• Users Online: 304
  • Print this page
  • Email this page

 Table of Contents  
Year : 2020  |  Volume : 37  |  Issue : 4  |  Page : 164-169

Long latency reflexes in patients with postural instability and ataxia

1 Department of Neurology, Adnan Menderes University Medical Faculty, Aydin, Turkey
2 Department of Clinical Neurophysiology, Adnan Menderes University Medical Faculty, Aydin, Turkey
3 Department of Neurology and Clinical Neurophysiology, Adnan Menderes University Medical Faculty, Aydin, Turkey

Date of Submission09-Apr-2020
Date of Decision21-May-2020
Date of Acceptance15-Jun-2020
Date of Web Publication29-Dec-2020

Correspondence Address:
Cengiz Tataroğlu
Department of Neurology, Adnan Menderes University Medical Faculty, 09100 Aydin
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/NSN.NSN_44_20

Rights and Permissions

Objectives: Distal electrical stimulation of an upper extremity mixed nerve can generate a reflex response from the trapezius muscle. This reflex response may have a central neural pathway and can be affected by postural changes. Materials and Methods: In this study, long latency reflexes (LLRs) from both distal and trapezius muscle were evaluated in patients with Parkinson's disease (PD) with and without postural dysfunction and in patients with cerebellar ataxias. Thirty-three patients with PD, 10 patients with degenerative cerebellar ataxia and 22 healthy volunteers were included in the study. LLRs were recorded from ipsilateral thenar and trapezius muscles. Latencies and amplitudes of LLRs obtained from thenar (thenar LLR) and trapezius (trapezius LLR) muscles were analyzed. Results: In patients with PD, thenar LLRs showed significant shortening in the onset latencies and significant increase in the amplitudes in comparison with healthy controls. Trapezius LLRs did not show any significant difference in latencies or amplitudes; however, these responses showed a significant absence in one or two components in patients with Parkinson's disease with postural dysfunction. Additionally, this reflex was not recorded in patients with cerebellar ataxia. Conclusion: Trapezius LLRs can give some information regarding the physiology of neural circuits responsible for postural arrangement. Cerebellar connections may have a major role in the generation of trapezius LLRs.

Keywords: Ataxia, long latency reflexes, Parkinson's disease, postural instability, sensorimotor integration, trapezius

How to cite this article:
Deneri E, Tilek N, Çoban A, Tataroğlu C. Long latency reflexes in patients with postural instability and ataxia. Neurol Sci Neurophysiol 2020;37:164-9

How to cite this URL:
Deneri E, Tilek N, Çoban A, Tataroğlu C. Long latency reflexes in patients with postural instability and ataxia. Neurol Sci Neurophysiol [serial online] 2020 [cited 2023 Mar 27];37:164-9. Available from: http://www.nsnjournal.org/text.asp?2020/37/4/164/305388

  Introduction Top

Long duration and low intensity electrical stimulation of a peripheral nerve can generate late reflex responses from a muscle undergoing a stable voluntary contraction. These responses are known as long latency reflexes (LLRs).[1],[2] These reflexes have been studied in hand muscles.[3],[4] LLRs obtained from intrinsic hand muscles following electrical stimulation of mixed nerves have an early spinal component (HR) and three late components. It is believed that HR is a synonym of monosynaptic H reflex. The second of the late components, which is the most stable (LLR2), is recorded at about 50 ms. It is believed that this component has a transcortical generator.[3],[4],[5] These reflex responses can be accepted as an electrophysiological parameter reflecting central sensorimotor integration.

Recently, LLRs have also been recorded from axial muscles, and some features of these reflexes have been investigated.[1] Electrical stimulation of upper extremity distal mixed nerves can generate a reflex response obtained from the trapezius muscles. This reflex response includes a series of components. The first and second components have been observed more frequently and their latencies are about 30 and 50 ms, respectively. The exact central neural pathway is not known; however, postural changes can affect these reflex responses. We observed in our previous report that postural changes modified the amplitudes of these responses.[1] Therefore, it is postulated that trapezius LLRs may give some information regarding the physiology of central postural adjustments.[1]

We became interested in the behavior of these reflexes in some neurological disorders which influence central postural organization. Postural instability due to Parkinson's disease (PD) and ataxia due to cerebellar involvement are prominent conditions causing posture and gait disturbances. The mechanism of postural instability in PD is not completely understood. However, it is suggested that the pedunculopontine tegmental nucleus might play a role as an interface between the basal ganglia and the cerebellum in stabilizing posture.[6] This nucleus may also have a role in sensorimotor integration.[7]

It seems that disturbances in sensorimotor integration due to neurological disorders can contribute to the development of postural instability. LLRs may give information regarding central sensorimotor integration, and so the analysis of these reflex studies may give valuable information about the appearance of postural instability.

In this study, analyses of LLRs obtained from distal extremity muscles and axial muscles were performed in patients with PD with and without postural instability and in patients with marked cerebellar involvement. The aim was to investigate the effects of different types of postural dysfunction on these reflex responses.

  Materials and Methods Top

Thirty-three patients with PD (14 females and 19 males), 10 patients with cerebellar ataxia (6 females and 4 males) and 22 healthy volunteers (13 females and 9 males) were included in the study. The mean ages of the healthy controls and patients (patients with PD and patients with cerebellar ataxia) were 57.0 ± 7.3, 60.6 ± 6.6, and 62.3 ± 9.0 years, respectively. There was no significant age difference between groups (P > 0.05). Fourteen patients with PD had postural instability, and the patients with PD were divided into two groups in accordance with this finding. The diagnostic criteria of the Movement Disorders Society for PD were used for the diagnosis of PD.[8]

Subjects with Parkinson-plus disease, secondary Parkinsonism, or any systemic disease were excluded from the study. Tremor dominant patients were excluded because this clinical feature may cause difficulty in the stability of voluntary muscle contraction. In addition, subjects with peripheral neuropathy were also excluded from the study.

Patients with both truncal and extremity ataxias on both sides were included to the ataxia group. Patients with pyramidal, extrapyramidal, or mental involvement and dysautonomia were not included in the cerebellar ataxia group. Magnetic resonance imaging investigations disclosed pure cerebellar atrophy in these patients.

All subjects gave informed consent for the study and the study was approved by the local ethics committee.

Clinical evaluation

Unified Parkinson Disease Rating Scale (UPRDS) scores were recorded for every patient with PD. Postural stability was evaluated visually by the pull test. For this test, the individual was moderately pushed backward from the shoulders by the examiner. If the individual could not maintain an upright position, this test was considered as positive and the individual was accepted as having postural instability.[9]

Electrophysiological evaluation

Routine sensory and motor nerve conduction studies of upper and lower extremity peripheral nerves (median, ulnar, tibial, peroneal nerves, and sensory nerve conduction of the sural nerve on one side) were performed in all individuals participating to the study. All patients with PD were in the “on” period of the disease during electrophysiological investigations.

Long latency reflexes

Initially, thenar LLRs were recorded, and then trapezius LLRs were recorded. The recordings of thenar LLR were performed on the right side and then on the left side. At least two traces were recorded and superimposed for each side. The recording was performed using surface cup electrodes with the belly-tendon technique from the abductor pollicis brevis muscle. Square wave electrical pulses were delivered to the median nerve at the wrist level by a standard surface stimulating electrode. Stimulus intensity was set as the stimulus intensity causing just visible motor activity on the median innervated distal muscles. Stimulus duration was 0.5 ms. The stimulus was delivered at random, and interstimulus intervals were about 2–5 s. At least 40 traces were recorded and averaged for each recording. Filter settings were set between 10 Hz and 2 kHz. Sweep duration was 20 ms/div. During the recording, individuals were instructed to maintain a moderate stable isometric muscle contraction (50% of maximal voluntary contraction).

Trapezius LLRs were recorded from the ipsilateral trapezius. Surface cup electrodes were used for recording. An active electrode was placed on the belly of the trapezius at the midpoint between the acromion and spinous process of vertebra C7. A reference electrode was placed over the acromion.

Stimulus intensity was set at twice the motor threshold intensity determined by the recording of the thenar muscle during the analysis of the LLRs of the distal muscle. Other stimulus parameters were similar to distal LLRs. First, right side and then left side stimulations and recordings were performed. During the recording, a moderate stable isometric voluntary contraction of the trapezius was maintained. For this, individuals were instructed to make a shoulder elevation with about 50% of maximal muscle force. The stability of voluntary electromyographic activity was monitored by visual and auditory feedback during the recordings of reflex responses from both the thenar and the trapezius muscles.

Data analysis

Peak-to-peak amplitudes and onset latencies of the early spinal component (HR) and the second long latency component (LLR2) were evaluated.

In the analysis of LLRs obtained from the trapezius muscle, amplitude, and onset latencies of the first and second components were evaluated. The frequency of these components was evaluated both in the patients with PD and in the healthy controls.

Statistical analysis

Descriptive analysis of electrophysiological and clinical data was performed. The Kolmogorov–Smirnov test was used to show normal distribution of variables. Electrophysiological data obtained from patient groups and controls were compared using the one-way analysis of variance test. Homogeneity of variances was tested by post hoc test. Tukey's test was used as post hoc analysis. The Mann–Whitney U -test was used as nonparametric tests. In addition, the Chi-square test was used to test the significance of the frequency of reflex response. Possible relationships between clinical and electrophysiological data were tested by Spearman correlation analysis. P < 0.05 was considered as statistically significant.

  Results Top

Clinical evaluation

The patients with PD included in the study had a duration of the disease ranging from 1 to 35 years. All patients with PD had rigidity and bradykinesia, and 14 out of the 33 patients with PD had postural instability. Seventeen of the patients with PD also had rest tremor. All patients had an akinetic-rigid dominant clinical picture of PD. The mean UPDRS score was 28.1 ± 21.7 (4–88). In addition, the mean motor score of UPDRS was 15.8 ± 10.9 (1–47). Motor findings were markedly unilateral in eight patients with PD. The right side was slightly more affected (in five subjects).

The ataxic patients included in the study had a duration of disease which ranged from 7 to 25 years. All patients had both extremity and truncal ataxia and cerebellar dysartria (pancerebellar syndrome). Ten patients were diagnosed with hereditary cerebellar ataxia and had a family history of degenerative ataxia.

Long latency reflexes obtained from the thenar muscle

The early spinal component of thenar LLR (HR) was recorded in all individuals. Among the later components, the second component of LLR (LLR2) was the most stable. The third component was not observed clearly in any subject, and LLR1 was observed clearly in only four subjects. LLR2 was recorded in all patients with PD.

The latencies of LLR2 obtained from the patients with PD were significantly shorter than those from the healthy controls (P : 0.001). The mean amplitude of the LLR2 was also higher than in the healthy controls [Figure 1]. This difference was more marked in the right sides of the patients and healthy controls. Slight clinical asymmetry between right and left sides may cause this difference. Differences in the thenar LLRs between subgroups are shown in [Table 1].
Figure 1: Long latency reflexes obtained from the thenar muscle (a) and both trapezius muscles (b) in a patient with Parkinson's disease who had rigidity especially on his left side. The second component of the thenar long latency reflex was increased. However, long latency reflexes obtained from the trapezius did not show a significant difference

Click here to view
Table 1: Differences in the thenar long latency reflexes between subgroups

Click here to view

When we compared electrophysiological data between patients with and without postural dysfunction, we found no significant difference.

In patients with ataxia, thenar LLRs showed no significant difference from those of healthy controls [Table 1].

Long latency reflexes obtained from the trapezius

Mean latencies and amplitudes of trapezius LLR did not show significant difference in patients with PD. Furthermore, no significant difference was observed in these parameters between both the patients with and without postural instability and the healthy controls. [Table 2] shows the electrophysiological findings in the patients and controls.
Table 2: Electrophysiological data of long latency reflexes obtained from the trapezius muscle in patients with and without postural instability

Click here to view

Trapezius LLR did not show high stability in healthy controls. Some components may be absent in some individuals. The first component of the trapezius LLR could not be recorded in six individuals (6/44). The second component of the trapezius LLR could not be recorded in nine healthy controls (9/44).

The most conspicuous abnormality of trapezius LLRs was observed in patients with ataxia. Trapezius LLRs were not recorded in any patient with prominent cerebellar dysfunction.

Some components of trapezius LLRs were absent more frequently in patients with PD. In patients with PD without postural instability, the first component of the trapezius LLR could not be recorded in seven extremities (7/38) (P > 0.05). The second component of the trapezius LLR could not be recorded in nine extremities (9/38) (P > 0.05).

In patients with PD with postural instability, the absence of the first component of the trapezius LLR was observed more frequently than in patients without postural instability (14/28 extremities, P : 0.001, χ2: 11.3). Furthermore, the absence of the second component was also observed in patients with postural instability 12/28 (P : 0.03, χ2: 4.2). These results suggest that there were significant decreases in the frequencies of trapezius LLRs in patients with PD with postural instability.

There was no significant correlation between the clinical scales and the electrophysiological data.

  Discussion Top

In the present study, LLRs elicited by electrical stimulation of the median mixed nerve from both axial and distal muscles of the upper extremity were analyzed in patients with cerebellar ataxia and in patients with PD with and without postural instability. We aimed to analyze the effects of postural dysfunction due to PD and diffuse cerebellar involvement on the trapezius and thenar LLRs. Possible effects of postural instability on the trapezius LLRs were our primary interest.

Mean amplitudes of LLR thenar and LLR trapezius showed some differences on the right and left sides in our individuals. However, these differences were not statistically significant. Slight clinical asymmetry in the patients with PD may explain partly this difference.

The trapezius as an axial muscle has an important role in postural adjustments.[10] LLRs obtained from the trapezius have recently been evaluated in various studies.[1],[9],[11] It has been observed that the trapezius muscle has some features which are different from the LLRs obtained from distal extremity muscles. These reflex responses can be influenced by postural changes.[1]

According to our results, cerebellar abnormalities had more impact on the trapezius LLRs than postural instability due to PD. LLRs obtained from distal muscles have been evaluated in a few studies in patients with cerebellar disorders. Claus et al. studied distal LLRs in patients with cerebellar dysfunction. Their patient group was not homogeneous, and patients with Friedreich's disease and focal cerebellar lesions were also included. In the cerebellar atrophy group in that study, some patients also had pyramidal dysfunction. They demonstrated an increase in the amplitudes of the third component of thenar LLR in patients with cerebellar atrophy.[12] However, later components of the reflex responses were not analyzed because it is recorded very rarely.

Disturbance in the coordination between different joints and extremities due to cerebellar dysfunction may be a reason for the missing trapezius LLRs in these patients. Our findings suggested that cerebellar connections may have a role in the generation of trapezius LLRs. The evaluation of trapezius LLR in patients with partial cerebellar involvement such as isolated hemispheric lesions or midline lesions may give additional information regarding the neural substrate of this reflex.

On the other hand, postural instability also had similar but less severe effects on trapezius LLR. This finding may be partly explained by subclinical cerebellar involvement in patients with PD.[13] However, loss of trapezius LLR was mainly observed in patients with postural instability, and degeneration of multiple neural substrates has been observed in PD. Therefore, we suggest that the analysis of trapezius LLRs in PD may give some information regarding the involvement of postural mechanisms.

The pathogenesis of postural instability is not exactly known. However, pedunculopontine nucleus cholinergic neuronal loss may have a role in the postural instability observed in PD.[14] On the other hand, this nucleus has connections with cerebellum and has a role in the integration of sensory inputs. Therefore, its involvement may be a reason for dysfunction in the sensorimotor integration and frequent loss in trapezius LLRs.

LLRs obtained from hand muscles have been studied many times previously in patients with PD.[2],[15],[16],[17] Enhanced amplitude and shortened latency of the second component of this reflex (LLR2) have also been observed previously.[18] In some studies, it was concluded that the main abnormality was increased excitability in the first component in patients with PD.[2] In our study, the LLR2 component was accepted as the most prominent waveform after HR. In some subjects with PD, the first component (LLR1) can be the more prominent waveform. In this condition, certain determination of LLR2 may be difficult, and LLR1 can be erroneously taken as LLR2. This is a limitation of our study.

The exact pathophysiological mechanism causing this finding has not yet been clarified.[16],[17],[19],[20] Increased excitability of the Group II reflex pathway may be responsible for this reflex alteration.[21],[22] Pasquereau and Turner concluded that segmental spinal circuits can be responsible for exaggeration of the long latency stretch reflex.[23] On the other hand, some studies suggest that an excessive corticospinal output and increased excitability of the primary motor cortex has been observed in PD.[24],[25],[26],[27],[28],[29]

In our patients, abnormalities in trapezius LLRs showed some discrepancies from those obtained from thenar LLRs as mentioned above. These differences between the behaviors of the reflexes suggested that the neural substrate or the generator of LLRs obtained from the trapezius is different from LLRs obtained from the distal hand muscle.

Continuation of stable muscle contraction of the trapezius can be more difficult in patients with ataxia and PD. This condition may cause a potential limitation in the evaluation of these reflex responses. Therefore, monitoring of stable voluntary muscle activity was an important issue. Voluntary activity was monitored in this study by visual and auditory feedback during electrophysiological recordings. In addition, tremor dominant patients were not included in the study.

  Conclusion Top

LLRs obtained from the trapezius muscle may reflect the physiology of central postural organization. Cerebellar connections may have a major role in the generation of this reflex. The analysis of this reflex in patients with partial cerebellar involvement may give additional information regarding its neural generator.


The authors would like to thank Mevlut Türe for statistical analysis and Alec Rylands for English revision in the study.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Tataroglu C, Kuçuk FK, Ozkul A. Upper and lower extremity proprioceptive inputs modulate EMG activity of the trapezius. J Electromyogr Kinesiol 2011;21:77-81.  Back to cited text no. 1
Cruccu G, Deuschl G. the clinical use of brainstem reflexes and hand-muscle reflexes. Clin Neurophysiol 2000;111:371-87.  Back to cited text no. 2
Tataroglu C, Sair A, Parlaz A, Deneri E. Effects of 1-hz repetitive transcranial magnetic stimulation on long-latency reflexes and cortical relay time. J Clin Neurophysiol 2011;28:319-22.  Back to cited text no. 3
Tsuji T, Rothwell JC. Long lasting effects of rTMS and associated peripheral sensory input on MEPs, SEPs and transcortical reflex excitability in humans. J Physiol 2002;540:367-76.  Back to cited text no. 4
Tataroglu C, Genc A, Idiman E, Cakmur R, Idiman F. Cortical relay time for long latency reflexes in patients with definite multiple sclerosis. Can J Neurol Sci 2004;31:229-34.  Back to cited text no. 5
Mori F, Okada KI, Nomura T, Kobayashi Y. The pedunculopontine tegmental nucleus as a motor and cognitive interface between the cerebellum and basal ganglia. Front Neuroanat 2016;10:109.  Back to cited text no. 6
Müller ML, Albin RL, Kotagal V, Koeppe RA, Scott PJ, Frey KA, et al . Thalamic cholinergic innervations and postural integration function in Parkinson's disease. Brain 2013;136:3282-9.  Back to cited text no. 7
Postuma RB, Berg D, Stern M, Poewe W, Olanow CW, Oertel W, et al . MDS clinical diagnostic criteria for Parkinson's disease. Mov Disord 2015;30:1591-9.  Back to cited text no. 8
Goetz CG, Tilley BC, Shaftman SR, Stebbins GT, Fahn S, Martinez-Martin P, et al . Movement disorder society UPDRS revision task force. Movement disorder society-sponsored revision of the unified Parkinson's disease rating scale (MDSUPDRS): Scale presentation and clinimetric testing results. Mov Disord 2008;23:2129-70.  Back to cited text no. 9
Dimitrova D, Horak FB, Nutt JG. Postural muscle responses to multidirectional translations in patients with Parkinson's disease. J Neurophysiol 2004;91:489-501.  Back to cited text no. 10
Alexander CM, Harrison PJ. Reflex connections from forearm and hand afferents to shoulder girdle muscles in humans. Exp Brain Res 2003;148:277-82.  Back to cited text no. 11
Claus D, Schöcklmann HO, Dietrich HJ. Long latency stretch responses in cerebellar diseases. Eur Arch Psychiatry Neurol Sci 1986;235:355-60.  Back to cited text no. 12
Wu T, Hallett M. The cerebellum in Parkinson's disease. Brain 2013;136:696-709.  Back to cited text no. 13
Muller ML, Bohnen NI. Cholinergic dysfunction in Parkinson's disease. Curr Neurol Neurosci Rep 2013;13:377-9.  Back to cited text no. 14
Lee RG, Tatton WG. Motor responses to sudden limb displacements in primates with specific CNS lesions and in human patients with motor system disorders. Can J Neurol Sci 1975;2:285-93.  Back to cited text no. 15
Berardelli A, Sabra AF, Hallett M. Physiological mechanisms of rigidity in Parkinson's disease. J Neurol Neurosurg Psychiatry 1983;46:45-53.  Back to cited text no. 16
Rothwell JC, Obeso JA, Traub MM, Marsden CD. The behaviour of the long-latency stretch reflex in patients with Parkinson's disease. J Neurol Neurosurg Psychiatry 1983;46:35-44.  Back to cited text no. 17
Yavuz D, Gündüz A, Ertan S, Apaydın H, Sifoglu A, Kiziltan G, et al . Specific brainstem and cortico-spinal reflex abnormalities in coexisting essential tremor and Parkinson's disease (ET-PD). Neurophysiol Clin 2015;45:143-9.  Back to cited text no. 18
Tatton WG, Bedingham W, Verrier MC, Blair RD. Characteristic alterations in responses to imposed wrist displacements in Parkinsonian rigidity and dystonia musculorum deformans. Can J Neurol Sci 1984;11:281-7.  Back to cited text no. 19
Haslinger B, Erhard P, Kämpfe N, Boecker H, Rummeny E, Schwaiger M, et al . Event-related functional magnetic resonance imaging in Parkinson's disease before and after levodopa. Brain 2001;124:558-70.  Back to cited text no. 20
Marchand-Pauvert V, Gerdelat-Mas A, Ory-Magne F, Calvas F, Mazevet D, Meunier S, et al . Both L-DOPA and HFS-STN restore the enhanced group ii spinal reflex excitation to a normal level in patients with Parkinson's disease. Clin Neurophysiol 2011;122:1019-26.  Back to cited text no. 21
Simonetta Moreau M, Meunier S, Vidailhet M, Pol S, Galitzky M, Rascol O. Transmission of group II heteronymous pathways is enhanced in rigid lower limb of de novo patients with Parkinson's disease. Brain 2002;125:2125-33.  Back to cited text no. 22
Pasquereau B, Turner RS. Primary motor cortex of the parkinsonian monkey: altered neuronal responses to muscle stretch. Frontiers Syst Neurosci 2013:7;1-14.  Back to cited text no. 23
Abbruzzese G, Berardelli A. Sensorimotor integration in movement disorders. Mov Disord 2003;18:231-40.  Back to cited text no. 24
Kandler RH, Jarratt JA, Sagar HJ, Gumpert EJ, Venables GS, Davies-Jones GA, et al . Abnormalities of central motor conduction in Parkinson's disease. J Neurol Sci 1990;100:94-7.  Back to cited text no. 25
Valls-Solé J, Pascual-Leone A, Brasil-Neto JP, Cammarota A, Mcshane L, Hallett M. Abnormal facilitation of the response to transcranial magnetic stimulation in patients with Parkinson's disease. Neurology 1994;44:735-41.  Back to cited text no. 26
Tremblay F, Tremblay LE. Cortico-motor excitability of the lower limb motor representation: A comparative study in Parkinson's disease and healthy controls. Clin Neurophysiol 2002;113:2006-12.  Back to cited text no. 27
Lou JS, Benice T, Kearns G, Sexton G, Nutt J. Levodopa normalizes exercise related cortico-motoneuron excitability abnormalities in Parkinson's disease. Clin Neurophysiol 2003;114:930-7.  Back to cited text no. 28
Lefaucheur JP. Motor cortex dysfunction revelaed by cortical excitability studies in Parkinson's disease: Influence of antiparkinsonian treatment and cortical stimulation. Clin Neurophysiol 2005;116:244-53.  Back to cited text no. 29


  [Figure 1]

  [Table 1], [Table 2]

This article has been cited by
1 Effects of Perturbation Velocity, Direction, Background Muscle Activation, and Task Instruction on Long-Latency Responses Measured From Forearm Muscles
Jacob Weinman,Paria Arfa-Fatollahkhani,Andrea Zonnino,Rebecca C. Nikonowicz,Fabrizio Sergi
Frontiers in Human Neuroscience. 2021; 15
[Pubmed] | [DOI]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Materials and Me...
Article Figures
Article Tables

 Article Access Statistics
    PDF Downloaded283    
    Comments [Add]    
    Cited by others 1    

Recommend this journal