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.

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.

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).

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.

To determine the clinical significance of arachnoid cysts.

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.

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.

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.

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.

Acute phase nystagmus and the appearance of neurological symptoms were retrospectively investigated in 11 patients with cerebellar stroke.

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.

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.

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.

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).

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.

We assessed NPS and NPSR mRNA levels in brains of rats treated with haloperidol using quantitative real-time polymerase chain reaction.

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.

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.

Tinnitus is a disturbing symptom and is often the main reason for otology referral. It is usually associated with hearing loss of varying aetiology, and is thought to begin in the cochlea, with later abnormal central activity. We hypothesise that tinnitus without hearing loss may be caused by central and subcortical abnormalities and altered outer hair cell function.

To compare the auditory brainstem responses, middle latency responses and otoacoustic emissions in normal-hearing individuals with and without tinnitus.

The audiological test results of 25 normal hearing subjects with tinnitus (age 18–45 years) were determined, and compared with those of a control group.

A statistically significant difference was found between study group tinnitus ears vs control group ears, as regards wave I latency prolongation, shortening of wave V and absolute I–III and I–V interpeak latency, enlargement of wave Na and Pa amplitude, and distortion product and transient evoked otoacoustic emission signal-to-noise ratios. There was no statistically significant difference between unilateral vs bilateral tinnitus ears.

The pathogenesis and optimum management of tinnitus are still unclear. It often occurs with primary ear disease, usually associated with hearing loss, but may occur in patients with normal hearing. Observed changes in auditory brainstem and middle latency responses indicate central auditory alterations. Tinnitus involves both peripheral and central activity, and complete audiological and neurophysiological investigation is required. Management should be based on both audiological and neurophysiological findings.