The neural substrates subserving optokinetic nystagmus (OKN) in mammalian brainstem are reviewed. The accessory optic system (AOS) consists of 3 terminal nuclei, lateral (LTN), medial (MTN) and dorsal terminal nucleus (DTN) which are distributed along the brachium of the superior colliculus. All the AOS nuclei receive direct retinal inputs from the contralateral eye and a weak input from the ipsilateral eye and connect strongly with the nucleus of the optic tract (NOT) which is thought to provide the afferent limb of the horizontal OKN. LTN is the only nucleus where electrophysiological experiments have been performed in mammals as follows : (1) LTN units are direction-selective, responding preferentially during upward vertical background movements, and show a parafoveal receptive field. Most LTN neurons can provide both direction and velocity information only at lower velocities, and differ significantly from NOT neurons, responding to over 200°/s OKN stimuli. Therefore, it remains unclear how the LTN might subserve for the generation of OKN, other oculomotor or visual roles. (2) Ablation study of the NOT revealed the NOT contributes to the slow buildup of OKN which is thought to underlie the brainstem of lower vertebrates. (3) Pretectofugal fibers investigated using either biocytine or WGA HRP demonstrated the following : 1) Fibers traversing the posterior commissure terminate in the contralateral NOT. 2) Fibers descend medially through the nucleus reticularis pontis oralis to reach the lateral part of the ipsilateral nucleus reticularis tegmenti pontis. 3) Fibers project into the dorsal cap of the inferior olive. At the level of the abducens nucleus, some fibers ascend through the nucleus pontis caudalis and reach the nucleus prepositus hypoglossi and medical vestibular nucleus. Consistent with the physiological data, direct terminals of the NOT neurons in themedial vestibular nucleus could drive storage mechanisms and produce OKN in the monkey.
Substantial advances in understanding of oculomotor function have come from basing models of the oculomotor system on the control system theory. In this model, vestibular nystagmus, OKN and OKAN are produced by combined activation of two important pathways. One process, called the direct-pathway, produced rapid changes in eye velocity. A second process (indirect pathway) causes only slow changes in eye velocity and contains a non-ideal integrator. This integrator, labeled a “velocity-storage integrator”, appears to hold or store activity related to slow phase eye velocity. Activities in the direct and indirect pathways combine to form the velocity signal (This signal drives the “velocity-to-position integrator”, which drives the oculomotor plant). The velocity storage mechanism serves as a focus for superimposing a variety of sensory inputs that signal motion and provide the central nervous system with a coordinate basis for interpreting continuous movement of the head relative to the environment. However, neural circuits underlying these mechanism are still unknown. The recent studies suggest that the velocity-storage integrator appears to lie in the vestibular nuclei (mainly medial vestibular nucleus, MVN), while the velocity-to-position-integrator is probably closely associated with the prepositus hypoglossi nuclei. The recent extracellular recording study shows that activities of “vestibular only” and “vestibular, plus saccade” units in the rostral MVN are likely to carry an eye velocity signal related to velocity storage.
This study investigated the characteristics of postural sway in cases of Parkinson's diesease (PK). We examined 16 patients previously diagnosed with PK. The subjects stood on a stabilometer with their eyes open or closed, and the sway of the center of gravity of the body was recorded for one minute. The sway pattern during standing posture in PK patients was analyzed. The subjects consisted of 16 patients, including two with positive symptoms (PK-P), while six (PK-Na) and eight (PK-Nb) had negative symptoms. Results 1) With eyes opened, the sway pattern was centripetal in six, right-left in two, diffuse in two, the displacement type in four and the multiple center type in two. With eyes closed, the sway pattern was centripetal in four, forward-backward in four, right-left in three, diffuse in one, the displacement type in two and the multiple center type in two. The displacement and multiple center types were representative of body sway in PK. 2) Considering the similarities in body sway with eyes open and closed, we divided body sway in PK into three groups (centripetal and forward-backward type, right-left and diffuse type, displacement and multiple center type). 3) Considering the relation between the classification by symptoms and body sway, we related PK-Na with displacement and multiple center type and PK-Nb with right-left and diffuse type. It was demonstrated that the centripetal and forward-backward type involved disorders in postural fixation and equilibrium, the right-left and diffuse type involved righting disorder, while the displacement and multiple center type involved tremor, akinesia and disorders in postural fixation and equilibrium.
It is thought that various factors are involved in the process of motion sickness. Using a combination of vestibulo-ocular reflex (VOR) and a method in which the line of fixation in smooth pursuit eye movement can be freely controlled using a face a mount display (FMD), the process of motion sickness induction was studied under conditions in which phase spaces of head movement and eye movement are either synchronized or not synchronized. Under the synchronous phase-space condition, no motion sickness was induced, when the lines of fixation controlled by VOR and FMD were in the equiphase or antiphase, while motion sickness was readily induced under the asynchronous phase-space condition. Moreover, when the head was moved under conditions in which eye movement was restricted, movement of the visual field was recognized as antiphase relative to the head movement. However, when eye movement was controlled by the subject himself/herself, motion sickness was not induced because head movement and recognition of the visual field were synchronized. On the other hand, when eye movement was controlled by the investigator, motion sickness could be induced. From the above findings based on the intrinsic model of motor command, it is assumed that asynchronous phases of head movement and eye movement generated by the inverse model and forward model of the forecast system are input information leading to motion sickness.
A patient with acute hearing loss and vertigo due to infarction involving the anterior--inferior cerebellar artery (AICA) is reported. A 64-year-old female complained of sudden-onset, severe, unilateral hearing loss and vertigo without any other neurological deficits. Neuro-otological examinations revealed a horizontal, spontaneous, positional, and gaze nystagmus toward the right. Pursuit eye movement and optokinetic nystagmus were unilaterally impaired and ABR showed the absence of waves II-IV and prolonged I-V interpeak latency difference. Based on finding of neuro-otological examination, brain stem lesion was suspected and neuroradiological examinations were performed. MRI showed a pontine infarction in the AICA area and angiography demonstrated stenosis of the right AICA thus the patient was diagnosed as having AICA syndrome. The clinical signs of AICA syndrome are occasionally similar to those of inner ear disorders. In such cases, neuro-otological examinations such as ENG and ABR are clinically useful in distinguishing AICA syndrome from inner ear diseases.
Introduction Vasovagal reflex (VVR) is a disease that has received attention in various fields. Recently, researchers have started to clarify its mechanism. Three patients with symptoms probably due to VVR were treated in this department and the Head up tilt test was used to diagnose dizziness due to VVR. Patients The three patients included a 21-year-old female (Case 1), a 26-year-old male (Case 2) and a 61-year-old female (Case 3). All three patients had chief complaints of spontaneous dizziness after standing or sitting for 5 to 30 minutes. Results The duration of standing before the onset of positive findings was 9.5 minutes in Case 1 and 11 minutes in Case 2. In Case 3, positive findings were obtained 9.5 minutes after isoproterenol administration. Discussion All three patients showed spontaneous dizziness in either the standing or sitting position and the results of the Head up tilt test were positive. Therefore, dizziness seemed to be due to VVR in these patients. The instantaneous decrease in blood volume due to paradoxical activation of the vagus nerve may have induced dizziness, loss of consciousness and faintness. Because of severe patient stress during the Head up tilt test, this examination should be indicated only in those who are strongly suspected of VVR.
Most large cerebello-pontine angle (CPA) tumors usually cause typical abnormal oculomotor findings on vestibular and oculomotor examinations, reflecting brainstem and cerebellar lesions. However, we encountered four patients with large CPA tumor without the typical abnormal neurotological findings and these cases are described in this report. Case 1 : A 63-year-old female. Chief compliment (CC) was double vision. Audiovestibular examinations showed normal findings except for slight nystagmus on ENG. MRI revealed a 4.8 × 4.7 cm lesion of the right CPA. The histopathological diagnosis was CPA meningioma.Case 2 : A 58-year-old female. CC was a tinnitus. Pure tone audiometry indicated right-sided sensorineural hearing loss (SNHL). Results of vestibular examination were normal. MRI revealed a 4.0 × 3.5 cm lesion from the clivus to the CPA that was diagnosed radiologically as a meningioma. Case 3 : A 50-year-old female. CC were tinnitus and head heaviness. Audiovestibular examinations were all unremarkable. MRI revealed a 3.0 × 2.7 cm lesion of the right CPA that was diagnosed as an epidermoid cyst. Case 4 : A 48-year-old female. CC were hearing loss and tinnitus. Audiometric studies indicated right-sided moderate-to-profound SNHL. There were no responses on ABR. Vestibular examinations were unremarkable. MRI revealed a 4.2 × 4.0 cm left-sided CPA mass that was diagnosed at surgery as an acoustic neuroma with cystic changes. Previous study showed that when the CPA tumor is larger than 3 cm, ETT and OKP demonstrate abnormal findings in 70 to 78% of patients, respectively. However, in our cases, despite pronounced compressions of the brainstem and cerebellum by large CPA tumors, vestibular examinations did not reveal any significant findings. These atypical findings might have resulted from the histological characteristics and slow growth of the CPA tomor, in addition to factors related to central vestibular compensation and indivisual differences in susceptibility to the lesions.
It has recently been demonstrated that the inner ear has a chemical control mechanism to regulate blood flow adequately, as in central organs. Impairment of blood flow regulation is supposed to be a cause of vertigo or hearing disturbance especially in elderly patients. In the present study, we investigated age-related impairment of chemical regulation in the inner ear. Using rats, cochlear blood flow (CoBF) was measured by laser Doppler flowmetry and chemical control was evaluated by blood flow reactivity to 7% CO2 + air inhalation. CoBF of young rats (2-to 3-month old) increased to 130±7.3% of pre-inhalation (mean± SE), aged rats (12-to 14-month old) to 123 ±2.9. Chemical Vasomotor index (Cl : ΔCoBF/ΔPCO2) of young rats was 1.67 ±0.33 (%/mmHg), and that of aged rats was 1.47 ±0.44. As shown by these results, chemical control in the aged group was weaker than that in the young group, although the difference in reactivity was not significant. Considering these results and the literature, we discuss the pathogenesis of vertigo and hearing disturbance in elderly patients.
A fifty-year-old woman began to complain of a dizzy sensation in March 1996. Thereafter, she became unable to do her house-work and often remained in bed. She first consulted our hospital in May. On the initial examination, she showed gaze nystagmus on rightward, leftward and upward gaze. At that time, electronystagmographic test showed abnormal pursuit ocular movement and optokinetic nystagmus was hardly provoked, although saccadic ocular movement appeared normal. She was soon admitted to our hospital. Two weeks later, a second electronystagmographic test recording was taken, demonstrating disappearance of optokinetic nystagmus provocation as well as visual suppression on caloric test. Stabilometer test showed remarkable regressive changes during these two weeks. Auditory brainstem response was normal at that time, even though electroencephalography typically showed a periodic synchronous discharge. We found that the patient had been taking some powdered bovine bone products daily for more than ten years. From these data, we diagnosed Creutzfeldt-Jakob disease. Thereafter, she became akinetic and mute and in July 1996 often took a decorticated posture, associated with periodic alternating gaze deviation.
Benign Paroxysmal positioning vertigo and acoustic tumors are thought to be related to the function of the vertical semicircular canal (VSCC). Therefore, we developed a new test to assess VSCC function by analyzing VSCC-induced nystagmus. We examined 11 healthy subjects, wearing goggles equipped with an infrared CCD camera and sitting on a chair designed to bilaterally stimulate the VSCCs by tilting the head backward during 45° rotation to the right on the sagital plane. The stimuli used were sinusoidal rotation with a maximal angular velocity of 100°/sec at a frequency of 0.033 Hz. The result was that the maximum slow phase eye velocity (MSPEV) of horizontal nystagmus decreased parallel to the head-tilted angle and the MSPEV of the vertical nystagmus was maximal when the head was tilted 60° or 70° backward. From the perspective of VSCC anatomy, the direction of horizontal nystagmus is reversed when head is tilted 60° backward. However, we could not observe the reverse of the direction of horizontal nystagmus even when head tilted 80° backward. We considered that vertical nystagmus was maximal when the head was tilted 60-70° backward because this position applied the optimal stimulation to the VSCC. This finding is in agreement with the position of the vertical VSCC in skull. We concluded that rotational test with respect to the VSCC can be used to analyze VSCC function.
The cause of delayed endolymphatic hydrops (DEH) has not been elucidated. Especially in contralateral DEH, it remains controversial whether the fluctuation of hearing loss and repetition of vertigo is due to hearing disturbance in the contralateral ear. We diagnosed 8 patients as the ipsilateral type of DEH and 5 patients as the contralateral type. We investigated the clinical manifestations of DEH and the manner of occurrence of hearing loss and vertigo. With regard to preexisting severe hearing loss, the contralateral type of DEH differed only slightly from the ipsilateral type. The contralateral type showed repeated vertigo less frequently than the ipsilateral type. When occurrence was investigated in patients with the contralateral type, we supposed that it was possible for some cases diagnosed as the ipsilateral type to shift to the contralateral type. On serologic and immunologic examination, all of patients with the contralateral type showed antinuclear antibodies.
Vestibular evoked myogenic potentials (VEMP) by tapping the head and by clicks were studied in 6 normal subjects (4 males and 2 females, age : 26 to 38 years old) and 11 patients with cochleo-vestibular disorders (4 males and 7 females, age : 22 to 66 years old). Diagnoses were acoustic neuroma in 5 patients, vestibular neuronitis in 2 patients, low tone sensorineural hearing loss in 2 patients, Meniere's disease in one patient and sensorineural hearing loss in one patient. All of the normal subjects had biphasic responses (p13-n23) to tapping the head as well as to clicks. We evaluated VEMPs in patients with cochleo-vestibular disorders with reference to the presence of p13-n23, amplitude ratio of p13-n23, and interaural latency differences of p13 and n23. In patients with cochleo-vestibular disorders, VEMPs by clicks were absent in 7 patients, decreased in amplitude in 2 patients and normal in 2 patients. VEMPs by tapping were absent in 3 patients, prolonged in latency of p13 in 5 patients and normal in 3 patients. Concerning differentiation of normal VEMPs from abnormal VEMPs, 10 of 11 patients showed the same VEMPs by tapping as by clicks. As long as interaural latency differences are included as parameters of evaluation, VEMP by tapping is a useful substitution for VEMP by clicks.