Vestibular exercises improve central vestibulospinal compensation after vestibular neuritis

OBJECTIVE AND BACKGROUND: Animal experiments have shown that central vestibular compensation of unilateral peripheral vestibular lesions can be improved by vestibular exercises. There are, however, no equivalent clinical studies on the efficacy of such specific physiotherapy on acute unilateral peripheral vestibular lesions in humans. DESIGN AND METHODS: To quantify the differential effects of specific vestibular exercises on central compensation in patients with an acute/subacute unilateral vestibular lesion (vestibular neuritis), we determined the time course of recovery of 1) the ocular torsion (OT) for the vestibulo-ocular system, 2) the subjective visual vertical (SVV) for perception, and 3) the total sway path (SP) values for postural control in 19 patients with and 20 patients without vestibular exercises. All patients had a persisting peripheral vestibular deficit for at least 30 days (statistical end point). RESULTS: Although normalization of OT and SVV was similar in the control and physiotherapy groups, the total SP values on day 30 after symptom onset differed significantly: 3.2 +/- 1.9 m/min in the physiotherapy group and 16.9 +/- 6.1 m/min in the control group (ANOVA, p < 0.001). CONCLUSIONS: This prospective clinical study suggests that specific vestibular exercises improve vestibulospinal compensation in patients with acute peripheral vestibular lesions.     

Selective ablation of immature blood vessels in established human tumors follows vascular endothelial growth factor withdrawal

In the guinea pig, lateral deviation of the head is a cardinal symptom of the vestibular syndrome caused by unilateral labyrinthectomy. In the course of recovery from this syndrome (vestibular compensation), lateral deviation of the head disappears completely in 2-3 days. Because this symptom is known to be due to the lesion of the horizontal semicircular canal system, and since obliquus capitis inferior (OCI) muscle is activated predominantly by yaw rotation (horizontal vestibulocollic reflex), we hypothesized that changes in the activity of this muscle could be at least in part responsible for the lateral head deviation caused by unilateral labyrinthectomy. In order to test this hypothesis, electromyographic (EMG) activities of the right and left OCI muscles, as well as eye movements, were recorded in 12 head-fixed alert guinea pigs at various times after left surgical labyrinthectomy (performed with the animals under halothane anesthesia). After the operation, a decrease in tonic EMG activity was observed in the right (contralateral to the lesion) OCI muscle while an increase in tonic EMG activity was detected in the left (ipsilateral) OCI muscle. In addition, phasic changes in EMG activity associated with ocular nystagmic beats occurred in the OCI muscles. These phasic changes were in the opposite direction to those of the tonic changes. There were bursts of activity in the right OCI and pauses in the left OCI. From measurements of rectified averaged EMG activities which took into account both parts (tonic and phasic) of the phenomenon, it was concluded that the labyrinthectomy-induced asymmetry between the activities of the left and right OCI muscles was high enough and lasted long enough to be an important mechanism in the lateral deviation of the head caused by unilateral labyrinthectomy.     

An update on peritoneal dialysis and hemodialysis in the pediatric population

Drugs acting as agonists (SKF38393 and quinpirol) or antagonists (SCH23390 and sulpiride) on dopamine receptors were administered at various doses (1, 2 or 4 mg kg-1 day-1) to aged male rats of the Sprague-Dawley strain subjected to labyrinth unilateral lesion. The time course of vestibular compensation was evaluated by recording spontaneous eye nystagmus and by scoring ambulation and rearing with the open field test and motor ability and coordination with the rotorod test. Treatment started 3 days prior to surgery and continued until day 7 after surgery. The vestibular compensation of untreated young male rats was also studied with the same methods. The decline of spontaneous nystagmus in aged animals was slower than that of young rats and was facilitated by the large doses of quinpirol (D2 receptor agonist) and inhibited by sulpiride (D2 receptor antagonist) 4 mg kg-1 day-1, while the other drugs did not affect this parameter. After operation, ambulation and rearing of aged rats increased more slowly as compared to that of young animals. Moreover, motor performance and coordination in aged rats improved less rapidly than those of young controls. Dopamine receptor agonists increased ambulation and improved motor performance and coordination in aged rats, while dopamine receptor antagonists exerted opposite effects. Rearing was not affected by any kind of drug treatment. These results suggest that dopamine neurotransmission plays a role in vestibular compensation process following unilateral labyrinthectomy in aged animals, and this may have clinical relevance in vestibular pathologies of peripheral origin that are associated to brain ageing.     

Polyamine changes in the vestibular nuclei of guinea pigs following labyrinthectomy

Vestibular compensation is a process of behavioral recovery from ocular, motor and postural disorders following unilateral damage to the vestibular end-organ. Although restoration of the normal resting discharge rate in the ipsilateral vestibular nuclei is important in compensation, the biochemical and molecular mechanisms mediating recovery are largely unknown. The ornithine decarboxylase polyamine pathway is activated in the nervous system following axotomy or denervation. The authors postulate that changes in polyamines mediate vestibular compensation. Within 150-micron brain stem coronal section micropunches analyzed by high performance liquid chromatography techniques, the polyamine spermidine was significantly increased in the ipsilateral lateral vestibular nucleus 8 hours following labyrinthectomy in the guinea pig model. Because naturally occurring polyamines modulate excitatory amino acid receptors (N-methyl-D-aspartate [NMDA]) which in turn mediate neurotransmission between primary afferents and second order vestibular neurons, stimulation of polyamine pathways following neural injury may play a critical role in compensation.     

Comparative approaches to the avian song system

The aim of this paper is to: i) review the behavioural, electrophysiological, pharmacological and biochemical evidence relating to the involvement of N-methyl-D-aspartate (NMDA) receptors in the vestibular compensation process which follows unilateral peripheral vestibular deafferentation (UVD); and ii) suggest a unifying hypothesis based on this literature and recent studies of long-term depression (LTD)-like phenomena in the brainstem vestibular nucleus complex (VNC). It is suggested that NMDA receptors may induce a form of heterosynaptic LTD in the ipsilateral VNC, which is partly responsible for the extent of the hypoactivity which occurs immediately following UVD, and the severity of the associated vestibular syndrome. It is also suggested that vestibular compensation may develop as this LTD dissipates, allowing remaining synaptic inputs and the intrinsic properties of ipsilateral VNC neurons to re-establish the resting activity which is responsible for static vestibular compensation. It is argued that this hypothesis accounts for the majority of the available data on NMDA receptors in relation to vestibular compensation, and may serve as a useful working hypothesis, in order to formulate further experiments to investigate the contribution of NMDA receptors to the compensation process.     

Phenotype, cytokine production and cytolytic capacity of fresh (uncultured) tumour-infiltrating T lymphocytes in human renal cell carcinoma

Abnormalities in the vestibulo-ocular reflex (VOR) after unilateral vestibular injury may cause symptomatic gaze instability. We compared five subjects who had unilateral vestibular lesions with normal control subjects. Gaze stability and VOR gain were measured in three axes using scleral magnetic search coils, in light and darkness, testing different planes of rotation (yaw and pitch), types of stimulus (sinusoids from 0.8 to 2.4 Hz, and transient accelerations) and methods of rotation (active and passive). Eye velocity during horizontal tests reached saturation during high-velocity/acceleration ipsilesional rotation. Rapid vertical head movements triggered anomalous torsional rotation of the eyes. Gaze instability was present even during active rotation in the light, resulting in oscillopsia. These abnormal VOR responses are a consequence of saturating nonlinearities, which limit the usefulness of frequency-domain analysis of rotational test data in describing these lesions.     

Vestibulo-ocular reflex deficits to rapid head turns following intratympanic gentamicin instillation

The response of the vestibulo-ocular reflex following unilateral vestibular deafferentation by gentamicin ablation was studied using transient stimuli. The response to these rapid passive head turns showed a strong asymmetry with permanent, reduced gains toward the side of lesion. These gain reductions have large variation (gains of 0.26 to 0.83), which may result from preferential sparing of regularly firing afferent fibers following gentamicin ablation. Based on the size and nature of the nonlinearity, an explanation based on Ewald's second law was discounted.     

Experimental study of vestibular neurectomy

The authors describe an experimental study carried out on baboons. After unilateral vestibular neurectomy, the behaviour disorders on the one hand, and on the other, modifications and temporal development of reflex muotatic excitability of the spine using Hoffmann's reflex method are analyzed. As far as behaviour is concerned, a four-day period of motor restriction following the operation causes more marked residual disorders in comparison with controls. From the neurophysiological point of view, neurectomy results in seriously disordered spinal reflexes characterized by ipsilateral hypo-excitability developing in there stages: a tw-day initial critical phase during which the disorders are at their worst, a four-day recuperative stage with partial regression of the disorders, finally a chronic compensation stage in which spinal excitability returns to normal after several months.     

Intraorbital conjunctival cyst after a penetrating orbital injury: a case report

We report a case of intraorbital conjunctival cyst following a penetrating orbitocranial injury. The patient was a 28-year-old male who was hospitalized with exophthalmos, retrobulbar pain and upper gaze disturbance of his left eye. When he was 4 years old, a thin iron rod had penetrated intracranially through the inner angle of his left orbit. He was hospitalized and treated conservatively for about two weeks. The left eye ball was intact and visual acuity was normal, although bloody fluid had continuously flowed out from the left inner angle of the conjunctival wound for a few days. He had been febrile to 39 degrees C and complained of headache for one week. Subsequentry, the symptoms gradually improved through conservative therapy. When he was a junior high school student, he noticed exophthalmos of his left eye. However, he had never been examined closely, until he was 28 years old. We suspect that he had suffered from meningitis caused by the penetrating orbitocranial injury, and had fortunately improved under the conservative therapy. On admission to our hospital, a craniogram showed fracture of the left orbital roof, and coronal and three-dimensional computed tomography (CT) scans clearly demonstrated the orbital fracture. CT revealed a cystic mass in the retrobulbar space, and a porencephalic cyst in the medial basal frontal lobe. On magnetic resonance imaging (MRI) scans, both cysts were of low intensity on T1-weighted imaging, and of high intensity on T2-weighted images. Coronal and sagittal MRI scans showed that the two cysts were connected with each other through the fracture in the orbital roof. We diagnosed therefore that the orbital cyst was a herniated porencephalic cyst of the frontal lobe. Surgery was performed by a transcranial approach. The porencephalic cyst adhered to the fractured lesion of the frontal base but did not extend into the orbita. The intraorbital cyst was totally removed by opening the orbital roof including the fractured lesion. The cyst contained milky fluid. Postoperatively, the exophthalmos, retrobulbar pain and upper gaze disturbance showed gradual improvement. On histological examination, the cyst was found to be lined by non-keratinized stratified squamous epithelium and was diagnosed as a conjunctival cyst. This case was considered to be one of traumatic conjunctival cysts caused by a penetrating orbitocranial injury. Orbital conjunctival cysts have been reported to comprise about 10% of orbital epidermoid and dermoid cysts. Of these cysts, traumatic conjunctival cysts are rare, and only a few cases have been described. The etiology and therapy of orbital conjunctival cysts are discussed.     

Brachytherapy in early prostate cancer--early experience

Intravenous lidocaine has been reported to alleviate vertigo in Meniere's disease and suggested as a possible antivertigo agent after unilateral labyrinthectomy in a study of cats. To further evaluate the effects of intravenous lidocaine on the acute phase of postural compensation, we subjected 13 pigmented guinea pigs to unilateral labyrinthectomy. Seven received intravenous lidocaine (4 mg/kg) immediately after labyrinthectomy. The other six served as controls and received an equivalent-volume injection of normal saline solution. Total body curvature, trunk curvature, yaw head tilt, and roll head tilt were measured at frequent intervals for up to 30 hours after surgery. Both groups had immediate difficulties with posturing that gradually improved. The lidocaine group tended to exhibit delayed postural compensation, but this was only statistically significant for roll head tilt. These results do not show improvement in postural compensation from unilateral labyrinthectomy after the administration of intravenous lidocaine. A species-specific effect on the vestibular pathways is suggested, and we conclude that further evaluation of lidocaine and the vestibular system is warranted.     

Polyamines increase in the brain stem and cerebellum following labyrinthectomy

The goal of this investigation was to test the hypothesis that unilateral damage to the vestibular end-organ (labyrinthectomy) stimulates polyamine synthesis in central vestibular neural structures that mediate the process of behavioral recovery (vestibular compensation). Pharmacological studies have shown that compensation can be altered by alpha-difluoromethylornithine (DFMO), a specific inhibitor of polyamine synthesis. Because polyamines are important in regeneration, development and modulation of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors, which mediate vestibular synaptic plasticity, we investigated changes in polyamines in specific central vestibular structures after unilateral labyrinthectomy. The supernatant fraction of brain tissue homogenates was reacted with dansyl chloride. Dansylated polyamine derivatives were quantified in the vestibular nuclei, cerebellum, and inferior olive in both the control and the unilaterally labyrinthectomized guinea pig by high-performance liquid chromatography-fluorometric detection. No left-right differences in putrescine, spermidine, or spermine were detected in any brain parenchyma of controls. Polyamine imbalance, characterized by increased spermidine in the ipsilateral medial and lateral vestibular nuclei, was noted 12 and 24 h after unilateral labyrinthectomy (UL). In contrast, spermidine, spermine, and putrescine were elevated bilaterally in the cerebellum and inferior olive after UL. These biochemical changes may represent neuronal modifications to establish a balance between the vestibular nuclei after unilateral labyrinthectomy. Elucidation of the role of polyamines in central vestibular function and in vestibular compensation offers promise for the development of novel therapeutic strategies for treatment of vestibular disorders.     

Compensation of the human vertical vestibulo-ocular reflex following occlusion of one vertical semicircular canal is incomplete

The vestibulo-ocular reflex (VOR) was studied in nine human subjects 2-15 months after permanent surgical occlusion of one posterior semicircular canal. The stimuli used were rapid, passive, unpredictable, low-amplitude (10-20 degrees), high-acceleration (3000-4000 degrees/s2) head rotations in pitch and yaw planes. The responses measured were vertical and horizontal eye rotations, and the results were compared with those from 19 normal subjects. After unilateral occlusion of the posterior semicircular canal, the gain of the head-up pitch vertical VOR--the vertical VOR generated by excitation from only one and disfacilitation from two vertical semicircular canals--was reduced to 0.61 +/- 0.06 (normal 0.92 +/- 0.06) at a head velocity of 200 degrees/s. In contrast the gain of the head-down pitch vertical VOR--the VOR still generated by excitation from two, but disfacilitation from only one vertical semicircular canal--was within normal limits: 0.86 +/- 0.11 (normal 0.96 +/- 0.04). The gain of the horizontal VOR in response to yaw head rotations--ipsilesion 0.81 +/- 0.06 (normal 0.88 +/- 0.05) and contralesion 0.80 +/- 0.11 (normal 0.92 +/- 0.11)--was within normal limits in both directions (group means +/- two-tailed 95% confidence intervals given in each case). These results show that occlusion of just one vertical semicircular canal produces a permanent deficit of about 30% in the vertical VOR gain in response to rapid pitch head rotations in the excitatory direction of the occluded canal. This observation indicates that, in response to a stimulus in the higher dynamic range, compensation of the human VOR for the loss of excitatory input from even one vertical semicircular canal is incomplete.     

Contribution of vestibular commissural pathways to spatial orientation of the angular vestibuloocular reflex

During nystagmus induced by the angular vestibuloocular reflex (aVOR), the axis of eye velocity tends to align with the direction of gravito-inertial acceleration (GIA), a process we term "spatial orientation of the aVOR." We studied spatial orientation of the aVOR in rhesus and cynomolgus monkeys before and after midline section of the rostral medulla abolished all oculomotor functions related to velocity storage, leaving the direct optokinetic and vestibular pathways intact. Optokinetic afternystagmus and the bias component of off-vertical-axis rotation were lost, and the aVOR time constant was reduced to a value commensurate with the time constants of primary semicircular canal afferents. Spatial orientation of the aVOR, induced either during optokinetic or vestibular stimulation, was also lost. Vertical and roll aVOR time constants could no longer be lengthened in side-down or supine/prone positions, and static and dynamic tilts of the GIA no longer produced cross-coupling from the yaw to pitch and yaw to roll axes. Consequently, the induced nystagmus remained entirely in head coordinates after the lesion, regardless of the direction of the resultant GIA vector. Gains of the aVOR and of optokinetic nystagmus to steps of velocity were unaffected or slightly increased. These results are consistent with a model in which the direct aVOR pathways are organized in semicircular canal coordinates and spatial orientation is restricted to the indirect (velocity storage) pathways.     

Torticollis due to disinhibition of the vestibulo-collic reflex in a patient with Steele-Richardson-Olszewski syndrome

A patient with the clinical picture of Steele-Richardson-Olszewski syndrome and an unusual intermittent neck twisting is reported. He had virtually no voluntary ocular movements and only very slow, low-amplitude voluntary head movements. However, in response to optokinetic or vestibular stimulation, he developed full eye deviations in the direction of the slow phase of the expected nystagmus. No quick phases were observed, and the deviation outlasted the duration of the vestibular stimuli because of defective saccades. The head also turned fully during these stimuli, quicker than on attempted voluntary movements, and remained deviated similarly to the eyes. This suggests that the neck deviations in this patient were due to a disinhibited vestibulo-collic reflex and a disturbed head position resetting mechanism. Neck electromyographic responses in response to whole-body rotation indicated that the vestibulocollic reflex responsible for the torticollis in this patient had a short latency of approximately 30 ms.     

Passive sustained turning of the head induces asymmetric gain of the vestibulo-ocular reflex in healthy subjects

In order to test the hypothesis of an interaction between neck proprioception and the vestibulo-ocular reflex (VOR), we rotated 16 healthy subjects both facing forward and with their heads passively turned 70 degrees to either side. We found that gain tended to be lower when the subjects were rotated with their heads turned opposite to the direction of rotation compared to when they were rotated in the same direction, but facing forward. Although our findings were not statistically significant, they suggest that there is a measurable interaction between neck proprioception and the VOR in subjects with normal vestibular function. Asymmetric neck muscle proprioceptive signals seem to give rise to asymmetric functioning of the VOR, which, at least in part, could be the pathogenesis of cervical dizziness. If so, this could lead to misinterpretation of vestibular assessments in patients with neck pain who also complain of dizziness.     

Evidence that short ACTH fragments enhance vestibular compensation via direct action on the ipsilateral vestibular nucleus

The aim of the present study was to determine whether administration of the synthetic ACTH-(4-9) analogue, Org 2766, directly into the ipsilateral vestibular nucleus complex (VNC), would enhance vestibular compensation following unilateral labyrinthectomy (UL). Either artificial cerebrospinal fluid (ACSF; n = 4) or Org 2766 (0.67 nmol kg-1 every 4 h for 52 h; n = 4), was administered directly into the VNC via a stainless steel cannula connected to an osmotic minipump implanted s.c. Three symptoms of UL, spontaneous ocular nystagmus (SN), roll head tilt (RHT) and yaw head tilt (YHT), were measured at 10, 20, 25, 30, 40, 45 and 50 h post-UL. Org 2766 produced a significant decrease in the frequency of SN and accelerated its compensation. Org 2766 had no significant effect on either the compensation of RHT or YHT. This result suggests that vestibular compensation is enhanced by short ACTH fragments as a result of direct action on the ipsilateral VNC itself.     

Primary bronchopulmonary fibrosarcoma: report of a case

We herein report a case of primary bronchopulmonary fibrosarcoma in a 70-year-old man. The patient was referred to our hospital for investigation of hemosputum and an abnormal shadow. On admission, chest radiograph and computed tomography scan showed a mass lesion in right S3 and an infiltrative shadow in the right upper lobe. Transbronchial biopsy specimens showed findings of malignancy, and adenocarcinoma was suspected. A right pneumonectomy was performed, and pathologic examination confirmed a diagnosis of fibrosarcoma. The patient had an uneventful recovery and no sign of recurrence has been found in the year since his operation, although strict follow-up is essential.     

The reflex sympathetic dystrophy syndrome in patients who have had a spinal cord injury

Patients suffering from a spinal cord injury often present with a pain syndrome. Although the reflex sympathetic syndrome is a common diagnosis in some forms of neurological disease such as patients with a stroke, it is less frequent in those with a spinal lesion. The authors report eight patients with reflex sympathetic dystrophy who had a spinal cord injury. The diagnosis and treatment are discussed along with a review of literature.     

Transient changes in flocculonodular lobe protein kinase C expression during vestibular compensation

Protein kinase C (PKC) is a family of intracellular signal transduction enzymes, comprising isoforms that vary in sensitivity to calcium, arachidonic acid, and diacylglycerol. PKC isoforms alpha, gamma, and delta are expressed by cerebellar Purkinje cells and neurons in the cerebellar nuclei and vestibular nuclei of the Long-Evans rat. In control rats, these PKCs are distributed symmetrically in the flocculonodular-lobe Purkinje cells. Behavioral recovery from vestibular dysfunction produced by unilateral labyrinthectomy (UL) is accompanied by asymmetric expression of PKC isoforms in these regions within 6 hr after UL. These expression changes were localized within parasagittal regions of the flocculus and nodulus. The distribution of PKCalpha, -gamma, and -delta were identical, suggesting that they are coregulated in cerebellar Purkinje cells during this early compensatory period. The pattern of Purkinje cell PKC expression returned to the control, symmetric distribution within 24 hr after UL. It is hypothesized that these regional changes in Purkinje cell PKC expression are an early intracellular signal contributing to vestibular compensation. In particular, regulation of PKC expression may contribute to changes in the efficacy of cerebellar synaptic plasticity during the acute post-UL period.