Biomedical subjects
M Gizzi
Publications and source records attributed to M Gizzi.
Vestibular control of sympathetic activity. An otolith-sympathetic reflex in humans.
It has been proposed that a vestibular reflex originating in the otolith organs and other body graviceptors modulates sympathetic activity during changes in posture with regard to gravity. To test this hypothesis, we selectively stimulated otolith and body graviceptors sinusoidally along different head axes in the coronal plane with off-vertical axis rotation (OVAR) and recorded sympathetic efferent activity in the peroneal nerve (muscle sympathetic nerve activity, MSNA), blood pressure, heart rate, and respiratory rate. All parameters were entrained during OVAR at the frequency of rotation, with MSNA increasing in nose-up positions during forward linear acceleration and decreasing when nose-down. MSNA was correlated closely with blood pressure when subjects were within +/-90 degrees of nose-down positions with a delay of 1.4 s, the normal latency of baroreflex-driven changes in MSNA. Thus, in the nose-down position, MSNA was probably driven by baroreflex afferents. In contrast, when subjects were within +/-45 degrees of the nose-up position, i.e., when positive linear acceleration was maximal along the naso-ocipital axis, MSNA was closely related to gravitational acceleration at a latency of 0.4 s. This delay is too short for MSNA changes to be mediated by the baroreflex, but it is compatible with the delay of a response originating in the vestibular system. We postulate that a vestibulosympathetic reflex, probably originating mainly in the otolith organs, contributes to blood pressure maintenance during forward linear acceleration. Because of its short latency, this reflex may be one of the earliest mechanisms to sustain blood pressure upon standing.
Functions of the nucleus of the optic tract (NOT). II. Control of ocular pursuit.
Ocular pursuit in monkeys, elicited by sinusoidal and triangular (constant velocity) stimuli, was studied before and after lesions of the nucleus of the optic tract (NOT). Before NOT lesions, pursuit gains (eye velocity/target velocity) were close to unity for sinusoidal and constant-velocity stimuli at frequencies up to 1 Hz. In this range, retinal slip was less than 2 degrees. Electrode tracks made to identify the location of NOT caused deficits in ipsilateral pursuit, which later recovered. Small electrolytic lesions of NOT reduced ipsilateral pursuit gains to below 0.5 in all tested conditions. Pursuit was better, however, when the eyes moved from the contralateral side toward the center (centripetal pursuit) than from the center ipsilaterally (centrifugal pursuit), although the eyes remained in close proximity to the target with saccadic tracking. Effects of lesions on ipsilateral pursuit were not permanent, and pursuit gains had generally recovered to 60-80% of baseline after about 2 weeks. One animal had bilateral NOT lesions and lost pursuit for 4 days. Thereafter, it had a centrifugal pursuit deficit that lasted for more than 2 months. Vertical pursuit and visually guided saccades were not affected by the bilateral NOT lesions in this animal. We also compared effects of these and similar NOT lesions on optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN). Correlation of functional deficits with NOT lesions from this and previous studies showed that rostral lesions of NOT in and around the pretectal olivary nucleus, which interrupted cortical input through the brachium of the superior colliculus (BSC), affected both smooth pursuit and OKN. In two animals in which it was tested, NOT lesions that caused a deficit in pursuit also decreased the rapid and slow components of OKN slow-phase velocity and affected OKAN. It was previously shown that slightly more caudal NOT lesions were more effective in altering gain adaptation of the angular vestibulo-ocular reflex (aVOR). The present findings suggest that cortical pathways through rostral NOT play an important role in maintenance of ipsilateral ocular pursuit. Since lesions that affected ocular pursuit had similar effects on ipsilateral OKN, processing for these two functions is probably closely linked in NOT, as it is elsewhere.
Neuro-otologic history.
Throughout medicine, the clinical history is the most important diagnostic tool. This is particularly true in vestibular disease, where pathologic confirmation of the disease process is rare. Many vestibular conditions are more appropriately called syndromes, rather than diseases, because the pathology is either variable or unknown. Knowledge of the anatomy and physiology provides the basis of understanding the control of balance and the symptoms that might occur should something go wrong. History taking should cover the elements of the balance system, including vestibular function, vision, hearing, somatosensation, and motor function.
The familial incidence of benign paroxysmal positional vertigo.
The goal of this investigation was to determine whether there is a familial tendency in the development of benign paroxysmal positional vertigo (BPPV). We hypothesized an increased frequency of BPPV among relatives of patients with the same diagnosis. BPPV is caused by dislodged otoconia from the utricular macula floating in the semicircular canals. At least half of BPPV cases are idiopathic and most pathological associations provide no clue as to the reason otoconia become dislodged. We have noted a number of BPPV patients with family histories of BPPV, suggesting a genetic predisposition to the condition. We surveyed 120 successive BPPV patients and 120 successive dizzy patients without BPPV regarding the frequency of dizziness and BPPV (diagnosed by a physician) among family members. Patients in our group with BPPV were 5 times as likely to have relatives with BPPV compared to the dizzy control group (chi2=5.95, DF=1, p=0.015). We have demonstrated that there is a familial tendency for the occurrence of BPPV. There is nothing in our data that would distinguish between a hereditary or environmental influence in the development of the disease, however.
Video-oculography as part of the ENG battery.
Recording and quantifying eye movement is the basis of audiologic balance testing. The ability to record and quantify eye movement is a key part of the electronystagmography (ENG) test battery. With computerization, eye movements can be more accurately detected and analysed--testing the limits of the standard recording technique. In response to this, manufacturers are introducing alternative recording protocols. Specifically, infra-red video technology allows an accurate and sophisticated recording and analysis of eye motion in response to balance-related stimuli. The purpose of this technical note is to discuss the limitations of the EOG recording method and discuss the advantages that video-oculography offers.
Benefit of active compression-decompression cardiopulmonary resuscitation as a prehospital advanced cardiac life support. A randomized multicenter study.
BACKGROUND: We compared short-term prognosis of active compression-decompression (ACD) and standard (STD) cardiopulmonary resuscitation (CPR) in out-of-hospital cardiac arrests. METHODS AND RESULTS: We randomized advanced cardiac life support (ACLS) with ACD ACLS CPR on odd days and STD ACLS CPR on even days. We measured the rates of return of spontaneous circulation (ROSC), survival at 1 hour (H1), at 24 hours (H24), and at 1 month (D30): hospital discharge (HD); neurological outcome; and complications. Mean times from collapse to basic cardiac life support CPR was 9 minutes and from collapse to ACLS CPR was 21 minutes. Compared with the STD ACLS patients (n = 258), ACD ACLS patients (n = 254) had higher survival rates (ROSC, 44.9% versus 29.8%, P = .0004; H1, 36.6% versus 24.8%, P = .003; H24, 26% versus 13.6%, P = .002; HD without neurological impairment, 5.5% versus 1.9%, P = .03) and a trend for improvement in neurological outcome at D30 (Glasgow-Pittsburgh Outcome Categories = 1.6 +/- 0.8 versus 2.3 +/- 1.1. P = .09). Sternal dislodgements (2.9% versus 0.4%, P = .03) and hemoptysis (5.4% versus 1.3%, P = .01) were more frequent in the ACD ACLS group. CONCLUSIONS: Despite long time intervals, ACD significantly improved short-term survival rates in out-of-hospital cardiac arrests compared with STD CPR.
The diagnostic value of imaging the patient with dizziness. A Bayesian approach.
BACKGROUND: Imaging studies are routinely used in the evaluation of patients with dizziness. A principal concern of the ordering physician is to rule out a cerebellopontine angle (CPA) mass. The incidence of such masses in patients presenting with dizziness is quite low, however, raising the question of the value of imaging this population. OBJECTIVE: To calculate the probability, using Bayes theorem, that a given patient with dizziness has a CPA mass. DESIGN: Meta-analysis of epidemiological data on CPA masses and of studies reporting the incidence of otologic symptoms in patients with these masses. We also conducted a study of consecutive patients with dizziness to determine the frequency of asymmetric hearing loss in this population. These data were combined in applications of Bayes theorem to calculate disease probabilities. RESULTS: The probability that a patient with dizziness has a CPA mass is 0.0004, indicating that 2500 imaging studies would have to be performed to identify 1 CPA mass. If patients with subjectively normal hearing are investigated (ie, those with isolated dizziness), the probability is 0.000107, indicating that 9307 scans would have to be performed to identify 1 CPA mass. If the search is restricted to those patients with dizziness and asymmetric hearing loss (the patients usually felt to be high risk), the probability is 0.00156, indicating that 638 scans would have to be performed to identify 1 CPA mass. CONCLUSIONS: Even when studying patients with dizziness and asymmetric hearing loss, the probability of identifying a CPA mass is sufficiently low that we do not feel imaging is generally warranted. When faced with a patient with dizziness, we recommend a careful neurologic and otologic examination. If abnormalities are detected on examination that suggest central nervous system disease or invasive otologic disease, imaging should be pursued as appropriate. In cases of acute vertigo, if the patient is at high risk for cerebrovascular disease by virtue of age and additional risk factors, imaging should probably be pursued. For the remainder of patients, if progression of hearing loss is not documented, we do not believe imaging is warranted. Progressive hearing loss with abnormal speech reception thresholds probably warrants a magnetic resonance imaging scan of the internal auditory canals.
Management of visual loss after optic nerve sheath decompression in patients with pseudotumor cerebri.
PURPOSE: To determine the appropriate management of patients with pseudotumor cerebri with early, progressive visual loss after optic nerve sheath decompression (ONSD). METHODS: The records of all patients with pseudotumor cerebri who underwent ONSD were reviewed retrospectively. Patients who showed visual loss within 1 month of surgery were studied. RESULTS: Five patients with pseudotumor cerebri, including two with renal failure and hypertension, had visual loss within 1 month of ONSD. The first patient had an abrupt decrease in vision 6 days after ONSD. In this patient, a vessel on the nerve sheath bled into the surgical site. At the time of ONSD, this patient had a visual acuity of 20/20 1 day after surgery. Six days later, visual acuity decreased to 20/200. After high-dose intravenous corticosteroids failed to improve vision, emergency lumboperitoneal shunt resulted in full visual recovery. An apparent infectious optic neuropathy developed in the second patient 3 days after surgery. After 72 hours of intravenous antibiotics, visual acuity improved from 20/600 to 20/15. The other three patients had gradual visual loss after ONSD, which stabilized after lumboperitoneal shunts. CONCLUSIONS: Avoidance of bleeding during ONSD may prevent fibrous occlusion of the surgical site. Patients with no identifiable cause for visual loss after ONSD, who do not respond to intravenous corticosteroids, should be evaluated for emergency lumboperitoneal shunting. Postoperative infectious optic neuropathy should be considered in the differential diagnosis of abrupt visual loss after ONSD.
Orientation of human optokinetic nystagmus to gravity: a model-based approach.
Optokinetic nystagmus (OKN) was induced by having subjects watch a moving display in a binocular, head-fixed apparatus. The display was composed of 3.3 degrees stripes moving at 35 degrees/s for 45 s. It subtended 88 degrees horizontally by 72 degrees vertically of the central visual field and could be oriented to rotate about axes that were upright or tilted 45 degrees or 90 degrees. The head was held upright or was tilted 45 degrees left or right on the body during stimulation. Head-horizontal (yaw axis) and head-vertical (pitch axis) components of OKN were recorded with electro-oculography (EOG). Slow phase velocity vectors were determined and compared with the axis of stimulation and the spatial vertical (gravity axis). With the head upright, the axis of eye rotation during yaw axis OKN was coincident with the stimulus axis and the spatial vertical. With the head tilted, a significant vertical component of eye velocity appeared during yaw axis stimulation. As a result the axis of eye rotation shifted from the stimulus axis toward the spatial vertical. Vertical components developed within 1-2 s of stimulus onset and persisted until the end of stimulation. In the six subjects there was a mean shift of the axis of eye rotation during yaw axis stimulation of approximately 18 degrees with the head tilted 45 degrees on the body. Oblique optokinetic stimulation with the head upright was associated with a mean shift of the axis of eye rotation toward the spatial vertical of 9.2 degrees. When the head was tilted and the same oblique stimulation was given, the axis of eye rotation rotated to the other side of the spatial vertical by 5.4 degrees. This counterrotation of the axis of eye rotation is similar to the "Müller (E) effect," in which the perception of the upright is counterrotated to the opposite side of the spatial vertical when subjects are tilted in darkness. The data were simulated by a model of OKN with a "direct" and "indirect" pathway. It was assumed that the direct visual pathway is oriented in a body, not a spatial frame of reference. Despite the short optokinetic after-nystagmus time constants, strong horizontal to vertical cross-coupling could be produced if the horizontal and vertical time constants were in proper ratio and there were no suppression of nystagmus in directions orthogonal to the stimulus direction. The model demonstrates that the spatial orientation of OKN can be achieved by restructuring the system matrix of velocity storage. We conclude that an important function of velocity storage is to orient slow-phase velocity toward the spatial vertical during movement in a terrestrial environment.
The representation of the spatial vertical in human optokinetic nystagmus.
With our stimulus conditions we were unable to record more than 2-3 beats of OKAN; therefore direct comparison to the data recorded from monkeys is not possible. We did, however, see cross-coupling in OKN. In monkeys, cross-coupling predominates in OKAN, indicating that velocity storage underlies this phenomenon. We consistently saw the axis of response shift towards the spatial vertical. This implies that although OKAN was weak, velocity storage contributed a representation of the spatial vertical to OKN that is dependent on the axis of the head or body with respect to gravity.
Ocular motor function in motor neuron disease.
We studied ocular motor function in 34 patients with motor neuron disease (MND) and in 18 age-matched controls. This included the latency, accuracy, and amplitude-velocity relationships of saccades. We also examined ocular pursuit, the slow phases of optokinetic nystagmus, and the ability to suppress the vestibulo-ocular reflex (VOR) with visual fixation of a head-mounted target. Five of the subjects with MND had pronounced parkinsonian features on neurologic examination. The nonparkinsonian MND subjects had normal ocular motor function for all measures. Most subjects suppressed the VOR completely. The parkinsonian-MND patients had impairment of both saccadic and pursuit eye movements, and one parkinsonian-MND patient with poor pursuit was unable to suppress the VOR. We conclude that ocular motor function is generally spared in MND. The occasional appearance of ocular motor dysfunction probably reflects the incidence of secondary abnormalities such as parkinsonism.
Ocular flutter in vidarabine toxicity.
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Suppression of vestibular nystagmus by forced convergence in normal human subjects.
BACKGROUND: It has been suggested that the principal mechanism of nystagmus suppression in the nystagmus blockage syndrome is either adduction of the eye or convergence. We examined this issue using the nystagmus of the vestibulo-ocular reflex (VOR) as a model. METHODS: A motorized, computer-controlled rotary chair was used to produce VOR in darkness, using either sinusoidal or velocity step stimulation. Left eye position was monitored and horizontal slow-phase eye velocity was calculated. Subjects were cued to converge or perform other gaze tasks. RESULTS: Convergence suppressed nystagmus. With sinusoidal stimulation, nystagmus was nearly extinguished in extreme lateroversion, probably due to mechanical tethering of the eye. However, VOR gain suppression of 47% during convergence was observed even when the monitored eye was close to primary position. With velocity step stimulation, nystagmus was nearly extinguished at moderate angles of adduction. CONCLUSIONS: Convergence is sufficient to suppress nystagmus, without vision and without regard to whether the eye is adducted.