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C Helmchen

Publications and source records attributed to C Helmchen.

At least 37 records · Page 2Linked to original sources
PubMed2002

Localizing value of torsional nystagmus in small midbrain lesions.

BACKGROUND: The topodiagnostic value and specificity of nystagmus in patients with mesencephalic lesions and its relation to tonic torsional deficits and vertical saccade deficits is controversial and anecdotal. METHODS: The authors examined 11 patients with vascular MRI-identified mesencephalic lesions and clinical evidence of vertical-torsional nystagmus on gaze straight ahead, focusing on the three-dimensional nystagmus components recorded with the three-dimensional search coil technique. RESULTS: Combined lesions of the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and the interstitial nucleus of Cajal (iC) are much more frequent than riMLF and, in particular, iC lesions alone. Eight patients showed contralesional torsional nystagmus with a conjugate vertical component on gaze straight ahead and had anatomic (MRI) and clinical evidence (slowing of vertical saccades) for riMLF involvement. Tonic ocular torsion and the subjective visual vertical were shifted to the contralesional side (n = 7). Torsional nystagmus to the ipsilesional side was uncommon (n = 3) and found in patients with midbrain lesions involving the iC, all of whom also had decreased time constants of the slow phases of gaze-evoked nystagmus. CONCLUSIONS: Contrary to previous proposals, contralesional torsional nystagmus was the most frequent direction and is probably not compensatory for contralesional tonic ocular torsion. Small amplitude vertical saccades with normal velocities in association with ipsilesional torsional nystagmus may indicate isolated iC lesions. Torsional nystagmus following mesencephalic lesions may last for years and may help to distinguish rostral (riMLF) from caudal (iC) midbrain lesions.

Adult↗
PubMed2002

Disappearance of central thalamic pain syndrome after contralateral parietal lobe lesion: implications for therapeutic brain stimulation.

At present there is hardly any appropriate therapy for central pain syndromes available. We report on a unique case of a central thalamic pain syndrome that did not respond to any therapy but disappeared after an additional contralateral parietal lobe lesion. This example indicates that lesions affecting the bilateral balance of thalamo-parietal circuits may lead to pain relief in patients with central pain syndrome, which probably constitutes a bilateral disorder of functional plasticity. This should be taken into account in chronic brain stimulation for persistent pain states.

Electric Stimulation Therapy↗
PubMed2002

Effects of voluntary blinks on saccades, vergence eye movements, and saccade-vergence interactions in humans.

Blinks are known to change the kinematic properties of horizontal saccades, probably by influencing the saccadic premotor circuit. The neuronal basis of this effect could be explained by changes in the activity of omnipause neurons in the nucleus raphe interpositus or in the saccade-related burst neurons of the superior colliculus. Omnipause neurons cease discharge during both saccades and vergence movements. Because eyelid blinks can influence both sets of neurons, we hypothesized that blinks would influence the kinematic parameters of saccades in all directions, vergence, and saccade-vergence interactions. To test this hypothesis, we investigated binocular eye and lid movements in five normal healthy subjects with the magnetic search coil technique. The subjects performed conjugate horizontal and vertical saccades from gaze straight ahead to targets at 20 degrees up, down, right, or left while either attempting not to blink or voluntarily blinking. While following the same blink instruction, subjects made horizontal vergence eye movements of 7 degrees and combined saccade-vergence movements with a version amplitude of 20 degrees. The movements were performed back and forth from two targets simultaneously presented nearby (38 cm) and more distant (145 cm). Small vertical saccades accompanied most vergence movements. These results show that blinks change the kinematics (saccade duration, peak velocity, peak acceleration, peak deceleration) of not only horizontal but also of vertical saccades, of horizontal vergence eye movements, and of combined saccade-vergence eye movements. Peak velocity, acceleration, and deceleration of eye movements were decreased on the average by 30%, and their duration increased by 43% on the average when they were accompanied by blinks. The blink effect was time dependent with respect to saccade and vergence onset: the greatest effect occurred 100 ms prior to saccade onset, whereas there was no effect when the blink started after saccade onset. The effects of blinks on saccades and vergence, which are tightly coupled to latency, support the hypothesis that blinks cause profound spatiotemporal perturbations of the eye movements by interfering with the normal saccade/vergence premotor circuits. However, the measured effect may to a certain degree but not exclusively be explained by mechanical interference.

Adult↗
PubMed2001

Perilymph fistula associated with pulse-synchronous eye oscillations.

Three-dimensional eye movements (scleral search coil system) were recorded in a patient with a surgically acquired perilymph fistula of the left horizontal semicircular canal. Spontaneous horizontal pendular nystagmus was found to be related to the heart rate and may be caused by pressure transfer of blood pulses to the labyrinth. In addition, a contralesional horizontal jerk nystagmus was elicited by Valsalva maneuver, indicating that Ewald's first law may not only be valid for excitation but also for inhibition.

Aged↗
PubMed2001

Convergence retraction nystagmus: a disorder of vergence?

The pathological mechanism of convergence retraction nystagmus (CRN) is not known. To determine whether CRN is a disorder of vergence or of the saccadic system, the scleral search coil technique was used to record binocularly the three-dimensional components of CRN in a patient with a left mesencephalic infarction involving the nucleus of the posterior commissure and the rostral interstitial nucleus of the medial longitudinal fascicle. CRN had disconjugate horizontal and torsional components. The horizontal amplitude/velocity relationship of CRN aligned with the main sequence of vergence responses of normal control subjects but not with that of saccades. Vergence responses of the right eye and left eye were not asynchronous. The slow phases of CRN showed an exponential decay with a time constant of 70 milliseconds. Thus, CRN is probably a disorder of vergence rather than of opposing adducting saccades.

Adult↗
PubMed2001

Extensive myelitis associated with Mycoplasma pneumoniae infection: magnetic resonance imaging and clinical long-term follow-up.

Myelitis is a severe neurological complication associated with Mycoplasma pneumoniae infections. Little is known about the extent and the reversibility of this myelitis, and reports on the value of spinal imaging are inconclusive. To obtain more information on the diagnostic and prognostic value of spinal magnetic resonance imaging (MRI) we studied the clinical course and MRI long-term follow-up of two patients with extensive myelitis associated with M. pneumoniae infection. The neuroradiological findings were correlated with the clinical extent of the spinal syndrome, but their reversibility preceded clinical improvement. These preliminary findings indicate that follow-up spinal MRI may give valuable prognostic information in cases of M. pneumoniae associated myelitis and warrant further more systematic studies to ascertain the relationship between spinal MRI findings and prognosis.

Adult↗
PubMed2000

Vestibular influence on the binocular control of vertical-torsional nystagmus after lesions in the interstitial nucleus of Cajal.

The interstitial nucleus of Cajal (iC) is a center of the velocity-to-position integration for vertical and torsional eye movements. In addition, iC has projections to and from the vestibular nuclei. Therefore the vestibular influence on the binocular alignment of vertical-torsional nystagmus after unilateral reversible iC inactivations was investigated in the alert monkey using 3D binocular search-coil recordings. The nystagmus was compared with the eye muscle rotation axes, which were corrected for the tonic ocular torsion elicited by the iC inactivation. Rotation axes of nystagmus were different for both eyes and revealed a co-activation of eye muscles similar to the effects of electrical stimulation of the anterior canal nerve. This suggests that, in addition to the deficient neural integrator, a vestibular imbalance contributes to the vertical-torsional nystagmus after iC inactivations.

Animals↗
PubMed1999

Unilateral muscimol inactivations of the interstitial nucleus of Cajal in the alert rhesus monkey do not elicit seesaw nystagmus.

Seesaw-nystagmus (SSN) is a unique form of nystagmus with disconjugate vertical and conjugate torsional eye movements. Although rare, this disorder serves as a model for neuronal binocular control of the alignment of vertical-torsional eye movements of both eyes. The pathomechanism of SSN, however, is unclear. Studies in patients have suggested that the jerk SSN is associated with a midbrain lesion, i.e. a lesion of the interstitial nucleus of Cajal (iC), a center of integration of vertical and torsional eye movements. To test this hypothesis, we examined three dimensional binocular eye movements after reversible local inactivations of the iC and its immediate vicinity in the midbrain of the alert monkey. Inactivations were induced by muscimol microinjections. Eye movements were recorded with binocular scleral search coils. Isolated inactivations of neither the iC nor its immediate vicinity in the midbrain (including the adjacent rostral interstitial nucleus of the medial longitudinal fascicle, riMLF) elicited a disconjugate vertical/torsional nystagmus (SSN). However, there was a direction-specific right/left asymmetry in which a larger vertical amplitude was associated with the contralesional eye and a larger torsional amplitude with the ipsilesional eye, indicating a vestibular imbalance. We conclude that, first, iC lesions do not elicit SSN and, second, that apart from the gaze holding deficit a vestibular imbalance contributes to the vertical/torsional nystagmus after iC lesions.

Animals↗
PubMed1999

Cogan's syndrome: clinical significance of antibodies against the inner ear and cornea.

The aim of this study was to evaluate the pathological significance of antibodies against cornea and inner ear tissue in the development of audiovestibular and ocular symptoms in patients with Cogan's syndrome (CS). We analysed the serum of 5 CS patients for binding of IgM and IgG to fresh cryosections of rat labyrinth (semicircular canals, ampulla, utricle, saccule) and cornea by indirect immunofluorescence (IF). The predominant pattern of anti-corneal IgM was staining of the superficial cell layer of the non-keratinizing squamous epithelium. IgM against cornea was found in 3 patients, all of whom had bilateral inflammatory eye signs at the start of the disease. However, IgM was also detected in the chronic stage of the disease when no clinical signs of eye involvement were apparent. The study includes the first follow-up examination of anti-corneal IgM and IgG antibodies during a complete episode of active CS. During the first episode of CS in 1 patient, anti-corneal IgM became detectable 1 week after the onset of interstitial keratitis and 3 weeks after the onset of audiovestibular symptoms. It increased over several weeks and then fell to very low levels. However, at no time was anti-corneal IgG found. In the course of follow-up examinations, the serum of 4 patients intermittently contained low titre IgG antibodies against inner ear labyrinthine tissue, but without any clear correlation with the active stages of CS. In addition, high-resolution MRI (HR-MRI) of the inner ear was performed in the acute and chronic stages of CS to evaluate the activity of CS. In the acute stage, HR-MRI revealed abnormal MRI signals in the vestibule, semicircular canals, vestibular nerve, or cochlea. In the chronic stage, patients showed narrowing or occlusion of semicircular canals and the cochlea on the 3D-CISS images, but no high signal lesions (T1) and no enhancement. Antibodies against cornea or labyrinthine tissue were not consistently detected in CS and the level of organ-specific antibodies did not correlate with the activity of the disease.

Acute Disease↗
PubMed1999

Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review.

Head positioning can lead to pathological nystagmus and vertigo. In most instances the cause is a peripheral vestibular disorder, as in benign paroxysmal positioning vertigo (BPPV). Central lesions can lead to positional nystagmus (central PN) or to paroxysmal positioning nystagmus and vertigo (central PPV). Lesions in central PPV are often found dorsolateral to the fourth ventricle or in the dorsal vermis. This localization, together with other clinical features (associated cerebellar and oculomotor signs), generally allows one to easily distinguish central PPV from BPPV. However, in individual cases this may prove difficult, since the two syndromes share many features. Even if only BPPV as a peripheral lesion is considered, differentiation based on such features as latency, course, and duration of nystagmus during an attack, fatigability, vertigo, vomiting, and time period during which nystagmus bouts occur, may be impossible. Only the direction of nystagmus during an attack can allow differentiation.

Diagnosis, Differential↗
PubMed1998

Slow vertical saccades in motor neuron disease: correlation of structure and function.

We studied eye movements and brainstem pathology in 2 patients with slow vertical saccades and autopsy-proven amyotrophic lateral sclerosis (ALS). In both patients, the main ocular motor finding was supranuclear vertical gaze impairment with slow vertical saccades. The second patient had difficulty opening his eyes on command, with preserved spontaneous eyelid opening. Postmortem examination in both patients demonstrated cell loss in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and substantia nigra, along with histopathological findings consistent with ALS. The extent of the pathological changes in the riMLF correlated well with the degree of functional impairment as reflected in the slow vertical saccades. We suggest that motor neuron disease with early involvement of vertical saccades represents a distinct clinicopathological entity.

Amyotrophic Lateral Sclerosis↗
PubMed1998

Deficits in vertical and torsional eye movements after uni- and bilateral muscimol inactivation of the interstitial nucleus of Cajal of the alert monkey.

The mesencephalic interstitial nucleus of Cajal (iC) is considered the neural integrator for vertical and torsional eye movements and has also been proposed to be involved in saccade generation. The aim of this study was to elucidate the function of iC in neural integration of different types of eye movements and to distinguish eye movement deficits due to iC impairment from that of the immediately adjacent rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). We addressed the following questions: (1) According to the neural integrator hypothesis, all eye movements including the saccadic system and the vestibulo-ocular reflex (VOR) share a common neural integrator. Do iC lesions impair gaze-holding function for vertical and torsional eye positions and the torsional and vertical VOR gain to a similar degree? (2) What are the dynamic properties of vertical and torsional eye movements deficits after iC lesions, e.g., the specificity of torsional and vertical nystagmus? (3) Is iC involved in saccade generation? We performed 13 uni- and three bilateral iC inactivations by muscimol microinjections in four alert monkeys. Three-dimensional eye movements were studied under head-stationary conditions during vertical and torsional VOR. Under static conditions, unilateral iC injections evoked a shift of Listing's plane to the contralesional side (up to 20 degrees), which increased (ipsilesional ear down) or decreased (ipsilesional ear up) by additional static vestibular stimulation in the roll plane, i.e., ocular counterroll was preserved. The monkeys showed a spontaneous torsional nystagmus with a profound downbeat component. The fast phases of torsional nystagmus always beat toward the lesion side (ipsilesional). Pronounced gaze-holding deficit for torsional and vertical eye positions (neural integrator failure) was reflected by the reduction of time constants of the exponential decay of the slow phase to 330-370 ms. Whereas the vertical oculomotor range was profoundly decreased (up to 50%) and vertical saccades were reduced in amplitude, saccade velocity remained normal and horizontal eye movements were not affected. Bilateral iC injections reduced the shift of Listing's plane caused by unilateral injections, i.e., back toward the plane of zero torsion. Torsional nystagmus reversed its direction and ceased, whereas vertical nystagmus persisted. In contrast to unilateral injection, there was additional upbeating nystagmus. Time constants of the position integrator of the gaze-holding system did not differ between unilateral and bilateral injections. The range of stable vertical eye positions and saccade amplitude was smaller when compared with unilateral injections, but the main sequence remained normal. Dynamic vestibular stimulation after unilateral iC injections had virtually no effect on torsional and vertical VOR gain and phase at the same time when time constants already indicated severe integrator failure. Torsional VOR elicited a constant slow-phase velocity offset up to 30 degrees toward the contralesional side, i.e., in the opposite direction to spontaneous torsional nystagmus. Likewise, vertical VOR showed a velocity offset in an upward direction, i.e., opposite to the spontaneous downbeat nystagmus. Contralesional torsional and upward vertical quick phases were missing or severely reduced in amplitude but showed normal velocity. In contrast, bilateral iC injections reduced the gain of the torsional and vertical VOR by 50% and caused a phase lead of 10-20 degrees (eye compared with head velocity). We propose that the slow-phase velocity offset during torsional and vertical VOR reflects a vestibular imbalance. It therefore appears likely that the vertical and torsional nystagmus after iC lesions is not only caused by a neural integrator failure but also by a vestibular imbalance. Unilateral iC injections have clearly differential effects on the VOR and the gaze-holding function. (ABSTRACT TRUNCATED)

Animals↗
PubMed1998

Seesaw nystagmus associated with involuntary torsional head oscillations.

OBJECTIVE: To assess the diagnostic value of eye-head coupling in seesaw nystagmus (SSN). BACKGROUND: SSN is a rare binocular disorder characterized by alternating skew deviation and conjugate ocular torsion. METHODS: We examined a patient with a congenital nystagmus that switched to a pendular SSN on near viewing and was associated with involuntary torsional head oscillations. RESULTS: The binocular torsional eye movements were in phase with the clinically visible head oscillations (i.e., head movements were not compensatory for the torsional eye movements). CONCLUSION: This finding suggests that torsional eye-head coupling in pendular SSN has a common pathologic origin. We suggest that alternating vertical disparity of both eyes in pendular SSN is compatible with an oscillating signal acting on an intact vestibular system. The absence of brainstem lesions on high-resolution MRI supports this assumption.

Adult↗
PubMed1997

Diverse effects of Purkinje cell loss on deep cerebellar and vestibular nuclei neurons in Purkinje cell degeneration mutant mice: a possible compensatory mechanism.

The genetic defect in the Purkinje cell degeneration (PCD) mutant mouse completely disrupts the cerebellar corticonuclear connection through intrinsic action on the final integrating unit of the cerebellar cortex, the Purkinje cell (PC). The postsynaptic target neurons of the PC in the deep cerebellar nuclei (DCN) and the vestibular nuclei (VN) are denervated by this PC loss by more than two-thirds of their total y-aminobutyric acid (GABA)-ergic innervation. This massive disinhibition should be reflected in an increased and thus electrophysiologically detectable activity of the respective neurons. To address this question, we performed extracellular recordings of PCD mutant and corresponding wild-type VN neurons under sinusoidal vestibular stimulation. The response amplitudes (neuronal response to sinusoidal rotation) of VN neurons in PCD mutant mice showed a decrease rather than the expected increase. The same was true for the mean resting rate, whereas the phase relationships were unaffected for the most part. This finding is a clear indication of compensatory reactions in the VN that substitute quantitatively for the lost PC inhibition. The expression of the calcium-binding protein parvalbumin (Parv) is assumed to correlate with the physiological activity of neurons, and Parv is localized predominantly in inhibitory neurons. Because inhibitory inter- or projecting neurons are also largely denervated by the PC loss, Parv immunocytochemistry also was performed. In wild-type mice, only very few Parv-immunopositive (Parv+) somata were present in the VN, and none were present in the DCN. In PCD mutant mice, a substantial number of Parv+ neuronal somata were visible in the VN, and even more were visible in the DCN. This increase in Parv+ somata in PCD mutant mice is closely related temporally and spatially to the extent of denervation caused by the PCD. Parv+ neuronal somata are first visible in the dentate nucleus at postnatal day (P) 24 and appear in the other cerebellar and VN up to P29. Direct double labeling of Parv and GABA and of Parv and glycine reveals that the large majority of Parv + neurons colocalize GABA, glycine, or both inhibitory transmitters. These results show that neurons that are postsynaptic to cerebellar PC develop diverse physiological and biochemical reactions in the course of genetically determined PCD. These mechanisms are likely to contribute to the phenotypically mild motor disturbances observed in PCD mutant mice.

Animals↗
PubMed1997

Pathological torsional eye deviation during voluntary saccades: a violation of Listing's law.

BACKGROUND: Under normal conditions, there are no torsional eye movements during voluntary saccades when the head is stationary (Listing's law). METHODS AND RESULTS: Using dual search coils for three dimensional eye movement recordings, a patient is reported who had direction specific rapid deviations of torsional eye position (up to 10.5 degrees) during voluntary saccades followed by a slow exponential torsional drift after the end of the saccade ("blip") towards the initial torsional eye position. In the absence of spontaneous nystagmus, this transient torsion means a violation of Listing's law for voluntary saccades and was associated with a lesion involving the cerebellar vermis, its deep nuclei, and the dorsolateral medulla. Amplitudes of the blip were larger for ipsilesional (hypermetric) than contralesional (hypometric) horizontal saccades. For comparison transient torsion during and after saccades was also examined in six normal subjects. Using the same in vivo calibration, there were no blips larger than 1.2 degrees in any of them. CONCLUSION: Transient torsion with large amplitudes can be clinically seen on bedside examination and might thus be a new clinical sign in the diagnosis of saccadic disorders.

Adult↗
PubMed1996

Saccade-related burst neurons with torsional and vertical on-directions in the interstitial nucleus of Cajal of the alert monkey.

The interstitial nucleus of Cajal (iC) is known to be the neural integrator for vertical and torsional eye movements. Burst-tonic neurons are thought to be the neural substrate for this function. Until now, the iC has not been specifically considered to play a part in saccade generation. The aim of this study was to characterize saccade-related burst neurons in the iC during torsional and vertical eye movements. Saccade-related burst neurons were recorded in the iC of macaque monkeys during fast phases of torsional and vertical vestibular nystagmus, spontaneous and visually guided eye movements, and in light and darkness. Burst neurons in the iC (n = 85) were found intermingled between burst-tonic and tonic neurons. They were not spontaneously active, showed no eye position sensitivity, and responded during saccades and quick phases of nystagmus with a burst of activity whose duration was closely correlated with saccade amplitude and hence saccade duration (correlation coefficients up to 0.9). Latency in the on-direction was, on average, 10.4 ms (range 5-23 ms); it decreased with different saccade directions and became negative in the off-direction. In a horizontal-vertical coordinate system, on-direction of the majority of neurons was either upward (n = 52) or downward (n = 33). There was no horizontal on-direction. Burst neurons of different vertical on-directions were found intermingled throughout the iC. In the vertical-torsional plane, on-direction always showed an ipsiversive torsional component, i.e., a clockwise (positive) torsion for neurons in the right iC and a counterclockwise (negative) torsional component when recorded in the left iC. The findings indicate that saccade-related burst neurons in the iC control coordinate axes for vertical and torsional quick eye rotations. As in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), burst neurons in the iC encode vertical saccades with an ipsitorsional direction with similar burst characteristics. It is suggested that iC burst neurons play a part in the local feedback loop of the reciprocal iC-riMLF projections.

Animals↗
PubMed1996

A simplified calibration method for three-dimensional eye movement recordings using search-coils.

An algorithm is presented which allows the calibration of three-dimensional eye movements in two magnetic fields with two search-coils in one eye, whose relative orientation does not have to be known. Prior to recordings a calibration cube is placed in front of the eye to measure real and apparent crosstalk, produced by imprecisely oriented horizontal or vertical magnetic fields, and to obtain a first approximation of offset voltages. For calibration it suffices if one point is fixated and, in addition, spontaneous eye movements for 30-60 sec are performed. Additional fixation points can be used to improve the calibration. Position quaternions are applied for computing eye movement recordings from man and monkey and to determine Listing's plane.

Algorithms↗