Recovery of nerve conduction following microvascular decompression for trigeminal neuralgia

OBJECTIVE: To assess the function of trigeminal nerve before and after microvascular decompression for trigeminal neuralgia. BACKGROUND: To date there is no direct evidence that microvascular decompression of the trigeminal root restores normal conduction in the nerve. METHODS: The authors examined 10 patients with trigeminal neuralgia in whom preoperative MRI and MR angiography demonstrated neurovascular contact. During microvascular decompression, the trigeminal nerve was monitored by recording early scalp trigeminal evoked potentials immediately before, during, and after decompression. Direct recordings from the root entry zone were also performed. RESULTS: In all patients preoperative scalp evoked potentials showed impaired conduction of the trigeminal root. Microvascular decompression was associated with immediate recovery of conduction in seven patients, demonstrated by both scalp evoked potentials and direct root recordings. All 10 patients were pain free postoperatively. CONCLUSIONS: Improvement in trigeminal neuralgia following microvascular decompression is often associated with normalization of neurophysiologic data, suggesting recovery of nerve function. Rapid electrophysiologic recovery and pain relief following microvascular decompression argue that neither phenomenon is linked to remyelination. It is possible that the trigeminal evoked potentials might predict an effective microvascular decompression.     

Correlations between clinical deficits, motor and sensory evoked potentials and radiologic aspects of MRI in malformative syringomyelia. 27 Cases

Twenty-seven patients (15 males, 12 females, age range: 16-66 years) were admitted for malformative syringomyelia diagnosed on MRI with measures of syrinx extending and transverse diameter. Posterior tibial somatosensory evoked potentials (PT SEP), median (M SEP), trigeminal (V3 SEP), brain stem auditory evoked potentials (BEAP), cortical and cervical motor evoked potentials (MEP) were correlated with clinical and radiological findings. SEP abnormalities were not correlated with the duration of symptoms. PT SEP proved to be more sensitive than M SEP. MEP abnormalities were very frequent (87% of the cases), even without clinical motor deficits. Trigeminal SEP were more sensitive than BEAP which were not related to the presence of associated cranio-vertebral abnormalities. We found no significative relationship between clinical and radiological results. Moreover, there was a positive relationship between electrophysiological and radiological results: abnormal trigeminal SEP were detected in 85% of the patients with high cervical syringomyelia. In all cases, trigeminal SEP and MEP should be done in association with M and PT SEP as both of them detect subclinical evidence of spinal cord dysfunction in syringomyelia.     

Usefulness of trigeminal somatosensory evoked potentials to detect subclinical trigeminal impairment in multiple sclerosis patients

Trigeminal somatosensory evoked potentials (TSEPs) by surface electric pulse stimulation were recorded in 30 normal subjects and in 70 multiple sclerosis (MS) patients, 13 of whom presenting clinical trigeminal impairment. We observed significant prolongation of all TSEPs parameters in MS group. TSEPs were abnormal in 45 patients (64.3%). Clinical and neurophysiological data agreed in 36 patients (51%) on 84 sides (60%). TSEPs were able to detect clinically silent lesions 54 times. TSEPs recording proves to be an additional useful test in MS multimodal evoked potential protocols.     

Quantitative analysis of the gustatory evoked potentials in the guinea pig

Gustatory evoked potentials were studied in anesthetized guinea pigs to develop an objective and quantitative taste examination for patients with taste disorders. A positive wave was recorded by the application of NaCl, HCl or quinine hydrochloride solution. There was little difference in latency, duration and waveform among these three solutions. No apparent change in activity was seen after the application of sucrose solution or distilled water. The gustatory evoked potentials that excluded the influence of the trigeminal nerve innervating the tongue surface were able to be reproducibly recorded on either the cortical surface or the skull surface. There was a linear relationship between logarithmic values of potential amplitude and those of taste solution concentration. Therefore, it is suspected that the quantitative evaluation of taste detection is possible by measuring the taste solution concentration-potential amplitude relationship.     

Inhibition of trigeminal neurons by intravenous administration of the serotonin (5HT)1B/D receptor agonist zolmitriptan (311C90): are brain stem sites therapeutic target in migraine?

Migraine is a common and debilitating condition. Its treatment has received considerable attention in recent times with the introduction into clinical use of the serotonin (5HT)1B/D-like agonist sumatriptan. It is known from human studies that the intracranial blood vessels and dura mater are important pain-sensitive structures since mechanical or electrical stimulation of these vessels, such as the superior sagittal sinus, causes pain. We have developed a model of craniovascular pain by stimulating the superior sagittal sinus and monitoring trigeminal neuronal activity using electrophysiological techniques. In this study we determined the effect of intravenous administration of the novel anti-migraine compound zolmitriptan (311C90) upon evoked neuronal activity in trigeminal neurons. Nine adult cats were anaesthetised with alpha-chloralose (60 mg/kg, i.p.; 20 mg/kg, i.v., 2-hourly) with all surgery being conducted under halothane (1-3%). The superior sagittal sinus was isolated for electrical stimulation. Recordings were made from caudal trigeminal neurons at the C2 level of the cervical spinal cord with tungsten-in-glass microelectrodes. Signals were amplified and analysed by a custom-written program that enabled software filtering and extraction of both evoked potential and single cell data. Data were collected before and after administration of zolmitriptan. Electrical stimulation of the superior sagittal sinus resulted in activation of neuronal elements within the trigeminal nucleus that could be monitored as single unit activity or as evoked potentials, the latter reflecting both primary afferent and trigeminal cell body activity. The evoked potential recorded from the trigeminal nucleus was 207 +/- 14 microV and was reduced by zolmitriptan (100 micrograms/kg, i.v.) to a mean of 98 +/- 17 microV. Similarly, the probability of firing for trigeminal neurons was reduced from a control level of 0.63 +/- 0.1 to 0.13 +/- 0.05 after a dose of 100 micrograms/kg intravenously. These effects were dose-dependent and were significantly different from the effect of vehicle (P < 0.05). These data demonstrate that systemically administered zolmitriptan can inhibit evoked trigeminovascular activity within the trigeminal nucleus. This inhibition of trigeminal activity may play a role in the anti-migraine actions of this compound and offers the prospect of a third pathophysiologically consistent target site for anti-migraine drug effects.     

Muscarine receptor activation in the substantia gelatinosa of the spinal trigeminal nucleus of the guinea pig

1. Intracellular recordings were made from slices of guinea pig spinal trigeminal nucleus pars caudalis (SG). 2. Muscarine [0.3-30 microM; half maximally effective concentration (EC50) = 2.9 microM] hyperpolarized 61% of SG neurons. The effect was mimicked by carbachol (0.3-30 microM; EC50 = 3.9 microM) and antagonized by pirenzepine (1 microM). Thirty-four percent of the neurons were depolarized by muscarine and carbachol (1-30 microM: EC50 = 5.7 microM), and the effect was antagonized by pirenzepine (100 nM). 3. In approximately 80% of recordings, muscarine (10-30 microM) evoked repetitive spontaneous inhibitory postsynaptic potentials (IPSPs) that were sensitive to bicuculline (10 microM). 4. Muscarine (1-30 microM; EC50 = 3 microM) decreased the amplitude of the majority of evoked excitatory postsynaptic potentials (EPSPs), and the effect was mimicked by carbachol and antagonized by pirenzepine (100 nM). 5. These results indicate that there are at least three mechanisms by which muscarine inhibits SG neurons: 1) hyperpolarization through activation of non-M1 receptors; 2) activation of gamma-amino-butyric acid-containing interneurons that mediate IPSPs in a subset of neurons; and 3) a decrease in evoked EPSP amplitude. Muscarine can also activate SG neurons via interaction with an M1-type receptor.     

MR of the spine with a fast T1-weighted fluid-attenuated inversion recovery sequence

Much is unclear about the pathophysiological mechanisms underlying painful temporomandibular disorders. In addition to various other theories, masticatory muscle dysfunction and pain have also been attributed to primary central nervous system hyperactivity. We assessed this possibility in a study using recent neurophysiological techniques. From among outpatients whose diagnosis of temporomandibular disorders had been obtained in stomatognathic facilities, we studied 10 patients with bilateral pain and 15 patients with unilateral pain, in whom electromyographic examination of the trigeminal reflexes disclosed normal findings except for absence or amplitude asymmetry of the jaw jerk. Transcranial magnetic stimulation yielded masseter motor evoked potentials of normal latency and amplitude, but five patients had to exert a near-maximum contraction to obtain their responses. The masseter silent periods elicited by the double-shock technique recovered normally. Because these tests measure the excitability of the masticatory system (including motor cortex, corticobulbar and corticoreticular connections, reticular interneurones and lower motoneurones), the lack of facilitation in these patients' responses excluded central hyperactivity as the primary cause of their masticatory dysfunction and pain.     

Kinetics and yield of singlet oxygen photosensitized by hypericin in organic and biological media

The recording of olfactory evoked potentials in healthy humans, using a continuous flow olfactory stimulator, is described. A stimulator pushed inert gas (N2) in a continuous flow through the nose at a rate of 4 l/min. At fixed 30-second intervals, (32 times) the flow was replaced by an equal amount of CO2, a trigeminal stimulant. Each pulse lasted 200 ms. An electronic timing circuit triggered both the stimulator and the recorder. Signal acquisition was performed using an Evoked Potential Recorder (Nicolet Compact Four by Nicolet Biomedical Instruments), triggered by the stimulator. Using this stimulator device reliable olfactory evoked potentials can be recorded in a clinical setting. Since this is a non invasive technique which can be used to test olfactory function whether or not the patient cooperates, it is expected to become widely used, particularly in non collaborating patients and in those suspected of malingering.     

Enzyme determination in vitro of inhibitor activity of beta-lactamase from tazobactam. Comparison with high performance liquid chromatography

Most physiological studies of the human olfactory system have concentrated on the cortical level; the olfactory bulbar level has been studied rarely. We attempted to stimulate the human olfactory mucosa by electrical pulse to detect the bulbar potentials. Electrical stimulation (2 mA, 0.5 ms) of the human olfactory mucosa evoked a change in potential recorded from the frontal sector of the head. A negative peak of the evoked potential that occurred at 19.4 ms (grand means, n = 5) after stimulation was the clearest. The highest amplitude of the potential was recorded from the frontal sector of the head on the stimulated side. Our findings were similar to the experimental results obtained from the olfactory bulbs of animals. This evoked potential was considered to be the human olfactory bulbar potential. When the subjects were stimulated by applying electricity to the olfactory mucosa, no sensation of smell occurred even though evoked potentials were recorded. Evoked potentials were recorded only when the stimulating electrode was located in the olfactory cleft. When the stimulating electrode was outside the olfactory cleft, the stimulation caused pain. The trigeminal nerve seemed to be stimulated by electricity. Olfactory evoked potentials produced by the electrical stimulation of the human olfactory mucosa should aid the research on human olfactory physiology, and may be applicable to clinical tests of olfactory dysfunction.     

Electrophysiological characteristics of asymptomatic relatives of patients with type 2 spinocerebellar ataxia

INTRODUCTION: Electrophysiological studies have been shown to be useful in hereditary ataxia, but only a small number of patients have been studied, and the duration of the illness, serial studies and molecular definition have not been taken into account. OBJECTIVE: We proposed, by means of electrophysiological techniques, to characterize the functional evolutionary state of the afferent and efferent systems in asymptomatic relations of patients with type 2 spinocerebellar ataxia (SCA2). Patients and methods. A 10 year longitudinal, prospective study was made of 59 children of patients with SCA2. The sequence included four studies: 1986, 1991, 1994 and 1996, all with informed consent for the investigation. The control group consisted of 108 volunteers. The electrophysiological studies recorded were: conduction studies in peripheral nerves and multimodal evoked potentials. For statistical analysis multivariate methods were used with a confidence interval of 95% (alpha = 0.05). RESULTS: Electrophysiological alterations were observed even in the absence of clinical signs, such as reduced amplitude of sensory potentials, morphological changes and prolonged latency of the central components of somatosensory evoked potentials, and of brain stem auditory evoked potentials, whilst the visual evoked potentials remained normal. Of 79 relations studied during the 10 year investigation, 17 had clinical signs and were considered to be patients with SCA2. CONCLUSIONS: Four stages of the illness were defined: 'healthy', presymptomatic, and patients with and without nerve conduction block. These characterized the degenerative mechanisms of the afferent and efferent systems of the relations of patients with SCA2 who became ill themselves.     

Ambulatory tonsillectomy. Is postoperative hemorrhage a risk factor?

The aim of this study was to investigate the usefulness of chemosensory event-related potentials (CSERPs) in response to both olfactory and intranasal trigeminal stimulation in the diagnosis of anosmia. Forty-four patients participated. Gaseous CO2 was used for trigeminal stimulation, vanillin and H2S were used as olfactory stimulants. Event-related potentials to olfactory stimuli could not be obtained in any of the anosmic patients, indicating the complete loss of the sense of smell. However, all patients responded to stimulation of the trigeminal nerve with CO2. These data clearly demonstrate the clinical significance of CSERPs in the assessment of anosmia.     

Functional connectivity in the rodent trigeminal pathway grown in vitro

In explant cocultures of the rat trigeminal pathway, embryonic trigeminal ganglion cells grow their axons into peripheral cutaneous and central nervous system targets (R.S. Erzurumlu, S. Jhaveri, Target influences on the morphology of trigeminal axons, Exp. Neurol, 135 (1995) 1-16; R.S. Erzurumlu, S. Jhaveri, H. Takahashi, R.D.G. McKay, Target-derived influences on axon growth modes in explant cocultures of trigeminal neurons, Proc. Natl. Acad. Sci. USA 90 (1993) 7235-7239). In heterochronic cocultures, composed of embryonic trigeminal ganglion, embryonic whisker pad and postnatal brainstem slice, trigeminal axons develop arbors and terminal boutons in the brainstem trigeminal nuclei. To determine whether these terminal arbors establish functional connections with the brainstem neurons, we examined the electrophysiological properties of brainstem neurons and their responsiveness to trigeminal ganglion stimulation. Intracellular recordings were done in vitro on cells of the trigeminal subnucleus interpolaris (SPI) in trigeminal pathway cocultures (E15 whisker pad, E15 trigeminal ganglion, and postnatal day (PND) 0-2 brainstem slice) or in the SPI of acutely prepared brainstem slices. Electrophysiological properties of SPI cells in both preparations were virtually identical. The voltage responses of SPI neurons to intracellular current injection were highly linear suggesting they lacked a number of voltage-dependent conductances. Depolarizing current injection produced trains of action potentials with a frequency that varied with stimulus intensity. In explant cocultures, electrical activation of the trigeminal ganglion evoked EPSPs, and EPSPs coupled with IPSPs in SPI cells. Bicuculline blockade of IPSP activity resulted in long lasting EPSPs whose duration increased with membrane depolarization. These results show that brainstem trigeminal neurons can retain their functional properties in culture and establish functional connections with primary sensory afferents.     

Visual evoked cortical potentials (V.E.C.P.) by television presentation of different patterned stimuli to patients with multiple sclerosis

Visual pattern reversal evoked potentials constitute a test that can reveal early pathological changes in multiple sclerosis. Sixty nine subjects (52 controls, and 17 patients) were studied with this technique. The transient potentials evoked by checkerboard pattern reversal reveal an increase in the CII peak latency (significantly different from the controls) in M.S., with single elements of 15 and 30 min of arc and 20%-50% of contrast depth. The steady state potentials are absent or show phase lags in some patients with transient responses within the normal limits. The delayed evoked responses are detectable in a high percentage of patients with M.S., even when ocular symptoms are not seen in the clinical observation. Transient and steady-state E.Ps can furnish early tools for evaluation of functionality of visual pathways related to retinal form- and movement-analyzers, the former being sensitive to high spatial frequencies but conducting more slowly than the latter.     

Cutaneous silent period in masseter muscles: a clinical and electrodiagnostic evaluation

In 35 normal subjects electromyographic silent periods were constantly evoked bilaterally in the masseter muscles during maximal contraction after unilateral electrical stimulation over the infraorbital or mental nerve. Findings in this study and data obtained in 30 patients suffering from trigeminal (26) and facial (four) nerve lesions suggest that the silent period evoked according to our methods is cutaneous in origin. The trigeminal sensory root forms the afferent limb of the silent period reflex. Its central pathway is thought to pass both crossed and uncrossed through the pons. Determination of the cutaneous silent period might be of value for the demonstration of trigeminal nerve lesions and to supplement results concerning other brain-stem reflexes.     

Inhibitory gating of an evoked response to repeated auditory stimuli in schizophrenic and normal subjects. Human recordings, computer simulation, and an animal model

BACKGROUND: Altered sensory response is a prominent feature of schizophrenia. Inhibitory gatting mechanisms, shown by diminished P50 evoked responses to repeated auditory stimuli, seem to be deficient in schizophrenic persons. These inhibitory mechanisms usually are studied by averaging the electroencephalographic responses to many presentations of pairs of stimuli. Although averaging increases signal-to-noise ratio, it may obscure trial-to-trial differences. We compared differences between schizophrenic and normal persons in single trials and averages of P50 response. METHODS: Recordings from 10 schizophrenic patients and 10 normal subjects were analyzed using conventional averaging and single-trial measurements. A computer simulation of both methods examined their ability to extract evoked responses from background activity. Related single-neuron activity in the hippocampus in an animal model also was studied, because neuronal action potentials can be reliably identified in single trials. RESULTS: Averaged evoked potentials showed significant suppression of the P50 response to the second stimulus of the pair in normal patients, but not in schizophrenic patients. Single-trial analysis did not detect a response above background activity. Computer simulations gave similar results, suggesting that failure to detect suppression in single trials comes from inadequate differentiation of signal from noise. Recordings in animals confirmed almost complete suppression of the response of hippocampal pyramidal neurons to the second stimulus. CONCLUSIONS: The normal inhibition of response to repeated auditory stimuli seems to be compromised in schizophrenia. This loss of inhibitory gating could reflect a physiological deficit of hippocampal interneurons that is consonant with other evidence for interneuron pathologic defects in schizophrenia.     

Activity of Dipernoids isolated from Azorella compacta (Llareta) on Trypanosoma cruzi amastigotes

This paper deals with studies of evoked potentials in diseases of the peripheral and central nervous system. Indications and clinical value of visual evoked potentials, brain stem auditory evoked potentials, somatosensory evoked potentials and motor evoked potentials are evaluated for frequent neurological diseases.     

Sequential analysis of transmission properties of the CNS during consecutive REM periods]

Auditory and visual evoked potentials during sleep were recorded in healthy subjects. After averaging of the evoked potentials separately for the different REM episodes, the corresponding so-called amplitude-frequency-characteristic was calculated. This function describes the transfer properties of the system in the frequency domain. Regarding the visual evoked potentials, no difference between consecutive REM episodes could be proven. Under auditory stimulation, a significant difference between the first and the following REM episodes was found in the beta frequency range (12.5 to 20 Hz). This indicates different mechanisms of information processing during consecutive REM episodes.     

The mechanisms of pain in root compression

It is shown that antidromic stimulation of peripheral nociceptors induced by radicular compression is the initial pathogenetic factor of pain in patients with so-called paralytic sciatica and trigeminal neuralgia. Subsequently, segmental and suprasegmental mechanisms of pain retention are involved. The prevalence of one or another pain mechanisms at different stages of trigeminal neuralgia may determine the choice of adequate therapy.     

Subacute combined degeneration: clinical, electrophysiological, and magnetic resonance imaging findings

OBJECTIVE: Vitamin B12 deficiency is a systemic disease that often affects the nervous system. One of the most prevalent manifestations is subacute combined degeneration (SCD) of the spinal cord. To access the clinical, electrophysiological, and structural abnormalities associated with SCD, a study was conducted in nine patients. METHODS: Clinical, electrophysiological (electroneurography, somatosensory and motor evoked potentials), and MRI evaluations were performed in patients before and after treatment. RESULTS: The most prominent clinical and electrophysiological findings in all patients were dysfunctions of the posterior column. Corresponding hyperintense lesions in the posterior column of the spinal cord were found in two patients by T2 weighted MRI. Damage to the central motor pathway was identified in four patients. Demyelinating neuropathy was present in one patient and axonal neuropathy in four. All patients showed improvement of their symptoms after treatment with cobalamin. Abnormalities of the spinal cord on MRI disappeared early in recovery. Motor evoked potentials and median somatosensory evoked potentials typically normalised after treatment, whereas tibial somatosensory evoked potentials remained abnormal in most patients. CONCLUSIONS: Clinical, electrophysiological, and MRI findings associated with SCD in vitamin B12 deficiency are diverse. Thus vitamin B12 deficiency should be considered in the differential diagnosis of all spinal cord, peripheral nerve, and neuropsychiatric disorders.     

The use of the auditory evoked potential in the diagnosis of multiple sclerosis

Auditory evoked potentials, both early and middle components, were recorded from 227 patients with a variety of conditions including multiple sclerosis, brain stem vascular disease, intracranial tumours and Arnold-Chiari malformation. Abnormalities were found in a substantial proportion of patients with definite multiple sclerosis and a smaller proportion of those in the less definite clinical categories of this condition. There was a high correlation between clinical evidence of brain stem involvement and an abnormal auditory evoked potential in multiple sclerosis. Abnormalities were also found in a few patients presenting with an isolated episode of central nervous system dysfunction involving the brain stem. The auditory evoked potential was abnormal in other patients with known diagnoses including half of those with Arnold-Chiari malformation. Tumours involving the brain stem caused abnormalities of the brain stem evoked potentials in some cases and more frequently distortion of the middle components. The specificity of these auditory evoked potential abnormalities to multiple slcerosis is discussed.