-
[show abstract]
[hide abstract]
ABSTRACT: Fibromyalgia syndrome is a clinically well-characterized chronic pain condition of high socio-economic impact. Although the pathophysiology is still unclear, there is increasing evidence for nervous system dysfunction in patients with fibromyalgia syndrome. In this case-control study we investigated function and morphology of small nerve fibres in 25 patients with fibromyalgia syndrome. Patients underwent comprehensive neurological and neurophysiological assessment. We examined small fibre function by quantitative sensory testing and pain-related evoked potentials, and quantified intraepidermal nerve fibre density and regenerating intraepidermal nerve fibres in skin punch biopsies of the lower leg and upper thigh. The results were compared with data from 10 patients with monopolar depression without pain and with healthy control subjects matched for age and gender. Neurological and standard neurophysiological examination was normal in all patients, excluding large fibre polyneuropathy. Patients with fibromyalgia syndrome had increased scores in neuropathic pain questionnaires compared with patients with depression and with control subjects (P < 0.001 each). Compared with control subjects, patients with fibromyalgia syndrome but not patients with depression had impaired small fibre function with increased cold and warm detection thresholds in quantitative sensory testing (P < 0.001). Investigation of pain-related evoked potentials revealed increased N1 latencies upon stimulation at the feet (P < 0.001) and reduced amplitudes of pain-related evoked potentials upon stimulation of face, hands and feet (P < 0.001) in patients with fibromyalgia syndrome compared to patients with depression and to control subjects, indicating abnormalities of small fibres or their central afferents. In skin biopsies total (P < 0.001) and regenerating intraepidermal nerve fibres (P < 0.01) at the lower leg and upper thigh were reduced in patients with fibromyalgia syndrome compared with control subjects. Accordingly, a reduction in dermal unmyelinated nerve fibre bundles was found in skin samples of patients with fibromyalgia syndrome compared with patients with depression and with healthy control subjects, whereas myelinated nerve fibres were spared. All three methods used support the concept of impaired small fibre function in patients with fibromyalgia syndrome, pointing towards a neuropathic nature of pain in fibromyalgia syndrome.
Brain 03/2013; · 9.46 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease with variable involvement of other systems. A pathogenetic
role of immune-mediated mechanisms has been suggested. We retrospectively analyzed sural nerve pathology and the clinical
course in 18 patients with ALS. These patients had undergone sural nerve biopsy because of clinical or neurophysiological
signs indicating sensory involvement (ALS+). Eleven of the 18 ALS+ patients had inflammatory cell infiltrates (ALSvasc) resembling infiltrates seen in patients with vasculitic neuropathy. Data were compared with the 7 patients without vasculitic
infiltrates (ALSnonvasc) and with those of 16 patients with isolated peripheral nerve vasculitis (NPvasc). Biopsy specimens were processed with standard histological stains and with immunohistochemistry for a panel of inflammatory
markers, with the hypothesis that the composition of infiltrates should differ between ALSvasc and NPvasc. Immunoreactive cells were quantified in a blinded manner. Unlike patients with NPvasc, those with ALSvasc had only minor neurophysiological abnormalities in the sural nerve and, except for the infiltrates, almost normal nerve morphology
on semithin sections. The difference in epineurial T cell count was significant between ALSvasc and ALSnonvasc (p=0.031). Surprisingly, the cellular composition of epineurial infiltrates in sural nerve biopsies was indistinguishable
between ALSvasc and NPvasc despite a significant difference in fiber pathology (p<0.0001). Standard immunosuppressive treatment did not prevent clinical progression of the motor neuron disease in any of
the patients with ALSvasc. ALSvasc appears as a neuropathological subtype in ALS+ suggesting immune-mediated disease components but without response to standard
immunosuppressive treatment.
KeywordsAmyotrophic lateral sclerosis (ALS)–Sural nerve biopsy–Nonsystemic vasculitic neuropathy
Acta Neuropathologica 04/2012; 122(3):343-352. · 9.32 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Fabry disease (FD) is an X-linked lysosomal storage disorder which may lead to impaired peripheral nerve function, mostly affecting small nerve fibers, and to neuropathic pain. Characteristics of the neuropathy associated with FD and the covariates for its development and temporal course have not been described in a large cohort. We studied small fiber function and morphology in 120 Fabry patients at baseline and in subgroups of these until 4-year follow-up. Baseline neurological (89/120) and electrophysiological (106/120) examination was mostly normal. Quantitative sensory testing revealed impaired cold detection thresholds in 84% of men and 39% of women. Lower leg intraepidermal nerve fiber density (IENFD) was reduced to 46% in Fabry patients compared to controls and to 12.5% in men with impaired renal function. Patients with abnormal IENFD more often had pain. Group means for IENFD did not improve under enzyme replacement therapy (ERT), but IENFD in the back increased under ERT in 4/15 patients with good renal function and clinical improvement. Cutaneous cytokine gene expression did not differ from controls. We conclude that ERT may improve proximal skin innervation in patients with good renal function, but does not protect small fiber function in men with impaired renal function.
Journal of the Peripheral Nervous System 12/2011; 16(4):304-14. · 2.80 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To obtain information on functional integrity of the facial nerve by transcranial electrical motor evoked potentials independent of nerve visualization and to improve prediction of postoperative function.
In a prospective clinical study, 68 patients with cerebello-pontine angle tumors and 5 patients with trigeminal neuralgia were investigated by facial motor evoked potentials (FMEP) elicited by multi-pulse transcranial electrical motor cortex stimulation. For recording the same electrode set-up was used as for continuous EMG monitoring of the orbicularis oculi and oris muscles. Pre-surgical FMEP amplitudes and latencies were correlated with tumor extensions. End to start amplitude ratios were compared to early and long-term facial nerve function by House-Brackmann-Grading (HB) documented by pre- and post-operative photo and video documentation.
Reliable FMEP were obtained in 57 patients. FMEP responses at the start of surgery correlated with the degree of tumor extension. Largest FMEP amplitudes and shortest latencies were found in patients with trigeminal neuralgia. FMEP quality was reduced with increasing tumor extension (P<0.05). The ratio of end-operative to start-operative FMEP-amplitude showed a positive correlation with early and late facial nerve function. Correlation was especially close with early function: an amplitude preservation rate of 86% led to HB°1 or HB°2, of 67% to HB°3, at 33% to HB°4 and at 15% or lower to HB°5 or HB°6.
Initial FMEP amplitudes correlate with the presumed pre-operative nerve affection by space occupying tumors, a phenomenon reported here for the first time. Intact FMEP are highly reliable for preserved nerve continuity and hereby are of special help to the neurosurgeon for those surgical phases where the facial nerve is not visible and still covered by tumor and where conventional EMG monitoring is of very limited use. The end-to-start amplitude ratio of the FMEP is closely related to early and late clinical function. Amplitude reduction by 30% or more should result in a change of microsurgical action to enable fast recovery.
As an adjunct to intraoperative EMG, FMEP are superior in two respects, first in identifying pre-surgical latent nerve lesions and second in monitoring nerve integrity without direct nerve visualization. FMEP are highly reliable in predicting early and late postoperative function.
Clinical neurology and neurosurgery 07/2011; 113(10):872-9. · 1.30 Impact Factor
-
Movement Disorders 02/2011; 26(2):357-8. · 4.51 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We report on magnetic resonance neurography (MRN) as a supplementary diagnostic tool in sciatic nerve injection injury. The object of the study was to test if T2-weighted (w) contrast within the sciatic nerve serves as an objective criterion for sciatic injection injury. Three patients presented with acute sensory and/or motor complaints in the distribution of the sciatic nerve after dorsogluteal injection and underwent MRN covering gluteal, thigh and knee levels. Native and contrast-enhanced T1-w images were employed to identify the tibial and peroneal division of the sciatic nerve while T2-w images with fat suppression allowed visualization of the site and extent of the nerve lesion. MRN in the two patients with clinically severe sensory and motor impairment correctly depicted sciatic injury: continuity of the T2-w lesion within the nerve at the lesion site and distal to it corresponded well to severe injury confirmed by NCS/EMG as axonotmetic or neurotmetic. Topography of the T2-w lesion on cross-section corresponded to predominant peroneal involvement; moreover, associated denervation patterns of distal target muscles were revealed. One of these patients completely recovered with concomitant complete regression of MRN abnormalities on follow-up. The third patient experienced transient sensory and mild motor impairment with complete recovery after 2 weeks. In this patient, T2-w signal within the nerve and distal target muscles remained normal indicating only mild, non-axonal nerve affliction. Our case series shows that MRN can be very useful in precisely determining the site of sciatic injection injury and may provide diagnostic criteria for the assessment of lesion severity and recovery.
Journal of Neurology 01/2011; 258(6):1120-5. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: In focal hand dystonia, long-term potentiation (LTP) and depression (LTD)-like neuronal plasticity, as assessed by paired associative stimulation (PAS) targeting the hand-associated motor cortex, is enhanced and the topographic organization of plasticity is lost. However, if any of these abnormalities alone is sufficient to cause focal dystonia (FD) remains unknown. Ten patients with cervical dystonia (CD), 9 with blepharospasm (BS) and 16 age- and sex-matched controls were examined. PAS was performed by combining repetitively electric stimulation of the median nerve with subsequent transcranial magnetic stimulation of the contralateral motor cortex at 21.5ms (PAS21.5) and 10ms (PAS10). Corticospinal excitability was indexed by the magnitude of motor evoked potentials (MEPs) recorded from abductor pollicis brevis (APB) and abductor digiti minimi (ADM) muscles. In controls, MEP size of the homotopically conditioned APB increased after PAS21.5 whereas the MEP size of the heterotopically conditioned ADM remained stable. PAS10 led to a decrease of MEP size of the APB and to an increase of the heterotopic ADM. In contrast, after PAS21.5 and PAS10 in CD and BS MEP size increased and decreased, respectively, in both muscles. The magnitude of excitability changes, however, did not differ between dystonic patients and healthy controls. In FD the topographic organization of PAS21.5 and PAS10-induced plasticity is deranged in cortical areas not involved in the control of the dystonic body part. Somatotopical disorganization of plasticity may represent an endophenotypic trait in FD but may not be sufficient to generate a dystonic phenotype. Development of a dystonic phenotype may require that the gain of plasticity is additionally enhanced. This article is part of a Special Issue entitled "Advances in dystonia".
Neurobiology of Disease 11/2010; 42(2):171-6. · 5.40 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We report on a 51-year-old woman with episodic ataxia type 2 (EA2) and a novel CaV2.1 C-terminal single amino acid substitution (R2090Q). She had a 4-year history of acute episodes with ataxia, hemihypesthesia and hemicrania. Furthermore, fluctuating neuromuscular transmission abnormalities rarely described in patients with EA2 were clinically and electrophysiologically documented in this patient. Upon initiation of acetazolamide treatment she experienced a dose-dependent severe increase of attack frequency and severity along with a shorter attack duration, while she responded well to subsequent therapy with 4-aminopyridine.
Journal of the neurological sciences 09/2010; 296(1-2):104-6. · 2.32 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We describe an inflammatory myopathy that was symmetrically restricted to both gastrocnemius muscles in a young man. Histopathological findings were typical for polymyositis, but there were neither signs of generalization nor muscle weakness and wasting. This condition was highly sensitive to steroids and has been kept in remission for more than a year using azathioprine. Our findings add another entity to the spectrum of spatially restricted inflammatory myopathies. Muscle Nerve 40: 309-312, 2009.
Muscle & Nerve 09/2009; 40(2):309-12. · 2.37 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Transcranial sonography (TCS) reveals abnormal spatial extension of substantia nigra (SN) echogenicity in a high proportion of patients with Parkinson's disease (PD). It has been proposed that this abnormality represents a structural trait that is mechanistically distinct from degeneration of dopaminergic nigrostriatal projection neurons. We sought to clarify the relationship between sonographic abnormalities of SN and dysfunction of striatal dopaminergic neurotransmission. We studied 50 patients with PD. The spatial extension of the echogenic SN area was compared with the activity of presynaptic striatal dopamine reuptake transporters, assessed in the same patients by I-123-2-beta-carbomethoxy-3-beta-(4-iodophenyl)-tropane (beta-CIT) single-photon emission computed tomography (SPECT). Extension of echogenic SN area correlated (inversely) with striatal activity of presynaptic dopamine reuptake transporter in PD patients (R = -0.417; P = 0.003) and with the equivalent levodopa dose (R = 0.380; P = 0.006; linear regression analysis). Findings support the hypothesis that in PD abnormal extension of echogenic SN area provides a direct structural marker of degeneration of SN neurons. Therefore, in PD, TCS and beta-CIT assess pathophysiologically related phenomena.
Movement Disorders 07/2009; 24(11):1669-75. · 4.51 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The pathophysiology of dystonia is incompletely understood. Unlike many other focal dystonias, cervical dystonia, a frequent dystonia leading to twisting of the head, does not appear to be related to overuse or acquisition of a demanding motor skill. Here, we report development of task-specific dystonia of the neck muscles in a 67-year-old patient following bilateral traumatic arm amputation at the age of 15. To compensate for the amputation, the patient learned to write with a pen held in his mouth. After several years of practicing this unusual and demanding skill, symptoms of task-specific cervical dystonia (CD) developed. This dystonia later became permanent, and independent of the motor activity that initially triggered the dystonic muscular contractions. This singular case raises the possibility that the pathophysiology of CD may share common elements with that of focal dystonias in different body regions.
Movement Disorders 06/2008; 23(7):1041-3. · 4.51 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We evaluated the effect of different manipulations on the performance of a standardized counting task in 7 patients with idiopathic jaw-opening dystonia. Patients used a small stick as sensory stimulus. Following conditions were examined: stick placed between teeth and cheek (CHEEK), biting on stick (TEETH), voluntary jaw occlusion without stick (OCCLUSION). Articulation was rated by patients and experimenters and surface electromyographic activity (EMG) was recorded. Patient-rating (CHEEK - 36.6%, TEETH - 48.1%) and EMG (-18.1%; -17.3%) were significantly improved for conditions using the stick, whereas experimenter-rating showed a trend for TEETH (-16.2%). Although jaw occlusion during speaking deteriorates articulation in healthy subjects, there was no further deterioration in patients and EMG was even significantly reduced (-18.6%). Comparable results were obtained in 1 patient using a special dental device. We conclude that sensory tricks significantly improve subjective and objective parameters. Besides tactile stimulation, altered proprioceptive feedback and antagonist activation may modulate hyperactive dystonic networks.
Movement Disorders 03/2007; 22(3):430-3. · 4.51 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Neuronal plasticity is to be kept within operational limits to serve its purpose as a safe memory system that shapes and focuses sensory and motor representations. Temporal and spatial properties of motor cortical plasticity were assessed in patients with writer's cramp using a model of long-term potentiation (LTP) and long-term depression (LTD) of synaptic efficacy. Paired associative stimulation (PAS) combined repetitive electric stimulation of the median or ulnar nerve (MN or UN) with subsequent transcranial magnetic stimulation of the contralateral dominant motor cortex at 21.5 ms (MN-PAS21.5; UN-PAS21.5) or 10 ms (MN-PAS10). Motor-evoked potentials were recorded from abductor pollicis brevis (APB) muscle and abductor digiti minimi (ADM) muscles in 10 patients with writer's cramp and 10 matched healthy control subjects. Following MN-PAS21.5 or UN-PAS21.5 in non-dystonic subjects, motor responses increased if the afferent PAS-component came from a homologous peripheral region and remained stable with a non-homologous input. In contrast, following either MN-PAS21.5 or UN-PAS21.5, both APB- and ADM-amplitudes increased in patients. Compared with controls, this increase started earlier, its magnitude was larger and its duration longer. Following MN-PAS10 in controls, APB-amplitudes decreased, while ADM-amplitudes increased. In writer's cramp, the decrease of APB-amplitudes started earlier and lasted longer. Of note, ADM-amplitudes were decreased, too. LTP-like as well as LTD-like plasticity is abnormal with respect to both gain and spatial organization. These findings may help to develop a pathophysiological model explaining core features of focal dystonia.
Brain 11/2006; 129(Pt 10):2709-21. · 9.46 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: A novel Hebbian stimulation paradigm was employed to examine physiological correlates of motor memory formation in humans. Repetitive pairing of median nerve stimulation with transcranial magnetic stimulation over the contralateral motor cortex (paired associative stimulation, PAS) may decrease human motor cortical excitability at interstimulus intervals of 10 ms (PAS10) or increase excitability at 25 ms (PAS25). The properties of this plasticity have previously been shown to resemble associative timing-dependent long-term depression (LTD) and long-term potentiation (LTP) as established in vitro. Immediately after training a novel dynamic motor task, the capacity of the motor cortex to undergo plasticity in response to PAS25 was abolished. PAS10-induced plasticity remained unchanged. When retested after 6 h, PAS25-induced plasticity recovered to baseline levels. After training, normal PAS25-induced plasticity was observed in the contralateral training-naive motor cortex. Motor training did not reduce the efficacy of PAS25 to enhance cortical excitability when PAS10 was interspersed between the training and application of the PAS25 protocol. This indicated that the mechanism supporting PAS25-induced plasticity had remained intact immediately after training. Behavioral evidence was obtained for continued optimization of force generation at a time when PAS25-induced plasticity was blocked in the training motor cortex. Application of the PAS protocols after motor training did not prevent the consolidation of motor skills evident as performance gains at later retesting. The results are consistent with a concept of temporary suppression of associative cortical plasticity by neuronal mechanisms involved in motor training. Although it remains an open question exactly which element of motor training was responsible for this effect, our findings may link dynamic properties of LTP formation, as established in animal experiments, with human motor memory formation and possibly dynamic motor learning.
Cerebral Cortex 04/2006; 16(3):376-85. · 6.54 Impact Factor
-
Clinical Autonomic Research 01/2006; 15(6):419; author reply 420. · 1.30 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Animal experiments suggest that cortical sensory representations may be remodelled as a consequence of changing synaptic efficacy by timing-dependent associative neuronal activity. Here we describe a timing-based associative form of plasticity in human somatosensory cortex. Paired associative stimulation (PAS) was performed by combining repetitive median nerve stimulation with transcranial magnetic stimulation (TMS) over the contralateral postcentral region. PAS increased exclusively the amplitude of the P25 component of the median nerve-evoked somatosensory-evoked potential (MN-SSEP), which is probably generated in the superficial cortical layers of area 3b. SSEP components reflecting neuronal activity in deeper cortical layers (N20 component) or subcortical regions (P14 component) remained constant. PAS-induced enhancement of P25 amplitude displayed topographical specificity both for the recording (MN-SSEP versus tibial nerve-SSEP) and the stimulation (magnetic stimulation targeting somatosensory versus motor cortex) arrangements. Modulation of P25 amplitude was confined to a narrow range of interstimulus intervals (ISIs) between the MN pulse and the TMS pulse, and the sign of the modulation changed with ISIs differing by only 15 ms. The function describing the ISI dependence of PAS effects on somatosensory cortex resembled one previously observed in motor cortex, shifted by approximately 7 ms. The findings suggest a simple model of modulation of excitability in human primary somatosensory cortex, possibly by mechanisms related to the spike-timing-dependent plasticity of neuronal synapses located in upper cortical layers.
The Journal of Physiology 07/2005; 565(Pt 3):1039-52. · 4.72 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: This pilot study aimed at exploring the effects of intrathecally administered brain derived neurotrophic factor (BDNF) on autonomic functions in patients with ALS. A battery of autonomic sympathetic and parasympathetic tests was performed at baseline and after nine months of treatment in 10 ALS patients participating in a double-blind placebo-controlled phase II/III study of intrathecally administered BDNF. Results of patients treated with BDNF (25 or 150 microg/day) were compared to those receiving placebo. Sudomotor function and blood pressure response to handgrip significantly worsened during the treatment period (55.4+/-26.1 vs. 38.9+/-23.9 g/m(2)h, p<0.05; 20+/-6 vs. 13+/-4 microHg, p<0.05) whereas other sympathetic and all parasympathetic function tests only tended to be more abnormal at follow-up. Serum norepinephrine levels increased significantly during the nine-months observation period. The results of autonomic function tests were not different between patients treated with BDNF and placebo, but norepinephrine levels were higher in the BDNF group. We conclude that autonomic nervous system function deteriorates along with poorer motor performance independently from treatment with BDNF. The elevation of norepinephrine levels might reflect a non-specific up-regulation, and its association with BDNF an autocrine effect.
Amyotrophic Lateral Sclerosis 06/2005; 6(2):100-3.
-
[show abstract]
[hide abstract]
ABSTRACT: Using transcranial sonography, an area of hyperechogenicity at the substantia nigra (SN) may be detected as a typical marker in patients with Parkinson's disease (PD) as well as in approximately 9% of healthy subjects vulnerable to nigrostriatal impairment. In this longitudinal study, we provide evidence that the area of SN hyperechogenicity does not change in the course of PD. In conjunction with earlier findings in children and adolescents, this evidence indicates that, from late adolescence onward, this ultrasound finding is a trait marker for nigrostriatal vulnerability.
Movement Disorders 04/2005; 20(3):383-5. · 4.51 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Myotonic dystrophy type 2/proximal myotonic myopathy (DM2/PROMM) is an autosomal dominant multisystem disorder. Musculoskeletal pain is one of its frequent symptoms but also occurs in other chronic noninflammatory muscle disorders (OMD).
To characterize the phenotype of DM2/PROMM-associated musculoskeletal pain and to test whether it shows features distinct from OMD.
Outpatient clinic for patients with neuromuscular disorders, university hospital.
Twenty-four patients with DM2/PROMM (12 women and 12 men; median age, 57 years) and 24 age- and sex-matched patients with OMD consecutively recruited during a 3-year period were examined for musculoskeletal pain.
Standardized pain assessment; McGill Pain Questionnaire; depression score; and quantification of pain thresholds to blunt pressure on limb muscles with analgometer.
Unlike patients with OMD who have musculoskeletal pain, patients with DM2/PROMM distinguished a wide spectrum of coexisting pain types. The major pain type in patients with DM2/PROMM was exercise-related, temperature-modulated, and palpation-induced, whereas, cramps were rare. In 8 of the patients with DM2/PROMM and in 3 of the patients with OMD, musculoskeletal pain was the most disabling symptom.
Besides many similarities, DM2/PROMM-associated musculoskeletal pain shows features distinct from OMD.
Archives of Neurology 01/2005; 61(12):1938-42. · 7.58 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Acute axonal nerve lesions cause a hyperintense signal on T2-weighted (T2-w) magnetic resonance imaging (MRI) at the nerve lesion site and distal to it. The aim of this experimental study was to investigate the spatiotemporal evolution and resolution of MR nerve signal changes following denervation and reinnervation, and to relate these findings to electrophysiology and histology. The proximal sciatic nerve of adult rats was ligated by a tight suture that was removed 1 week later to induce complete axotomy and nerve regeneration upon release. Serial electromyography (EMG) and motor nerve conduction studies were performed parallel to MRI at multiple points of time. Moreover, sciatic nerves were taken for quantitative histological evaluation. Nerve hyperintensity on T2-w MRI was present distal to the lesion at thigh level 24 h after denervation preceding the occurrence of spontaneous activity on EMG by 24 h. After 48 h, the entire sciatic nerve and its branches showed an increased signal down to the level of the lower leg. The increased nerve signal regressed with a proximo-distal gradient beginning from week 2 after onset of nerve regeneration in the thigh. On EMG, the first reinnervation potentials were detected at that time at the respective level. Compound muscle action potential (CMAP) in the foot muscle fully recovered 12 weeks after onset of nerve regeneration, that is, 2 weeks after resolution of the hyperintensity along the entire nerve on MRI. Histology revealed axonal degeneration in the acute phase and later nerve oedema parallel to the increased nerve signal on MRI. MR signal alterations occur as early as 24 h after an axonal nerve lesion and correlate with nerve fiber degeneration and later with nerve oedema on histology. MR findings in denervation and reinnervation parallel the electrophysiological changes. Thus, MRI is a promising diagnostic tool for the early detection of acute axonal nerve lesions and monitoring of nerve regeneration.
Experimental Neurology 08/2004; 188(1):171-7. · 4.70 Impact Factor
