Parental care behaviour in response to perceived paternity is not mediated by 11-ketotestosterone in bluegill sunfish.

Parental care is critical for the survival of many young animals, but parental care can be costly to the individual providing care. To balance this cost, parents can allocate their care to offspring based on their value, which can be dependent on the offspring's relatedness to the parent. Bluegill (Lepomis macrochirus) is a fish characterized by uniparental male care and high levels of cuckoldry. While parental males of this species have been shown to adaptively adjust their care in response to paternity, the mechanisms for this adjustment are not well understood. Androgens are steroid hormones that are associated with parental care behaviours in many species including bluegill. Here, we test the hypothesis that circulating androgen concentrations mediate the adjustment in care provided by bluegill parental males by manipulating perceived paternity and then measuring circulating 11-ketotestosterone concentration and parental care behaviour. We show that males with higher perceived paternity provide higher levels of nurturing and nest defense behaviour, but contrary to expectations, we found that these males had lower concentrations of 11-ketotestosterone. Furthermore, we found positive correlations between individual circulating plasma 11-ketotestosterone concentrations and nurturing behaviour, but not with the aggressive behaviours that differed between paternity treatments. While bluegill make behavioural changes in response to perceived paternity, these changes do not appear to be modulated by 11-ketotestosterone.

Severity of Downgaze Palsy in the Context of Disease Duration Could Estimate Survival Duration in Patients With Progressive Supranuclear Palsy.

It is an unmet need to estimate survival duration for patients with progressive supranuclear palsy (PSP). The objective of this study was to identify factors associated with the survival duration in patients with PSP. We followed up 23 patients with probable PSP-RS (Richardson syndrome) or PSP-P (parkinsonism) in our PSP center until death from 2011 to 2019. We prospectively and quantitatively rated their downgaze palsy whenever first noticed in our clinic. This was utilized along with the disease duration, motor function, medication use for parkinsonism, sex, age at onset of PSP, comorbid pulmonary and cardiovascular diseases, and the total survival duration from the onset of PSP to death for prediction analysis. A well-fitted linear regression model and a multivariant Cox model were applied to identify predicting factors for total survival duration. All patients had the specific hummingbird sign on brain MRI for PSP when downgaze palsy was documented. We found that the severity of downgaze palsy and the disease duration at the assessment were consistently correlated with the total survival duration in both models. The total survival duration could be further estimated by a formed regression equation. We conclude that severity and time to develop downgaze palsy could help to estimate the total survival duration in patients with probable PSP-RS and PSP-P, the major forms of PSP, which has significant clinical applications in clinical counseling and trial enrollment.

Vestibular Testing.

PURPOSE OF REVIEW: Vestibular testing, both at the bedside and in the laboratory, is often critical in diagnosing patients with symptoms of vertigo, dizziness, unsteadiness, and oscillopsia. This article introduces readers to core concepts, as well as recent advances, in bedside and instrumented vestibular assessments. RECENT FINDINGS: Vestibular testing has improved immensely in the past 2 decades. While history and bedside testing is still the primary method of differential diagnosis in patients with dizziness, advances in technology such as the ocular vestibular-evoked myogenic potential test for superior canal dehiscence and the video head impulse test for vestibular neuritis have capabilities that go far beyond the bedside examination. Current vestibular testing now allows clinicians to test all five vestibular sensors in the inner ear. SUMMARY: Contemporary vestibular testing technology can now assess the entire vestibular periphery. Relatively subtle conditions, such as superior canal dehiscence or a subtle vestibular neuritis, can now be diagnosed with far greater certainty.

Square wave manoeuvre for apogeotropic variant of horizontal canal benign paroxysmal positional vertigo in neck restricted patients.

OBJECTIVE: We aimed to describe the clinical features of the apogeotropic variant of horizontal canal benign paroxysmal positional vertigo (HC BPPV-AG) in a cluster of patients with restrictive neck movement disorders and a new therapeutic manoeuvre for its management. METHODS: In a retrospective review of cases from an ambulatory tertiary referral center, patients with HC BPPV-AG in combination with neck movement restriction that prevented any classical manual repositioning procedure or who were refractory to canalith repositioning manoeuvres, were treated with a new manoeuvre comprised of sequential square-wave pattern of head and body supine rotations while nystagmus was being monitored, until either an apogeotropic to geotropic conversion or resolution of the nystagmus was observed. RESULTS: Fifteen patients were studied. All but one [14/15 cases] showed a positive therapeutic response to the repositioning procedure in a single session. In two cases, a direct relief of vertigo and elimination of nystagmus was observed without an intermediate geotropic phase. Although in three patients the affected ear was not initially identified, it was ultimately identified and successfully treated by the square wave manoeuvre in all of them. CONCLUSIONS: The square-wave manoeuvre is an alternative for HC BPPV-AG treatment in either cases with neck restriction, where the affected side is not well identified at the bedside or when other manoeuvres fail to resolve the HC BPPV-AG.

Loss-of-function BK channel mutation causes impaired mitochondria and progressive cerebellar ataxia.

Despite a growing number of ion channel genes implicated in hereditary ataxia, it remains unclear how ion channel mutations lead to loss-of-function or death of cerebellar neurons. Mutations in the gene KCNMA1, encoding the α-subunit of the BK channel have emerged as responsible for a variety of neurological phenotypes. We describe a mutation (BKG354S) in KCNMA1, in a child with congenital and progressive cerebellar ataxia with cognitive impairment. The mutation in the BK channel selectivity filter dramatically reduced single-channel conductance and ion selectivity. The BKG354S channel trafficked normally to plasma, nuclear, and mitochondrial membranes, but caused reduced neurite outgrowth, cell viability, and mitochondrial content. Small interfering RNA (siRNA) knockdown of endogenous BK channels had similar effects. The BK activator, NS1619, rescued BKG354S cells but not siRNA-treated cells, by selectively blocking the mutant channels. When expressed in cerebellum via adenoassociated virus (AAV) viral transfection in mice, the mutant BKG354S channel, but not the BKWT channel, caused progressive impairment of several gait parameters consistent with cerebellar dysfunction from 40- to 80-d-old mice. Finally, treatment of the patient with chlorzoxazone, a BK/SK channel activator, partially improved motor function, but ataxia continued to progress. These studies indicate that a loss-of-function BK channel mutation causes ataxia and acts by reducing mitochondrial and subsequently cellular viability.

Is Cerebellar Ataxia, Neuropathy, and Vestibular Areflexia Syndrome (CANVAS) a Vestibular Ganglionopathy?

OBJECTIVES: CANVAS is an acronym for cerebellar ataxia, neuropathy and vestibular areflexia syndrome. Limited autopsy data has suggested that CANVAS is caused by a focal dorsal root ganglionopathy that damages Scarpa's (vestibular) ganglion, but spares the Spiral (hearing) ganglion. If the vestibular areflexia of CANVAS is in fact due to ganglionopathy, then there should be global reduction of all vestibular responses. MATERIALS AND METHODS: With this hypothesis in mind, a retrospective review of 5 subjects who met the clinical criteria for CANVAS was performed. Recent advances in vestibular testing have made it possible to quantify responses from all 5 vestibular end organs in the inner ear. Results of the Video head impulse test (VHIT), video oculography, caloric test and vestibular evoked myogenic potential (VEMP) were examined to determine if all 5 end organs are nonfunctional in CANVAS. RESULTS: Severe reduction of function of the six semicircular canals and ocular VEMPs were observed. Only the cervical VEMPs were present and reproducible, consistent with either partial sparing of the inferior vestibular ganglia, specific embryologic resistance of the saccule to the degeneration or a mechanism for cervical VEMPs that does not require an intact vestibular ganglion. CONCLUSION: Our results suggest that Scarpa´s ganglia dysfunction could be the mechanism for loss of semicircular canal and utricular function in CANVAS patients, but the preservation of the cervical VEMP response is unexplained.

Migraine Associated Vertigo.

This chapter is a brief overview of migraine associated vertigo (MAV), focusing on the points most relevant to the practicing clinician. We review the definition of MAV, theories regarding its underlying pathophysiology, clinical presentation, epidemiology, findings on physical examination and oto vestibular testing, differential diagnosis, management and prognosis.

Symptoms in cervical vertigo.

OBJECTIVE: To use a unique, 41-question survey to identify patient features distinguishing cervical vertigo from vestibular causes of vertigo and vestibular migraine. METHODS: In this study, a unique, 41-question survey was administered to 48 patients diagnosed with cervical vertigo (n = 16), migraine (n = 16), and vestibular vertigo (eg, unilateral vestibular paresis, Meniere's disease) (n = 16) to test the hypothesis that a set of distinct symptoms can characterize cervical vertigo. Responses between the three diagnostic groups were compared to identify questions which differentiated patients based on their symptoms. RESULTS: Eight questions were successful in differentiating vestibular vertigo from migraine and cervical vertigo. Symptoms endorsed by subjects with cervical vertigo overlapped substantially with subjects with well-established vestibular disturbances as well as symptoms of subjects with migraine. Twenty-seven percent of cervical vertigo subjects reported having true vertigo, 50% having headache, and 94% having neck pain. CONCLUSION: Lacking knowledge of neck disturbance, the symptoms we elicited in our questionnaire suggest that cervical vertigo subjects may resemble migraine subjects who also have evidence of neck injury. Whether or not subjects with "cervical vertigo" also overlap with other diagnoses defined by a combination of symptoms and exclusion of objective findings such as chronic subjective dizziness and other variants of psychogenic dizziness remain to be established. LEVEL OF EVIDENCE: IV.

The Gain-Time Constant Product Quantifies Total Vestibular Output in Bilateral Vestibular Loss.

Patients with inner ear damage associated with bilateral vestibular impairment often ask "how much damage do I have." Although there are presently three clinical methods of measuring semicircular canal vestibular function; electronystagmography (ENG or VENG), rotatory chair and video head-impulse (VHIT) testing; none of these methods provides a method of measuring total vestibular output. Theory suggests that the slow cumulative eye position can be derived from the rotatory chair test by multiplying the high frequency gain by the time constant, or the "GainTc product." In this retrospective study, we compared the GainTc in three groups, 30 normal subjects, 25 patients with surgically induced unilateral vestibular loss, and 24 patients with absent or nearly absent vestibular responses due to gentamicin exposure. We found that the GainTc product correlated better with remaining vestibular function than either the gain or the time constant alone. The fraction of remaining vestibular function was predicted by the equation R = (GainTc/11.3) - 0.6. We suggest that the GainTc product answers the question "how much damage do I have," and is a better measure than other clinical tests of vestibular function.

Bilateral Vestibular Weakness.

Bilateral vestibular weakness (BVW) is a rare cause of imbalance. Patients with BVW complain of oscillopsia. In approximately half of the patients with BVW, the cause remains undetermined; in the remainder, the most common etiology by far is gentamicin ototoxicity, followed by much rarer entities such as autoimmune inner ear disease, meningitis, bilateral Ménière's disease, bilateral vestibular neuritis, and bilateral vestibular schwannomas. While a number of bedside tests may raise the suspicion of BVW, the diagnosis should be confirmed by rotatory chair testing. Treatment of BVW is largely supportive. Medications with the unintended effect of vestibular suppression should be avoided.

Characteristics of vestibular corrective saccades in patients with slow visual saccades, vestibular disorders and controls: A descriptive analysis.

OBJECTIVE: Our aim was to determine whether overt catch up saccades (OS) provoked by vestibular stimuli, as observed in the video head impulse test (vHIT), have comparable metrics as visually triggered horizontal saccades (VS), indicating a common saccadic brainstem generator. METHODS: Three groups of patients were studied: patients with neurological disorders causing slow saccades (group 1, n = 12), patients with peripheral vestibular lesions (group 2, n = 43), and normal controls (group 3, = 24). All patients underwent vHIT and Videooculographic testing. OS velocity, acceleration, amplitude and duration and VS velocity in this group was compared between the groups. RESULTS: There was significant reduction in the velocity of visually guided saccades in group 1, as expected from the patient selection constraints of this study. Group 1 also exhibited saccades which were longer in duration and of reduced acceleration when compared to subjects without saccadic slowing to visual targets (Group 2 and 3). There were significant positive correlations between OS acceleration and amplitude in both normal saccade groups (2 and 3) which was not observed in the slow saccade group (1). CONCLUSIONS: The metrics of overt saccades measured by the vHIT in patients with slow saccades and normal controls are similar to visually guided saccades. This supports the hypothesis that overt saccades associated with vestibular stimuli and visually triggered saccades share common circuitry that controls metrics.

Evolution of kin recognition mechanisms in a fish.

Both selection and phylogenetic history can influence the evolution of phenotypic traits. Here we used recently characterized variation in kin recognition mechanisms among six guppy populations to explore the phylogenetic history of this trait. Guppies can use two different kin recognition mechanisms: either phenotype matching, in which individuals are identified based on comparison with a recognition template, or familiarity, in which individuals are remembered based on previous interactions. Across the six populations, we identified four transitions in recognition mechanism: phenotype matching evolved once and was subsequently lost in a single population, whereas familiarity evolved twice. Based on a molecular clock, these transitions occurred among populations that had diverged on a timescale of hundreds of thousands of years, which is two orders of magnitude faster than previously documented transitions in recognition mechanisms. A randomization test provided no evidence that recognition mechanisms were constrained by phylogeny, suggesting that recognition mechanisms have the capacity to evolve rapidly, although the specific selection pressures that may be contributing to variation in recognition mechanisms across populations remain unknown.

Fluctuating Vestibulo-Ocular Reflex in Ménière's Disease.

OBJECTIVES: To describe the fluctuating high velocity vestibular ocular-reflex (VOR) during the Ménière's attacks and correlate those features with pathophysiology. PATIENTS: A patient with unilateral Ménière's disease (MD) was evaluated closely during and after acute vertigo episodes. MAIN OUTCOME MEASURES: The spontaneous nystagmus and the dynamic VOR changes were measured by the video head impulse test (VHIT) at different stages of the vertigo crisis and during the quiescent phase of the condition. RESULTS: During the Ménière's attack, the VOR gain showed large changes on the affected side; however, on recovery a return to the normal value was evident. The VOR gain also showed fluctuation on follow up, paralleling symptoms. The greatest reduction of the VOR was during the paralytic nystagmus phase. CONCLUSIONS: The present case documents rapid vestibular fluctuation documented with VHIT testing in MD. The ionic-chemical perilymphatic intoxication and the endolymphatic space collapse due to membrane rupture could explain those features. VHIT fluctuation is a promising tool for diagnosis of patients with episodic vestibular symptoms.

Cervicogenic causes of vertigo.

PURPOSE OF REVIEW: Herein we discuss the recent literature concerning cervicogenic vertigo including vertigo associated with rotational vertebral artery syndrome, as well as whiplash and degenerative disturbances of the cervical spine. We conclude with a summary of progress regarding diagnostic methods for cervicogenic vertigo. RECENT FINDINGS: Several additional single case studies of the exceedingly rare rotational vertebral artery syndrome have been added to the literature over the last year. Concerning whiplash and degenerative disturbances of the cervical spine, four reviews were published concerning using physical therapy as treatment, and two reviews reported successful surgical management. Publications regarding diagnostic methodology remain few and unconvincing, but the cervical torsion test appears the most promising. SUMMARY: Little progress has been made over the last year concerning cervicogenic vertigo. As neck disturbances combined with dizziness are commonly encountered in the clinic, the lack of a diagnostic test that establishes that a neck disturbance causes vertigo remains the critical problem that must be solved.

Bilateral vestibular loss.

Bilateral vestibular loss is a rare cause of visual disturbance (oscillopsia) and imbalance. When severe, the most common cause is iatrogenic-gentamicin ototoxicity. Bilateral loss is easily diagnosed at the bedside with the dynamic illegible E test. If this test is omitted, it can easily be misdiagnosed as a cerebellar syndrome. Treatment is largely supportive. Care should be taken to avoid medications that suppress vestibular function, and to encourage activity.

Clinical characteristics of cervicogenic-related dizziness and vertigo.

Cervical vertigo has long been a controversial entity and its very existence as a medical entity has advocates and opponents. Supporters of cervical vertigo claim that its actual prevalence is underestimated due to the overestimation of other diagnostic categories in clinics. Furthermore, different pathophysiological mechanisms have been attributed to cervical vertigo. Here the authors discuss the clinical characteristics of rotational vertebral artery vertigo, postwhiplash vertigo, proprioceptive cervical vertigo, and cervicogenic vertigo of old age. A clinical entity named subclinical vertebrobasilar insufficiency appears in the context of cervical osteoarticular changes. Migraine-associated vertigo may explain why some patients suffering from cervical pain have vertigo while others do not.

Neurophysiology of vestibular rehabilitation.

The vestibular system is a sophisticated human control system. Accurate processing of sensory input about rapid head and postural motion is critical. Not surprisingly, the body uses multiple, partially redundant sensory inputs and motor outputs, combined with a very competent central repair capability. The system as a whole can adapt to substantial peripheral vestibular dysfunction. The Achilles' heel of the vestibular system is a relative inability to repair central vestibular dysfunction.

Migraine-associated vertigo.

This article presents a brief overview of migraine-associated vertigo for the practicing otolaryngologist. Discussion includes the definition of migraine-associated vertigo and its pathophysiology, clinical features, demographics, findings on physical examination, use of otologic and vestibular testing, differential diagnosis, treatment, and prognosis.

Effectiveness of particle repositioning maneuvers in the treatment of benign paroxysmal positional vertigo: a systematic review.

BACKGROUND: Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo. PURPOSE: The purpose of this systematic review was to determine whether patients diagnosed with posterior canal (PC) BPPV, based on positional testing, and treated with a particle repositioning maneuver will show the resolution of benign paroxysmal positional nystagmus (BPPN) on the Dix-Hallpike Test performed 24 hours or more after treatment. DATA SOURCES: Data were obtained from an electronic search of the MEDLINE, EMBASE, and CINAHL databases from 1966 through September 2009. STUDY SELECTION: The study topics were randomized controlled trials (RCTs), quasi-RCTs, the diagnosis of PC BPPV, treatment with the particle repositioning maneuver, and outcome measured with a positional test 24 hours or more after treatment. DATA EXTRACTION: Data extracted were study descriptors and the information used to code for effect size. DATA SYNTHESIS: In 2 double-blind RCTs, the odds in favor of the resolution of BPPN were 22 times (95% confidence interval=3.41-141.73) and 37 times (95% confidence interval=8.75-159.22) higher in people receiving the canalith repositioning procedure (CRP) than in people receiving a sham treatment. This finding was supported by the results reported in 8 nonmasked quasi-RCTs. Studies with limited methodological quality suggested that a liberatory maneuver (LM) was more effective than a control intervention; there was no significant difference in the effectiveness of the LM and the effectiveness of the CRP; the self-administered CRP was more effective than the self-administered LM; and the CRP administered together with the self-administered CRP was more effective than the CRP administered alone. The Brandt-Daroff exercises were the least effective self-administered treatments. LIMITATIONS: The limitations included the methodological quality of the studies, the lack of quality-of-life measures, and confounding factors in reporting vertigo. CONCLUSIONS: Randomized controlled trials provided strong evidence that the CRP resolves PC BPPN, and quasi-RCTs suggested that the CRP or the LM performed by a clinician or with proper instruction at home by the patient resolves PC BPPN. There were no data on the effects of the maneuvers on outcomes relevant to patients.