Oral fluoroquinolones for maintenance treatment of melioidosis

Fifty-three hands with carpal tunnel syndrome had pre- and postoperative evaluations of median nerve distal motor latency (from wrist to thenar muscles) and orthodromic sensory nerve conduction velocity (from thumb and middle finger to wrist). At 6 months we observed a neurophysiological return to normal in all cases with normal preoperative distal motor latency and in about 50% of the hands with preoperative distal motor latency between 4 and 6 ms. Prolongation of the distal motor latency over 6 ms was not followed by return to neurophysiological normality, although some degree of sensory function was restored in the majority of cases.     

The usefulness of central motor conduction studies in the localization of cord involvement in cervical spondylytic myelopathy

Cervical spondylytic myelopathy (CSM) is common. Magnetic resonance imaging (MRI), although sensitive, often reveals extensive and sometimes clinically irrelevant findings. The purpose of this study was to investigate the usefulness of central motor conduction studies in localizing the rostral level of cord involvement in 6 patients with CSM. Central motor conduction was assessed using high-voltage stimulation for the spinal roots and magnetoelectrical stimulation for the motor cortex, recording from "marker muscles" innervated by successively higher cervical cord segments. Abnormal central motor conduction affected all subjects at C8-T1, 5 subjects at C7, but none at the C5-C6 levels. The MRI showed abnormalities at multiple levels as high as C4. Our results suggest that central motor conduction studies are helpful in localizing the clinically relevant levels of spinal cord compression in CSM and correlate well with motor abnormalities on clinical examination.     

Gleanings about dentistry from the world of literature

Due to the motor evoked potentials recorded in limb muscles after transcranial and spinal magnetic stimulation, conduction in the central motor pathways can now be evaluated safely and painlessly in man. The central motor conduction time obtained includes the time required for transmission, along the fast pyramidal fibres, from the cortex to the spinal motoneurons, the synaptic transmission to motoneurons and the conduction on a short segment of the motor nerve root. Lengthening of this time almost always reflects dysfunction of the central motor pathways. The abnormalities observed are not specific of any particular cause, and they must be interpreted in relation to the context. The usefulness of this new electrophysiological technique is being tested by radiological and anatomico-clinical correlations in various diseases of the central nervous system (e.g. disseminated sclerosis, cerebral infarction, spinal cord injury) and the locomotor apparatus (e.g. cervical myelopathy, radiculopathy).     

Central motor conduction in motor neuron disease

Central motor conduction time (CMCT) to abductor digiti minimi (ADM) and tibialis anterior (TA) was measured in 21 patients of motor neuron disease (MND). In the upper limb, the motor pathways were inexcitable in 13 and central motor conduction time (CMCT-ADM) was prolonged in 7 sides. In the lower limbs the motor pathways were inexcitable in 10 and CMCT-TA was prolonged in 14 sides. The CMCT abnormalities did not follow a constant pattern but were randomly distributed and were asymmetric in the upper limbs in 7 and lower limbs in 3 patients. Asymmetric and randomly focal abnormalities in central motor conduction in our patients are consistent with asymmetric and focal neuronopathy in MND.     

Cancer incidence of sulfite pulp workers in Denmark

A follow-up clinical study, peripheral motor and sensory nerve conduction velocities and central motor conduction by magnetic stimulation of the cortex were performed in 13 patients with classical Friedreich's ataxia (FA) phenotype, for a period of 9-12 years. Clinical worsening was unrelated to peripheral nerve abnormalities. The amplitude of the nerve action potentials and delayed conduction velocity remained unchanged for several years. Central motor conduction times were abnormal in all patients. Clinical conditions worsened significantly between successive examinations with significant increments in threshold and significant decrement of the amplitude of motor evoked potentials. The results are consistent with progressive pyramidal and cerebellar pathways involvement as the cause of clinical worsening in FA.     

Subacute multifocal painful neuropathy with spontaneous remission

We present the cases of two patients with subacute onset of multifocal painful neuropathy with spontaneous remission and no relapse. The distribution of pain in patient 1 was hands (median > ulnar nerve region) and feet (peroneal and terminal tibial nerve regions), and in patient 2, hands (ulnar nerve region) and feet, left worse than in right. Both patients experienced facial numbness. Deep tendon reflexes were intact except for absent ankle jerks in patient 2. Motor nerve conduction studies demonstrated a marked prolongation of the distal motor latencies with normal proximal segment conduction velocities, suggesting distal demyelination. Cerebrospinal fluid protein concentration was elevated in patient 2, but no definite abnormality was found on sural nerve biopsy. A demyelinating neuropathy with a monophasic self-limited course may be consistent with Guillain-Barre syndrome (GBS). However, the multifocal painful sensory symptoms with facial numbness and the marked distal nerve conduction slowing in our cases are not consistent with GBS.     

Effects of birch pollen-specific immunotherapy on apple allergy in birch pollen-hypersensitive patients

Electrophysiological testing remains an important efficacy parameter in clinical neuropathy trials. The quality of nerve conduction studies in reported trials varies greatly, and may be responsible for negative results. We report the utilization of an expert core lab for electrophysiological testing. With the core lab, the variability of repeat testing is comparable to that of a single, excellent laboratory. Motor conduction velocities demonstrated a coefficient of variation of 3% and sensory conduction velocities 4% across 60 study sites. The distal motor evoked potential amplitudes varied by 13% at the ankle, and 10% at the wrist. The sensory potential amplitudes varied by 16% at the ankle, and 11% at the wrist in 60 sites. The overall monitoring rate in all submitted nerve conduction tracings was 36.6%. Our results show that an expert core lab can improve the electrophysiological quality of clinical trial data with the potential to show small changes in nerve conduction velocities and in both motor and sensory potential amplitudes.     

Abdominal wall metastases in incidental gallbladder carcinoma--different incidence after laparoscopic and open surgery?

We investigated 303 diabetic patients in order to clarify the relationship between progression of diabetic polyneuropathy and conduction delay across the carpal tunnel. Distal latency ratio (DLR) was determined by comparison of distal motor latency of the median nerve with that of the ulnar nerve. Lower extremity polyneuropathy index (LPNI), expressed as a mean percentage of the normal for six indices over two nerves obtained by motor nerve conduction studies, was 82.9% on the average in the patients. Their DLR (1.44 +/- 0.24) was larger than the normal value (1.29 +/- 0.10). About 30% of the diabetics had abnormal DLR, especially in women its incidence was as high as 39%. The lower the LPNI level, the larger the incidence of abnormal DLR. In diabetic polyneuropathy patients peripheral nerves will become fragile, which might increase the incidence of conduction delay across the carpal tunnel. This phenomenon might also be called as 'double crush syndrome'.     

Reversal of defective nerve conduction with vitamin E supplementation in type 2 diabetes: a preliminary study

OBJECTIVE: The present study has examined the effect of vitamin E, the principal modulator of free radical activity, on electrophysiological parameters in patients with diabetic peripheral sensorimotor polyneuropathy, matched for duration of disease and metabolic control. RESEARCH DESIGN AND METHODS: A total of 21 subjects with type 2 diabetes were enrolled in this double-blind randomized placebo-controlled study (vitamin E, 11 patients; placebo, 10 patients). Patients were randomly assigned to receive either 900 mg vitamin E or placebo for 6 months. The average dietary vitamin E consumption of the subjects was similar during the study. The main outcome measure was the electrophysiological tests assessing nerve conduction. Fasting plasma glucose, HbA1, postprandial plasma glucose, and electrophysiological parameters in the basal state and after 6 months of treatment were studied. RESULTS: Glycemic indexes did not show any significant changes during the study, whereas nerve conduction improved significantly in 2 of the 12 studied electrophysiological parameters after 6 months in patients on vitamin E supplementation. The changes in the electrophysiological parameters were obvious in the median motor nerve fibers and tibial motor nerve fibers. Nerve conduction velocity in the median motor nerve fibers (P = 0.0019) and tibial motor nerve distal latency (P = 0.0284) improved significantly after 6 months of vitamin E supplementation. CONCLUSIONS: This study shows that defective nerve conduction in diabetic subjects with mild-to-moderate peripheral neuropathy may be improved by pharmacological doses of vitamin E supplementation. Further studies with a larger number of patients for longer periods of time are needed.     

BDNF attenuates functional and structural disorders in nerves of galactose-fed rats

Galactose intoxication of rats was used to disrupt metabolism of Schwann cells and skeletal muscle, two sites that contain the polyol-forming enzyme aldose reductase (AR). Galactose-fed rats develop a neuropathy characterized by nerve conduction deficits and axonal atrophy. To investigate the possibility that galactose metabolism by AR influences axonal function and structure by altering production of neurotrophic factors, the impact of galactose intoxication on nerve and muscle BDNF levels and the effects of exogenous BDNF treatment on galactose neuropathy were examined using biochemical, electrophysiologic and morphometric techniques. Galactose feeding increased BDNF protein in peripheral nerve and muscle. Exogenous BDNF treatment attenuated motor nerve conduction velocity deficits in the sciatic nerve of galactose-fed animals and myelin splitting of motor axons in the ventral root. In contrast, sensory nerve conduction velocity (SNCV) deficits in the sciatic nerve and myelin splitting in the central projections of sensory neurons were not prevented by BDNF treatment. BDNF treatment did not attenuate reduced axonal caliber in the sciatic nerve, but did ameliorate the diminution of the caliber of central sensory projections in the dorsal root. These findings point to the potential use of BDNF in the treatment of peripheral neuropathies.     

A family with neurogenic atrophy of the distal muscles of the upper limbs: clinical and electrophysiological studies

A Chinese family manifested mild neurogenic atrophy of the distal muscles of the upper limbs. None of the affected members had sensory abnormalities, or pyramidal tract or bulbar involvement. The onset of the illness was in the middle of the second decade of life. The muscle atrophy was more severe in the female members. Electromyographic examination of the atrophic muscles showed evidence denervation. One female patient demonstrated slow motor conduction velocity in the right median nerve.     

Mechanisms of motor dysfunction after transient MCA occlusion: persistent transmission failure in cortical synapses is a major determinant

BACKGROUND AND PURPOSE: Failure of prompt motor recovery after spontaneous recirculation or thrombolytic therapy may be due to an unsatisfactory restoration of synaptic activity within cortex and/or blockade of electrical impulses at the severely ischemic subcortical region. METHODS: Afferent, efferent, and synaptic activities were focally examined within the rat sensorimotor cortex by recording the somatosensory-evoked potential (SEP) and motor area response evoked by stimulation of premotor afferents (PmEP) intracortically and the motor-evoked potential (MEP) generated by stimulation of the forelimb area from the brain stem. The effect of ischemia on electrical activity in the cortex and on axonal conduction in the subcortical region was studied differentially by proximal or distal occlusion of the MCA. RESULTS: MEP consisted of direct and indirect waves generated by direct activation of pyramidal axons and indirect excitation of pyramidal neurons via cortical synapses, respectively. MEP, PmEP, and SEP disappeared on proximal occlusion. Following reperfusion after 1 to 3 hours of ischemia, the direct wave of MEP readily recovered but the indirect wave showed no improvement, suggesting a restored axonal conduction but impaired cortical synaptic transmission. The synaptic defect, which also caused a poor recovery in PmEP and SEP and on electrocorticogram, was persistent and detected 24 hours after 1 hour of proximal occlusion. CONCLUSIONS: Our data suggest that motor dysfunction is caused by loss of cortical excitability and blockade of motor action potentials at the subcortical level during ischemia. After brief transient ischemia, axonal conduction readily recovers; however, a persistent transmission failure at cortical synapses leads to motor dysfunction.     

Hydroxylamine blocks adenosine A1 receptor-mediated inhibition of synaptic transmission in rat hippocampus

BACKGROUND AND PURPOSE: Stroke-induced hemiparesis involving the arm and hand results in regular, repeated overuse of the opposite hand and wrist. Because repetitive hand and wrist movement is a common cause of carpal tunnel syndrome (CTS), we examined the nonparetic upper limb in stroke patients for evidence of CTS. METHODS: We measured bilaterally sensory nerve conduction velocity (SNCV), motor nerve conduction velocity (MNCV), sensory nerve action potentials (SNAP) at the wrist, palm-to-wrist distal sensory latency (DSL), palm-to-wrist SNAP, compound motor action potentials (CMAP), and distal motor latency (DML) in stroke patients and control subjects. Controls were right-handed, >/=65 years old, lucid, independent in their activities of daily living, and had no disease known to cause CTS. Stroke patients were divided into a functioning hand group (n=61) and a disused hand group (n=71). All patients had hemiplegia. RESULTS: Tinel's sign was observed on the nonparetic side in 57.7% of patients with a disused hand and in 31.1% of those with a functioning hand. All electrophysiological indices were significantly more abnormal on the nonparetic side than on the hemiparetic side or in controls. Patients with a disused hand showed greater abnormality on the nonparetic side in SNCV, SNAP, palm-to-wrist DSL, DML, and CMAP than patients with a functioning hand. CONCLUSIONS: Overuse of the nonparetic hand and wrist of the nonparetic side may result in CTS in stroke patients, especially when the paretic hand is not functional. Wrist splinting or other prophylactic treatments beginning soon after stroke might help to prevent CTS.     

A new method to determine pudendal nerve motor latency and central motor conduction time to the external anal sphincter

By placing the earth electrode between the site of the stimulus and the site of derivation, peripheral motor latency to the external anal sphincter can be determined and thus central motor conduction time (CMCT) can be calculated. In 18 volunteers we found a total motor conduction time of 19.4 msec (S.D. 1.71) after stimulation of the motor cortex and recording above the external anal sphincter. Latency was 5.6 msec (S.D. 0.66) when stimulated above L1 and pudendal latency (MEPuL) after stimulation above S3 was 2.5 msec (S.D. 0.32). CMCT to L1 (TMCT minus MCT to L1) was 13.8 msec (S.D. 1.13) and to S3 (TMCT minus MEPuL) it was 16.9 msec (S.D. 1.67). This method allows us to locate spinal dysfunction more precisely and also improves diagnosis of a possible neuropathy of the pudendal nerve.     

Computer in child psychotherapy--on the use of computer games in child guidance counseling]

The authors report a comparative study of peripheral nerve conductions and nerve biopsy and somatosensory evoked potentials between 15 patients with Friedreich's ataxia and 15 patients with Friedreich's ataxia phenotype with selective vitamin E deficiency. The patients in the two groups are of similar age, age of onset, and clinical phenotype. Peripheral motor nerve action potential amplitude, and conduction velocities are within normal ranges in the two groups. In the Friedreich's ataxia group there is an early and severe peripheral sensory axonal neuronopathy, characterised by an important reduction of the amplitude of sensory action potential, and important loss of myelinated fibres with complete disappearance of large myelinated fibres without any regenerative process. In the Friedreich's ataxia phenotype with selective vitamin E deficiency group there is slight-to-moderate axonal sensory neuropathy with normal to moderate decrease of large myelinated fibre density and important regeneration in nerve biopsy. Somatosensory evoked potentials are markedly involved in the two groups asserting a severe involvement of somatosensory pathway in lumbar, thoracic and cervical spinal cord. These findings suggest that the pathological mechanism involved in the two diseases are different: central peripheral axonopathy in Friedreich's ataxia and central distal axonopathy in Friedreich's ataxia phenotype with selective vitamin E deficiency.     

Segmental motor conduction time for abductor of the fifth finger muscle: methods and normative values

Electrical stimulation of the ulnar nerves (60 nerves) and magnetic stimulation of the roots (C7) and motor cortex were performed on 30 normal controls. The muscle responses and F wave (peripheral stimulation) were recorded from abductor digiti minimi muscle (60 muscles). The parameters of examined potentials were measured and the central, root, peripheral motor conduction times were estimated. The normative values were established as well as formulae of linear regression within the observed correlations with height. The method may be used for electrophysiological diagnosis of patients with motor pathway impairment at the different levels.     

Physiopathology of amyotrophic lateral sclerosis: the contribution from transcranial magnetic stimulation

INTRODUCTION/OBJECTIVE: The introduction of the technique of magnetic stimulation for the study of motor disorders has led to a better understanding of the pathophysiological mechanisms involved in amyotrophic lateral sclerosis (ALS). MATERIAL AND METHODS: Thirty two patients with ALS were studied in order to describe the behaviour of the variables: central conduction time (CCT), amplitude ratio (Ar) and motor threshold (MT) evaluated by means of motor evoked potentials (MEP). RESULTS: Analysis of these variables showed the great sensitivity of MEP for the detection of abnormalities in the corticospinal tract with 95% of the results being abnormal. Subclinical abnormalities were detected in 22.4% of recordings. Axonal degeneration was the commonest kind of conduction disorder seen. A significant lineal relationship between the evolution time and the variables MT, Ar and CCT (p < 0.05) was demonstrated. This suggests that there is a progressive deterioration of the voluntary motor pathway which begins with an excitotoxic mechanism at the onset of the disease and ends with the death of motor neurones. CONCLUSIONS: The electrophysiological results discussed, together with observations on isolated cases provide evidence in favour of the hypothesis of degeneration of the upper motor neurone. Although it is recognized that this alone does not explain the whole degenerative phenomenon of the motor system which occurs in ALS.     

Conduction velocity along the afferent vagal dendrites: a new type of fibre

1. We systematically calculated the conduction velocity along the peripheral extensions of sensory vagal neurones in cats (the dendrites). In addition, a study of excitability cycle and light microscopic investigation were also conducted on these neurones. 2. The conduction velocity of the three known types of fibres (A, B and C) remains uniform along the dendrites. 3. Another mixed type of fibres exists with a C conduction velocity (mean value 1-5 m/sec) along its distal pathway and a B conduction velocity (mean value 6 m/sec) along its proximal pathway. The change in conduction velocity progressively occurs in the thoraco-cervical portion of the vagus nerve at least 20 mm from the receptor and at least 40 mm from the T cell. 4. The mixed fibres exhibited a C type excitability cycle in their peripheral pathway and a B type excitability cycle in their central pathway. 5. The histological study using the teasing method demonstrated the existence of unmyelinated fibres, in the thoraco-cervical region of the vagus nerve, becoming progressively myelinated from the periphery to the nodose ganglion. These fibres are likely to be the ones showing mixed electrophysiological properties. They represent (approximately) 10% of the vagal nerve population. 6. We propose to call the mixed fibres BC because they present electrophysiological and morphological properties of C fibres in their distal part and properties of B fibres in their proximal part.     

Distribution and latency of muscle responses to transcranial magnetic stimulation of motor cortex after spinal cord injury in humans

Noninvasive transcranial magnetic stimulation (TMS) of the motor cortex was used to evoke electromyographic (EMG) responses in persons with spinal cord injury (n = 97) and able-bodied subjects (n = 20, for comparative data). Our goal was to evaluate, for different levels and severity of spinal cord injury, potential differences in the distribution and latency of motor responses in a large sample of muscles affected by the injury. The spinal cord injury (SCI) population was divided into subgroups based upon injury location (cervical, thoracic, and thoracolumbar) and clinical status (motor-complete versus motor-incomplete). Cortical stimuli were delivered while subjects attempted to contract individual muscles, in order to both maximize the probability of a response to TMS and minimize the response latency. Subjects with motor-incomplete injuries to the cervical or thoracic spinal cord were more likely to demonstrate volitional and TMS-evoked contractions in muscles controlling their foot and ankle (i.e., distal lower limb muscles) compared to muscles of the thigh (i.e., proximal lower limb muscles). When TMS did evoke responses in muscles innervated at levels caudal to the spinal cord lesion, response latencies of muscles in the lower limbs were delayed equally for persons with injury to the cervical or thoracic spinal cord, suggesting normal central motor conduction velocity in motor axons caudal to the lesion. In fact, motor response distribution and latencies were essentially indistinguishable for injuries to the cervical or thoracic (at or rostral to T10) levels of the spine. In contrast, motor-incomplete SCI subjects with injuries at the thoracolumbar level showed a higher probability of preserved volitional movements and TMS-evoked contractions in proximal muscles of the lower limb, and absent responses in distal muscles. When responses to TMS were seen in this group, the latencies were not significantly longer than those of able-bodied (AB) subjects, strongly suggestive of "root sparing" as a basis for motor function in subjects with injury at or caudal to the T11 vertebral body. Both the distribution and latency of TMS-evoked responses are consistent with highly focal lesions to the spinal cord in the subjects examined. The pattern of preserved responsiveness predominating in the distal leg muscles is consistent with a greater role of corticospinal tract innervation of these muscles compared to more proximal muscles of the thigh and hip.     

Histomorphometric study in children with idiopathic nephrotic syndrome

There is agreement on the clinical diagnostic criteria for acute inflammatory demyelinating polyneuropathy (AIDP/GBS) however, there is lack of consensus for detection of demyelination. In order to critically evaluate the prevailing criteria, sixty-six patients who fulfilled NINCDS criteria and had typical features of GBS were studied for electrophysiological abnormalities of peripheral nerves by using standard methods (median, common peroneal, sural and ulnar) between 1 to 12 weeks after the onset of symptoms. The commonest abnormality on motor nerve conduction study was prolonged distal latency (75%-83%) followed by reduction in CMAP amplitude (63%-82%), decreased velocity (48%-62%), conduction block (17%-39%) and f-wave abnormalities (37.8%-59%). Sensory conduction abnormalities were detected in over 20% of median, 25% of ulnar and 33% of sural nerves. All the patients had abnormality of at least two motor conduction parameters in one nerve when values beyond 2 SD of the mean were considered abnormal and over 70% of patients had three abnormalities in two nerves or two abnormalities in three nerves. Comparison with the prevailing criteria for demyelination revealed that the number of patients fulfilling them varied widely: Albers et al. (1985): 74.2%, Albers et al. (1989): 40.9% and Cornblath: 30.3%. We believe that the current criteria for detection of demyelination in acute neuropathy are too strict, underestimate the underlying pathology in GBS and need reassessment.