Anatomy of optic nerve radiations as assessed by static perimetry and MRI after tailored temporal lobectomy.

AIMS: To determine the course of optic nerve radiations in the temporal lobe, especially their retinotopic organisation and the anterior limit of the Meyer's loop. METHODS: 18 adult patients who had undergone a tailored temporal lobectomy for epilepsy were included in this study between 1994 and 1998. The rostrocaudal extent of the lateral temporal lobe resection assessed intraoperatively by the surgeon and by postoperative MRI was compared with the postoperative visual fields determined by automated static perimetry (ASP). RESULTS: 15 patients (83%) presented a postoperative visual field deficit (VFD) confined to the superior homonymous field contralateral to the side of the resection. All degrees from a minimal upper field loss to a complete quadrantanopia were observed. The VFDs were somewhat stereotyped, predominating along the vertical meridian. The smallest anteroposterior resection resulting in a VFD was limited to 20 mm from the tip of the temporal lobe. A relation was observed between the extent of the lateral resection in front of the second and third convolutions and the occurrence and extent of postoperative VFDs. No patient reported persisting subjective visual impairment. CONCLUSION: The high frequency of postoperative VFDs appears to be due to the greater sensitivity of ASP. The characteristics of the stereotyped VFDs allow new conclusions about the course and retinotopy of optic nerve radiations. The anterior limit of Meyer's loop is likely to be located more rostrally than previously believed.

Course of valvular strands in patients with stroke: cooperative study with transesophageal echocardiography.

BACKGROUND: Native valve strands might be related to the acute stage of thrombosis or might suggest a long-term valvular change. We aimed to estimate changes in the strands in patients with stroke through a serial transesophageal echocardiographic (TEE) study. METHODS AND RESULTS: A study was conducted among patients who were referred for TEE for stroke or cardiac pathology. Patients had TEE examinations with a 5-MHz multiplane TEE probe. Echocardiography was repeated 3 months later in patients with stroke. TEE was performed in 180 patients admitted to cardiology units and in 160 patients referred to neurology units. Among 34 patients with valvular strands, 30 were referred to neurology for stroke, whereas 4 patients were admitted to cardiology (18.8% versus 2.2%, difference 16.5%, 95% confidence interval 10% to 22.9%, P =.001). Strands were located on the mitral valve in 16 patients, the aortic valve in 6 patients, and both left heart valves in 8 patients. Among the 38 valves with strands, 17 (44. 7%) were morphologically normal, 4 (10.5%) were thickened, 7 (18.4%) were redundant, and 10 (26.3%) had both abnormalities. TEE showed other abnormalities in 16 (53.3%) patients, whereas 14 patients had only strands. Twenty-six (86.6%) patients had a second TEE study 3 months later. Strands were not found in 4 (15.4%) patients (95% confidence interval 4.3% to 34.9%). CONCLUSIONS: Valvular thickening or redundancy may predispose valves to strand formation. Native valve strands usually persist and thus reflect a chronic valvular change.

Postural asymmetry reduction by vestibular caloric stimulation in left hemiparetic patients.

The purpose of this study was to investigate the effects of caloric vestibular stimulation on the postural sway characteristics of hemiparetic patients. Two groups of 15 hemiparetic patients each (right and left) were compared to a group of 15 control subjects. Hemiplegic patients were selected for the study if they showed ability to stand without external support for at least 30 seconds. Posturographic evaluation was performed on a statokinesimetric platform just before and after a cold contralesional ear irrigation (20 degrees C) during 60 seconds. Two quantitative parameters were analysed: the antero-posterior difference and the lateral difference, reflecting the asymmetry of standing in the antero-posterior and frontal planes, respectively. The results of the 3 groups studied were compared with a Student's t-test. Before stimulation, as previously reported, left hemiparetic patients showed a predominant lateral displacement of the centre of pressure toward the side of the lesion, as compared to right hemiparetic patients. After vestibular stimulation, the lateral displacement was reduced in both patient groups, predominantly in the left hemiparetic group. After vestibular stimulation, the lateral displacement thus was not different in both patient groups and in the control group. Antero-posterior differences were not significantly different in the patient groups and in the control group before stimulation and were not affected by vestibular stimulation. The suggestion is made that greatest postural imbalance produced by right brain damage could reflect a persistent distorsion of a "spatial postural representation". Vestibular stimulation may restore symmetrical activity in the cerebral structures involved in the generation of this "spatial postural representation".

Predominance of postural imbalance in left hemiparetic patients.

Postural sway characteristics in a group of 15 left hemiparetic patients were compared with those in a group of 15 right hemiparetic patients using a statokinesimetric platform. The results in the two patient groups were also compared with those derived from a group of 15 age-matched healthy control subjects. Three postural sway parameters were used: the total sway area, the anteroposterior sway and the lateral sway. Hemiparetic patients showed a larger sway area and a lateral displacement of the center of pressure toward the side of the lesion compared to normal subjects. Furthermore, left hemiparetic patients showed greater sway area and lateral displacement compared to right hemiparetic patients. We suggest that the predominance of postural imbalance in left hemiparetic patients could be due to a displacement of postural reference toward the lesion's side.

Room tilt illusion. A central otolith dysfunction.

BACKGROUND: We report a sudden 90 degrees room tilt illusion (RTI) following vestibular stimulation in 3 patients with persistent skew deviation caused by a brain stem lesion. Room tilt illusion is a transient tilt perception of the visual surrounding, on its side or even upside down, that is often reported with brain stem lesions. Although its pathophysiologic cause is not well known, the RTI suggests an impairment of otolith pathways, as reported in skew deviation. METHODS: The 3 patients with brain stem lesions were reexamined as part of a follow-up of patients with signs of otolith dysfunction. A registration of vestibular function was performed with a rotatory chair, including earth-vertical axis rotation for canal stimulation and off-vertical axis rotation (OVAR) for otolith stimulation. Measurement of the subjective visual vertical (SVV) was also performed. RESULTS: The otolith-ocular reflex registered by OVAR was impaired in the 3 patients with skew deviation and the SVV in 2 patients. After each direction of OVAR stimulation, the 3 patients reported an RTI as the room was illuminated. CONCLUSIONS: The coexistence of otolith oculomotor (skew deviation and impaired otolith-ocular reflex) and perceptual (tilt of SVV and RTI) disorders suggests a common otolith dysfunction. However, an RTI occurred specifically after vestibular stimulation and when the room was illuminated. We thus suggest that RTI reflects a dynamic visuo-otolith mismatch.

Clinical and radiological aspects of Villaret's syndrome.

A 68-year-old man with a history of large cell lung carcinoma presented 1 year after surgical management of the initial lesion, with a complete unilateral IX-XII cranial nerve palsy with Horner's sign. This rare multiple cranial nerve palsy is called Villaret's syndrome. It suggests an extracranial lesion located in the retroparotid space. Complete basal skull radiology work up including computed tomography and magnetic resonance imaging confirmed the location of the causal lesion in the retroparotid space.

Short-term vestibulo-ocular reflex adaptation in humans. I. Effect on the ocular motor velocity-to-position neural integrator.

We investigated the effect of short-term vestibulo-ocular reflex (VOR) adaptation in normal human subjects on the dynamic properties of the velocity-to-position ocular motor integrator that holds positions of gaze. Subjects sat in a sinusoidally rotating chair surrounded by an optokinetic nystagmus drum. The movement of the visual surround (drum) was manipulated relative to the chair to produce an increase (x 1.7 viewing), decrease (x 0.5, x 0 viewing), or reversal (x (-2.5) viewing) of VOR gain. Before and after 1 h of training, VOR gain and gaze-holding after eccentric saccades in darkness were measured. Depending on the training paradigm, eccentric saccades could be followed by centrifugal drift (after x 0.5 viewing), implying an unstable integrator, or by centripetal drift [after x 1.7 or x (-2.5) viewing], implying a leaky integrator. The changes in the neural integrator appear to be context specific, so that when the VOR was tested in non-training head orientations, both the adaptive change in VOR gain and the changes in the neural integrator were much smaller. The changes in VOR gain were on the order of 10% and the induced drift velocities were several degrees per second at 20 deg eccentric positions in the orbit. We propose that (1) the changes in the dynamic properties of the neural integrator reflect an attempt to modify the phase (timing) relationships of the VOR and (2) the relative directions of retinal slip and eye velocity during head rotation determine whether the integrator becomes unstable (and introduces more phase lag) or leaky (and introduces less phase lag).

Short-term vestibulo-ocular reflex adaptation in humans. II. Error signals.

We oscillated humans sinusoidally at 0.2 Hz for 1 h, using various combinations of rotations of the head and visual surround to elicit short-term adaptation of the gain of the vestibulo-ocular reflex (VOR). Before and after each period of training, the gain of the VOR was measured in darkness, in response to a position step of head rotation. A small foveal target served as well as a full-field stimulus at driving VOR adaptation. Oscillation of the visual surround alone produced a substantial increase in the VOR gain. When the visual scene was rotated in phase with the head but with a larger amplitude to produce a reversal of the VOR, the VOR gain increased if the movement of the visual scene was much greater than that of the head, otherwise the gain decreased. We interpreted these results with a model of VOR adaptation that uses as its "error signal" the combination of motion of images on the retina (retinal slip) and any additional slow-phase eye velocity, beyond that generated by the VOR through the vestibular nuclei, necessary to prevent such retinal slip during head rotation. The slow phase velocity generated by the VOR is derived from "inferred head rotation", a signal based on the discharge of neurons in the vestibular nuclei that receive both labyrinthine and visual (optokinetic) inputs. The amplitude and sign of the ratio of the "error signal" to "inferred head velocity" determined the amplitude and the direction (increase or decrease) of VOR gain adaptation.

Adaptation of the vestibulo-ocular reflex with the head in different orientations and positions relative to the axis of body rotation.

We investigated the influence of static head orientation and position, relative to the axis of body rotation, upon vestibular adaptation. With the head centered, displaced anterior to the axis of body rotation, or tilted 40 degrees to 45 degrees in roll or pitch, the gain of the vestibulo-ocular reflex (VOR) was trained (to go either up or down) for one hour using artificial manipulation of the visual surround to produce a visual-vestibular mismatch. Before and after each training session, the VOR was measured in darkness with the head in the training as well as in several non-training positions. We found that transfer of VOR adaptation to non-training positions was almost complete when comparing head eccentric versus head-centered rotations. For tilts, however, transfer of VOR learning was far less complete suggesting that static otolith signals provide a strong contextual cue that gates the expression of an adaptive VOR response. Finally, following training to increase the VOR, gain was greater for centripetally than centrifugally directed slow phases. Centripetally directed postsaccadic drift also developed. These findings imply that the gain increase paradigm also leads to abnormal function of the velocity-to-position neural integrator, which holds eccentric positions of gaze.