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Bickerstaff brainstem encephalitis and Fisher syndrome: anti-GQ1b antibody syndrome

Shahrizaila N, Yuki N

J Neurol Neurosurg Psychiatry, 2013 May;84(5):576-83.
PMID: 22984203 DOI: 10.1136/jnnp-2012-302824

In the 1950s, Bickerstaff and Fisher independently described cases with a unique presentation of ophthalmoplegia and ataxia. The neurological features were typically preceded by an antecedent infection and the majority of patients made a spontaneous recovery. In the cases with Bickerstaff brainstem encephalitis, there was associated altered consciousness and in some, hyperreflexia, in support of a central pathology whereas in Fisher syndrome, patients were areflexic in keeping with a peripheral aetiology. However, both authors recognised certain similarities to Guillain-Barré syndrome such as the presence of peripheral neuropathy and cerebrospinal fluid albuminocytological dissociation. The discovery of immunoglobulin G anti-GQ1b antibodies in patients with Fisher syndrome and later in Bickerstaff brainstem encephalitis was crucial in providing the necessary evidence to conclude that both conditions were in fact part of the same spectrum of disease by virtue of their common clinical and immunological profiles. Following this, other neurological presentations that share anti-GQ1b antibodies emerged in the literature. These include acute ophthalmoparesis and acute ataxic neuropathy, which represent the less extensive spectrum of the disease whereas pharyngeal-cervical-brachial weakness and Fisher syndrome overlap with Guillain-Barré syndrome represent the more extensive end of the spectrum. The conditions can be referred to as the 'anti-GQ1b antibody syndrome'. In this review, we look back at the historical descriptions and describe how our understanding of Fisher syndrome and Bickerstaff brainstem encephalitis has evolved from their initial descriptions more than half a century ago.
Amyotrophic lateral sclerosis and motor neuron syndromes in Asia

Shahrizaila N, Sobue G, Kuwabara S, Kim SH, Birks C, Fan DS, et al.

J Neurol Neurosurg Psychiatry, 2016 08;87(8):821-30.
PMID: 27093948 DOI: 10.1136/jnnp-2015-312751

While the past 2 decades have witnessed an increasing understanding of amyotrophic lateral sclerosis (ALS) arising from East Asia, particularly Japan, South Korea, Taiwan and China, knowledge of ALS throughout the whole of Asia remains limited. Asia represents >50% of the world population, making it host to the largest patient cohort of ALS. Furthermore, Asia represents a diverse population in terms of ethnic, social and cultural backgrounds. In this review, an overview is presented that covers what is currently known of ALS in Asia from basic epidemiology and genetic influences, through to disease characteristics including atypical phenotypes which manifest a predilection for Asians. With the recent establishment of the Pan-Asian Consortium for Treatment and Research in ALS to facilitate collaborations between clinicians and researchers across the region, it is anticipated that Asia and the Pacific will contribute to unravelling the uncertainties in ALS.
Late presentation of Nipah virus encephalitis and kinetics of the humoral immune response

Wong SC, Ooi MH, Wong MN, Tio PH, Solomon T, Cardosa MJ

J Neurol Neurosurg Psychiatry, 2001 Oct;71(4):552-4.
PMID: 11561048

Nipah virus is a newly discovered paramyxovirus transmitted directly from pigs to humans. During a large encephalitis outbreak in Malaysia and Singapore in 1998-9, most patients presented acutely. A 12 year old child is described who developed encephalitis 4 months after exposure to the virus. She was diagnosed by a new indirect IgG enzyme linked immunosorbent assay (ELISA), which is also described. The late presentation and IgG subclass responses had similarities to subacute sclerosing panencephalitis. Nipah virus should be considered in patients with encephalitis even months after their possible exposure.
Late clinical and magnetic resonance imaging follow up of Nipah virus infection

Lim CC, Lee WL, Leo YS, Lee KE, Chan KP, Ling AE, et al.

J Neurol Neurosurg Psychiatry, 2003 Jan;74(1):131-3.
PMID: 12486285

The Nipah virus is a newly identified paramyxovirus responsible for an outbreak of fatal encephalitis in Malaysia and Singapore. This paper reports the follow up clinical and magnetic resonance imaging findings in 22 affected subjects. Of 13 patients with encephalitis, one died, one was lost to follow up, and seven recovered. Among the four remaining patients, one had residual sixth nerve palsy, another suffered from severe clinical depression, and a third patient had evidence of retinal artery occlusion. One patient with delayed onset Horner syndrome had a single lesion in the cervical spinal cord. The brain magnetic resonance findings were stable or improved in nine patients over 18 months of follow up. Among a second group of nine asymptomatic seropositive abattoir workers, magnetic resonance examination in seven subjects revealed discrete small lesions in the brain; similar to those detected in encephalitis patients. These findings suggest that in addition to encephalitis, the newly discovered Nipah virus affects the spinal cord and the retina. Late clinical and radiological findings can occur in Nipah virus infections as with other paramyxoviruses.
Intracranial hypertension causing visual failure in cryptococcus meningitis

Tan CT

J Neurol Neurosurg Psychiatry, 1988 Jul;51(7):944-6.
PMID: 3204403

Thirty four patients with cryptococcal meningitis seen in the University of Malaya medical centre since 1980 were reviewed. Eleven patients had bilateral papilloedema and visual impairment but eventually survived. Seven patients had intensive aggressive measures, including shunting to reduce intracranial hypertension irrespective of ventricular size shown in CT scan, and showed substantial improvement in vision. It is concluded that papilloedema and visual failure in cryptococcal meningitis reflects raised intracranial pressure and that this should be treated vigorously.
Juvenile muscular atrophy of distal upper extremities

Tan CT

J Neurol Neurosurg Psychiatry, 1985 Mar;48(3):285-6.
PMID: 3981204
Brain imaging abnormalities and outcome after acute ischaemic stroke: the ENCHANTED trial

Delcourt C, Wang X, Zhou Z, Wardlaw JM, Mair G, Robinson TG, et al.

J Neurol Neurosurg Psychiatry, 2020 12;91(12):1290-1296.
PMID: 33055145 DOI: 10.1136/jnnp-2020-323015

OBJECTIVE: To test the hypothesis that imaging signs of 'brain frailty' and acute ischaemia predict clinical outcomes and symptomatic intracranial haemorrhage (sICH) after thrombolysis for acute ischaemic stroke (AIS) in the alteplase dose arm of ENhanced Control of Hypertension ANd Thrombolysis strokE stuDy (ENCHANTED).
METHODS: Blinded assessors coded baseline images for acute ischaemic signs (presence, extent, swelling and attenuation of acute lesions; and hyperattenuated arteries) and pre-existing changes (atrophy, leucoaraiosis and old ischaemic lesions). Logistic regression models assessed associations between imaging features and death at 7 and 90 days; good recovery (modified Rankin Scale scores 0-2 at 90 days) and sICH. Data are reported with adjusted ORs and 95% CIs.
RESULTS: 2916 patients (67±13 years, National Institutes of Health Stroke Scale 8 (5-14)) were included. Visible ischaemic lesions, severe hypoattenuation, large ischaemic lesion, swelling and hyperattenuated arteries were associated with 7-day death (OR (95% CI): 1.52 (1.06 to 2.18); 1.51 (1.01 to 2.18); 2.67 (1.52 to 4.71); 1.49 (1.03 to 2.14) and 2.17 (1.48 to 3.18)) and inversely with good outcome. Severe atrophy was inversely associated with 7-day death (0.52 (0.29 to 0.96)). Atrophy (1.52 (1.08 to 2.15)) and severe leucoaraiosis (1.74 (1.20 to 2.54)) were associated with 90-day death. Hyperattenuated arteries were associated with sICH (1.71 (1.01 to 2.89)). No imaging features modified the effect of alteplase dose.
CONCLUSIONS: Non-expert-defined brain imaging signs of brain frailty and acute ischaemia contribute to the prognosis of thrombolysis-treated AIS patients for sICH and mortality. However, these imaging features showed no interaction with alteplase dose.
Zika virus infection and Guillain-Barré syndrome: a review focused on clinical and electrophysiological subtypes

Uncini A, Shahrizaila N, Kuwabara S

J Neurol Neurosurg Psychiatry, 2017 03;88(3):266-271.
PMID: 27799296 DOI: 10.1136/jnnp-2016-314310

In 2016, we have seen a rapid emergence of Zika virus-associated Guillain-Barré syndrome (GBS) since its first description in a French-Polynesian patient in 2014. Current evidence estimates the incidence of GBS at 24 cases per 100 000 persons infected by Zika virus. This will result in a sharp rise in the number of GBS cases worldwide with the anticipated global spread of Zika virus. A better understanding of the pathogenesis of Zika-associated GBS is crucial to prepare us for the current epidemic. In this review, we evaluate the existing literature on GBS in association with Zika and other flavivirus to better define its clinical subtypes and electrophysiological characteristics, demonstrating a demyelinating subtype of GBS in most cases. We also recommend measures that will help reduce the gaps in knowledge that currently exist.
Cerebral cryptococcosis in Malaysia

Richardson PM, Mohandas A, Arumugasamy N

J Neurol Neurosurg Psychiatry, 1976 Apr;39(4):330-7.
PMID: 932751

Cryptococcal infection of the brain as encountered in a tropical country is reviewed. The meningitic form is not uncommon and there has been, in the last decade, an apparent, if not real, rise in incidence in Malaysia as in Singapore. Only exceptionally was there overt evidence of immunological deficiency. Hydrocephalus was present in about three-quarters of the patients with meningitis and shunts were employed readily. The presence of multiple small intracerebral cysts could be suspected clinically but treatment for this complication was ineffective. The antifungal agent used most frequently was 5-fluorocytosine. Resistance to this drug developed in about one patient in four. There is a need for further epidemiological studies and for a continuing search for new antifungal agents.
Association of dengue infection and Guillain-Barré syndrome in Malaysia

Tan CY, Razali SNO, Goh KJ, Sam IC, Shahrizaila N

J Neurol Neurosurg Psychiatry, 2019 11;90(11):1298-1300.
PMID: 31085583 DOI: 10.1136/jnnp-2019-320756
Fulltext Early lowering of blood pressure after acute intracerebral haemorrhage: a systematic review and meta-analysis of individual patient data

Moullaali TJ, Wang X, Sandset EC, Woodhouse LJ, Law ZK, Arima H, et al.

J Neurol Neurosurg Psychiatry, 2022 01;93(1):6-13.
PMID: 34732465 DOI: 10.1136/jnnp-2021-327195

OBJECTIVE: To summarise evidence of the effects of blood pressure (BP)-lowering interventions after acute spontaneous intracerebral haemorrhage (ICH).
METHODS: A prespecified systematic review of the Cochrane Central Register of Controlled Trials, EMBASE and MEDLINE databases from inception to 23 June 2020 to identify randomised controlled trials that compared active BP-lowering agents versus placebo or intensive versus guideline BP-lowering targets for adults <7 days after ICH onset. The primary outcome was function (distribution of scores on the modified Rankin scale) 90 days after randomisation. Radiological outcomes were absolute (>6 mL) and proportional (>33%) haematoma growth at 24 hours. Meta-analysis used a one-stage approach, adjusted using generalised linear mixed models with prespecified covariables and trial as a random effect.
RESULTS: Of 7094 studies identified, 50 trials involving 11 494 patients were eligible and 16 (32.0%) shared patient-level data from 6221 (54.1%) patients (mean age 64.2 [SD 12.9], 2266 [36.4%] females) with a median time from symptom onset to randomisation of 3.8 hours (IQR 2.6-5.3). Active/intensive BP-lowering interventions had no effect on the primary outcome compared with placebo/guideline treatment (adjusted OR for unfavourable shift in modified Rankin scale scores: 0.97, 95% CI 0.88 to 1.06; p=0.50), but there was significant heterogeneity by strategy (pinteraction=0.031) and agent (pinteraction<0.0001). Active/intensive BP-lowering interventions clearly reduced absolute (>6 ml, adjusted OR 0.75, 95%CI 0.60 to 0.92; p=0.0077) and relative (≥33%, adjusted OR 0.82, 95%CI 0.68 to 0.99; p=0.034) haematoma growth.
INTERPRETATION: Overall, a broad range of interventions to lower BP within 7 days of ICH onset had no overall benefit on functional recovery, despite reducing bleeding. The treatment effect appeared to vary according to strategy and agent.
PROSPERO REGISTRATION NUMBER: CRD42019141136.
Fulltext Prevalence of dementia in ischaemic or mixed stroke populations: systematic review and meta-analysis

Craig L, Hoo ZL, Yan TZ, Wardlaw J, Quinn TJ

J Neurol Neurosurg Psychiatry, 2022 02;93(2):180-187.
PMID: 34782389 DOI: 10.1136/jnnp-2020-325796

An understanding of the epidemiology of poststroke dementia (PSD) is necessary to inform research, practice and policy. With increasing primary studies, a contemporary review of PSD could allow for analyses of incidence and prevalence trends. Databases were searched using a prespecified search strategy. Eligible studies described an ischaemic or mixed stroke cohort with prospective clinical assessment for dementia. Pooled prevalence of dementia was calculated using random-effects models at any time after stroke (primary outcome) and at 1 year (range: 6-18 months), stratified for inclusion of prestroke dementia. Meta-regression explored the effect of year of study. Sensitivity analyses removed low-quality or outlier studies. Of 12 505 titles assessed, 44 studies were included in the quantitative analyses. At any time point after stroke, the prevalence of PSD was 16.5% (95% CI 10.4% to 25.1%) excluding prestroke dementia and 22.3% (95% CI 18.8% to 26.2%) including prestroke dementia. At 1 year, the prevalence of PSD was 18.4% (95% CI 7.4% to 38.7%) and 20.4% (95% CI 14.2% to 28.2%) with prestroke dementia included. In studies including prestroke dementia there was a negative association between dementia prevalence and year of study (slope coefficient=-0.05 (SD: 0.01), p<0.0001). Estimates were robust to sensitivity analyses. Dementia is common following stroke. At any point following stroke, more than one in five people will have dementia, although a proportion of this dementia predates the stroke. Declining prevalence of prestroke dementia may explain apparent reduction in PSD over time. Risk of dementia following stroke remains substantial and front-loaded, with high prevalence at 1 year post event.