Bilateral medial medullary infarction presented with monoplegia of the lower limb, followed by paraplegia and finally by tetraplegia]

A 69-year-old Japanese man suddenly developed monoplegia of left lower extremity, followed by paraplegia and finally by tetraplegia. MRI revealed an infarction in bilateral medial medulla extending from the cervicomedullary junction up to the upper limit of the medulla. Both hypoglossal nerve palsy and sensory disturbance were absent. At the pyramidal decussation, fibers to the lower extremities cross caudal to the fibers going to the upper extremities, therefore right below the decussation, fibers to the lower extremities run medial side of the fibers to the upper extremities, but later the former run lateral side of the latter. In this patient, the authors considered that the lesion initially damaged the pyramidal decussation at a slightly lower level, involving the tract to left lower extremity, and then extended to right lower extremity, to the left upper extremity, finally to the right upper extremity. Bilateral medial medullary infarction must be considered in the clinical course seen as in this patient.     

Effect of transcutaneous electrical nerve stimulation (TENS) on central nervous system amplification of somatosensory input

The effect of transcutaneous electrical nerve stimulation (TENS) on the central nervous system amplification process was investigated focusing on the dorsal column-medial lemniscal pathway, because the dorsal column nucleus was recently shown to receive multiple sources of sensory information, including pain. Short latency somatosensory evoked potentials (SSEPs) were recorded in ten healthy normal volunteers. Amplitude changes in each SSEP component (the N9 brachial plexus potential, the P14 potential that originates from the cervicomedullary junction, spinal N13/P13 generated by the cervical dorsal horn and the cortical N20/P25 potential) were studied at stimulus strenghts ranging from the threshold (40% maximum stimulus) to 2.5 times the threshold (maximum). The findings suggest that sensory amplification begins at the P14 generator source near the cuneate nucleus. There was no statistically significant difference in sensory amplification between P14 and cortical N20/P25, indicating that the cuneate nucleus is the main site of the central amplifying process. When TENS was applied to the palm distal to the median nerve stimulation used for SSEP, cortical N20/P25 amplification disappeared, evidence that TENS suppresses the central amplification phenomenon, most probably at the level of the cuneate nucleus. Received: 29 October 1996 Received in revised form: 13 October 1997 Accepted: 6 November 1997     

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.

     

Dorsally exophytic cervicomedullary glioblastoma

Spinal glioblastoma multiforme is a rare entity comprising 1.5% of all spinal cord tumors. We report a 57-year-old man presenting with a 1.5 month history of left sided radiculopathy, lower cranial nerve weakness and difficulty in walking. MRI of the brain and spine showed an exophytic intramedullary lesion extending from the cervicomedullary junction to the lower margin of C4. To our knowledge, we report the first patient with dorsally exophytic cervicomedullary and cervical intramedullary glioblastoma multiforme.     

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.     

Electrophysiological evaluation in 4 patients with diabetic pseudotabes

BACKGROUND: Researches on diabetic nervous system lesion are mainly focus on peripheral nerve and vegetative nerve, so there are few investigations on diabetic pseudotabes. OBJECTIVE: To investigate the electrophysiological examinations on the diagnosis of diabetic pseudotabes. DESIGN: Case study. SETTING: Department of Electrophysiology and Department of Neurology, Zhongshan Hospital Affiliated to Xiamen University. PARTICIPANTS: A total of 4 patients with type 2 diabetes mellitus, including 3 males and 1 female aged from 50 to 72 years, were selected from Department of Neurology, Zhongshan Hospital Affiliated to Xiamen University from March 2002 to February 2005. All accepted subjects met the modified diagnostic criteria of diabetes mellitus, which was set by American Diabetes Mellitus Association (ADA) in 1997. Otherwise, the subjects had typical symptoms and physical signs of spinal posterior funiculus damage. However, patients with spinal cord lesion which was caused by other factors were excluded. All accepted subjects provided the confirmed consent. METHODS: Nicolet NT electromyography (EMG)/evoked potential meter (made in the USA) was used to detect spinal cord conduction velocity (SCCV), somatosensory evoked potential (SEP) of lower limbs, motor nerve conduction velocity (MNCV) and sensory nerve conduction velocity (SNCV) of extremities. Determining criteria: Measurements were performed based on the laboratory standards. SCCV, which was less than lower limit of normal value (T2–12: 40–55 m/s, T12–L4: 20–41 m/s, T2–L4: 36–45 m/s), was regarded as abnormal. SEP value of lower limbs: P40, P60 and PF, which were more than standard deviation of normal value (x(—)+2.5), were regarded as the abnormality. Normal value of P40, P60 and PF latencies (x(—)±s) in this study: P40, P60 and PF in males were (37.6±1.9) ms, (59.8±3.9) ms and (7.6±0.9) ms, respectively; meanwhile, those in females were (35.5±1.7) ms, (55.2±2.7) ms and (6.3±0.7) ms, respectively. MNCV and SNCV, which were less than 50 m/s in upper limbs and 40 m/s in lower limbs, were regarded as the abnormality. MAIN OUTCOME MEASURES: Electrophysiological examinations. RESULTS: All 4 patients with type 2 diabetes mellitus were involved in the final analysis. ① SCCV: Among 4 patients, SCCV of three patients was decreased in T2–12, T12–L4 and T2–L4, and that of the other one was decreased in T2–12 and T2–L4; however, SCCV in T12–L4 was normal. There was significant difference as compared with normal value (P < 0.01). ② SEP of lower limbs: SEP values of lower limbs were abnormal in all 4 patients. Among them, P40, P60 and PF latencies of two patients were delayed; P40 of one patient was delayed and PF was not drained out; P40 and P60 of the last one were delayed and PF was normal. ③ MNCV and SNCV: The MNCV and SNCV were normal in one patient and abnormal in three patients. The results demonstrated that MNCV and SNCV of extremities decreased; especially, sensory nerve action potential (SNAP) of both lower extremities of one patient were not drained out. CONCLUSION: Detections of SCCV, SEP of lower limbs, MNCV and SNCV of extremities are helpful to investigate whether peripheral nerve and deep sensory passage are damaged or not and determine whether deep sensory damage is caused by peripheral nerve and spinal posterior funiculus.     

Lower cervical origin of the P13-like potential in median SSEPS.

The authors studied the origin of the scalp P13-like potential in median somatosensory evoked potentials, which have been reported to be preserved in patients with cervicomedullary lesions or in brain death. There were five patients with high to middle cervical lesions (C2/3 or C3/4 level). Small P13-like potentials after P11 were identified for all patients with a noncephalic reference but not with an ear reference. Their onset latencies were slightly earlier than the expected latency of the true P13/14 onset. In two patients, delayed true P13/14s followed by N18s were identified with both noncephalic and ear references. The authors argue that the P13-like potential observed in these patients is a different entity from scalp P13 in normal subjects. Because the C3/4 vertebral level corresponds to the C5 cord level, the origin of the P13-like potential must be below C5, contradicting the previous opinion that it is generated at the cervicomedullary junction or at the high cervical dorsal column. The authors named this potential lower cervical P13 (or lcP13), and present an opinion that it is generated by the beginning of the second spinal ascending volley, which has been described by direct-recording studies in humans.     

Involvement of peripheral sensory fibers in amyotrophic lateral sclerosis: Electro-physiological study of 64 cases

We report electrophysiological findings of conduction along peripheral sensory fibers in 64 patients with amyotrophic lateral sclerosis. Distribution of the values of action potential amplitudes and conduction velocities of peripheral afferent fibers were significantly lower than in normal age-matched controls. Sensory action potential amplitudes (SAPas) were more affected than sensory conduction velocities (SCVs). When single patients were considered, SAPas were slightly but significantly reduced in 22% of the cases (median nerve 17%, ulnar nerve 11%, and sural nerve 22%). A parallel decrease in SCVs and MCVs in 14 patients in whom the study was repeated over a period of time was also found. All these electrophysiological findings are due to progressive neuronopathy of peripheral sensory fibers. A pathogenetic mechanism is proposed. © 1993 John Wiley & Sons, Inc.     

Evidence for an abnormal cortical sensory processing in dystonia: selective enhancement of lower limb P37-N50 somatosensory evoked potential.

We evaluated brain stem P30, contralateral frontal N37, and the vertex-ipsilateral central P37, N50 somatosensory evoked potentials (SEPs) obtained in response to stimulation of the tibial nerve in 10 patients with idiopathic dystonia. Results were compared with those obtained in 10 healthy subjects matched for age and sex. The amplitude of the brain stem P30 potential and of the contralateral frontal N37 response in dystonic patients was not significantly different from that recorded in normal subjects. The vertex- ipsilateral central P37-N50 complex, which is thought to originate in the pre-rolandic cortex, was significantly enhanced in patients compared with the control group. These results suggest the enhancement of the vertex-ipsilateral central P37-N50 complex might reflect an abnormal response to somatosensory inputs of a precentral cortex which is excessively activated because of a disorder of the basal ganglia. Such inefficient sensory processing in motor areas might contribute to motor impairment in dystonia.     

Determination of nerve conduction abnormalities in patients with impaired glucose tolerance

Recent studies have shown that impaired glucose tolerance (IGT) is associated with dysfunction in the peripheral and autonomic nerves. The aim of this study was to determine the electrophysiological abnormalities of IGT. To determine electrophysiological abnormality in the large sensorimotor and sudomotor autonomic nerves with IGT patients, 43 patients and 34 healthy subjects have been studied. Subjective neuropathy symptoms, neurological examination and the electrophysiological findings were evaluated. When conduction of large somatic fibers only was evaluated, the ratio of electrophysiological abnormality was found to be 21%. In addition, where sympathetic skin response was evaluated the sudomotor autonomic abnormality ratio was 28% in upper extremities, 53% in lower extremities, and 16% in upper and lower extremities together. The percentages of abnormal electrophysiological parameters in different motor and sensory nerves were 39.5% in the peroneal motor nerve, 20.9% in the median motor and sural sensory nerves, 18.6% in the median sensory nerve, 16.3% in the tibial motor nerve, 14% in the ulnar sensory nerve, and 2.3% in the ulnar motor nerve. While distal motor latency was the most frequent abnormal parameter in the median and tibial motor nerves, the amplitude changes in the peroneal and ulnar motor nerves were also prominent. In sensory evaluation, the onset latency in the median-ulnar sensory nerves and the amplitude in the sural sensory nerve were found to be evident abnormalities.     

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     

Absent median nerve P14 far-field somatosensory evoked potential with persistent tibial nerve P30 component in a patient with ischemic pontine lesion

In a patient with an ischemic lesion of the right paramedian region of the pons, somatosensory evoked potential (SEP) recording to median nerve stimulation showed an absent P14 response with still preserved P13 and N18 potentials. The tibial nerve P30 and N33 SEP components were normal. Our results suggest that the median nerve P14 potential, absent in our patient, has a different origin from the tibial nerve P30 response, normal in the present case.     

Effect of movement on dipolar source activities of somatosensory evoked potentials.

The early scalp somatosensory evoked potentials (SEPs) to median and tibial nerve stimulation were recorded at rest and during voluntary movement of the stimulated hand and foot, respectively. Both tibial and median nerve SEP distributions at rest could be explained by four-dipole models, in which one dipole was activated at the same latency as the subcortical far field and the three remaining dipolar sources were located in the perirolandic region contralateral to the stimulated side. Voluntary movement reduced all cortical dipoles in strength, while the subcortical one remained unchanged, suggesting that the effect of movement occurs above the cervicomedullary junction. In animals, cutaneous inputs are suppressed during movement and we therefore interpreted the depression of activity in the primary somatosensory cortex induced by movement as due to selective "gating" of cutaneous afferents. Because the reduction in strength of the cortical dipoles was generally lower during passive than active movement, both centrifugal and centripetal mechanisms probably contribute to the phenomenon of "gating." Copyright 1999 John Wiley & Sons, Inc.     

Anomalies in early somatosensory evoked potentials in brain stem lesions (study of 64 cases)

Short latency somatosensory evoked potentials (SEPs) have been recorded in 64 patients with brainstem lesions documented by neuroimaging techniques. Patients were classified in four groups according to the lesion topography: cervico-medullary junction and medulla (16 cases), pons (19 cases), mesencephalon (8 cases), extensive (21 cases). SEPs were abnormal in 57.8% of cases either bilaterally (17.2%), or unilaterally (40.6%). The different components were affected as follows, P14: 34.4%; N20: 56.9%; P22 and N30: 54.7%, peripheral and spinal responses were always spared: N18 and P14 abnormalities were highly correlated. In cervico-medullary lesions P14 and N20 were constantly abnormal, P14 was normal in strictly mesencephalic lesions but could be abnormal in cases of subthalamic lesions with mesencephalic extension; in pontic lesions, P14 could be normal or not, and N20 was always very reduced. These results confirm that P14 has a supra-spinal origin and may have two generators. SEPs detected a subclinical dysfunction of the lemniscal pathways in 18% of patients with normal somatosensory performances and, as BAEPs (abnormal in 54% of the 54 recordings performed in this series) deserve to be recorded for the routine investigation of brainstem function.     

Short latency somatosensory evoked potentials from radial, median and ulnar nerve stimulation in man

Short latency somatosensory evoked potentials (SEPs) were elicited by stimulation at the wrist of median, radial, and ulnar nerves, singly or in combination, using normal subjects. Amplitude of P10 was strikingly lower with radial stimulation than with median stimulation, while ulnar-derived P10 was intermediate in amplitude. This difference probably reflects the antidromic firing of motor fibers contained in median nerves as compared with the superficial branch of radial nerve, which is entirely sensory. Beyond P10, there appear to be no significant differences between median, radial and ulnar-derived SEPs. With simultaneous stimulation of several nerves within one arm, larger potentials were sometimes achieved but with poorer definition of P12 and P14. The clinical utility of radial, ulnar, and median stimulation for localizing peripheral lesions derives from the distinct anatomical pathways of the stimulated fibers through the brachial plexus and from the separable motor and sensory components of P10. SEP is less invasive than EMG; this fact, plus its freedom from sampling error, make it potentially more suitable than conventional EMG for sequentially following a patient's clinical course.     

The "Gulf War syndrome". Is there evidence of dysfunction in the nervous system?

In a pilot study, 14 Gulf War veterans were randomly selected from a large list of those with unexplained illness, to compare the functional integrity of the peripheral and central nervous system with a group of 13 healthy civilian control subjects using predetermined outcome measures. The controls were matched closely for age, sex, handedness, and physical activity. Outcome measures included scoring of symptoms and clinical neurological signs, quantitative sensory testing of heat, cold and vibration sensibilities, motor and sensory nerve conduction studies on upper and lower limbs, needle EMG of distal and proximal muscles and multimodality evoked potential (visual, brainstem, and somatosensory) studies. Three measurements, all related to peripheral nerve function (cold threshold (P = 0.0002), sural nerve latency (P = 0.034), and median nerve sensory action potential (P = 0.030) were abnormal in the veterans compared with the controls. There may be a dysfunction in the veterans but more studies are required to investigate the findings further and to characterise the dysfunction if confirmed.     

138例糖尿病患者神经电图分析

目的探讨2型糖尿病患者周围神经病变(DPN)的神经电生理特点及其与病程的关系。方法连续记录138例血糖控制良好的糖尿病患者神经电图(包括感觉神经传导速度SCV和运动神经传导速度MCV)的检测结果,并根据糖尿病病程将其分组进行比较。结果共检测周围神经1669条,异常神经313条(18.75%),下肢异常率(132/530,24.9%)明显高于上肢(59/517,11.4%)(P<0.0001),感觉神经(122/622,19.6%)与运动神经(191/1047,18.2%)受累无差异(P=0.5665);糖尿病病程10年以上者运动、感觉神经异常率(24.3%,33%)明显高于病程小于10年组(14.2%,14%)(P<0.001)。病程大于10年组神经传导速度均较病程小于10年组减慢,正中神经、胫后神经运动传导速度和尺神经、腓肠神经感觉传导速度有统计学意义(P<0.05);除尺神经外所查运动神经近远端复合肌肉动作电位波幅(CAMP)病程≥10年组均明显低于病程<10年组。结论尽管受检时血糖控制良好,但依然有周围神经电生理异常变化。2型糖尿病患者下肢神经传导异常率高于上肢,尤以运动神经明显。病程是糖尿病周围神经损害的危险因素,随着病程增加神经传导异常率和损伤严重程度增高。     

糖尿病周围神经病病情分级与电生理的相关性

目的探讨糖尿病周围神经病病情分级与电生理的相关性。方法依据糖尿病性周围神经病的诊断标准确定入选对象;依据糖尿病周围神经病病情分级对入选对象进行临床分级;应用丹麦产DANTEC CANTATA型肌电图仪,进行运动神经和感觉神经传导功能检查。结果腓肠神经、正中神经诱发感觉动作电位波幅(SNAP)和腓总神经复合肌肉动作电位波幅(CMAP)随病情分级的升高而明显减低(P<0.05);腓肠神经、正中神经感觉传导速度(SCV)和腓总神经、正中神经运动传导速度(MCV)3级与1、2两级比较显著减慢(P<0.05)。结论神经电生理改变,尤其感觉神经电生理改变,易此作为糖尿病周围神经病情程度评定的指标。     

The utility of various sensory nerve conduction responses in assessing brachial plexopathies

To determine which sensory nerve conduction studies (S-NCS) are helpful in detecting supraclavicular axon loss brachial plexopathies, we selected 53 cases (of 417 reviewed) in whom complicating factors were absent and which, by needle electrode examination findings, involved only a single “truncal” element (upper, middle, or lower) of the brachial plexus. Extensive S-NCS included: median, recording thumb (Med-D1), index (Med-D2), and middle fingers (Med-D3); ulnar, recording fifth finger (Uln-D5); dorsal ulnar cutaneous, recording dorsum of the hand (DUC); radial, recording base of thumb; and both medial and lateral antebrachial cutaneous (MABC, LABC), recording forearm. Except for the median sensory fibers, the “cord” elements traversed by the sensory fibers assessed during the S-NOS listed above are anatomically defined (i.e., the sensory fibers enter the brachial plexus at only one cord). In regard to the median sensory fibers, however, there are two possible pathways through the infraclavicular plexus: (1) the lateral cord and/or (2) the medial cord. Because the lower trunk is only accessible via the medial cord, any sensory fibers found to be traversing the lower trunk had to first traverse the medial cord. Similarly, those traversing the upper and middle trunks must first be a component of the lateral cord. The frequency that the various S-NCS responses were abnormal (unelicitable, below laboratory normal value, or ≤ 50% of the contralateral response) for a given brachial plexus element lesion was as follows: (1) upper trunk (UT): 25 of 26 Med-D1, 25 of 26 LABC, 15 of 26 radial, 5 of 26 Med-D2, 2 of 26 Med-D3; (2) middle trunk (MT): 1 of 1 Med-D3; (3) lower trunk (LT): 25 of 26 Uln-D5, 22 of 23 DUC, 11 of 17 MABC, 3 of 23 Med-D3. With lower trunk brachial plexopathies, both “routine” (Uln-D5) and “uncommon” (DUC; MABC) S-NCS are abnormal. With upper trunk brachial plexopathies, in contrast, only the “uncommon” S-NCS (Med-D1; LABC) are consistently affected. The “routine” median S-NCS recording digit 2 (Med-D2) is far less reliable than the median S-NCS recording digit 2 (Med-D1) in detecting upper trunk axon loss brachial plexopathies. Additionally, the various pathways traversed by the fibers contributing to the individual S-NCS responses can be predicted, an important point when the full extent of a brachial plexus lesion is sought. © 1995 John Wiley & Sons, Inc.     

A case of left third nerve palsy and contralateral vertical gaze palsy with medial midbrain infarction]

An 81-year-old man developed oculomotor nerve palsy of the left eye and vertical gaze palsy of the right eye due to left medial midbrain infarction. His left eyelid was ptotic and the pupil was dilated. His right eye showed normal horizontal movement and Bell's phenomenon was preserved although the oculocephalic reflex was incomplete. There were no other abnormal neurological findings. The brain MRI revealed a high-intensity lesion in left medial midbrain on T2 weighted image. This lesion involved the oculomotor nerve nucleus, the interstitial nucleus of Cajal, and the rostral intersititial nucleus of the medial longitudinal fasciculus (riMLF). We thought that upward gaze palsy of the right eye was resulted from the infarction of the left riMLF or disruption of the axonal collateral of upward gaze fibers in the left oculomotor nucleus. Downward gaze palsy was resulted from the damage of the downward gaze fibers before their decussation, or the damage of the left interstitial nucleus of Cajal. This case provides evidence that unilateral lesion of the midbrain could cause contralateral vertical gaze palsy.