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The topodiagnostic implications of hemiataxia following lesions of the human brainstem are only incompletely understood. We performed a voxel-based statistical analysis of lesions documented on standardised MRI in 49 prospectively recruited patients with acute hemiataxia due to isolated unilateral brainstem infarction. For statistical analysis individual MRI lesions were normalised and imported in a three-dimensional voxel-based anatomical model of the human brainstem. Statistical analysis revealed hemiataxia to be associated with lesions of three distinct brainstem areas. The strongest correlation referred to ipsilateral rostral and dorsolateral medullary infarcts affecting the inferior cerebellar peduncle, and the dorsal and ventral spinocerebellar tracts. Secondly, lesions of the ventral pontine base resulted in contralateral limb ataxia, especially when ataxia was accompanied by motor hemiparesis. In patients with bilateral hemiataxia, lesions were located in a paramedian region between the upper pons and lower midbrain, involving the decussation of dentato-rubro-thalamic tracts. We conclude that ataxia following brainstem infarction may reflect three different pathophysiological mechanisms. (1) Ipsilateral hemiataxia following dorsolateral medullary infarctions results from a lesion of the dorsal spinocerebellar tract and the inferior cerebellar peduncle conveying afferent information from the ipsilateral arm and leg. (2) Pontine lesions cause contralateral and not bilateral ataxia presumably due to major damage to the descending corticopontine projections and pontine base nuclei, while already crossed pontocerebellar fibres are not completely interrupted. (3) Finally, bilateral ataxia probably reflects a lesion of cerebellar outflow on a central, rostral pontomesencephalic level.

Somatosensory evoked potentials (SEPs) play a less important role in the diagnosis of multiple sclerosis (MS) than visually evoked potentials. Since standard SEPs only reflect the dorsal column function, we now investigated spinothalamic tract function in patients with MS using laser-evoked potentials (LEPs).LEPs to thulium laser stimuli (3ms, 540 mJ, 5mm diameter) were recorded from 3 midline positions (Fz, Cz, Pz) in 20 patients with MS, and 6 patients with possible but unconfirmed MS. Peak latencies and peak-to-peak amplitude of the vertex potential negativity (N2) and positivity (P2) were evaluated and compared with normative values from 22 healthy control subjects. Median and tibial nerve SEPs were recorded with standard methods. Depending on the results of sensory testing, two skin areas (both hands, both feet, or one hand and foot of the same body side) were assessed in each patient.In group comparisons, LEPs in patients with MS were significantly delayed and reduced in amplitude compared with healthy subjects (P0.001) or patients with suspected but unconfirmed MS (P0.05). In intraindividual comparisons within the patients with MS, LEP amplitude was significantly lower (P0.01) and latencies were significantly longer (N2: P0.01; P2: P0.05) for a clinically hypoalgesic skin area than an unaffected control area. On a single case basis, LEPs were abnormal in 12 (60%) and SEPs in 8 (40%) of the patients with MS; combined analysis of LEPs and SEPs raised sensitivity to 75% (15 patients). LEPs were also abnormal for 7 skin areas with clinically normal nociception and thermal sensitivity, indicating subclinical lesions. Standard SEPs detected subclinical lesions in 5 areas with normal tactile sensitivity.In patients with multiple sclerosis, spinothalamic tract function and LEPs were impaired more often than dorsal column function and SEPs. LEPs also detected subclinical lesions. Combined assessment of LEPs and SEPs can help to document dissemination of demyelinating CNS lesions and thus contribute to the diagnosis of multiple sclerosis.

Backgroud: Small brainstem infarctions are increasingly recognized as a cause of isolated ocular motor and vestibular nerve palsies in diabetic and/or hypertensive patients. This raises the question whether there are also isolated 7th nerve palsies due to pontine infarctions in patients with such risk factors for the development of cerebrovascular diseases. Methods: Over an 11-year-period, we retrospectively identified 10 diabetic and/or hypertensive patients with isolated 7th nerve palsies and electrophysiological abnormalities indicating pontine dysfunction. All patients had examinations of masseter and blink reflexes, brainstem auditory evoked potentials, direct current electro-oculography including bithermal caloric testing, and T1- and T2-weighted MRI (slice thickness: 4–7 mm). Results: Electrophysiological abnormalities on the side of the 7th nerve palsy included delayed masseter reflex latencies (4 patients), slowed abduction saccades (4 patients), vestibular paresis (2 patients), and abnormal following eye movements (2 patients). Electrophysiological abnormalities were always improved or normalized at re-examination, which was always associated with clinical improvement. MRI revealed an ipsilateral pontine infarction in 2 patients. Another 2 had bilateral hyperintense intrapontine lesions, and one an ipsilateral cerebellar infarction. Conclusions: Simultaneous improvement or recovery of abnormal clinical and electrophysiological findings strongly indicated that both were caused by the same actual pontine lesions. A 7th nerve palsy may be the only clinical sign of a pontine infarction in diabetic and/or hypertensive patients. Such mechanism may be underestimated if based on MRI only.

Patients with sensory disturbances of painful and non-painful character show distinct changes in touch and/or pain sensitivity. The patterns of sensory changes were compared to those of human surrogate models of neuropathic pain to assess the underlying mechanisms. We investigated 30 consecutive in-patients with dysaesthesia of various origins (peripheral, spinal, and brainstem lesions) and 15 healthy subjects. Tactile thresholds were determined with calibrated von Frey hairs (1.1mm). Thresholds and stimulus-response functions for pricking pain were determined with a series of calibrated punctate mechanical stimulators (0.2mm). Allodynia was tested by light stroking with a brush, Q-tip, and cotton wisp. Perceptual wind-up was tested by trains of punctate stimuli at 0.2 or 1Hz. Intradermal injection of capsaicin (n=7) and A-fiber conduction blockade (n=8) served as human surrogate models for neurogenic hyperalgesia and partial nociceptive deafferentation, respectively. Patients without pain (18/30) showed a continuous distribution of threshold shifts in the dysaesthetic skin area with a low to moderate increase in pain threshold (by 1.52+/-0.45 log2 units). Patients with painful dysaesthesia presented as two separate groups (six patients each): one showing lowered pain thresholds (by -1.94+/-0.46 log2 units, hyperalgesia) and the other elevated pain thresholds (by 3.02+/-0.48 log2 units, hypoalgesia). The human surrogate model of neurogenic hyperalgesia revealed nearly identical leftward shifts in stimulus-response function for pricking pain as patients with spontaneous pain and hyperalgesia (by a factor of about 5 each). The sensory changes in the human surrogate model of deafferentation were similar to patients with hypoalgesia and spontaneous pain (rightward shift of the stimulus-response function with a decrease in slope). Perceptual wind-up did not differ between symptomatic and control areas. There was no exclusive association of any parameter obtained by quantitative sensory testing with a particular disease (of either peripheral or central origin). Our findings suggest that neuropathic pain is based on two distinct mechanisms: (I) central sensitization (neurogenic hyperalgesia; in patients with minor sensory impairment) and (II) partial nociceptive deafferentation (painful hypoalgesia; in patients with major sensory deficit). This distinction as previously postulated for postherpetic neuralgia, is obviously valid also for other conditions. Our findings emphasize the significance of a mechanism-based classification of neuropathic pain.

There is a significant number of individual patients with cranial nerve palsies as the sole manifestation of MRI- and, less frequently, CT-documented small brainstem infarctions or hemorrhages. The 3rd and 6th nerves are most commonly involved and, less frequently, the 4th, 5th, 7th, and 8th nerves. An intra-axial basis for such lesions may be underestimated if the diagnosis is based solely on MRI. The electrophysiologic abnormalities indicating brainstem lesions may be independent of MRI-documented morphological lesions. This paper reviews the literature on cerebrovascular brainstem diseases manifesting as isolated cranial nerve palsies. It supports the concept that small pontine and mesencephalic infarctions are the main cause of non-traumatic cranial nerve palsies in the middle-aged and elderly population. Microvascular infarction of the respective extra-axial cranial nerve segments seem to be less important.

The purpose of this study was to identify clinical predictors and anatomical structures involved in patients with pain after dorsolateral medullary infarction. Eight out of 12 patients (67%) developed poststroke pain within 12 days to 24 months after infarction. The pain occurred in the ipsilateral face (6 patients) and/or the contralateral limbs and trunk (5 patients, 3 of whom also had facial pain). Ipsilateral facial pain was significantly correlated with lower medullary lesions, including those of the spinal trigeminal tract and/or nucleus, as documented by magnetic resonance imaging. The R2 blink reflex component was abnormal only in patients with facial pain. Likewise, pain and temperature sensation in the ipsilateral face was decreased in all patients with facial pain but not in patients without pain. Ipsilateral touch sensation in the face was also decreased in all patients with facial pain, but the lesions revealed on magnetic resonance imaging did not involve the principal sensory nucleus of the fifth cranial nerve, and the R1 blink reflex latencies were normal. Although facial pain was correlated with lesions of the spinal trigeminal tract and/or nucleus, none of the lesions involved the subnucleus caudalis, which contains most nociceptive neurons. These findings suggest that facial pain after medullary infarction is due to lesions of the lower spinal trigeminal tract (axons of primary afferent neurons), leading to deafferentation of spinal trigeminal nucleus neurons.

Objectives: Normative values of the masseter reflex are scarce. We studied the latencies, amplitudes and side differences of the masseter reflex in 105 healthy volunteers between the ages of 5 and 78 years. Methods: Latencies were calculated as the mean of 10 single sweeps and, simultaneously, measured from the summation curve. Short-term reproducibility was determined in 33 volunteers by retesting the reflex after 1 week. Results: There was a positive correlation between age and latencies and a negative correlation between age and amplitude. Maximal normal latencies were 8.3 ms for men and 7.9 ms for women in the age group below 50 years and 9.1 and 9.2 ms for the age group above 50 years. Latency differences between the right and left sides of >0.4 ms for subjects aged below 50 years and >0.5 ms for subjects aged above 50 years exceeded the 95% confidence interval. Amplitudes did not depend on gender. Calculated as a percentage of the side with higher amplitude, differences above one third could be accepted as abnormal. Conclusion: The masseter reflex appears to be a stable and robust clinical test, if age and gender differences are taken into account.

Brainstem dysfunction was evaluated in 67 patients with myelomeningocele and Chiari II malformation using brainstem auditory evoked potentials (BAEP), blink reflex (BR) and masseter reflex (MR). Signs and symptoms related to Chiari II malformation were observed in 18 patients while 49 patients had normal brainstem findings. BAEP and BR showed a higher sensitivity of brainstem involvement than MR (BAEP=1.0, BR=0.83, MR=0.50). BR, and in particular, MR were of higher accuracy (BR=0.52, MR=0.72) than BAEP (0.39) in separating patients with brainstem signs and symptoms related to Chiari II malformation. We feel that this is due to anatomic and physiologic peculiarities of the brainstem structures mediating BR and MR. Our results suggest that brainstem reflexes can support the decision of further treatment.

In einer prospektiven Studie untersuchetn wir 106 konsekutiv eingeschlossene Patienten mit apoplektiform auftretender Dysarthrophonie aufgrund eines im MRT gesicherten singluaren, nicht raumfordernden Infarkts.

Over a 13.5-year period, we observed 10 patients with isolated superior oblique palsies in whom electrophysiological abnormalities indicated brainstem lesions. In 7 patients unilateral masseter reflex abnormalities were seen, and were located on the side of the superior oblique palsy in 2 patients and on the opposite side in 5 patients. Two patients had slowed gain of following eye movements to the side contralateral to the superior oblique palsy. Slowed adduction saccades in the eye contralateral to the superior oblique palsy were seen in 1 patient. Clinical improvement was frequently (in 7 of 10 patients) associated with improvement or normalization of electrophysiologic findings. Magnetic resonance imaging (MRI) was normal, showing no evidence of brainstem lesions in 6 patients. Unilateral superior oblique palsy may be the only clinical sign of a brainstem lesion. Although such a cause may be underdiagnosed if based on MRI-documented lesions only, it remains a rare condition.

Objectives : Intra-individual variability of SEP parameters was investigated by serial SEP recordings. Methods : Median nerve SEP of 53 normal subjects (mean age 25.5±2.7 years) were evaluated. Recordings were repeated 1 week, 2 weeks, and 6 months after the initial recording. Results : Mean values of latencies from right median nerve stimulation were slightly longer (+0.1 ms) as compared to the left. The intra-individual (within stimulation side) variance did not depend on the time interval between recordings. The total within-stimulation-side variance of latencies was 0.056 ms 2 for N20 (C 3/4 ′ vs. F z ), 0.070 ms 2 for N13 (C 7 vs. F z ), 0.048 ms 2 for N10 (Erb's point vs. F z ), 0.111 ms 2 for P9 (C 3/4 ′ vs. contralateral forearm), and 0.148 ms 2 for P14 (C 3/4 ′ vs. contralateral forearm), and was about 3 times smaller than between-side variability with regard to cortical or spinal potentials. Upper limits for latency differences and lower limits for amplitude ratios in repeated recordings, as well as upper and lower limits for between-side latency differences and amplitude ratios were calculated, using F distributions with worst-case assumptions for degrees of freedom and error probability P =0.05. Upper limits of within-stimulation-side latency differences were 0.55 ms for N20, 0.62 ms for N13, 0.51 ms for N10, 0.78 ms for P9, and 0.90 ms for P14, and corresponding lower limits of amplitude ratios were 0.69, 0.62, 0.66, 0.45, and 0.50, respectively. Conclusions : Our results demonstrate a small systematic, and a larger random difference between right and left side stimulation, one arising from the peripheral, and the other one from the central pathway proximal to the source of N10.

During a 10 year period 24 patients with definite multiple sclerosis with isolated cranial nerve palsies were studied (third and fourth nerve: one patient each, sixth nerve: 12 patients, seventh nerve: three patients, eighth nerve: seven patients), in whom cranial nerve palsies were the presenting sign in 14 and the only clinical sign of an exacerbation in 10 patients. MRI was carried out in 20 patients and substantiated corresponding brainstem lesions in seven patients (third nerve: one patient, sixth nerve: four patients, eighth nerve: two patients). Additional abnormal findings of electro-oculography, or masseter reflex, or blink reflex, or combinations of these were found in 20 patients and interpreted in favour of a brainstem lesion at the level of the respective cranial nerve. In 11 of 14 patients with isolated cranial nerve palsies as the presenting sign of multiple sclerosis, dissemination in space was documented by MRI, and in the remaining three by evoked potentials. In patients with multiple sclerosis with isolated cranial nerve palsies, MRI is the most sensitive method of documenting dissemination in space and electrophysiological testing the most sensitive at disclosing brainstem lesions.

Electrical stimulation of the mental nerve evokes two suppression periods SP1 and SP2 in masseter muscle activity bilaterally. In order to investigate a possible nociceptive origin of the suppression periods, we compared the reflex responses evoked by electrical stimulation and by selective activation of nociceptors in hairy skin using painful infrared laser stimuli. The SP was elicited during more than 90% maximal voluntary contraction. Thresholds for detection, pain, and SP in the mental nerve area were determined by the method of limits. A suppression period was evoked by laser stimuli in nine of ten subjects bilaterally. The mean onset latency was 46.9 ms, the mean duration 58.9 ms. The electrical threshold of SP1 (9 mA) was 7.7 x I(0), about 20% smaller than I(P), and significantly higher than I(SP2) (4.7 mA). The onset latencies and durations were 11.7 ms and 21 ms for SP1, and 45 ms and 42.7 ms for SP2 (stimulus intensity 2 x I(P)). The mean difference in onset latencies between laser SP and electrically evoked SP1 was 35.1 +/- 6.2 ms, which closely matches the nociceptor response latency to a laser heat pulse. Based on the threshold and the onset latency we conclude that at least SP1 and laser SP are nociceptive in origin and mediated by group III fibers.

The electrically evoked blink reflex (BR) consists of an ipsilateral R1 component (R1) at 11 ms and two bilateral components R2 at 33 ms and R3 at 83 ms. It is still unclear whether the R2 is mediated by activation of tactile or nociceptive afferents. For testing the nociceptive hypothesis, nociceptors of the supraorbital nerve were selectively activated by infrared laser stimuli in 10 subjects. Only painful laser stimuli evoked a bilateral early polyphasic BR response (LR2) at 71 ms. Stimulation of infraorbital and mental nerve dermatomes was equally effective. A late bilateral reflex response at 130 ms was occasionally observed. Regarding the nociceptor activation time of about 40 ms, onset latencies were within the range of the electrically evoked R2 and R3, respectively. The good accordance of R2 and LR2 may be due to activation of identical nociceptive fibers or to convergence of electrically evoked tactile and laser-elicited nociceptive input onto common multireceptive neurons.

The difference between the median nerve latency to the second lumbrical muscle and the ulnar nerve latency to the second interosseous muscle (L-I DIFF) was tested in a prospective study to discriminate whether prolonged distal motor latency of the median nerve in patients with polyneuropathy (PNP) reflects an additional carpal tunnel syndrome (CTS). We investigated 92 patients (107 hands) with CTS, 30 patients (34 hands) with PNP, 22 patients (27 hands) with CTS and coexisting PNP (PNP+CTS), and 77 controls (87 hands). L-I DIFF was significantly prolonged in both the CTS and PNP+CTS patients as compared to PNP patients and controls. It proved to be the most specific test to differentiate between diffuse (PNP) and focal (entrapment) nerve disorder. © 1997 John Wiley & Sons, Inc. Muscle Nerve, 20, 153–157, 1997.

We investigated the supranuclear tracts involved in speech production in 8 patients with dysarthria associated with a single lacunar stroke.Magnetic resonance imaging revealed the lesion site in 7 out of 8 patients. We tested corticobulbar tract function using transcranial magnetic stimulation and demonstrated impairment of the corticolingual projections in all the patients and in 5 patients impairment of the corticofacial projections. Sensory function in the oral cavity was impaired in 1 out of 8 patients.99m Tc hexamethyl-propylene amine oxime-single-photon emission computerized tomography (HMPAO-SPECT) imaging, performed in 5 patients, showed cerebellar diaschisis in 1, suggesting additional cerebropontocerebellar tract impairment. Dysarthria observed in the 2 patients with impaired sensation in the oral cavity or with cerebellar diaschisis did not differ from the dysarthria found in the other patients. We conclude that interruption of the corticolingual pathways to the tongue is crucial in the pathogenesis of dysarthria following extracerebellar lacunar stroke.NEUROLOGY 1996;47: 1135-1141

Thirty-seven patients with risk factors for the development of cerebrovascular diseases had sudden onset isolated third nerve palsy and abnormal masseter reflex and/or electro-oculographic findings indicating a causative midbrain lesion. Improvement or recovery of the third nerve palsies was accompanied by improvement or recovery of the abnormal electrophysiologic findings pointing to their functional significance. Magnetic resonance imaging (MRI) in 29 of these patients demonstrated corresponding ischemic midbrain lesions in eight, ipsilateral in five patients, bilateral in three. In another three patients with MRI proven midbrain lesions (ipsilateral in two, bilateral in one) electrophysiological examinations were normal. Computer assisted tomography in 27 patients showed no brainstem lesion.

Dem klinisch tatigen Arzt erscheinen rechtliche Fragen fachfremd und werden haufig auch nicht wahrend des Studiums oder in der Weiterbildung vermittelt. Nicht selten betrifft dies sogar die durch die eigene Tatigkeit begrundete Arzthaftung, deren wichtigste Fallstricke allenfalls marginal bekannt sind. Seit Wegfall der Forderung nach einer Mindestzahl selbst erstatteter Gutachten in der Weiterbildungsordnung besteht bei jungeren Arzten oft auch nur noch ein geringes Interesse an der Durchfuhrung von Begutachtungen, obwohl diese – zumindest in einigen Rechtsgebieten – durchaus adaquat honoriert werden. Versicherte haben jedoch nicht nur Anspruch auf eine sachgerechte arztliche Behandlung, sondern im Krankheits- oder Schadensfall gleichermasen auch auf eine kompetente arztliche Begutachtung. Daruber hinaus liegen die volkswirtschaftlichen Kosten fur – haufig durch Gutachten induzierte – Renten- und Entschadigungszahlungen in derselben Grosenordnung wie die der Krankenversicherung. Ein wesentlicher Grund fur das geringe Interesse an Begutachtungen mag darin liegen, dass viele Arzte sich im Bereich rechtlicher Fragen ausgesprochen unsicher fuhlen und dann lieber die Hande davon lassen, um nicht in eine der zahlreichen „Fallgruben“ zu sturzen. Der nachfolgende Beitrag versucht ein Grundgerust fur den Umgang mit Begutachtungen zu vermitteln.

A technique for eliciting and recording the stretch reflex (R) of the medial pterygoid muscle (Pter) is described. The latency was 6.9 ± 0.43 ms in 23 healthy volunteers (mean age 23.7 years) showing a side-to-side difference of 0.29 ± 0.21 ms. The PterR latencies were little shorter and side-to-side difference little greater than of the masseter reflex. Observations in 5 selected patients with small brainstem lesions suggest that the neurons of the PterR afferents form a cluster within the caudal portion of the trigeminal mesencephalic nucleus. Testing the masseter and pterygoid reflexes provides a more precise localization of small ponto-mesencephalic lesions. © 1992 John Wiley & Sons, Inc.

Neuromuscular transmission was studied in the rat phrenic nerve-hemidiaphragm preparation with acetylcholinesterase (AChE) partially inactivated. Enzyme inhibition resulted in (1) increased single-twitch tension of the diaphragm; (2) compound muscle action potential (CMAP) containing repetitive discharges; (3) stimulus-induced antidromic backfiring (SIAB) seen in the phrenic nerve; and (4) repetitive nerve stimulation (RNS) eliciting a decrement-increment (D-I) phenomenon (i.e., amplitude reduction maximal with the second CMAP). Using a high-calcium and low-magnesium solution, SIAB and the decrement of the second CMAP during RNS were intensified, whereas closely spaced trains and (+)-tubocurarine (TC) abolished SIAB and simultaneously prevented the decrement of the second CMAP. Importantly, low concentrations of (+)-TC prevented SIAB in the phrenic nerve, while the repetitive discharges of the CMAP and the increase in twitch tension remained unaffected. This observation suggests that preterminal nicotinic receptors stimulated by released acetylcholine induce SIAB, whereas postsynaptic events are less important in the generation of SIAB. SIAB, a presynaptic event, appears to be responsible for the transient impairment of the neuromuscular transmission, i.e., the D-I phenomenon.

Horizontal eye movements were investigated in 65 patients with bilateral internuclear ophthalmoplegia utilizing direct current electro-oculography. Abduction saccades were slowed in 35 patients (53.8%), being hypermetric in 65.7% of them. Slowing of abduction saccades is attributed to impaired inhibition of the tonic resting activity of the antagonistic medial rectus muscle. Experimental data indicate that this slowing results from a lesion of an uncrossed connection between the pontine reticular formation and the oculomotor nucleus. The prevalence of hypermetric abduction saccades increased with increasing severity of adduction paresis on the opposite eye. This confirms the view that medial rectus paresis induces an increased phasic innervation proportional to the deficit in adduction. A commensurate increase in the phasic innervation of the agonistic lateral rectus muscle causes hypermetric abduction saccades.

Borreliosis seems a good example to use in furthering this discussion. Professor Bautsch gives a probability of borreliosis of about 85% after a positive test result in cases where an indication for a blood test is given (for example, facial paresis). The range of symptoms that is associated with borreliosis by doctors, patients, and self help groups is extremely broad, however, and many symptoms are also reported for diseases with a psychosomatic origin. For this reason, the question is how these individual symptoms are weighted when an indication is defined. Spontaneously, “hard” indicators that spring to mind include particular dermatological changes (erythema migrans, benign lymphocytoma, acrodermatitis chronica atrophicans), arthritis, and cardiomyopathy, as well as individual neurological disorders (for example, meningo radiculitis and paresis of the facialis muscle, although the latter is rare in adults). If other indicators are selected then the assessment of the result may more closely resemble that of a “population screening,” because often no consensus exists about whether individual symptoms are considered to be associated with borreliosis. In everyday clinical practice, it is easy to lose sight of this. Epidemiological studies assume that 35% of the population will come into contact with borreliosis depending on the region, but mostly this population never develops apparent signs of illness. If it is true that no clear distinction is possible between active and cured borreliosis (p 405, right hand column) then that makes it even more difficult to reach reliable conclusions. Even if such conditions can be included in the statistical estimates, just which conclusions could possibly be drawn?

Masseter (MR) and blink reflexes (BL) were investigated in 51 patients with internuclear ophthalmoplegia (INO) due to multiple sclerosis (28) and lacunar infarction (23). The MR was abnormal in 20 of 23 cases with bilateral INO and in 21 of 28 with unilateral INO. The R1 component of the BL (BL-R1) was abnormal in 7 of 23 patients with bilateral INO and 10 of 28 with unilateral INO. Combined MR and BL-R1 changes occurred in 8 of 28 cases with unilateral INO and 7 of 23 with bilateral INO. The findings provide evidence for a rostral/caudal localization of lesions within the medial longitudinal fasciculus causing INO on the basis of MR and BL-R1 abnormalities. An abnormality limited to MR suggests a midbrain location in 58.8% of patients while abnormal BL-R1 with or without an associated MR change suggests a rostral pontine location in 35.3%.