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The effect of surgical medicaments on peripheral nerve function.

Surgical medicaments are often placed in close proximity to peripheral nerves and may be responsible for some postoperative sensory disturbances. In this study we investigated the effect of four medicaments -- BIPP, (bismuth iodoform paraffin paste), Whitehead's varnish (compound iodoform paint), Surgicel (oxidized regenerated cellulose) and Carnoy's solution (ethanol, chloroform and acetic acid) -- on peripheral nerve function. The experiments were carried out on the saphenous nerve in anaesthetized adult rats. Electrical stimuli (30 V, 0.1 ms duration) were applied to the saphenous nerve through electrodes placed distally (at the ankle) to evoke a compound action potential (CAP) which was recorded proximally (in the thigh). The CAP was recorded before, and for 2 h after, the application of the medicament to a 1 cm length of nerve between the electrodes. In other animals (n = 4 in each group) recordings were made after the medicament had been placed in a connective tissue pocket immediately overlying the nerve for a 2-week period. BIPP (n = 4) had no immediate or delayed effect on neural function, whereas Whitehead's varnish (n = 4) and Carnoy's (n = 4) solution both blocked neural conduction within 2 min of being placed adjacent to the nerve. The effect of Surgicel (n = 8) was more variable; axonal conduction was blocked within 2 h in five of the eight experiments undertaken. After the application of Whitehead's varnish or Surgicel for 2 weeks, the CAPs had regained characteristics which were similar to those of the controls, but after the application of Carnoy's solution they remained significantly diminished (P < 0.004). These results suggest that, with the exception of BIPP, the medicaments tested could be responsible for some postoperative sensory disturbances, and the effects of Carnoy's solution on neural function may be persistent.

Acetic Acid↗

Electrophysiologic responses of human sural nerve to temperature.

The purpose of this study was to assess the conduction, specifically the latency and amplitude of the sensory nerve action potential (SNAP), of the sural nerve as a function of intraneural temperature of the leg. The electrophysiologic responses of the sural nerve were determined at different temperatures in 22 healthy adults. Distal sensory latency and amplitude of the sural SNAP was determined at 1 degree C intervals over a limb temperature range of 23 degrees to 40 degrees C. Limb temperature was monitored with a thermistor probe placed subcutaneously near the sural nerve. Ice bath soaks were used for cooling and infrared radiation for warming the limbs. An analysis of covariance was performed for the SNAP latencies and amplitudes to determine the effect of gender and leg (right or left) at each temperature level. No effect of gender or leg on neural conduction was detected in individual subjects. A regression analysis was then used on pooled data to determine the effect of temperature on sural SNAP latency and amplitude. An inverse linear change in the latency of sural SNAP was observed over the temperature ranges used. Mean latency increased 0.1 msec per 1 degree C increase in subcutaneous temperature. A direct relationship between amplitude of the SNAP and temperature was determined. Mean amplitude increased 0.3 muV per 1 degree C increase in subcutaneous temperature. The results of this study support previous reports, which state that SNAP latency is indirectly related to the intraneural temperature. Clinical electromyographers must monitor the temperature of the lower leg and foot whenever sensorineural conduction of the lower limbs is performed.

Action Potentials↗

Early detection of diabetic visceral neuropathy. An electrophysiologic study of bladder and urethral innervation.

The segmental and supraspinal innervation of the detrusor muscle and periurethral striated musculature was studied in 27 patients with diabetes mellitus by gas cystometry, integrated sphincter electromyography, and spinal evoked-response latency measurements. Slowing of neural conduction velocities was a consistent finding in all the patients, even when cystometry did not show abnormalities. Thus, neuropathy in the segmental innervation of the bladder and urethra was documented.

Adolescent↗

Visual electrophysiological responses in subjects with cerebral autosomal arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).

OBJECTIVES: To evaluate visual electrophysiological responses in subjects with cerebral autosomal arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). METHODS: Three subjects (one male and two females, mean age 55.3+/-2.9 years) belonging to an Italian family already diagnosed with CADASIL through clinicopathological and genetic studies and 14 control subjects (6 males and 8 females, mean age 52.7+/-3.6 years) were enrolled in the study. Flash electroretinogram (ERG), oscillatory potentials (OPs) and simultaneous recordings of pattern electroretinogram (PERG) and visual evoked potentials (VEPs) were assessed in all 3 subjects with CADASIL and age-matched controls. RESULTS: Subjects with CADASIL showed: reduced ERG, OP and PERG (N35-P50, P50-N95) amplitudes with respect to our normal limits; delayed PERG (N35, P50) and VEP (P100) implicit times when compared with our normal limits; and VEP (N75-P100) amplitudes and retinocortical times within our normal limits. CONCLUSIONS: Subjects with CADASIL present a dysfunction in the outer, middle and innermost retinal layers when the index of neural conduction in the postretinal visual pathways is normal. The delay in visual cortical responses observed in subjects with CADASIL may be ascribable to retinal impairment with a possible functional sparing of the postretinal visual structures.

Dementia, Multi-Infarct↗

[Neurophysiologic findings in radio-humeral epicondyle pathology].

A number of authors assumed a compression syndrome of the radial nerve or its branches to be responsible for the heterogenous classified picture of radiohumeral epicondylopathy. Various structural and functional stenoses have been discussed as possible causes. We performed electromyographies on the extensor muscles, subdividing from the radial epicondyle and found significant (p < 0.05) changes in 27/51 patients regarding latency, velocity of neural conduction and rate of polyphasic potentials. Especially affected were the extensor carpi radialis brevis and extensor digitorum muscle. These findings were confirmed by torque measurements and histologic observations from both muscular and tendon biopsies. In summary, we believe the model of a neurogenous origin of radio-humeral epicondylopathy to be an appropriate explanation.

Biopsy↗

Chronic placental insufficiency has long-term effects on auditory function in the guinea pig.

Very low birth weight and growth-restricted infants have an increased risk of auditory impairments. It is uncertain whether these impairments are related to adverse pre-, peri- or postnatal events. We aimed to determine whether a period of chronic placental insufficiency (CPI) in the guinea pig results in long-term alterations to auditory function. Near mid-gestation, CPI was induced via unilateral ligation of the uterine artery. At 8 weeks of age, auditory brainstem responses (ABRs) were recorded in response to unilateral acoustic stimulation in prenatally-compromised (PC, n=8) and control animals (n=8). Stimuli consisted of 100 micros clicks, presented at 33 pulses per second (pps) and tone pip stimuli at frequencies of 2, 4, 8, 16 and 32 kHz. To examine temporal response properties, click stimuli were also presented at rates of 66, 132 and 200 pps. Normal ABR waveforms were elicited by both click and tone pip stimuli in all animals. Moreover, there was no difference between control and PC animals in stimulus detection thresholds across the frequencies examined. Using high rate click stimuli, PC animals demonstrated a significant increase in both the latency of wave III (normalised to 33 pps) and the wave I-III inter-peak interval compared to the controls. We hypothesise that these functional changes reflect alterations in myelination of the auditory brainstem and/or changes in synaptic efficacy. The results suggest subtle deficits in neural conduction in the PC guinea pig at maturity, and may have implications for speech perception abilities of low birth weight or prenatally affected infants.

Acoustic Stimulation↗

Correlation of acetylator phenotype with peripheral, autonomic and central neuropathy in Northern Indian non-insulin-dependent diabetes mellitus patients.

OBJECTIVES: Genetic susceptibility to diabetic neuropathy has been suspected and tentatively explored; however, diabetic autonomic and central neuropathies are poorly investigated areas. Previous trials correlating types of diabetes and diabetic neuropathy with acetylator dimorphisms have not been conclusive. The present study was designed to test peripheral neuropathy, autonomic neuropathy and integrity of central conduction pathways in patients of non-insulin-dependent diabetes mellitus (NIDDM), and to correlate the findings with the acetylator phenotype. METHODS: Twenty-six patients of NIDDM with stable glycaemic control and 11 age- and sex-matched control subjects were recruited, clinically examined and investigated with glycaemic and lipid profile, renal function tests, nerve conduction studies (sensory and motor), auditory brain stem evoked responses (ABERs) and somatosensory evoked potentials (SEPs). Acetylator status of the subjects was determined by sulphadimidine test. RESULTS: Out of 26 NIDDM patients, eight (30.7%; group 1A) were slow acetylators and 18 (69.3%; group 1B) were fast acetylators. The distribution of slow and rapid acetylators in both the groups was similar. Glycaemic and lipid profiles and 24-h urinary albumin excretion in groups 1A and 1B were also similar. Motor nerve conduction velocity, latency of F wave, sensory nerve conduction and amplitudes of sensory nerve action potentials were not different between fast and slow acetylator NIDDM patients. On testing for ABERs, there were no statistically significant differences in peak latencies of waves I, III and V; interpeak latencies (IPLs) I-III, III-V and I-V; amplitude of waves I, III and V on both sides between NIDDM patients and controls. However, peak latencies of wave III (P < 0.01), wave V (P < 0.005), IPLs I-III and I-V (P < 0.005), IPLs III-V (P < 0.05), and amplitudes of wave I (P < 0.05) and wave V (P < 0.05) on the left side were significantly different in slow acetylator NIDDM patients. Increase on the right side for the same group was statistically significant for IPLs I-III and I-V (P < 0.05). SEPs showed no statistically significant difference between NIDDM patients and controls, and slow and fast acetylator NIDDM patients. CONCLUSIONS: No significant association of acetylator status with peripheral neuropathy in NIDDM subjects was observed in the present study. However, central neural conduction, primarily tested by ABERs, was significantly delayed in slow acetylators compared with fast acetylator NIDDM patients. Hence, there may be a predisposition to neuropathy in this group of patients, and such a predisposition may be better detected by studying central rather than peripheral nervous conduction pathways in NIDDM patients.

Adult↗

Relative vulnerability of the brain and spinal cord to ischemia.

In this experiment CER and SER were monitored as blood flow was progressively lowered by lowering the systemic arterial pressure below the lower limits of autoregulation (bleeding). Blood flow in the brain and dorsal column of the spinal cord was monitored and recorded with the hydrogen clearance method. Long tract neural conduction in the spinal cord appeared quite refractory to the effects of ischemia and disappeared only after 8--18 min of essentially absolute ischemia. The CER was more sensitive to the effects of ischemia, disappearing first in one animal and returning later in all of the animals. The SER returned in all animals after re-infusion of the blood and re-establishment of the blood flow even after a 13--23 min period of absolute ischemia and a 5 min period of electrical silence.

Animals↗

Mice with disrupted GM2/GD2 synthase gene lack complex gangliosides but exhibit only subtle defects in their nervous system.

Gangliosides, sialic acid-containing glycosphingolipids, are abundant in the vertebrate (mammalian) nervous system. Their composition is spatially and developmentally regulated, and gangliosides have been widely believed to lay essential roles in establishment of the nervous system, especially in neuritogenesis and synaptogenesis. However, this has never been tested directly. Here we report the generation of mice with a disrupted beta 1,4-N-acetylgalactosaminyltransferase (GM2/GD2 synthase; EC 2.4.1.92) gene. The mice lacked all complex gangliosides. Nevertheless, they did not show any major histological defects in their nervous systems or in gross behavior. Just a slight reduction in the neural conduction velocity from the tibial nerve to the somatosensory cortex, but not to the lumbar spine, was detected. These findings suggest that complex gangliosides are required in neuronal functions but not in the morphogenesis and organogenesis of the brain. The higher levels of GM3 and GD3 expressed in the brains of these mutant mice may be able to compensate for the lack of complex gangliosides.

Animals↗

Electrophysiologic evaluation of the facial nerve in Bell's palsy. A review.

Facial nerve paralysis is the most common mononeuropathy and idiopathic facial paralysis (Bell's palsy) the most common seventh nerve disease electromyographers may be asked to evaluate. The electrophysiologic method of choice to assess the facial nerve is side-to-side evoked amplitude comparison with the affected side expressed as a percentage of the nonaffected side. This examination should be performed on days 3, 5, 7, 9, 11 and 13 after onset of paralysis. If the percentage of surviving axons falls below 10% within the first 14 days, an incomplete recovery is suggested. Electromyography may assist in prognosticating a functional return, determining neural conduction across the site of injury and following reinervation in the recovery period. The persistence or early return of an absent R1 component of the blink reflex may qualitatively suggest a satisfactory functional outcome in facial paralysis. Supramaximally exciting the facial nerve at the stylomastoid foramen and comparing the clinical response on the affected and nonaffected side, maximum stimulation test, can also predict eventual seventh nerve return. Observing a minimal twitch, utilizing the nerve excitability test or measuring the facial nerve latency have yielded poor correlations with functional return and are of limited usefulness in the prognostication of acute facial palsies. Trigeminal somatosensory evoked potentials can be employed to evaluate the status of the trigeminal nerve as approximately 50% of patients with Bell's palsy also have lesions involving the fifth nerve. Side-to-side amplitude comparison and electromyography are the two most valuable electrophysiologic methods of assessing facial nerve functioning.

Action Potentials↗

Interaction between conducted vasodilation and sympathetic nerve activation in arterioles of hamster striated muscle.

We tested the hypothesis that sympathetic nerve activity can influence the conduction of vasodilation along the arteriolar wall. Arterioles in the superfused cremaster muscle of anesthetized male hamsters (n = 21, 109 +/- 4 g) were studied. Microelectrodes were positioned adjacent to the distal end of primary arterioles to stimulate sympathetic nerves throughout arteriolar networks (perivascular nerve stimulation [PNS]). Microiontophoresis micropipettes (tip outer diameter, 1 to 2 microns) filled with acetylcholine (ACh, 1 mol/L) were positioned adjacent to the wall of second-order (2A) or third-order (3A) arterioles approximately 1 mm distal to their origin to induce local and conducted vasodilation; diameter responses were recorded at the micropipette tip and at vessel origins, respectively. For 2A and 3A arterioles (resting diameters, 15 to 54 and 9 to 30 microns, respectively), vasoconstriction with PNS was frequency dependent (0.5 to 32 Hz); this was attenuated by 65% (P < .05) with alpha-adrenoceptor blockade (phentolamine, 1 mumol/L). Conducted vasodilation was attenuated by > 40% during 16-Hz PNS (P < .05); this effect was reversed by phentolamine. In a reciprocal fashion, conducted vasodilation diminished PNS-induced vasoconstriction by approximately 50% (P < .05). Elevating oxygen (from 0% to 10%) in the superfusion solution induced vasoconstriction similar to that with 16-Hz PNS yet had no effect on conduction. Neural blockade with tetrodotoxin (1 mumol/L) eliminated PNS-induced vasoconstriction and enhanced (P < .05) conducted vasodilation. These findings indicate that perivascular nerves in striated muscle can influence cell-to-cell communication along the arteriolar wall both at rest and during enhanced sympathetic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Transplantation of cryopreserved human embryonal carcinoma-derived neurons (NT2N cells) promotes functional recovery in ischemic rats.

This study was designed to explore the efficacy of a human clone cell line as an alternative neural graft source and to validate the practice of cryopreservation and xenografting as logistical approaches toward conducting neural transplantation. We investigated the biological effects of transplanting cultured human neurons (NT2N cells) derived from a well-characterized embryonal carcinoma cell line into the brains of rats subjected to transient, focal cerebral ischemia induced by embolic occlusion of the middle cerebral artery. At 1 month and extending throughout the 6-month posttransplantation test period, ischemic animals that were transplanted with NT2N cells and treated with an immunosuppressive drug displayed a significant improvement in a passive avoidance task as well as a normalization of asymmetrical motor behavior compared to ischemic animals that received rat fetal cerebellar cell grafts or vehicle alone. Remarkably, cryopreserved NT2N cell grafts compared with fresh NT2N cell grafts, remained viable in the immunosuppressed rat brain and effective in producing behavioral recovery in immunosuppressed ischemic animals. The long-term viability of cryopreserved NT2N cell xenografts in vivo and their sustained effectiveness in promoting behavioral recovery suggest potential utilization of xenografting and cryopreservation as useful protocols for establishing clone cell lines as graft source in neural transplantation therapies for central nervous system disorders.

Animals↗

Co-existence and elimination of convergent motor nerve terminals in reinnervated and paralysed adult rat skeletal muscle.

1. Experiments were carried out to determine whether neuromuscular synapse elimination can occur in skeletal muscle in the complete absence of conducted neural activity, using reinnervation of partially denervated adult muscle as a paradigm. Partially denervated rat lumbrical muscles were paralysed with a nerve conduction block applied to the sciatic nerve during regeneration of injured sural nerve motor axons. Both intact (lateral plantar nerve) and regenerating motor axons converging on the same muscle fibres were therefore inactive. 2. Paralysed muscles expressed prolonged twitch contractions, low tetanus-to-twitch ratios, prolonged synaptic potentials and marked post-tetanic potentiation of frequency of miniature endplate potentials compared with control muscles and neuromuscular junctions. 3. Isometric tension and intracellular recording data suggest that regenerating axons reinnervated more muscle fibres in paralysed muscles than in controls. A greater proportion of muscle fibres was polyneuronally innervated in the paralysed muscles, but significant numbers of muscle fibres acquired a mononeuronal innervation by regenerated, inactive motor nerve terminals. 4. The data suggest that muscle paralysis enhances the regeneration of motor axons when they grow into partially denervated muscles, but activity-independent competition may also be important in the mechanism of synapse elimination at neuromuscular junctions. The data further imply that when nerve endings expressing identical patterns of activity converge on a postsynaptic cell, Hebbian rules may not be sufficient to predict the outcome of the competition, contrary to specific postulates of the neurotrophic theory of development and maintenance of neural connections.

Animals↗

Estrogen reduces the excitability of the female rat medial amygdala afferents from the medial preoptic area but not those from the lateral septum.

Electrical stimulation of the medial amygdala (AMY) elicited antidromic action potentials in neurons in the preoptic area (POA) and the lateral septum (LS) of 36 urethane-anesthetized ovariectomized female rats, which were either treated with estrogen o not treated. The extracellular potentials from the two sites showed similar characteristics, with the exception of the sensitivity to estrogen: they had latencies between 3 and 35 ms. Thresholds were as low as 100 microA. The mean relative refractory period was 2.2 ms. The peak-to-peak amplitudes of the positive-negative biphasic potential ranged from 1.0 mV to 12.0 mV. Estrogen had site-specific effects on parameters of antidromic activation in the POA. Estrogen-treated rats had a significantly higher threshold (937 vs 664 microA) and a longer refractory period (2.5 vs 2.1 ms) than the ovariectomized rats (P < 0.05 for each). The effects were absent in the LS. Selective cutting of the stria terminalis diminished the AMY-induced antidromic responses in the POA and LS. Electrical stimulation of the stria blocked the AMY-induced antidromic potentials by collision. Thus, estrogen-sensitive POA efferents as well as non-estrogen-sensitive LS efferents project to the AMY via the stria terminalis. Reductions in axonal excitability would inhibit neural conduction and transmission. Estrogen may therefore reduce the AMY inputs from the POA, without affecting those from the LS. Such alterations in the neural impulse flow may underlie estrogen-dependent neuroendocrine or behavioral regulation.

Amygdala↗

Transtympanic and surface recordings in the diagnosis of retrocochlear disorders.

A series of patients presenting with subsequently surgically confirmed central tumour involving the auditory pathways were investigated using both transtympanic electrocochleography (TT ECochG) and surface recordings of brainstem evoked responses (BER). While ECochG allows a detailed study of peripheral function, BER allow the investigation of neural conduction up to the level of the inferior colliculus. Valuable information can be obtained from: (1) comparison of the amplitudes of the sensory and neural components of the ECochG; (2) comparison of ECochG, BER and auditory thresholds; (3) time interval measurements between the auditory nerve response (N1 on the ECochG) and the inferior colliculus (wave P4-5 on BER); (4) contralateral comparisons. Similar measurements performed in pure cochlear pathologies, mainly in Meniere's disease, yielded very significant differences.

Audiometry↗

Electrophysiologic evidence for an intersegmental reflex pathway between lumbar paraspinal tissues.

STUDY DESIGN: Electrophysiologic recordings were obtained from a lumbar paraspinal nerve or muscle in the anesthetized cat while electrically stimulating a paraspinal nerve or facet capsule in an adjacent lumbar segment. A variety of approaches were used to demonstrate the reflex nature of both the nerve and the muscle response. OBJECTIVE: The primary purpose of this study was to seek electrophysiologic evidence for the presence of intersegmental reflexes between adjacent lumbar vertebral segments. A second purpose of this study was to confirm a previous procedure used to evoke paraspinal reflexes. This previous work had shown that electrical stimulation of the L1-L2 facet joint capsule elicits electromyographic activity from multifidus muscle one to two vertebral segments caudal to the stimulated facet in a porcine preparation. SUMMARY OF BACKGROUND DATA: Biomechanical approaches have stressed the need for spinal stability to avoid conditions that could give rise to low back dysfunction. It seems reasonable to believe that reflex interactions between vertebral segments contribute to the sensorimotor integration of lumbar paraspinal tissues. It also seems reasonable to believe that alterations or abnormal elicitation of these reflexes could contribute to biomechanical changes associated with low back pain and paraspinal muscle spasm. METHODS: Experiments were performed on 23 alpha-chloralose anesthetized adult cats. In eight cats the L3, L4, and L5 medial branch from each dorsal ramus was exposed and placed on a bipolar hook electrode. In six cats the L4 medial branch was stimulated and a compound action potential was recorded from the L3 medial branch. In three of the six cats the L5 medial branch was stimulated and a compound action potential was recorded from the L3 medial branch. In one cat the L4 medial branch was stimulated and a compound action potential was recorded from the L5 medial branch. In one cat the L3 medial branch was stimulated and a compound action potential was recorded from the L5 medial branch. At the end of each protocol the medial branch was cut just proximal to the stimulating electrode to confirm that the compound action potential was reflexive in nature and not initiated by volume conduction. In 15 cats three approaches were used to confirm that multifidus electromyographic activity evoked by electrical stimulation of a lumbar facet capsule was reflexive in nature: 1) by anesthetizing the site of the sensory endings, i.e., the facet capsule, 2) by injecting lidocaine intrathecally to block neural conduction centrally, i.e., within the spinal canal, or 3) by cutting the afferent pathway, i.e., the medial branch of the dorsal ramus. RESULTS: Electrical stimulation of the medial branch of the dorsal ramus innervating the medial-most lumbar paraspinal tissues evoked a compound action potential in the medial branch innervating the medial-most paraspinal tissues one and two segments away. Stimulating voltages between 2 and 70 V were necessary to evoke the compound action potential. Each compound action potential was reflexive in nature because cutting the lumbar medial branch proximal to its contact with the stimulating electrode abolished each compound action potential. The conduction velocity of the reflex ranged from 3.5 to 6.1 m/sec. Electrical stimulation of a lumbar facet capsule evoked lumbar multifidus muscle electromyographic activity. However, injecting lidocaine intrathecally or transecting the medial branch of the dorsal ramus had no effect on electromyographic activity. Injecting lidocaine into the facet or into the multifidus muscle around the facet joint (near the stimulating electrode) significantly decreased the magnitude of the multifidus electromyography. CONCLUSION: These results indicate that afferent impulses conveyed by the medial branch of the dorsal ramus reflexly altered efferent activity to an adjacent lumbar segment. This intersegmental paraspinal reflex may span at least one or two vertebral segments. The data suggest that electrical stimulation of the facet joint capsule may not have reflexly elicited multifidus activity because neither chemical interruption (intrathecal lidocaine) nor physical interruption (nerve transection) of the presumed reflex pathway diminished or abolished the electromyographic response. Volume conduction of the stimulating currents likely elicited multifidus activity during electrical stimulation of the facet capsule. When using electrical stimulation of neural paraspinal tissues to evoke reflex muscle activity, appropriate control experiments must be performed to clearly demonstrate the reflexive nature of the response.

Action Potentials↗

The effects of carbamazepine and sodium valproate on SEPs and BAEPs.

SEPs and BAEPs were studied in 36 previously untreated epileptics receiving either carbamazepine (CBZ) or sodium valproate (VPA) monotherapy. CBZ prolonged central conduction times in SEPs and BAEPs. SEP latency prolongation correlated with serum CBZ levels. VPA had minimal effects on evoked potentials. The present study gives evidence of similar effects of carbamazepine and phenytoin on central neural conduction.

Adult↗

Evoked potential abnormalities in postoperative patients with biliary atresia.

The somatosensory evoked potentials from the lower extremities were measured postoperatively in 15 patients with biliary atresia to investigate whether they were free of neurologic dysfunction. Because long-standing cholestasis causes progressive neuropathy due to malabsorption of vitamin E, the serum vitamin E, D, and A levels were also examined to evaluate the fat-soluble vitamin status. The cerebral evoked potentials to posterior tibial nerve stimulation were recorded in all 15 patients as well as in 45 controls, but spinal evoked potentials examined at the level of the cauda equina could not be recorded in five patients more than 8 years of age with long-standing icterus. The remaining 10 patients exhibited spinal evoked potentials as observed in the controls, but the mean neural conduction velocity at the cauda equina was significantly lower than that of the 45 controls (42.0 +/- 5.1 m/s vs 52.3 +/- 6.8 m/s, P = .0002). The serum vitamin E, D, and A levels were within the normal range in 13, 9, and 1 of 15 patients, respectively. These results suggest that the patients with long-term follow-up are still at risk of developing neural disturbances even with normal serum vitamin E status.

Adolescent↗