Silent period in the mentalis muscle induced by facial nerve and cutaneous stimulation.

The aim of this study was to demonstrate that silent periods of the mentalis muscle are induced after facial nerve stimulation and cutaneous stimulation in normal subjects. When the marginal mandibular branch of the facial nerve and the cutaneous nerve in areas adjacent to the lower lip were stimulated during slight voluntary contraction of the mentalis muscle, silent periods were elicited with surface electrodes on the mentalis muscle. The early phase and the late phase of the silent period were elicited by marginal mandibular branch stimulation. The early phase of the silent period was recognized following the F waves and it disappeared at 36.3 msec. The average duration of the late phase of the silent period was 59.2 msec, with an average latency of 62.5 msec. Only the late phase of the silent period after cutaneous stimulation could be elicited, with a duration and latency of 55.9 msec and 54.0 msec respectively. The authors conclude that the silent period is able to be elicited in the mentalis muscle by peripheral nerve stimulation, and is one of the late responses in facial muscles.

Delayed resolution of residual hemifacial spasm after microvascular decompression operations.

OBJECTIVE: After microvascular decompression to treat hemifacial spasm (HFS), resolution of the HFS is often gradual. We carefully investigated the course of the gradual resolution of HFS and examined the differences between patients with and without postoperative HFS. METHODS: One hundred seventy-five patients with HFS were monitored, for observation of 1) whether postoperative HFS occurred, 2) when it occurred, and 3) when it disappeared after microvascular decompression. For two groups of patients, with (Group I) and without (Group II) postoperative HFS, we investigated age, sex, spasm side, preoperative facial nerve block (botulinum toxin treatment), decompression material, preoperative HFS period, offender (compressing vessel), temporary and permanent postoperative complications, and electromyographic findings. RESULTS: In Group I (88 patients), postoperative HFS began within 4 days after surgery, a period that we have termed the silent period of postoperative HFS; the median value for the time to resolution was 28 days. The other 87 patients exhibited no postoperative HFS (Group II). There was a significantly higher incidence of postoperative facial weakness in Group II (Group II, 41.3%; Group I, 25.5%; P = 0.02 by logistic regression analysis). In Group I, there was no statistically significant relationship between the investigated parameters and the silent period or the postoperative HFS period, as determined by Cox proportional-hazards regression analysis, except for the number of preoperative facial nerve blocks. Electromyographic investigation of F waves revealed facial paresis during the silent period in a patient. CONCLUSION: Approximately 50% of patients with HFS exhibited residual spasm postoperatively. An immediate postoperative silent period of 4 days without spasm was characteristic. One-quarter, one-half, and 90% of the residual spasm resolved by 1 week, 1 month, and 8 months after surgery, respectively.

F-waves and facilitated late responses of the mentalis muscle in patients with a cerebrovascular accident.

F-waves in the extremities result from the backfiring of antidromically activated anterior horn cells and F-waves of the mentalis muscle can be also elicited after stimulation of the marginal mandibular branch of the facial nerve. In order to investigate the influence of the descending pathway of the excitability of the facial motonucleus, the F-wave of the mentalis muscle and the facilitated late response, which follows F-waves and which seems to be the snout reflex due to their similar latency and habituation, were studied in 11 conscious patients with a hemispheric cerebrovascular accident (CVA) presenting with hemiparesis, and in 10 unconscious patients with CVA or head injury. The duration and the persistence of the F-waves increased significantly statistically on the normal side in the CVA patients compared with those of the palsy side and the normal subjects. In comatose patients the F-waves and the facilitated late response were not elicited. The latency (46.1 +/- 13.3 msec) of the facilitated late responses in the unconscious patients tended to increase compared with the latency (36.6 +/- 4.3 msec) in the conscious patients. These findings suggest that the hyperexcitability of the facial motoneuron is ipsilateral to any hemispheric lesion; the hemispheric lesion exerts a bilateral excitatory influence on the interneuron of the facilitated late response: and that the reticular formation may influence the facial motoneuron and any interneurons concerned in the facilitated late response. F-waves and facilitated late responses should be further examined as neurophysiologically useful diagnostic methods.

Effect of brain-derived neurotrophic factor, nerve growth factor, and neurotrophin-3 on functional recovery and regeneration after spinal cord injury in adult rats.

This study examined whether continuous intramedullary infusion of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), or neurotrophin-3 (NT-3) had either an early neuroprotective effect or a delayed effect on regeneration after spinal cord injury (SCI) in adult rats. BDNF, NGF, NT-3 or vehicle was infused at a rate of 625 ng/h into the SCI site at T3 through an implanted cannula attached to an osmotic pump. This infusion was maintained for 14 days after a 35-g clip compression injury. At 4 weeks after injury, the axonal tracer fluorogold (FG) was introduced into the spinal cord caudal to the lesion and the animals sacrificed 3 days later following behavioral assessment. The inclined plane score was significantly higher in BDNF-treated animals (45 +/- 3 degrees) compared to control animals (36 -/+ 1 degrees) at 1 week after injury (p < 0.05), although the scores were not significantly different at later times. BDNF-treated animals also showed more FG-labeled cells in the red nucleus and sensorimotor cortex (1,638 +/- 350 and 124 +/- 83, respectively) compared to controls (1,228 +/- 217 and 36 +/- 15, respectively) and a lower percent cavitation at the injury site (21.4 +/- 10.4%) compared to control animals (32.3 +/- 11.7%). Invasion & proliferation of Schwann cells and formation of peripheral myelin were more prominent at the injury site in the BDNF-treated animals than in the other groups. These results indicate that continuous intramedullary infusion of BDNF provides neuroprotection and enhances some regenerative activity after SCI.

F-waves of the facial muscles in healthy control subjects and in patients with peripheral facial nerve disturbance.

F-waves were recorded from the mentalis muscles with surface electrodes following stimulation of the marginal mandibular branch of the facial nerve in healthy control subjects during wakefulness, non-REM (rapid eye movement) sleep and voluntary contraction and in patients with Bell's palsy and acoustic neurinoma. The F-wave of the facial muscles results from the backfiring of antidromically activated alpha motoneurons in the facial motonucleus. Therefore, first, the F-waves were not easily elicited in patients with any disturbance in the proximal segment of the facial nerve (Bell's palsy and acoustic neurinoma). Second, the F-waves were affected by excitability of the facial motonucleus; the F-waves were inhibited significantly during sleep and enhanced significantly during voluntary contraction compared with those at rest during wakefulness. When the stimulation strength was set submaximum for M-waves, F-waves were elicited but H-waves, which have lower threshold than M-waves, were not elicited in the facial muscles, unlike the case of the extremities. Measurement of the F-waves of facial muscles is a new method for estimating excitability of the facial motonucleus unless there is any disturbance of the proximal segment. Fundamental characteristics of the facial F-waves were shown in the present study and measuring facial F-waves is clinically applicable for investigation of both excitability of the facial motonucleus and facial peripheral nerve disturbance.

Cell proliferation and nestin expression in the ependyma of the adult rat spinal cord after injury.

A population of precursor cells is known to exist in the subependyma of the lateral ventricles in adult rodents. However, the source of the precursor cells in the adult mammalian spinal cord has not been identified in vivo, although the adult spinal cord was recently reported to contain neural stem cells in vitro. In this study we found active cell proliferation and nestin expression in the adult ependyma of the central canal after spinal cord injury. The normal ependyma showed limited proliferative activity indicated by a low Ki-67 labeling index (1.5% at T1 level) and no immunoreactivity to nestin, a marker for neural precursor cells. In contrast, the spinal cord injured by clip compression demonstrated a dramatic increase in ependymal proliferation indicated by a high Ki-67 labeling index (maximum of 26% at 3 days [d] after injury) and concomitant strong nestin expression in the ependyma. These responses were downregulated by 7 d after injury. The increased cell proliferation in the ependyma was observed only at sites immediately adjacent to the lesion. After injury, nestin positive, GFAP negative cell populations were found in areas surrounding the ependymal layer, which suggests migration of the ependymal cells. These results indicate the precursor cell qualities of the adult ependyma after injury. Thus, we propose the ependyma of the central canal, which is normally latent but activates locally and temporally in response to spinal cord injury, as the in vivo source for precursor cells in the adult mammalian spinal cord.

Central neurocytoma presenting with intratumoral hemorrhage 15 years after initial treatment by partial removal and irradiation.

A 50-year-old male presented with a central neurocytoma with intratumoral homorrhage. He had undergone partial removal of the tumor and postoperative radiation therapy 15 years previously. He was followed as an outpatient after the initial treatment, and there was no evidence of regrowth of the residual tumor. Removal of the hematoma and biopsy of the tumor were performed. Abnormally developed blood capillaries in the tumor may have undergone disturbances of circulation caused by irradiation which resulted in bleeding. Patients with partially resected central neurocytomas which have low proliferative potential may not require radiation therapy, due to the benign nature and the risk of delayed complications of irradiation including intratumoral hemorrhage.

Electrophysiological investigation of hemifacial spasm after microvascular decompression: F waves of the facial muscles, blink reflexes, and abnormal muscle responses.

In patients with hemifacial spasm, it has been said that the spasm is due to cross compression of the facial nerve by a blood vessel and that microvascular decompression (MVD) of the facial nerve is an effective treatment. The F waves, which result from backfiring of antidromically activated motor neurons of the facial motor nucleus, are indices of the excitability of the facial motor nucleus and are enhanced in patients with hemifacial spasm. Measuring blink reflexes and abnormal muscle responses (lateral spread), a characteristic sign of hemifacial spasm, has been used to investigate the mechanism of hemifacial spasm pathophysiologically. Thus the authors measured F waves of the facial muscle, blink reflexes, and abnormal muscle responses before and after MVD in patients suffering from hemifacial spasm to investigate the excitability of the facial motor nucleus and the course of the cure of hemifacial spasm after MVD. The authors obtained facial nerve-evoked electromyograms in 20 patients with hemifacial spasm before and after the MVD procedure. On the spasm side, the F waves and blink reflexes were enhanced preoperatively compared to those on the normal side and abnormal muscle responses were recorded in all patients. In 12 patients whose hemifacial spasm had not disappeared completely for 5.1 +/- 1.7 (mean +/- standard error) months following the MVD procedure, F waves were still enhanced significantly and abnormal muscle responses were still recordable, albeit at lower amplitude. Within 1 month after the hemifacial spasm had disappeared completely. F waves were still significantly enhanced in 17 patients and abnormal muscle responses were recorded in seven of 15 patients. Subsequently, the enhanced F waves and abnormal muscle responses disappeared completely. The authors' study supports the hypothesis that the cause of hemifacial spasm is hyperexcitability of the facial motor nucleus and suggests that additional surgery should not be performed for at least 2 years after MVD, because that period is necessary for the disappearance of the hyperexcitability of the facial motor nucleus.

[Practical localization of the central sulcus using a video display during surgery by cortical somatosensory evoked potentials and how to discern precentral P20 and central P25].

In patients with lesions around the central sulcus, cortical surface somatosensory evoked potentials (SEPs) have been applied for the purpose of localization of the central sulcus based on the polarity inversion of postcentral N20 to precentral P20 across the central sulcus. We have intraoperatively monitored SEPs to infer the location of the central sulcus in 16 cases since December 1988. Intraoperative localization of the central sulcus has been most useful in patients with frontal lobe gliomas in which the localization of the central sulcus enables the surgeon to extensively resect tumor without postoperative motor weakness. The localization of the central sulcus, however, might be misjudged by using the polarity inversion criterion alone, because central P25 following N20 and P20 complicates SEP waveforms. It is significant that P25, which is recorded also posterior to the central sulcus, is discerned from the precentral P20. In order to solve this matter, we regarded only the positivity in SEP waveforms having the identical peak latency to that of N20 as the precentral P20. Positive potentials having a later peak latency than that of N20 are the superposition of P20 and P25, and might also be recorded posterior to the central sulcus. For the observation of the polarity inversion of N20 to P20 across the central sulcus, a multi-channel SEP should be recorded using a sheet of silicone rubber embedded in a 16-electrode array consisting of a 4 by 4 grid. We projected the exposed cortical surface on the video display through the microscope apparatus and marked the locations of the recording electrodes on the video display. This enabled the location of the recording electrodes to correspond easily and precisely to the cortical surface. Our reliable and simple method of intraoperative localization of the central sulcus by cortical SEPs monitoring is presented in a practical case.

Effect of repetitive stimulation on lateral spreads and F-waves in hemifacial spasm.

The lateral spread (LS) response, which can be elicited in muscles innervated by other branches of the facial nerve, is electromyographycally specific for patients with hemifacial spasm (HFS), occurring about 10 ms after stimulus. The F-wave in facial muscles, which is a late response that antidromicaly propagates to the facial motonucleus and returns orthodromicaly down the same axon, revealed a trend toward enhancement in patients with HFS. The LSs were facilitated by repetitive stimulation during the microvascular decompression (MVD) operation, which has proved to be a successful treatment, and the F-waves were also facilitated by repetitive stimulation on the spasm side more than on the normal side. Greater facilitation of these responses was in direct proportion to higher stimulation rates and greater numbers of stimulations. The repetitive stimulation of the facial nerve may result in activation of the motoneuron pool and in the lowering of the threshold of somatic membranes. These results support the hypothesis that hemifacial spasm is caused by hyperexcitability of the facial motonucleus, which is increased by antidromic repetitive stimulation.

Abnormal muscle response (lateral spread) and F-wave in patients with hemifacial spasm.

In patients with hemifacial spasm (HFS) the spasm is due to cross compression of the facial nerve by a blood vessel and microvascular decompression (MVD) has proved to be a successful treatment. Abnormal muscle response (AMR), which can be elicited by one facial nerve branch stimulation in muscles innervated by other branches of the facial nerve, is specific for patients with HFS, and the AMR consists of a constant response occurring about 10 ms after stimulus and an afterdischarge with long duration (variable response, autoexcitation). The F-wave in facial muscles is a small recurrent discharge that antidromically propagates to the facial motonucleus and returns orthodromically down the same axon. We measured the AMRs and F-waves of facial muscles in HFS patients in order to investigate the relationship of both potentials and the origin of the AMRs. We obtained facial nerve evoked electromyograms from 10 HFS patients. The afterdischarges of the AMRs and the enhanced F-waves were always elicited at the same time by marginal mandibular branch stimulation of the facial nerve. There was a linear correlation between the duration of these two potentials in each case. Between the duration of the afterdischarge of the AMRs elicited in the mentalis muscles by the zygomatic branch stimulation of the facial nerve and that of the F-waves in the mentalis muscles, there was also a linear correlation in 10 cases. These results suggest that the F-wave and the afterdischarge have the same origin and that the AMR is an exaggerated F-wave.

F-wave in patients with hemifacial spasm: observations during microvascular decompression operations.

In patients with hemifacial spasm (HFS), the spasm is due to cross compression of the facial nerve by a blood vessel. There are currently two hypotheses how the cross compression can cause HFS: 1. the spasm is caused by ephaptic transmission and hyperexcitability at the site of compression; and 2. the spasm is caused by hyperexcitability in the facial motonucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of anterior horn cell excitability. Enhancement of the F-waves in facial muscles also indicates increased excitability of the facial motonucleus. On the other hand, abnormal muscle response (AMR), which can be elicited by stimulating one branch of the facial nerve and recording electromyographically from muscles innervated by other branches of the facial nerve, is specific for patients with HFS. We have therefore measured the AMRs and the F-waves in the facial muscle of HFS patients under anesthesia in order to investigate the excitability of the facial motonucleus. We obtained facial nerve evoked electromyograms from 14 HFS patients during microvascular decompression (MVD) operation. The F-waves, obtained with surface electrodes from the mentalis muscle, were defined as the second response after the M-wave. The F-waves in facial muscles cannot usually be elicited during surgical anesthesia using inhalation anesthetics. However, the F-waves were elicited on the spasm side in 10 out of 14 patients with HFS and the F-waves disappeared after MVD under anesthesia, as the early responses (R1) of the blink reflex were elicited on the spasm side before MVD under anesthesia. The F-waves elicited during anesthesia were suppressed significantly, compared with those before MVD. These results suggest that excitability in facial motonucleus increased on the spasm side.

Electrophysiological investigation of hemifacial spasm: F-waves of the facial muscles.

In patients with hemifacial spasm (HFS), the spasm is due to cross-compression of the facial nerve by a blood vessel. There are currently two hypotheses for the mechanism of HFS: 1) the spasm is caused by ephaptic transmission and an increase in excitability at the site of compression; and 2) the spasm is caused by hyperexcitability in the facial nerve nucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of proximal motoneuron conduction and anterior horn cell excitability. Enhancement of the F-waves indicates increased anterior horn cell excitability. We have therefore measured F-waves in the facial muscle of HFS patients in order to investigate the excitability of the facial nerve nucleus. The authors obtained facial nerve evoked responses from 20 HFS patients before microvascular decompression (MVD), 10 HFS patients after MVD and 10 healthy controls. The F-waves, obtained with surface electrodes from the mentalis muscle, were the second response after the M-wave. On the patient's spasm side, the F-wave duration, F/M amplitude ratio and frequency of F-wave appearance significantly increased compared with those of the normal side or healthy controls; minimum latency and chronodispersion did not significantly differ between these groups. In patients whose spasm disappeared completely following MVD, the abnormal muscle response (lateral spread), which is a characteristic sign of HFS, and the enhancement of the F-wave eventually also disappeared. Because of the correlation between HFS and F-waves, the authors' study supports the hypothesis that the cause of HFS is hyperexcitability of the facial motonucleus.

The neural origin generating early cortical components of SEP: topographical analysis using temporal-second-order-differentiation of cortical SEPs.

In order to identify dipole generators of the N20/P20 and P25, we employed second-order-differentiation in the temporal dimension (temporal-second-order-differentiation; TSOD) with delta t = 2 msec. The rate of variation in the voltage of cortical SEPs calculated by TSOD identified responses of each dipole, reflecting the density of neuronal firing. On topographic analysis, the distributions of N20/P20 and P25 conformed to the shape of gyrus better in the TSOD maps than in the isovoltage maps. The TSOD maps indicated that N20 and P25 were post-central components and that P20 was a pre-central one. Therefore, we concluded that the two dipoles generating N20/P20 and P25 were located in the posterior wall of the central sulcus (area 3b) and the crown (areas 1 and 2) of the post-central gyrus, respectively.

[Neurophysiological study of hemifacial spasm--F wave of the facial muscles].

We studied the F wave of the facial muscles on both the normal side and the spastic side in 14 patients with hemifacial spasm. The purpose of this study was to determine if the mechanism of hemifacials spasm originates in ephaptic transmission in the facial nerve at the site of vascular compression or in a hyperexcited facial motor nucleus. Larger amplitude, longer duration and shorter latency F waves in the peripheral nerves than in normals indicate anterior horn cell hyperexcitability. We found abnormal potentials exhibiting synkinesis (lateral spread), a typical electrophysiological finding in hemifacial spasm, in the facial nerve evoked electromyograms of the 14 patients, none of whom had experienced facial palsy or facial nerve block. Electrical stimulation was delivered transcutaneously to the most distal portion of the marginal mandibular branch of the facial nerve. Using surface electrodes the F waves were obtained over the mentalis muscle as the second response after the M wave. While the F waves were normal on the patients' normal side, on the spastic side, their duration was longer (mean duration about 1.9 times that of the normal side), their onset latency was slightly shorter, and their F/M amplitude latency was greater than on the normal side. After microvascular decompression, the facial spasm and abnormal F-wave findings resolved. Onset latency was not increased, and on the spastic side some patients displayed facial spasm clinically and electrophysiologically for one year after MVD. In other words, there was hardly any focal demyelination of the facial nerve, so it is possible that ephaptic transmission and ectopic excitation are the mechanism of HFS.(ABSTRACT TRUNCATED AT 250 WORDS)

[Transcranial magnetic stimulation of the facial nerve--identification of the actual excitation site in the cat].

The site where transcranial magnetic stimulation excites the facial nerve was studied in 6 cats. Transcranial magnetic stimulation of the facial nerve was recorded from the left mentalis muscle. A figure-of-eight shaped magnetic coil was used, and coil induction direction had more influence on the facial nerve evoked compound muscle action potentials (CMAPs) than the coil position. No change could be detected in the CMAPs before and after craniotomy, after cerebellar lobectomy and after exposure of the facial nerve in the facial canal. The facial nerve was stimulated electrically at the porus, meatal portion, geniculum and horizontal portion. The latencies of the CMAPs for each portion were measured and compared with the magnetic response, which was coincidental with that of the meatal portion. The facial nerve was then transected distally from the porus, and CMAPs following magnetic stimulation were recorded at each step. The CMAPs disappeared when the nerve was transected at the fundus. The results of both approaches in this study led to the conclusion that transcranial magnetic stimulation excites the facial nerve at the meatal portion.

[A case of food-dependent exercise-induced anaphylaxis associated with repeated episodes of syncope].

This report describes a patient with food-dependent exercise-induced anaphylaxis (FEA). A 25-year-old female has had three episodes of syncopal attack associated with urticaria in the past two years: the attacks have been developed by exercise after taking meals made of wheat flour. She has an allergic predisposition to metals. No abnormal findings were observed in the routine work up for syncope including, ECG, 24-hour Holter ECG, UCG, tilt table test, and EEG examinations. A provocative test for FEA was performed. It included food (sandwich) intake followed by exercise. The serum histamine concentration was elevated to a three times higher than the control value after the provocation. Accordingly, she was diagnosed as FEA and advised not to take wheat flour prior to physical exercise. No syncopal episode has been observed during the 16 months since the diagnosis.

[Natural history for residual intracranial AVM: compared with that for conservatively treated AVM].

It is generally accepted that the most suitable treatment of AVM is surgical removal which does not cause neurological deficits. But in some cases, it is impossible to treat surgically because of size or location, so the patient is unfortunately discharged with some part of the nidus remaining. In this paper, we report the natural history of residual AVMs in which part of the nidus remained after initial therapy, and try to ascertain whether therapeutic reduction of the nidus is more effective in preventing intracranial hemorrhage than conservative treatment. Of 362 cases, residual AVMs were found in 35 cases, and were followed up for 9.2 years on average. Eighty cases treated with only conservative therapy were also followed up for 10.9 years on average. The annual risk of intracranial hemorrhage for residual AVMs was 2.9% and that for conservatively treated AVMs was 3.0%, not a significant difference. There was no difference between the two groups in mortality or ADL. We conclude that therapeutic reduction of the nidus was not effective in preventing intracranial hemorrhage.