A novel variant in the tropomyosin 3 gene presenting as an adult-onset distal myopathy - a case report.

BACKGROUND: We report a patient with a novel c.737 C > T variant (p.Ser246Leu) of the TPM3 gene presenting with adult-onset distal myopathy. CASE PRESENTATION: A 35-year-old Chinese male patient presented with a history of progressive finger weakness. Physical examination revealed differential finger extension weakness, together with predominant finger abduction, elbow flexion, ankle dorsiflexion and toe extension weakness. Muscle MRI showed disproportionate fatty infiltration of the glutei, sartorius and extensor digitorum longus muscles without significant wasting. Muscle biopsy and ultrastructural examination showed a non-specific myopathic pattern without nemaline or cap inclusions. Genetic sequencing revealed a novel heterozygous p.Ser246Leu variant (c.737C>T) of the TPM3 gene which is predicted to be pathogenic. This variant is located in the area of the TPM3 gene where the protein product interacts with actin at position Asp25 of actin. Mutations of TPM3 in these loci have been shown to alter the sensitivity of thin filaments to the influx of calcium ions. CONCLUSION: This report further expands the phenotypic spectrum of myopathies associated with TPM3 mutations, as mutations in TPM3 had not previously been reported with adult-onset distal myopathy. We also discuss the interpretation of variants of unknown significance in patients with TPM3 mutations and summarise the typical muscle MRI findings of patients with TPM3 mutations.

Syphilitic Spinal Disease: An Old Nemesis Revisited. A Case Series and Review of Literature.

ABSTRACT: Syphilitic spinal disease is a rare condition caused by the spirochete Treponema pallidum, either from direct spirochete involvement of the cord or as a consequence of indirect spirochete involvement of the meninges, blood vessels, or the vertebral column. After the introduction of penicillin therapy in the 1940s, it has become an increasingly rare condition. We report 3 challenging cases of syphilitic spinal disease presenting as myelopathy-1 with an extra-axial gumma of tertiary syphilis causing cord compression and 2 with tabes dorsalis complicated by tabetic spinal neuroarthropathy-each presenting a diagnostic dilemma to their treating physicians. We also review the literature for updates on modern investigative modalities and discuss pitfalls physicians need to avoid to arrive at the diagnosis.

Facial Nerve Involvement Accompanying Optic Neuritis Secondary to Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disorder.

ABSTRACT: We present the first reported case of facial nerve involvement accompanying an optic neuritis in myelin oligodendrocyte glycoprotein antibody-associated disorder.

Use of Twitter in Neurology: Boon or Bane?

Twitter is a free, open access social media platform that is widely used in medicine by physicians, scientists, and patients. It provides an opportunity for advocacy, education, and collaboration. However, it is likely not utilized to its full advantage by many disciplines in medicine, and pitfalls exist in its use. In particular, there has not been a review of Twitter use and its applications in the field of neurology. This review seeks to provide an understanding of the current use of Twitter in the field of neurology to assist neurologists in engaging with this potentially powerful application to support their work.

Acute flaccid paralysis: Do not forget beriberi neuropathy.

We aimed to elucidate characteristics of beriberi neuropathy (BB) in a general hospital (GH) setting. Nerve conduction studies (NCS), cross-referenced with clinical records of patients admitted to a GH (May 2011-July 2017), were reviewed for diagnosis of BB. Thirteen patients (age range 23-64 years; five women) were diagnosed with BB. Eleven were incarcerated (2-24 months) at time of index event. Eleven reported prior, severe anorexia (2-6 months); five reported significant weight loss, three had recurrent vomiting, and three reported alcohol misuse. Commonest presentation was weakness (12/13); nine had symptom evolution over ≥3 weeks. At nadir, 11/13 could not walk independently. Other features included numbness/paraesthesiae (10/13), dysautonomia (6/13), vocal cord dysfunction/dysphagia (4/13), nystagmus (3/13). Pain was not prominent. Cerebrospinal fluid, tested in five patients, was acellular; one showed mildly increased protein. NCS showed predominantly sensorimotor, axonal polyneuropathy, rarely asymmetric. Only one patient had sural-sparing pattern. All received high dose thiamine. Two of the thirteen received intravenous immunoglobulin for suspicion of Guillain-Barré syndrome (GBS). Eleven improved to independent ambulation. One patient died from pulmonary embolism; one was lost to follow-up. Two of the thirteen had residual neurocognitive effects; both misused alcohol. Besides GBS, BB is an important cause of acute to subacute flaccid paralysis, especially in incarcerated patients and those with significant dietary deprivation. Features favoring BB over GBS are ≥3 weeks of symptoms, nystagmus, confusion, vocal cord dysfunction, volume overload, normal spinal fluid, elevated lactate, and absence of sural-sparing pattern in NCS.

Prevalence and Risk Factors of Acute Incidental Infarcts.

BACKGROUND AND PURPOSE: The study of silent stroke has been limited to imaging of chronic infarcts; acute incidental infarcts (AII) detected on brain magnetic resonance imaging have been less investigated. This study aims to describe prevalence and risk factors of AII in a community and a clinic-based population. METHODS: Subjects were drawn from 2 ongoing studies: Epidemiology of Dementia in Singapore study, which is a subsample from a population-based study, and a clinic-based case-control study. Subjects from both studies underwent similar clinical and neuropsychological assessments and brain magnetic resonance imaging. Prevalence of AII from these studies was determined. Subsequently, risk factors of AII were examined using multivariable logistic regression models. RESULTS: AII were seen in 7 of 623 (1.2%) subjects in Epidemiology of Dementia in Singapore (mean age, 70.9±6.8 years; 45% men) and in 12 of 389 (3.2%) subjects (mean age, 72.1±8.3 years; 46% men) in the clinic-based study. AII were present in 0.8% of subjects with no cognitive impairment, 1.9% of those with cognitive impairment not dementia, and 4.2% of subjects with dementia. Significant association of AII was found with cerebral microbleeds (≥5) in the Epidemiology of Dementia in Singapore (odds ratio, 6.76; 95% confidence interval, 1.28-35.65; P=0.02) and in the clinic-based cohort (odds ratio, 4.65; 95% confidence interval, 1.39-15.53; P=0.01). There was no association of AII with hypertension, diabetes mellitus, or hyperlipidemia. CONCLUSIONS: AII are more likely to be present in those with cognitive impairment. Although a cause-effect relationship between the presence of AII and cognitive impairment is plausible, the association may be because of under-reporting of symptoms by individuals with cognitive impairment. The association between AII and cerebral microbleeds may indicate cerebral vasculopathy, independent of traditional vascular risk factors.

Intracranial stenosis, cerebrovascular diseases, and cognitive impairment in chinese.

Extracranial carotid artery disease has been shown to be related to cognitive deficits. However, limited data are available on intracranial stenosis (ICS) and cognitive impairment. We investigate the association between ICS and cognitive impairment in Chinese. Subjects (n=278), recruited from the Epidemiology of Dementia in Singapore Study, underwent comprehensive clinical evaluation, neuropsychological testing, and brain magnetic resonance imaging (MRI), including 3-dimensional-time-of-flight magnetic resonance angiography (MRA). Cognitive function was expressed as composite and domain-specific Z-scores. Cognitive impairment no dementia and dementia were diagnosed according to internationally accepted diagnostic criteria. Linear and logistic regression models were adjusted for age, sex, education, vascular risk factors, and other MRI markers. A total of 29 (10.4%) persons had ICS on MRA, which was significantly associated with both composite cognitive Z-scores [mean difference in Z-score, presence vs. absence of ICS: -0.37 (95% confidence interval: -0.63, -0.12)] and specific domains including executive function, language, visuomotor speed, verbal memory, and visual memory. ICS was also related to significant cognitive impairment (odds ratio: 5.10 [1.24 to 21.02]). With respect to other MRI markers, adjusted for the presence of lacunar infarcts, the associations of ICS with both composite and domain-specific Z-scores, and significant cognitive impairment became nonsignificant; however, adjustment for other MRI markers did not alter these associations. In this Chinese population, presence of ICS was associated with cognitive impairment independent of vascular risk factors. These associations may be mediated through the presence of infarcts.

Abnormalities of cortical thickness, subcortical shapes, and white matter integrity in subcortical vascular cognitive impairment.

Subcortical vascular cognitive impairment (sVCI) is caused by lacunar infarcts or extensive and/or diffuse lesions in the white matter that may disrupt the white matter circuitry connecting cortical and subcortical regions and result in the degeneration of neurons in these regions. This study used structural magnetic resonance imaging (MRI) and high angular resolution diffusion imaging (HARDI) techniques to examine cortical thickness, subcortical shapes, and white matter integrity in mild vascular cognitive impairment no dementia (VCIND Mild) and moderate-to-severe VCI (MSVCI). Our study found that compared to controls (n = 25), VCIND Mild (n = 25), and MSVCI (n = 30) showed thinner cortex predominantly in the frontal cortex. The cortex in MSVCI was thinner in the parietal and lateral temporal cortices than that in VCIND Mild. Moreover, compared to controls, VCIND Mild and MSVCI showed smaller shapes (i.e., volume reduction) in the thalamus, putamen, and globus pallidus and ventricular enlargement. Finally, compared to controls, VCIND Mild, and MSVCI showed an increased mean diffusivity in the white matter, while decreased generalized fractional anisotropy was only found in the MSVCI subjects. The major axonal bundles involved in the white matter abnormalities were mainly toward the frontal regions, including the internal capsule/corona radiata, uncinate fasciculus, and anterior section of the inferior fronto-occipital fasciculus, and were anatomically connected to the affected cortical and subcortical structures. Our findings suggest that abnormalities in cortical, subcortical, and white matter morphology in sVCI occur in anatomically connected structures, and that abnormalities progress along a similar trajectory from the mild to moderate and severe conditions.

Ankle-brachial index, cognitive impairment and cerebrovascular disease in a Chinese population.

BACKGROUND: Previous studies have assessed the association between ankle-brachial index (ABI) and cognition, mainly using brief cognitive tests. We investigated whether ABI was associated with cognition independent of neuroimaging markers of cerebrovascular disease. METHODS: Chinese subjects (n = 278, aged ≥60 years) were recruited from the ongoing Epidemiology of Dementia in Singapore (EDIS) Study. Ankle and brachial blood pressures were measured, and low ABI was defined as ≤0.9. A neuropsychological battery was utilized to determine cognition. Cognitive impairment no dementia (CIND) and dementia were diagnosed according to standard diagnostic criteria. Magnetic resonance imaging (MRI) was used to obtain semiquantitative and quantitative markers of cerebrovascular disease and atrophy. RESULTS: A low ABI was related to the presence of intracranial stenosis (odds ratio, OR = 1.71; 95% confidence interval, CI: 1.13-2.59), but not with the presence of infarcts, microbleeds or grey matter, white matter and white matter lesion volumes. Furthermore, a low ABI was associated with poorer overall cognitive function and CIND-moderate/dementia (OR = 2.26; 95% CI: 1.11-4.59), independent of cardiovascular risk factors, and the MRI markers related to cerebrovascular disease and atrophy. CONCLUSION: We found an association between a low ABI and cognitive impairment, independent of any MRI marker of cerebral small vessel disease or large artery atherosclerotic disease.

Cerebral microbleeds and cognition: the epidemiology of dementia in Singapore study.

Cerebral microbleeds (CMBs) are considered to be a novel marker of cerebral small vessel disease. However, the link with cognitive impairment remains unclear. We investigated whether CMBs-independent of other traditional markers of cerebral small vessel disease-are related to cognition. Chinese subjects from the population-based Singapore Chinese Eye Study, who failed an initial cognitive screening and were recruited into the ongoing Epidemiology of Dementia in Singapore Study, underwent neuropsychological testing and 3 T brain magnetic resonance imaging. The presence and number of CMBs were graded using Brain Observer Microbleed Scale on susceptibility-weighted images. Other magnetic resonance imaging lesions that were graded included presence of lacunes, white matter lesion, and total brain volumes. A comprehensive neuropsychological battery was administered and cognitive function was summarized as composite and domain-specific Z-scores. Among 282 subjects, 91 had any CMBs (32.3%), of whom 36 (12.8%) had multiple CMBs. CMBs were-independent of cardiovascular risk factors and other markers of cerebral small vessel disease-significantly associated with poorer cognitive function as reflected by composite Z-score (mean difference per CMB increase: -0.06; 95% confidence interval: -0.11, -0.01] and with domain-specific Z-scores including executive function, attention, and visuoconstruction. Among Chinese subjects CMBs were, independent of other concomitant markers of cerebral small vessel disease, associated with poorer cognitive function.

Computer tomography for prediction of cognitive outcomes after ischemic cerebrovascular events.

BACKGROUND: The aim of this study was to evaluate whether parameters noted on a single, acute computed tomographic (CT) scan, are associated with significant cognitive impairment (SCogI), and can help in the prediction of SCogI 3-6 months after stroke or transient ischemic attack (TIA). METHODS: Patients with a recent (≤14 days) ischemic stroke or TIA, without preexisting dementia, underwent noncontrast CT scan within 24 hours of admission. A formal neuropsychologic battery was administered 3-6 months from index stroke. SCogI was defined as moderate cognitively impaired, not demented (CIND) (≥3 domains impaired), and dementia diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria. Logistic regression models were used to examine associations between CT parameters and SCogI. Receiver operating characteristic analysis with an area under the curve (AUC) was performed to assess discriminatory ability of radiological parameters for SCogI. RESULTS: In all, 318 patients were included: 250 (78.6 %) with ischemic stroke and 68 (21.4%) with TIA; the mean age was 59.8 (±11.4) years. At 3-6 months, 76 (23.9 %) had SCogI (67 CIND moderate and 9 dementia). The presence of significant atrophy (P = .02) and chronic infarcts (P = .03) were associated with SCogI at 3-6 months. A significant increase in AUC was noted after addition of summarized CT results to a clinical score derived from age and baseline Montreal Cognitive Assessment (cutoff 21 of 22) for detection of SCogI: .83 (.78-.89) to .86 (.82-.91); P = .03. CONCLUSIONS: CT parameters are independently associated with SCogI at 3-6 months after an ischemic cerebrovascular event and may be a clinically useful component in predicting for SCogI after stroke.

Prevalence of cognitive impairment in Chinese: epidemiology of dementia in Singapore study.

OBJECTIVE: To study the prevalence of and associated factors for cognitive impairment and dementia in community dwelling Chinese from Singapore. METHODS: This study includes Chinese subjects from the Epidemiology of Dementia in Singapore (EDIS) study, aged ≥60 years, who underwent comprehensive examinations, including cognitive screening with the locally validated Abbreviated Mental Test and Progressive Forgetfulness Questionnaire. Screen positive participants subsequently underwent extensive neuropsychological testing and cerebral MRI. Cognitive impairment no dementia (CIND) and dementia were diagnosed according to internationally accepted criteria. The prevalence of cognitive impairment and dementia were computed per 5 year age categories and gender. To examine the relationship between baseline associated factors and cognitive impairment, we used logistic regression models to compute odd ratios with 95% CI. RESULTS: 1538 Chinese subjects, aged ≥60 years, underwent cognitive screening: 171 (15.2%) were diagnosed with any cognitive impairment, of whom 84 were CIND mild, 80 CIND moderate and seven had dementia. The overall age adjusted prevalence of CIND mild was 7.2%; CIND moderate/dementia was 7.9%. The prevalence increased with age, from 5.9% in those aged 60-64 years to 31.3% in those aged 75-79 years and 44.1% in those aged ≥80 years. Multivariate analysis revealed age, diabetes and hyperlipidaemia to be independently associated with cognitive impairment. CONCLUSIONS: In present study, the overall prevalence of cognitive impairment and dementia in Chinese was 15.2%, which is in the same range as the prevalence reported in Caucasian and other Asian populations.

Comparison of the Montreal Cognitive Assessment and the Mini-Mental State Examination in detecting multi-domain mild cognitive impairment in a Chinese sub-sample drawn from a population-based study.

BACKGROUND: We examined the discriminant validity of the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE) in detecting multiple-domain mild cognitive impairment (md-MCI) in a Chinese sub-sample drawn from elderly population-based study. METHODS: This study included Chinese participants from the Epidemiology of Dementia in Singapore (EDIS) study aged ≥ 60 years who underwent cognitive screening with the Abbreviated Mental Test and Progressive Forgetfulness Questionnaire. Screen-positive participants subsequently underwent MoCA, MMSE, and a comprehensive formal neuropsychological battery. MCI was defined by Petersen's criteria and further classified into single-domain MCI (sd-MCI) and md-MCI. Area under the receiver operating characteristic curve (AUC) with 95% confidence intervals (CIs) was computed for the MoCA and the MMSE in detecting md-MCI. RESULTS: A total of 300 participants were recruited: 128 (42.7%) were diagnosed with no cognitive impairment (NCI), 47 (15.7%) with sd-MCI, and 83 (28.0%) with md-MCI. Forty-one participants were excluded, 7 (2.3%) had dementia, and 34 (11.3%) had only objective cognitive impairment without subjective complaints. Although the MoCA had a significantly larger AUC than the MMSE (0.94 (95% CI = 0.91-0.97) vs. 0.91 (95% CI = 0.86-0.95), p= 0.04), at optimal cut-off points, the MoCA (19/20) was equivalent to the MMSE (25/26) in detecting md-MCI (sensitivity: 0.80 vs. 0.87, specificity: 0.92 vs. 0.80). CONCLUSION: Both screening tests had good discriminant validity and can be used in detecting md-MCI in a sub-sample of Chinese drawn from a population-based study.

Unique Clinical, Radiological and Histopathological Characteristics of a Southeast Asian Cohort of Patients with Limb-Girdle Muscular Dystrophy 2G/LGMD-R7-Telethonin-Related.

AIM: We describe a cohort of five patients with limb-girdle muscular dystrophy (LGMD) 2G/LGMD-R7 in a South-east Asian cohort. BACKGROUND: LGMD2G/LGMD-R7-telethonin-related is caused by mutations in the TCAP gene that encodes for telethonin. METHODS: We identified consecutive patients with LGMD2G/LGMD-R7-telethonin-related, diagnosed at the National Neuroscience Institute (NNI) and National University Hospital (NUH) between January 2000 and June 2021. RESULTS: At onset, three patients presented with proximal lower limb weakness, one patient presented with Achilles tendon contractures, and one patient presented with delayed gross motor milestones. At last follow up, three patients had a limb girdle pattern of muscle weakness and two had a facioscapular humeral pattern of weakness. Whole body muscle MRI performed for one patient with a facioscapular-humeral pattern of weakness showed a pattern of muscle atrophy similar to facioscapular-humeral dystrophy. One patient had histological features consistent with myofibrillar myopathy; electron microscopy confirmed the disruption of myofibrillar architecture. One patients also had reduced staining to telethonin antibody on immunohistochemistry. CONCLUSION: We report the unique clinical and histological features of a Southeast Asian cohort of five patients with LGMD2G/LGMD-R7-telethonin-related muscular dystrophy and further expand its clinical and histopathological spectrum.

Silent stroke: not listened to rather than silent.

BACKGROUND AND PURPOSE: The prevalence of silent brain infarcts varies from 8% to 28% in the general elderly population. Silent brain infarcts are associated with increased risk of subsequent stroke and cognitive dysfunction. By definition, silent strokes lack clinically overt stroke-like symptoms and fail to come to clinical attention; however, impaired recall of symptoms may be a potential confounder. Our aim is to report a series of patients with incidentally detected acute and subacute strokes and examine whether they were truly asymptomatic. METHODS: Subjects included in this study were drawn from ongoing dementia research studies at the Memory Ageing and Cognition Center, in which all participants underwent a cranial MRI. Incidental hyperintense lesions on diffusion-weighted imaging with corresponding apparent diffusion coefficient defects indicative of acute/subacute silent stroke were identified. Clinical data for individuals with incidental hyperintense lesions on diffusion-weighted imaging were collated. RESULTS: Six of 649 subjects had incidental hyperintense lesions on diffusion-weighted imaging; on retrospective questioning, 3 recalled symptoms temporally correlated with MRI lesions, which had been reported to but ignored by family members. Two subjects had focal neurological signs. A majority of the subjects with incidental hyperintense lesions on diffusion-weighted imaging had significant cognitive impairment. CONCLUSIONS: A significant number of strokes may be "silent" due to lack of awareness of stroke-like symptoms in the elderly and their families. Enhanced stroke prevention education strategies are needed for the elderly population and, in particular, for their families.

Acute to Subacute Atraumatic Entrapment Neuropathies in Patients With CMT1A: A Report of a Distinct Phenotypic Variant of CMT1A.

Charcot-Marie-Tooth type 1A (CMT1A) is typically characterised as a childhood-onset, symmetrical, length-dependent polyneuropathy with a gradual progressive clinical course. Acute to subacute neurological deterioration in CMT1A is rare, and has been reported secondary to overlap pathologies including inflammatory neuropathy. We identified two patients with CMT1A who presented with acute to subacute, atraumatic, entrapment neuropathies as an initial symptom. A superimposed inflammatory neuropathy was excluded. Both patients had a diffuse demyelinating polyneuropathy, with markedly low motor nerve conduction velocities (<20 m/s). In both patients, we demonstrated symptomatic and asymptomatic partial conduction blocks at multiple entrapment sites. Nerve ultrasound findings in our patients demonstrated marked diffuse nerve enlargement, more pronounced at non-entrapment sites compared to entrapment sites. We discuss ways to distinguish this condition from its other differentials. We propose pathophysiological mechanisms underlying this condition. We propose that CMT1A with acute to subacute, atraumatic, entrapment neuropathies to be a distinct phenotypic variant of CMT1A.

Acute perfusion and diffusion abnormalities predict early new MRI lesions 1 week after minor stroke and transient ischemic attack.

BACKGROUND AND PURPOSE: Transient ischemic attack and minor stroke are associated with high ischemic recurrence in the first week. We prospectively studied the correlation between baseline diffusion/perfusion deficits and development of new ischemic lesions. METHODS: Patients with transient ischemic attack and those with minor stroke (n=50) underwent MRI at admission. Acute perfusion-weighted imaging deficit (Tmax+2-second delay) and diffusion-weighted imaging (DWI) lesion volumes were measured planimetrically. Follow-up scans were examined for new DWI/fluid-attenuated inversion recovery lesions at Days 7 and 30. RESULTS: Twenty-eight patients (56%) had acute DWI lesions. New DWI lesions developed in 9 of 50 patients (18%) at 1 week and 11 of 50 (cumulative 22%) at 4 weeks. Patients with new infarcts were more likely to have baseline DWI lesions (χ²=8.264, P=0.003). Baseline DWI lesion volume was significantly larger in those who developed new lesions at Day 7 (median, 13.2 mL; interquartile range, 12 versus median 0.1 mL; interquartile range, 2 mL; P<0.001) and Day 30 (11.1 mL; interquartile range, 13 mL versus 0.1 mL; interquartile range, 13 mL; P<0.001). Thirty-eight patients had baseline perfusion-weighted imaging. Patients with recurrent lesions were more likely to have baseline perfusion deficits (χ²=19.5, P<0.0001). All new lesions developed within the baseline hypoperfused regions. Baseline DWI lesion volume predicted new lesion development at day 7 (OR, 1.17 per mL; CI, 1.05 to 1.30; P=0.005) and Day 30 (OR, 1.39 per mL; CI, 1.03 to 1.26; P=0.009) by regression analysis. CONCLUSIONS: Early recurrence of stroke is much more likely in patients with larger baseline DWI and perfusion-weighted imaging lesions. MRI lesion "recurrence" appears to be related to completion of the natural history of the original cerebrovascular syndrome rather than de novo events in most patients.

Low body temperature does not compromise the treatment effect of alteplase.

BACKGROUND AND PURPOSE: Hypothermia is neuroprotective in ischemic stroke models. The influence of baseline body temperature on outcomes after thrombolytic therapy is unclear. We examined outcomes after alteplase treatment across baseline body temperature for patients with ischemic stroke in data held within the Virtual International Stroke Trials Archive (VISTA; 1998 to 2007). METHODS: We collated data on age, baseline severity (National Institutes of Health Stroke Scale), and 90-day modified Rankin Scale score on patients presenting with acute ischemic stroke. We compared 90-day modified Rankin Scale score between thrombolyzed and nonthrombolyzed comparators across baseline body temperature. We report age and baseline National Institutes of Health Stroke Scale-adjusted Cochran-Mantel-Haenszel probability value and proportional OR with 95% CI for improved modified Rankin Scale distribution. We report temperature profiles over 72 hours after stroke by treatment group. RESULTS: Rankin data were available for 5586 patients with acute ischemic stroke in VISTA (1980 received alteplase). Age and baseline severity were similar (age 68.0±13.0 years versus 69.9±12.3 years, National Institutes of Health Stroke Scale 14.2±5.2 versus 13.0±5.6). Alteplase was associated with improved outcome (OR, 1.49; 95% CI, 1.35 to 1.65, P<0.0001). Alteplase treatment effect was not associated with baseline temperature (P=0.14). Point estimates showed benefit of alteplase treatment across 35.5°C to 37.5°C but showed a negative trend >37.5°C. Alteplase did not influence temperature profiles over 72 hours after stroke. CONCLUSIONS: There is no evidence of influence of body temperature on alteplase treatment response. These results are reassuring that low temperatures across a physiological range do not compromise therapeutic effect of alteplase.

Oxfordshire community stroke project classification poorly differentiates small cortical and subcortical infarcts.

BACKGROUND AND PURPOSE: The Oxfordshire Community Stroke Project (OCSP) is a common clinical stroke classification tool. We evaluated the accuracy of OCSP classification with a prospective magnetic resonance imaging (MRI) study. METHODS: Stroke/transient ischemic attack patients presenting within 48 hours of onset were included in the study (n=130). Following computed tomography scan, OCSP classification, total anterior circulation infarcts (TACI), partial anterior circulation infarcts (PACI), lacunar circulation infarcts (LACI), and posterior circulation infarcts (POCI) were performed by 3 independent examiners. All patients underwent diffusion-weighted MRI with planimetric volume measurement and classification into OCSP categories, organized by lesion location. RESULTS: Patients were clinically classified as TACI (12 patients), PACI (62 patients), LACI (38 patients), and POCI (18 patients). In 101 patients with diffusion-weighted MRI lesions, correct classification rates were: TACI (83.3%), PACI (83%), LACI (39%), and POCI (86%). OCSP had the following sensitivity (SE), specificity (SP), and positive predictive value (PPV): TACI (SE, 100%; SP, 98%; PPV, 83%), PACI (SE, 73%; SP, 78%; PPV, 83%), LACI (SE, 47%; SP, 83%; PPV, 39%), and POCI (SE, 92%; SP, 98%; PPV, 86%). Sixty-one percent of patients in the LACI group had radiographic appearances consistent with PACI, and 15% of those classified as PACI had lacunar infarcts. No differences in stroke severity existed between patients classified correctly (median National Institutes of Health Stroke Scale [NIHSS]=4; interquartile range [IQR]=7) or incorrectly (median NIHSS=3; IQR=3). Patients classified correctly had larger infarct volume (median=6.75 mL; IQR=33.2) than did those who were incorrectly classified (1.86 mL; IQR=5; P=0.008). CONCLUSIONS: OCSP classification does not permit accurate discrimination between lacunar and small-volume cortical infarcts. Differential patterns of investigation for stroke etiology should not be based solely on clinical criteria.

Transient global amnesia and focal diffusion weighted imaging lesions in mesiotemporal region: A ten-year experience.

OBJECTIVE: To determine prevalence and characteristics of mesiotemporal diffusion weighted imaging (DWI) lesions in transient global amnesia (TGA), and to determine prevalence of "missed" DWI lesions on routine radiological reporting. METHODS: This is a retrospective study of patients with TGA admitted to a tertiary care hospital over ten years. Patients with TGA, who underwent magnetic resonance imaging (MRI) of the brain within one week of index event, were included in this study. MRI's were reviewed by two independent raters. Clinical data and other investigations were collated. RESULTS: Of the 55 patients of TGA, 19 (35 %) had hyperintense DWI lesions with concordant apparent diffusion coefficient (ADC) hypointensity in the mesiotemporal region. Fifteen out of 19 (79 %) had unilateral lesions (6 left, 9 right). Twelve out of 19 DWI lesions were reported at the time of index scan. The false negative reporting rate was 36.8 %. DWI slice thickness (5 mm versus 3 mm), MRI machine strength (1.5 versus 3 T) and time interval from symptom onset to MRI brain (>24 h versus ≤ 24 h) were not significantly different between patients with or without DWI lesions and as well between patients with DWI lesions missed and initially reported at the time of index scan. CONCLUSION: Punctuate DWI mesiotemporal lesions in TGA are prone to under-reporting. These lesions need to be categorically searched for at the time of reporting MRI Brain.