Cutaneous and mixed nerve silent periods in syringomyelia.

OBJECTIVES AND METHODS: We studied cutaneous and mixed nerve silent periods (CSP, MNSP) in 4 patients with cervical syringomyelia documented by magnetic resonance imaging who on clinical examination presented with unilateral hypalgesia and hypothermesthesia. In addition, we recorded upper and lower extremity somatosensory and motor evoked potentials (SEP, MEP), and cortical silent periods. RESULTS: In all patients, CSP and the later portion of MNSP were absent or shortened on their affected side, while both were normal on their unaffected side. In all patients, SEP latencies were normal following both median and tibial nerve stimulation. In two patients, the amplitude N13 (median nerve SEP), and in one patient each the amplitudes N20 (median nerve SEP) and P37 (tibial nerve SEP) were reduced. Central motor conduction time was prolonged to abductor digiti minimi muscle in one patient on the affected side, but was normal to tibialis anterior muscle in all patients. Cortical silent periods where present bilaterally in spite of unilateral complete absence of CSP and MNSP in two subjects tested. Loss of CSP and MNSP were a sensitive parameter of spinal cord dysfunction in syringomyelia. The cervical median nerve SEP response N13 reflected gray matter involvement, while corticospinal tract dysfunction was less frequently observed. CONCLUSION: Our data suggest that CSP and later portion of MNSP are generated at the spinal level by the same small myelinated A-delta fibers, and that their central network is distinct from large diameter fiber afferents and efferents.     

Neural generator of P14 far-field somatosensory evoked potential studied in a patient with a pontine lesion

Somatosensory evoked potentials (SEPs) to electrical stimulation of the right and the left median nerves were studied in a patient with a pontine lesion. At first there was mainly right medial lemniscus involvement. Four months later the left medial lemniscus was found to be also involved. SEPs to stimulation of the right median nerve had normal wave forms and latencies while N20 was lacking and P14 was abnormal after stimulation of the left median nerve in the first SEP record. N20 and P14 were absent with preservation of P9 and P11 after stimulation of both left and right median nerves in the second SEP record. Therefore the P14 component has been found abnormal, then absent, in a patient with a pontine lesion.     

Color imaging of parietal and frontal somatosensory potential fields evoked by stimulation of median or posterior tibial nerve in man

Somatosensory evoked potentials (SEPs) to median or fingers or posterior tibial nerve stimulation were recorded with earlobe reference in normal young adults. A system of 16 electrodes on the scalp served to create bit-mapped images of the potential fields at 1 msec intervals. The P14 (median SEP) or P30 (tibial SEP) far fields thought to reflect the afferent volley in the medial lemniscus produced widespread positivity over the scalp. Subsequent components had a characteristic focal distribution suggesting that they reflected one or more generators in cortical areas. For the median SEP, the parietal N20 and the prerolandic P22 showed differences in onset and offset times as well as distribution that precluded their being related to the same generator. While N20 was contralateral, P22 extended ipsilaterally. P22 may be generated in the motor area 4 and the supplementary motor area. P22 was also distinct from the P27 field restricted to the contralateral parietal region. The frontal N30 had a bilateral distribution and the P45 presented variable features. For the tibial SEP, no phase reversal was confirmed between the parietal P38 (midline-ipsilateral focus) and N33 (contralateral focus). N37 over the contralateral prerolandic region might reflect a generator in the motor region. P58 was more symmetrically distributed than P38, possibly because it reflected generators more posteriorly on the parietal convexity. N75 had a widespread field with focus on the ipsilateral side of midline.     

Giant somatosensory evoked potentials in a patient with the anterior spinal artery syndrome

We studied a previously healthy 25-year-old woman with the anterior spinal artery syndrome, a rare thoracocervical myelopathy with multiple potential etiologies. Quantitative and clinical sensory examination showed dissociated loss of pin-prick and temperature discrimination below the level of the lesion, with normal light touch, vibratory, and position sense. Magnetic resonance imaging was consistent with cervical spinal cord infarction. Median SEPs showed normal Erb's potential with absent spinal N—₁₃ and normal scalp N—₂₀ latency. Tibial SEPs showed normal lumbosacral responses and normal scalp P—₃₀ latency. Both median and tibial nerve stimulation produced cortical responses of unusually large amplitude (median 38 m?V, tibial 17 m?V). We hypothesize that large SEP amplitudes in this patient resulted from loss of anterolateral inhibitory influences on the dorsal column–medial lemniscal system. © 1993 John Wiley & Soncs, Inc.     

Assessment of intraspinal and intracranial conduction by P30 and P39 tibial nerve somatosensory evoked potentials in cervical cord, brainstem, and hemispheric lesions.

In routine recordings of tibial nerve somatosensory evoked potentials (SEPs), a global central conduction time is evaluated by measuring the interval between the segmental spinal N22 potential, recorded in the lumbar region, and the cortical P39 potential. In this study, we tested the reliability of the scalp far-field P30 potential, which originates in the vicinity of the cervico-medullary junction, in order to evaluate separately intraspinal and intracranial conduction in normal subjects and patients with cervical cord and intracranial lesions. P30 and cortical P39 potentials were studied in 23 healthy subjects and in 70 patients with cervical cord (n = 47), brainstem (n = 11) or hemispheric lesions (n = 12) selected on the basis of neuroimaging--computed tomography (CT) or magnetic resonance (MR)--findings. Median nerve SEPs were also recorded in all patients. Of the several montages tested to obtain the P30 potential, the Fpz-Cv6 derivation gave the highest signal-to-noise ratio; it permitted to obtain a P30 potential that peaked at 29.2 +/- 1.6 ms in all normal subjects. P30 abnormalities were observed only in patients with cervical or cervico-medullary lesions; these were associated with a normal P39 in only two of 33 abnormal recordings. Conversely, P30 was consistently normal in lesions situated above the cervico-medullary junction whether associated with normal, delayed, or reduced P39. P30 abnormalities were subclinical in 42% of abnormal recordings. All patients with normal tibial and median nerve SEPs on both sides had normal touch, joint, and vibration sensation in the four limbs. There was a strong correlation between tibial nerve P30 and median nerve P14 data in the whole series of patients; both potentials behaved similarly in all cases of intracranial supramedullary lesions. Combined abnormalities of P30 and P39 potentials thus indicate that conduction is impaired at the spinal level and proved to be particularly informative for detecting spinal cord dysfunction in patients with neuroimaging evidence of a narrowed cervical canal. Recording of abnormal N13, P14, or P30 potentials provided evidence of a cervical cord dysfunction in 66% of patients who had a suspected spondylotic myelopathy. Recording of tibial nerve P30 potential has proven to give reliable and useful information when a separate assessment of intraspinal and intracranial somatosensory conduction is needed; it merits inclusion, as does the upper limb N13 potential, in the evaluation of patients whose MR image indicates cervical canal narrowing.     

Somatosensory evoked potentials,sensory nerve potentials and sensory nerve conduction in hereditary motor and sensory neuropathy type I

Summary Thirty-nine patients from six families with hereditary motor and sensory neuropathy type I and control subjects were included in this study. A neurological deficit score (NDS) was derived from a neurological examination and compared with neurophysiological test findings. Further, sensory nerve conduction velocities (SNCV) were compared with the motor nerve conduction velocities (MNCV). Five patients whom peaks of N11/N13 complex and N20 of the median nerve sensory evoked potential (SEP) could be recorded showed normal interpeak latency. The interpeak separation P14 N20 measured in six patients was normal. These findings point to the normal function of the central conductive pathways. Erb and cervical potentials of the median nerve SEP could be recorded in 10% and 12% of the patients, respectively. In contrast, about half of the patients showed a scalp N20, while in most of them no SNCV could be measured. In six patients far-field potential P14 of the median nerve SEP was the first detectable potential. Therefore, we argue in view of the anatomical structure of the thalamus, that the first generator for synchronizing and amplification of impulses is probably located in the thalamus. A third of the patients had a cortical sural nerve SEP, while no sural nerve potentials could be recorded. No association was found between the SEP findings and the NDS. There was an inverse correlation between median SNCV and the NDS, but no relationship between the former and sensory deficit alone. In 40% of the patients median SNCV and in 13% sural SNCV could be recorded and considered to be severely decreased. In contrast, the majority of the patients had mild to moderate sensory deficit. Furthermore, patients with measurable SNCVs had higher MNCVs and lower NDS than patients without measurable SNCVs.     

Intraoperative neurophysiologic discovery of uncrossed sensory and motor pathways in a patient with horizontal gaze palsy and scoliosis.

OBJECTIVE: To report the intraoperative neurophysiologic discovery of clinically unsuspected non-decussation of the somatosensory and motor pathways. METHODS: We performed somatosensory evoked potential (SEP) and transcranial electric stimulation (TES) muscle motor evoked potential (MEP) monitoring during scoliosis surgery for a 16 year old patient with familial horizontal gaze palsy and progressive scoliosis. Our routine procedures included optimizing tibial cortical SEP monitoring derivations through saggital and coronal (C4', C2', Cz', C1', C3'-mastoid) P37 mapping, which surprisingly indicated non-decussation. Consequently, we also obtained coronal median nerve SEPs and simultaneous bilateral muscle recordings to lateralized TES (C3-Cz, C4-Cz) intraoperatively and focal hand area transcranial magnetic stimulation (TMS) postoperatively. RESULTS: For each nerve, tibial P37/N37 distribution was contralateral/ipsilateral and median N20 ipsilateral. For each hemisphere, ipsilateral TES MEPs had lower thresholds and TMS MEPs were exclusively ipsilateral. Accurate monitoring required reversed montages. Reevaluation of an MRI (previously reported normal) disclosed a ventral midline cleft of the medulla. CONCLUSIONS: The results indicate uncrossed dorsal column-medial lemniscal and corticospinal pathways due to brain-stem malformation with absent internal arcuate and pyramidal decussations. SIGNIFICANCE: Simultaneous bilateral recording to unilateral stimulation demonstrates SEP/MEP hemispheric origin and is important for accurate interpretation and monitoring because decussation anomalies exist.     

EDSS correlated analysis of median nerve somatosensory evoked potentials in multiple sclerosis

Median nerve somatosensory evoked potentials (SEP) were recorded in 30 patients with multiple sclerosis. The examined patients had an expanded disability status scale (EDSS) between 0 and 6. The primary cortical potential N20, the subcortical potentials P14, N13b, N13a and the peripheral potential P9 were recorded simultaneously. In 5 patients normal SEP were observed (group 1) and in 6 patients there were consecutive disturbances of the somatosensory pathway (group 3). In 19 patients subcortical potentials were abnormal or absent while the following potentials were normal or identified which pattern corresponds to amplification within CNS structures (group 2). The EDSS of groups 1 and 2 were similar and lower than the EDSS of group 3, which indicates that amplification mechanisms could represent a positive prognostic factor in SEP diagnosis of multiple sclerosis. Received: 15 March 2000 / Accepted in revised form: 4 September 2000     

Delayed somatosensory conduction in acute painful neuropathy of diabetes

We examined the peripheral–central sensory conduction by using somatosensory evoked potential (SEP) in a 48 year old diabetic patient with acute painful neuropathy. The sural, ulnar and median sensory nerve conduction and SEP elicited by wrist stimulation showed no abnormalities, nevertheless, the tibial nerve SEP revealed absent spinal N19 and a remarkable delay of the cortical arrival time. These findings suggest involvement of the dorsal roots or the dorsal column in the acute painful neuropathy of diabetes.     

Neural generators of N18 and P14 far-field somatosensory evoked potentials studied in patients with lesion of thalamus or thalamo-cortical radiations

Somatosensory evoked potentials (SEPs) to electrical stimulation of the right or left median nerve were studied in 4 patients with hemianesthesia and a severe thalamic or suprathalamic vascular lesion on one side. The SEPs were recorded with a non-cephalic reference. The normal side of each patient served as his or her own control. The lesion consistently abolished the parietal N20-P27-P45 and the prerolandic P22-N30 SEP components. It did not significantly affect the P9-P11-P14 positive far fields, nor the widespread bilateral N18 SEP component. This allowed N18 features to be studied without interference from cortical components. It is proposed that N18 reflects several deeply located generators in brain stem and/or thalamus whereas N20 represents the earliest cortical response of the contralateral post-central receiving areas.     

The dissociation of early SEP components in lesions of the cervico-medullary junction: a cue for routine interpretation of abnormal cervical responses to median nerve stimulation

In non-cephalic reference records the lesions of upper cervical cord and medulla dissociate SEPs to median nerve stimulation, cervical N11 and N13 potentials being preserved whereas later components, generated above the foramen magnum, are absent or desynchronized and delayed. This was observed in 4 patients with space occupying lesions of the cervico-medullary junction. In three of them serial postoperative SEP records demonstrated a progressive normalization of the responses following decompression. During normalization delayed cortical components could reappear on the scalp before the far-field P14 positivity. Before surgery the widespread N18 potential was absent, at least on one side, in the 4 patients and was never found to be dissociated from the P14 component. The reversibility of early SEP dissociations after surgery allowed a documented study of the abnormal patterns of cervical to Fz responses that may be observed with various lesions of the cervical cord, including demyelination. When the P14 component is delayed because of conduction slowing it is injected as an abnormal 'N14' in the Cv6-Fz response; in this situation the use of a non-cephalic reference is necessary to make the distinction between the cervical N13 potential and brain-stem 'N14' negativity.     

Subcortical P30 potential following tibial nerve stimulation: Detection and normative data

Stimulation of the tibial nerve evokes a P30 far-field potential over the scalp which, like the median nerve P14, probably originates in the vicinity of the cervico-medullary junction. Unlike the P14 potential. P30 recording has not been systematically performed in clinical practice, probably because of doubts about the generator of the potential and the possibility of consistently recording it on the scalp after the unilateral stimulation of the tibial nerve. In this study, we tested the reliability of the tibial nerve scalp far-field P30 potential in 34 normal subjects using different montages, of which the Fpz-Cv6 derivation gave the highest signal to noise ratio, making it possible to obtain a P30 potential peaking at 29.2 ± 1.6 msec in all normal subjects. This suggests that this component should to be included in the routine recording of tibial nerve SEPs in order to evaluate the spinal and intracranial conduction of the somatosensory pathway separately.

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Sommario La stimolazione del nervo tibiale posteriore genera sullo scalpo un potenziale far-field P30 che origina, come il potenziale P14 da stimazione del nervo mediano, in prossimità della giunzione cervicomidollare.A differenza della componente P14, la risposta P30 non viene sistematicamente valutata nella pratica clinica, probabilmente per le incertezze relative alla sua precisa origine e alla possibilità di registrare in modo consistente questa componente dopo stimolazione unilaterale del nervo tibiale. In questo studio abbiamo valutato l'affidabilità della registrazione del potenziale P30 in 34 soggetti normali utilizzando differenti montaggi.Tra i diversi montaggi utilizzati la migliore risposta in termini di rapporto segnale/rumore veniva registrata nella derivazione Fpz-Cv6 che permetteva di ottenere un potenziale P30 con una latenza di 29.2±1.6 msec in tutti i soggetti normali.Questo studio suggerisce che la registrazione di questa componente merita di essere inclusa nello studio dei PESS del nervo tibiale per una valutazione separata della conduzione sensitiva midollare e intracranica.

     

Somatosensory tibial nerve evoked potentials with parasagittal tumours: a contribution to the problem of generators

Somatosensory evoked potentials following stimulation of the median nerve at the wrist and the tibial nerve at the ankle were recorded in 5 patients with parasagittal tumours, 4 in the fronto-parietal and 1 in the frontal region. Three had intracerebral tumours and 2 parasagittal meningiomas. The extent of each lesion was determined by CT scan, showing a unilateral process involving predominantly the paracentral lobule and adjacent parts of the post- and precentral gyri ("Mantelkante') in 4 patients and a more frontal location of one meningioma affecting mainly the superior frontal gyrus. SEPs recorded from the patients with fronto-parietal tumours showed a uniform pattern with a complete absence of the wave N70 of the tibial SEP elicited by stimulating the nerve contralateral to the lesion. All other waves, including the P40-N50 complex on both sides and the median SEP, were in the normal range. In contrast, the frontal meningioma led to an only slightly altered from of the waves immediately following the initial P40-N50 complex. It is concluded that the tumour abolished the generators of the wave N70 which are apparently located in the cortical somatosensory leg area. Therefore unilateral loss of the wave N70 is indicative of parasagittal lesions. The results may give good evidence that the P40-N50 complex is generated in the thalamus or thalamo-cortical connections.     

Origin of the early components of somatosensory evoked potentials by the posterior tibial nerve stimulation--a comparative study of median nerve stimulation in clinical cases

In order to determine the generation sites of short latency somatosensory evoked potentials to the posterior tibial nerve stimulation, scalp topography was performed on 10 normal subjects in the two different band-pass recordings, i.e., wide band-pass filter (5-3000 Hz) and narrow band-pass filter (100-1000 Hz). Furthermore, comparative study of the changes of evoked potentials between posterior tibial nerve stimulation and median nerve stimulation was carried out in 22 cases with well localized lesion of the central nervous system in the same wide band-pass filter setting. The early components of somatosensory evoked potentials elicited by the posterior tibial nerve stimulation were obtained as P 30, N 34, and P 38 in the wide band-pass filter, and P 29, N 32, P 36 in the narrow band-pass filter. Components P 30, N 34 and components P 29, N 32 were widely distributed on the scalp, but were disappeared on the scalp-scalp recording. These results suggested all those components were generated from the deep subcortical structures. In the case with high cervical lesion, component P 30 at the posterior tibial nerve stimulation was remarkably prolonged in latency, and component P 13 at the median nerve stimulation was disappeared. P 30-N 34 interpeak latency at the posterior tibial nerve stimulation was prolonged in the case with pontine lesion, while P 13-N 16 interpeak latency at the median nerve stimulation was also prolonged. In the cases with thalamic and internal capsular lesion, P 30 and N 34 at the posterior tibial nerve stimulation and P 13 and N 16 at the median nerve stimulation were all preserved in normal range. These results revealed that components P 30 and N 34 were almost identical to components P 13 and N 16, respectively. On the other hand, component P 38 at the posterior tibial nerve stimulation was suppressed or disappeared in the cases with well localized lesion at the midcentro parietal region, that includes the primary foot sensory area.(ABSTRACT TRUNCATED AT 400 WORDS)     

Origin of the widespread N18 in median nerve SEP.

The widespread N18 potential in median nerve SEP was studied in normal subjects and in patients with high cervical, brain-stem and thalamic lesions who had profound disturbances of deep sensation. N18 was well identified in the HSi-CV2 derivation in every normal subject as a broad elevation from the baseline lasting about 20 msec. The cortical N20 was absent in all patients. N18 was absent in a patient with a dorsal column lesion at C1-2 level. The amplitude and configuration of N18 were normal in all other patients with brain-stem and thalamic lesions, including a patient with a lesion at the ponto-medullary junction. The sagittal distribution of N18 was studied in a patient with a thalamic lesion and an oblique distribution with the maximum region between Cz and nasion was demonstrated. The present results indicate that at least the greater part of N18 is generated at the caudal most brain-stem or through branches from this level. Taking previous animal and intraoperative studies into consideration, we think it most probable that the main part of N18 corresponds to the ventro-rostral negative pole of the dipolar potential generated at the cuneate nucleus by the primary afferent depolarization of presynaptic terminals of dorsal column fibers.     

Current source density mapping of somatosensory evoked responses following median and tibial nerve stimulation.

Potential recording of brain activities always encounters the problem resulting from the activation of reference electrodes. Current source density (CSD) computation does not take reference sites into account and consequently may better localize the generator sources. In the past, several attempts have been made to record CSDs of the somatosensory evoked responses (SERs) following median nerve stimulation. In order to compare the generating mechanisms of SERs following median nerve and tibial nerve stimulation, the scalp CSD distributions of the median nerve SER and the tibial nerve SER were compared in 5 normal subjects. In the median nerve SER, far-field potentials such as P14 and N16 were abolished in the CSD records. N20, P25 and N35 showed almost identical CSD distributions, albeit P25 had a reversed polarity. By contrast, the tibial nerve SER showed similar distributions for P40 and P60 CSDs, but N50 had a different distribution from the others. In the potential records, P40 and P60 were distributed predominantly ipsilateral to the stimulus (paradoxical lateralization), whereas the P40 and P60 CSDs formed a dipole localized over the contralateral foot somatosensory area. N50 disclosed the same tendency, although it had a slightly different CSD pattern from that of P40 and P60. These findings suggest that the median nerve and tibial nerve SER components are not necessarily comparable and that under certain circumstances CSDs are better indicators of local electrical events than the corresponding potentials.     

Somatosensory evoked potentials correlate with genetics in Huntington's disease

Abnormalities of somatosensory evoked potentials (SEPs) have been reported in Huntington's disease, a neuropsychiatric disorder caused by the expansion of a CAG trinucleotide repeat. The aim of our study was to determine the relationship between these electrophysiological changes and the length of the nucleotide repeat. We found a striking correlation between the decrease in the early component amplitudes (N20 and N30) of the median nerve SEP and the repeat length, suggesting that these SEP alterations are indeed related to the genetically determined pathological process. The cortical components of the tibial nerve SEP exhibited a dramatic alteration in the patient group and were the only SEP changes found in the group of asymptomatic carriers of the mutation, being more sensitive than the median nerve SEPs.     

Neural generators of tibial nerve P30 somatosensory evoked potential studied in patients with a focal lesion of the cervicomedullary junction

The tibial nerve P30 potential was studied in 6 patients with focal lesions located in the vicinity of the cervicomedullary junction. P30 potential was unaffected while cortical P39 was abnormal in the patients with a supramedullary lesion affecting the somatosensory pathway just above its decussation. Conversely, P30 was abnormal in the presence of a lesion situated caudally to the cervicomedullary junction affecting the lower limb sensory fibers just below their decussation. Median nerve P14 behaved similarly to the P30 potential in these cases. These clinical observations suggest that P30 potential, as P14 of median nerve somatosensory evoked potentials, is generated in the lower brain stern probably before the decussation of the sensory fibers; nucleus gracilis and medial lemniscus fibers in the lower brain stem are probably the anatomical structures generating P30 potential. This suggests that P30 potential may be used to study intraspinal and intracranial conduction times separately in the afferent somatosensory pathways. © 1996 John Wiley & Sons, Inc.     

Abnormalities of somatosensory and motor evoked potentials in adrenomyeloneuropathy: Comparison with magnetic resonance imaging and clinical findings

We studied 6 patients with adrenomyeloneuropathy (AMN) showing mild signs of central nervous system involvement. All patients underwent brain and spinal magnetic resonance imaging (MRI) and somatosensory (SEP) and motor (MEP) evoked potential study. Whereas SEPs and MEPs were abnormal in all patients, only 1 patient showed brain MRI abnormalities; spinal MRI showed hypotrophy without focal abnormalities in 4 of 6 patients. Median nerve SEPs, which were recorded with noncephalic reference montage, revealed delayed or absent scalp P14 far-field potential in all patients and abnormal spinal N13 in 2. Moreover, tibial nerve SEPs revealed abnormalities of the subcortical P30 response in all 4 patients in whom scalp-to-ear recording was employed. These findings strongly suggest that in the early stages of disease neurological dysfunction is localized in the spinal cord, where it is difficult to assess using MRI. However, SEPs and MEPs, which show a typical pattern of abnormality in these patients, could be useful in disclosing signs of long tract involvement and in monitoring treatment. © 1997 John Wiley & Sons, Inc. Muscle Nerve 20: 1249–1257, 1997     

Parkinson's disease and lower limb somatosensory evoked potentials: apomorphine-induced relief of the akinetic-rigid syndrome and vertex P37-N50 potentials.

We evaluated brainstem P30, vertex-central P37-N50 and contralateral frontal N37 somatosensory evoked potentials (SEPs) from the tibial nerve in 14 patients affected by Parkinson's disease (PD) with akinetic-rigid syndrome. In seven patients SEPs were recorded after administration of apomorphine. The cortical P37-N50 complex was either absent (five patients, eight tested sides) or significantly smaller in patients as compared to the control group (n = 18). There was a relationship between abnormalities of early vertex potentials and degree of motor impairment. Administration of apomorphine was followed by an increase in amplitude of P37-N50 response, which was maximal after 15-30 min and then progressively returned to basal values in parallel with clinical improvement. Amplitude of brainstem P30 and frontal N37 responses was within normal values and did not vary following drug administration. These results suggest that the P37-N50 complex arises from independent cortical generators, probably located in the pre-rolandic cortex, which may be selectively affected by basal ganglia dysfunction. Amplitude decrease of the P37-50 complex may reflect an abnormal processing of somatosensory inputs within the pre-central cortex due to defective modulation exerted by basal ganglia circuitry on cortical excitability. SEP potentiation following apomorphine, besides indicating that this dysfunction is partly reversible, might suggest objective method to measure therapeutic efficacy.