCV studies included median, peroneal, and sural nerves. Results of QST and NCV were compared among clinical groups using survival methodology. The log-rank statistic showed significant differences among the groups; the direction of the differences were consonant with clinical severity. For each diabetic patient, the result of each measurement was classified as normal or abnormal; more diabetic patients had abnormal NCV than either vibration tests or thermal tests. In conclusion, findings of QST and NCV are in keeping with clinical categorization of patients, QST and NCV are complementary tests, and the sural sensory study is the best single predictor of DSP.