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This study aimed to characterise the ipsilateral, contralateral and bilateral masseter vestibular-evoked myogenic potential using clicks and 500 Hz tone burst stimuli in healthy adults.
Method
Masseter vestibular-evoked myogenic potential was recorded from 20 healthy participants aged 19–28 years (11 males and 9 females). Masseter vestibular-evoked myogenic potential was recorded using 500 Hz tone burst and click stimuli in ipsilateral, contralateral and bilateral modes.
Results
A statistically significant difference was observed between ipsilateral and contralateral stimulation for p11 latency, n21 latency and p11-n21 amplitude for both click and 500 Hz tone burst stimuli. The amplitude of the p11-n21 complex was higher for ipsilateral, contralateral and bilateral stimulations for 500 Hz tone burst than for click stimulus.
Conclusion
This study showed a significant difference for p11-n21 amplitude between click and 500 Hz tone burst evoked masseter vestibular-evoked myogenic potential. In addition, bilateral stimulation elicited a larger response than ipsilateral and contralateral stimulation.
Currently recommended landmarks for captive-bolt euthanasia of cattle often result in failure to penetrate the brainstem. The purpose of this study was to evaluate the ability to disrupt the brainstem by placing the shot at a higher position on the head. Intact heads from euthanased animals or natural mortalities were used for this study. Heads were grouped as adult (> 2 years), young (6-24 months) and neonate (< 1 month) and randomly assigned to either the LOW group (the intersection of two lines drawn from the medial canthus to the top of the opposite ear) or the HIGH group (midline halfway between the top of the poll and an imaginary line connecting each lateral canthus). Each head received a single shot from a CASH penetrating captive bolt with bolt length and power load selected based on manufacturer's recommendations. Computed tomography images of each head were evaluated independently by two veterinary radiologists. Brainstem disruption was assumed to occur if the bolt passed caudal to the presphenoid bone and deep to the third ventricle and was within 1.5 cm of midline. Brainstem disruption occurred in 16/18 adult HIGH and 7/14 adult LOW heads, 13/16 young HIGH and 11/19 young LOW heads, and 11/11 neonate HIGH and 14/14 neonate LOW heads. The higher shot location landmarks used in this study increased the probability of disrupting the brainstem when adult cattle were shot with a penetrating captive bolt which should reduce the risk of regaining sensibility. Reliable brainstem disruption is a precondition for considering penetrating captive bolt as a single-step euthanasia method. Further research is needed to determine if this method will reliably ensure a humane death.
Humane euthanasia of cattle under field conditions presents special challenges for veterinarians and producers. The purpose of this study was to evaluate the effectiveness of the CASH Dispatch Kit captive-bolt system combined with improved shot placement landmarks as a single-step euthanasia method for cattle. Cattle destined for euthanasia for reasons unrelated to the study were utilised. Adult (> 2 years), young (6-24 months) and neonatal (< 1 month) cattle each received a single shot from the CASH penetrating captive-bolt pistol. An additional group of neonatal animals was shot with a non-penetrating muzzle attachment. The shot was placed on midline halfway between the top of the poll and an imaginary line connecting the lateral canthus of each eye. Following the shot, the animals were immediately assessed for loss of consciousness based upon: i) immediate collapse (if standing); ii) loss of eye reflexes with a centered, dilated pupil; iii) lack of co-ordinated respiration; iv) lack of vocalisation; and v) lack of a righting reflex. Lack of consciousness and heartbeat were assessed at 1-min intervals until cardiac arrest. All animals were adequately stunned by a single shot. Euthanasia via a single shot was successful in 28/31, 17/19, 8/10, and 9/10 adult, young, neonate (penetrating) and neonate (non-penetrating) animals, respectively. Reasons for failure included return of co-ordinated respiration and prolonged time until cardiac arrest. A single shot from the CASH Dispatch captive-bolt system will humanely euthanase most animals. However, the results of this study indicate that application of a follow-up step to ensure death is still needed in certain instances.
The motor thalamus is interconnected with the brainstem, cortex, and basal ganglia and plays major roles in planning, sequencing, and executing action. In this chapter, I highlight roles of input-defined thalamic circuits in motor sequence production and learning. Brainstem–motor thalamic pathways carry efference copy signals important for the production of both innate and learned motor sequences, for example, during saccades, grooming, and birdsong. Basal ganglia thalamocortical loops implement aspects of reinforcement learning, including the generation of motor exploration during vocal babbling. Classic "gating" models of basal ganglia–thalamic transmission fail to explain thalamic discharge during behavior, which instead appears strongly driven by cortical inputs. A challenge going forward is to determine if there are conserved principles of thalamic function across diverse motor thalamic subregions.
There is international variability in whether neurological determination of death (NDD) is conceptually defined based on permanent loss of brainstem function or “whole brain death.” Canadian guidelines are not definitive. Patients with infratentorial stroke may meet clinical criteria for NDD despite persistent cerebral blood flow (CBF) and relative absence of supratentorial injury.
Methods:
We performed a multicenter cohort study involving patients that died from ischemic or hemorrhagic stroke in Alberta intensive care units from 2013 to 2019, focusing on those with infratentorial involvement. Medical records were reviewed to determine the incidence and proportion of patients that met clinical criteria for NDD; whether ancillary testing was performed; and if so, whether this demonstrated the absence of CBF.
Results:
There were 95 (27%) deaths from infratentorial and 263 (73%) from supratentorial stroke. Sixteen patients (17%) with infratentorial stroke had neurological examination consistent with NDD (0.55 cases per million per year). Among patients that underwent confirmatory evaluation for NDD with an apnea test, ancillary test (radionuclide scan), or both, ancillary testing was more common with infratentorial compared with supratentorial stroke (10/12 (85%) vs. 25/47 (53%), p = 0.04). Persistent CBF was detected in 6/10 (60%) patients with infratentorial compared with 0/25 with supratentorial stroke (p = 0.0001).
Conclusions:
Infratentorial stroke leading to clinical criteria for NDD occurs with an annual incidence of about 0.55 per million. There is variability in clinicians’ use of ancillary testing. Persistent CBF was detected in more than half of patients that underwent radionuclide scans. Canadian consensus is needed to guide clinical practice.
This chapter looks at the state of sleep and its biology. it begins by looking at what comprises the state of sleep, and examines comparatively which, and how, other animals sleep. It looks at circadian rhythms, and how the sleep--wake cycle is controlled, with melatonin manufactured by the pineal gland. There is emphasis on the electrophysiology of sleep (sleep EEG), and a description of the stages of sleep and how they are characterised by different EEG profiles, particularly the distinction between REM and non-REM sleep. The neurology of sleep looks at the role of structures such as the brainstem and reticular activating system, and the effect of damage at different levels of the brain on sleeping behaviour. The psychopharmacology of sleep looks at the changing role of neurotransmitters throughout the day and night, and in dreaming and dreamless sleep. The chapter then examines the range of sleep disorders, including problems getting to sleep, as well as sleep walking and sleep talking. It then looks at the effects of sleep deprivation. The chapter concludes with a discussion of why we sleep, covering the possible evolutionary functions of sleep, with focus on the role of sleep in learning and memory consolidation.
To determine the clinical significance of arachnoid cysts.
Methods
The scans of 6978 patients undergoing magnetic resonance imaging of the internal acoustic meatus for unilateral cochleovestibular symptoms were retrospectively reviewed. We identified the scans with arachnoid cysts, and assessed the statistical associations between the laterality, location and size of the arachnoid cyst, the laterality of symptoms, the patients’ age and gender.
Results
In a total of 37 arachnoid cysts identified in 36 patients (0.5 per cent), no associations were identified between the laterality of symptoms and the laterality of the arachnoid cyst, regardless of its size or location. There were no significant associations between the location of the arachnoid cyst and the age (p = 0.99) or gender of the patient (p = 0.13), or size (p = 0.656) or side of the cyst (p = 0.61). None of the cysts with repeat imaging scans (17 cysts) demonstrated growth.
Conclusion
Our results suggest that most, if not all, arachnoid cysts are of no clinical significance. Given their indolent behaviour, even serial imaging is not essential.
Earlier findings in patients with a small supratentorial white matter infarct demonstrated subtle impairments of cognition. This is in line with reported difficulties in regaining premorbid level of functioning in daily life activities, even though any physical neurological deficits are no longer present. Either a “bystander effect” of adjoining gray matter or a long distance effect through hypometabolism or other neurochemical changes might underlie these impairments. To find the best explanation, a group of 17 patients with a lacunar infarct in the brainstem was neuropsychologically evaluated and compared with a closely matched control group. The patients demonstrated significantly impaired task performance on a constellation of neuropsychological tasks that was very similar to the findings previously found in patients with a supratentorial lacunar infarct (Boston Naming Test, TEA visual elevator, category fluency, Trailmaking Test). We conclude that a small white-matter infarct may affect cognitive functioning in a nonspecific way independently of its location. (JINS, 2003, 9, 490–494.)
To determine the characteristics of acute phase nystagmus in patients with cerebellar lesions, and to identify a useful indicator for differentiating central lesions from peripheral lesions.
Methods:
Acute phase nystagmus and the appearance of neurological symptoms were retrospectively investigated in 11 patients with cerebellar stroke.
Results:
At the initial visit, there were no patients with vertical nystagmus, direction-changing gaze evoked nystagmus or pure rotatory nystagmus. There were four cases with no nystagmus and seven cases with horizontal nystagmus at the initial visit. There were no neurological symptoms, except for vertigo and hearing loss, in any cases at the initial visit. The direction and type of nystagmus changed with time, and neurological symptoms other than vertigo appeared subsequently to admission.
Conclusion:
It is important to observe the changes in nystagmus and other neurological findings for the differential diagnosis of central lesions.
The nasal cycle exhibits mainly reciprocal changes in nasal airflow that may be controlled from centres in the hypothalamus and brainstem. This study aims to gather new knowledge about the nasal cycle to help develop a control model.
Method:
Right and left nasal airflow was measured in healthy human subjects by rhinomanometry. This was performed over 7-hour periods on 2 study days separated by approximately 1 week. The correlation coefficient for nasal airflow was calculated for day 1 and day 2.
Results:
Thirty subjects (mean age, 22.7 years) completed the study. The correlation coefficient for nasal airflow varied between r = 0.97 with in-phase changes in airflow and r = −0.89 with reciprocal changes in airflow. The majority of r values were negative, indicating reciprocal changes in airflow (50 out of 60). There was a tendency for r values to become more negative between day 1 and day 2 (p < 0.001).
Conclusion:
A control model involving a hypothalamic centre and two brainstem half centres is proposed to explain both the in-phase and reciprocal changes in airflow associated with the nasal cycle.
The brainstem-derived neuropeptide S (NPS) has a multidirectional regulatory activity, especially as a potent anxiolytic factor. Accumulating data suggests that neuroleptics affect peptidergic signalling in various brain structures. However, there is no information regarding the influence of haloperidol on NPS and NPS receptor (NPSR) expression.
Methods
We assessed NPS and NPSR mRNA levels in brains of rats treated with haloperidol using quantitative real-time polymerase chain reaction.
Results
Chronic haloperidol treatment (4 weeks) led to a striking upregulation of NPS and NPSR expression in the rat brainstem. Conversely, the NPSR mRNA expression was decreased in the hippocampus and striatum.
Conclusions
This stark increase of NPS in response to haloperidol treatment supports the hypothesis that this neuropeptide is involved in the dopamine-dependent anxiolytic actions of neuroleptics and possibly also in the pathophysiology of mental disorders. Furthermore, our findings underline the complex nature of potential interactions between dopamine receptors and brain peptidergic pathways, which has potential clinical applications.
There is some experimental evidence to support the existence of a connection between panic and respiration. However, only recent studies investigating the complexity of respiratory physiology have revealed consistent irregularities in respiratory pattern, suggesting that these abnormalities might be a vulnerability factor to panic attacks. The source of the high irregularity observed, together with unpleasant respiratory sensations in patients with panic disorder (PD), is still unclear and different underlying mechanisms might be hypothesized. It could be the result of compensatory responses to abnormal respiratory inputs or an intrinsic deranged activity in the brainstem network shaping the respiratory rhythm. Moreover, since basic physiological functions in the organism are strictly interrelated, with reciprocal modulations and abnormalities in cardiac and balance system function having been described in PD, the respiratory findings might arise from perturbations of these other basic systems or a more general dysfunction of the homeostatic brain. Phylogenetically ancient brain circuits process physiological perceptions/sensations linked to homeostatic functions, such as respiration, and the parabrachial nucleus might filter and integrate interoceptive information from the basic homeostatic functions. These physiological processes take place continuously and subconsciously and only occasionally do they pervade the conscious awareness as ‘primal emotions’. Panic attacks could be the expression of primal emotion arising from an abnormal modulation of the respiratory/homeostatic functions.
Numerous findings of brain structural changes in obstructive sleep apnea (OSA) give strong support to the notion that the disorder does cause brain injury. This chapter describes findings by technique, influences of factors other than the sleep disordered breathing on structural changes in OSA, and a summary of the brain regions shown across multiple studies to be affected in the disorder. Psychological symptoms of depression and anxiety are associated with neural changes in non-OSA populations, so one can hypothesize that the structural changes in OSA would be exacerbated in the presence of these symptoms. Many areas in the brain show structural impairments in OSA, including cortical, limbic, brainstem and cerebellar regions. Neuroimaging methods give numerical measures that are associated with a variety of biological pathologies, and technical limitations due to scanning and analysis issues limit the interpretability of the data.
This chapter reviews brain imaging studies that comment on whether or not there is abnormal brain function in insomnia patients that may in some way relate to their difficulty in sleeping. It provides a systems neuroscience view of a hierarchical arousal network in the central nervous system. Human sleep neuroimaging studies in healthy subjects support the involvement of these basic arousal networks in non-rapid eye movement (NREM) sleep. Blood flow has been shown to correlate negatively with the presence of NREM sleep in the pontine reticular formation, and in the basal forebrain/hypothalamus. Pharmacotherapy for insomnia may have some of its mechanism of action on the limbic and paralimbic structures, especially the antidepressant medications. Traditional sedative-hypnotic approaches appear to target brainstem and hypothalamic arousal networks in insomnia patients while behavioral treatments and frontal cerebral hypothermia appear to target frontal hyperarousal in insomnia patients.
This chapter focuses on aspects of structural and functional neuroanatomy relevant to Behavioral Neurology & Neuropsychiatry (BN&NP). It considers the general structure of the brain from the brainstem through the cerebral cortex, including a review of white matter anatomy, the cerebral vasculature, and the ventricular system. The brainstem comprises the medulla oblongata, pons and cerebellum, and midbrain. Each of these areas and the neurobehaviorally salient structures they contain are reviewed briefly in the chapter. The reticular formation (which is contributed to by several brainstem substructures) and the cranial nerves (some, but not all, of which are located within the brainstem) also are discussed in the chapter. The diencephalon includes the thalamus, metathalamus (medial and lateral geniculate nuclei), epithalamus (habenula, stria medullaris, and pineal body), and subthalamus. The chapter considers briefly the thalamus, hypothalamus (and pituitary), and the epithalamus.
The advent of neuroimaging has allowed clinicians to improve clinico-anatomical correlations in stroke patients. Arterial trunks supplying the brainstem include: the vertebral artery, basilar artery, anterior and posterior spinal arteries, posterior inferior cerebellar artery, anterior inferior cerebellar artery, superior cerebellar artery, posterior cerebral artery, and anterior choroidal artery. The arterial supply of the medulla oblongata comes from the vertebral arteries that form the middle rami of the lateral medullary fossa, the posterior inferior cerebellar artery that gives rise to the inferior rami of the lateral medullary fossa, and the anterior and posterior spinal arteries. Different arterial trunks supply blood to the pons, including the vertebral arteries, anterior inferior cerebellar artery, superior cerebellar artery, and basilar artery. The leptomeningeal arteries consist of the terminal branches of the anterior, middle, and posterior cerebral arteries forming an anastomotic network on the surface of the hemispheres.
Severe ischemic stroke with progressive edema development is frequently life-threatening and associated with a poor prognosis due to limited expandability within the cranial cavity. This chapter describes the relevant aspects of supra- and infratentorial space-occupying strokes with particular emphasis on the role of decompressive surgery. Large ischemic infarction of the middle cerebral artery (MCA) territory can lead to a clinical syndrome called malignant MCA stroke. Cranial computed tomography (CT) is still the most widely used radiological modality to diagnose and monitor malignant MCA infarction. The only specific treatment option for this type of stroke with a solid base of evidence and major impact on the clinical course to date is decompressive surgery, that is, hemicraniectomy. Swelling of a large space-occupying cerebellar infarct appears within a few days from symptom onset and can lead to compression of the brainstem and midbrain or cause a hydrocephalus.
This chapter talks about a 54-year-old right-handed man who was brought to medical attention by his daughter because of progressive speech difficulty over the last 2 years. The patient was clinically diagnosed with fronto-temporal dementia with non-fluent progressive aphasia as well as behavioral symptoms. Sensory and motor nerve conduction studies were normal. EMG needle electromyography showed mixed denervation pattern in the right FDI and left biceps with 2_ fasciculation potentials, positive sharp waves, and fibrillations. Motor units were polyphasic with increase in sharp waves. External examination of the formalin-fixed brain showed no obvious cerebral atrophy or no focal lesions. The base of the brain was unremarkable apart from mild patchy atherosclerosis. Serial coronal sections through the cerebral hemispheres showed a normal ventricular system and deep gray structures. Sections of the brainstem and cerebellum were also unremarkable apart from mild loss of pigmentation of substantia nigra.