Acute vestibular neuritis may provoke atrial fibrillation.

BACKGROUND: Exclusion of stroke is the focus of guidelines in the emergency department assessment of acute vertigo, especially with new-onset atrial fibrillation (AF). Early diagnosis of vestibular neuritis (VN) is also important but may be deferred awaiting brain magnetic resonance imaging (MRI) for exclusion of stroke. This may delay potentially beneficial corticosteroid therapy. AIMS: To highlight that VN can provoke acute AF. METHODS: In the course of a prospective study of acute vertigo in patients assessable within 24 h of admission, we encountered three patients with acute onset transient AF associated with VN. We performed a detailed neurological examination and quantitated the vestibulo-ocular reflex (VOR) gain with video-oculography. Brain MRI was performed in all patients. RESULTS: There were two men and one woman, aged 58-66 (mean 61) years. All patients had typical non-direction-changing rotatory nystagmus and positive head impulse tests. The horizontal VOR gains ranged 0.38-0.62 (mean 0.47). Diffusion-weighted MRI within 36 h was normal in all. AF reverted in all three within 24 h. CONCLUSIONS: Acute AF can be precipitated by vertigo such as in VN. In VN, the concurrence of acute AF may distract from the correct neurological diagnosis, delaying potentially beneficial corticosteroid therapy, especially if exclusion of stroke is dependent on MRI, which may be delayed.

Cerebral amyloid angiopathy: Review of clinico-radiological features and mimics.

Cerebral amyloid angiopathy (CAA) is an important cause of lobar intracerebral haemorrhage (ICH) in the elderly, but has other clinico-radiological manifestations. In the last two decades, certain magnetic resonance imaging (MRI) sequences, namely gradient-recalled echo imaging and the newer and more sensitive susceptibility-weighted imaging, have been utilised to detect susceptibility-sensitive lesions such as cerebral microbleeds and cortical superficial siderosis. These can be utilised sensitively and specifically by the Modified Boston Criteria to make a diagnosis of CAA without the need for 'gold-standard' histopathology from biopsy. However, recently, other promising MRI biomarkers of CAA have been described which may further increase precision of radiological diagnosis, namely chronic white matter ischaemia, cerebral microinfarcts and lobar lacunes, cortical atrophy, and increased dilated perivascular spaces in the centrum semiovale. However, the radiological manifestations of CAA, as well as their clinical correlates, may have other aetiologies and mimics. It is important for the radiologist to be aware of these clinico-radiological features and mimics to accurately diagnose CAA. This is increasingly important in a patient demographic that has a high prevalence for use of antiplatelet and antithrombotic medications for other comorbidities which inherently carries an increased risk of ICH in patients with CAA.

Importance of spontaneous nystagmus detection in the differential diagnosis of acute vertigo.

Vertigo is a common cause of emergency department attendance. Detection of spontaneous nystagmus may be a useful sign in distinguishing vestibular neuritis from other vestibular diagnoses. We aimed to assess the contribution of spontaneous nystagmus in the diagnosis of acute vertigo. We enrolled consecutive consenting patients arriving at a single emergency department with acute vertigo. There was no declared protocol for the emergency department staff. A standardized history and examination was conducted by the investigators. Observation for spontaneous nystagmus, its response to visual fixation, and testing the vestibulo-ocular reflex with the horizontal head impulse test were the chief examination components. MRI was obtained within 24 hours. Clinical criteria and MRI were used to reach the final diagnosis. The investigators' physical findings and final neurological diagnosis were compared with the initial emergency department examination findings and the referral diagnosis. There were 28 patients, 15 with vestibular neuritis, six with benign paroxysmal positional vertigo, one with stroke, suspected clinically, and three with migraine. In three the diagnosis remained uncertain. Spontaneous nystagmus was seen in all 15 patients with vestibular neuritis, fixation-suppressed in eight of 11 tested for this. The head impulse test was positive in 12 of 15 with vestibular neuritis. The emergency department referral diagnosis was correct in six of 23 patients. The ability to detect spontaneous nystagmus is useful in vestibular diagnosis, both in support of a diagnosis of vestibular neuritis and in avoiding false positive diagnoses of benign paroxysmal positional vertigo.

A 19-year-old male with cerebellar ataxia and cognitive impairment following glandular fever.

A 19-year-old male, who was previously functionally independent, presented with cerebellar ataxia and cognitive impairment following glandular fever. This case highlights the importance of considering an Epstein-Barr virus aetiology in children or young adults with acute cerebellar ataxia.

Late-adult onset Leigh syndrome.

We report an illustrative case of a 74-year-old man who, in the absence of intercurrent illness, presented with rapid cognitive decline. MRI showed bilateral, symmetrical, high T2-weighted signal in the anterior basal ganglia and medial thalami, extending to the periaqueductal grey matter, basal ganglia and basal frontal lobes. A (18)F-fluorodeoxyglucose-positron emission tomography scan showed widespread reduction of metabolism in the cortex of the frontal, temporal and parietal lobes, posterior cingulate gyrus, precuneus and caudate nuclei, with sparing of the sensorimotor cortex, thalami and lentiform nuclei. A mild vitamin B12 deficiency was found and despite normal thiamine levels, intravenous (IV) thiamine and vitamin B therapy was commenced, with a short course of IV methylprednisolone and tetracycline. Repeat neuropsychological assessment four weeks following treatment revealed increased alertness and interactiveness but significant cognitive decline persisted. Unexpectedly, the patient suffered a transmural anterior myocardial infarction six weeks after presentation and died within 24hours. An a autopsy showed: global reduction in cytochrome oxidase (COX) activity in all skeletal muscles examined; bilateral, symmetrical, hypervascular, focally necrotizing lesions in the substantia nigra, periaqueductal grey matter, superior colliculi, medial thalami anteriorly and posteriorly, as well as in the putamena but the mammillary bodies were not affected. Biochemical analysis of fresh muscle confirmed selective deficiency of complex IV of the oxidative phosphorylation chain. A diagnosis of late-adult onset Leigh syndrome was made. Multiple genetic studies failed to identify the specific underlying mutation. The relevant literature is reviewed.

When to measure lipid profile after stroke?

BACKGROUND: Although acute decreases in total cholesterol (TC) are well documented in myocardial infarction, previous stroke studies have produced conflicting results. The timing of lipid estimation in ischemic stroke is becoming important with recent trial results indicating the benefits of statins. We therefore aimed to determine the optimal time for lipid measurements after stroke. We hypothesized that TC would acutely decrease after stroke and return to baseline by 12 weeks. METHODS AND RESULTS: We performed a prospective, observational study of 50 patients (age 68.5 +/- 11.2 years) who presented with acute ischemic stroke. Of these, 22 (44%) were HMG-CoA reductase (statin) naïve, 15 (30%) had already been on statins and 13 (26%) were commenced on statins. Of the 50 patients, 38 (76%) completed 12 weeks of follow-up, 5 died, and 7 were lost to follow-up. Fasting lipid profile (TC, low-density lipoprotein, high-density lipoprotein, triglyceride) was measured <48 h, 4 weeks and 12 weeks following ictus. In patients who were statin naïve, there was a significant increase in TC at the week 12 evaluation. CONCLUSIONS: Cholesterol levels in acute stroke are an unreliable measure of lipid status. Initiation of statins should ideally be based on measurements taken 12 weeks after stroke.

Management of the elderly cardiac surgical patient: neurological sequelae.

The main neurological complications after cardiac surgery and non-surgical cardiac procedures include stroke, encephalopathy and neuropsychological deficits. Embolism from aortic atherosclerosis is the most common pathogenic mechanism. This article reviews the incidence, risk factors, and mechanisms of these complications.