Prolactin modulates changes in parental care behaviour in response to perceived paternity in bluegill sunfish (Lepomis macrochirus).

Prolactin is a hormone conserved across all vertebrates and is renowned for its role in reproduction and parental care. Previous studies on prolactin in fish have primarily relied on administration of mammalian prolactin and have suggested that increases in prolactin lead to greater parental care. However, the influence of endogenous prolactin on fish parental care remains unknown. Here, we measure circulating concentrations of endogenous prolactin during parental care in a fish and link these concentrations to parental care behaviour. We provide evidence that male bluegill sunfish with higher circulating concentrations of prolactin provide more parental care to their offspring. Furthermore, we show that nesting males with experimentally reduced perceived paternity have lower circulating prolactin concentrations and perform fewer parental behaviours, facilitating an adaptive investment in offspring in response to paternity cues. Our findings not only confirm the role of endogenous prolactin in modulating parental care behaviour in a fish but also provide a mechanism underlying the adaptive changes in parental care made in response to perceived paternity.

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.

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.

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.

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.

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.

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.

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.

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.

Promiscuity drives self-referent kin recognition.

Kin selection theory has been one of the most significant advances in our understanding of social behavior . However, the discovery of widespread promiscuity has challenged the evolutionary importance of kin selection because it reduces the benefit associated with helping nestmates . This challenge would be resolved if promiscuous species evolved a self-referent kin-recognition mechanism that enables individuals to differentiate kin and nonkin . Here, we take advantage of an asymmetry in the level of promiscuity among males of alternative life histories in the bluegill sunfish (Lepomis macrochirus). We show that, as a consequence of this asymmetry, offspring of "parental" males have a high level of relatedness to nestmates, whereas offspring of "cuckolder" males have a low level of relatedness to nestmates. We find that offspring of parentals do not use a direct recognition mechanism to discriminate among nestmates, whereas offspring of cuckolders use kin recognition by self-referent phenotype matching to differentiate between kin and nonkin. Furthermore, we estimate that the cost of utilizing such self-referent kin recognition is equivalent to a relatedness (R) of at least 0.06. These results provide compelling evidence for adaptive use of kin recognition by self-referent phenotype matching and confirm the importance of kinship in social behavior.

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.

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.

Interactions between auditory and somatosensory feedback for voice F0 control.

Previous studies have demonstrated the importance of both kinesthetic and auditory feedback for control of voice fundamental frequency (F0). In the present study, a possible interaction between auditory feedback and kinesthetic feedback for control of voice F0 was tested by administering local anesthetic to the vocal folds in the presence of perturbations in voice pitch feedback. Responses to pitch-shifted voice feedback were larger when the vocal fold mucosa was anesthetized than during normal kinesthesia. A mathematical model incorporating a linear combination of kinesthesia and pitch feedback simulated the main aspects of our experimental results. This model indicates that a feasible explanation for the increase in response magnitude with vocal fold anesthesia is that the vocal motor system uses both pitch and kinesthesia to stabilize voice F0 shortly after a perturbation of voice pitch feedback has been perceived.

Role of loading on head stability and effective neck stiffness and viscosity.

This experiment tests the hypothesis that loading the head would increase head stability. In particular, we hypothesized that an arrangement of the head so that muscle activation is required to counteract a load would significantly increase effective neck stiffness and viscosity, which would be associated with lower peak head angular velocity following abrupt force perturbations applied to the head. Seven young healthy subjects had their head loaded (preload) using a weight/pulley apparatus. Then, the head was pulled either forward or backward by dropping an additional weight onto the preload, causing an impulse of force followed by an increase in load. We recorded the applied force and head angular velocity. Neck viscoelastic properties as a function of loading were estimated by fitting experimental data to a second-order mathematical model of the head biomechanics. Across preloads varying from 2.22 to 8.89 N, peak head angular velocity decreased by 18.2% for the backward and by 19.9% for forward perturbations. As preload increased, simulated effective neck stiffness and viscosity significantly increased leading to lower peak angular velocity. These results demonstrated that loading reduces peak head angular velocity and that change in muscle stiffness and viscosity is a feasible explanation for this effect. We propose that reduction in peak head velocity could be caused by modulation of the strength of the vestibulo-collic reflex.

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.

Pairing virtual reality with dynamic posturography serves to differentiate between patients experiencing visual vertigo.

BACKGROUND: To determine if increased visual dependence can be quantified through its impact on automatic postural responses, we have measured the combined effect on the latencies and magnitudes of postural response kinematics of transient optic flow in the pitch plane with platform rotations and translations. METHODS: Six healthy (29-31 yrs) and 4 visually sensitive (27-57 yrs) subjects stood on a platform rotated (6 deg of dorsiflexion at 30 deg/sec) or translated (5 cm at 5 deg/sec) for 200 msec. Subjects either had eyes closed or viewed an immersive, stereo, wide field of view virtual environment (scene) moved in upward pitch for a 200 msec period for three 30 sec trials at 5 velocities. RMS values and peak velocities of head, trunk, and head with respect to trunk were calculated. EMG responses of 6 trunk and lower limb muscles were collected and latencies and magnitudes of responses determined. RESULTS: No effect of visual velocity was observed in EMG response latencies and magnitudes. Healthy subjects exhibited significant effects (p < 0.05) of visual field velocity on peak angular velocities of the head. Head and trunk velocities and RMS values of visually sensitive subjects were significantly larger than healthy subjects (p < 0.05), but their responses were not modulated by visual field velocity. When examined individually, patients with no history of vestibular disorder demonstrated exceedingly large head velocities; patients with a history of vestibular disorder exhibited head velocities that fell within the bandwidth of healthy subjects. CONCLUSION: Differentiation of postural kinematics in visually sensitive subjects when exposed to the combined perturbations suggests that virtual reality technology could be useful for differential diagnosis and specifically designed interventions for individuals whose chief complaint is sensitivity to visual motion.