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Magnetic resonance imaging (MRI) is as good as, if not better than, X-ray Computed Tomography (CT) for providing useful information about cerebral infarction [1±3]. In particular, newer techniques such as diffusion weighted imaging are very sensitive to the earliest changes of cerebral ischaemia but are not widely available because of hardware limitations [4]. Most centres, therefore, continue to rely on T2-weighted images to recognize the early ischaemic lesion. Most MRI studies emphasize changes that occur acutely; much less is known about the sub-acute changes that occur. Previous observations have established that changes in T2-weighted imaging occur within the ®rst 24 h after the onset of infarction and it has been assumed that these changes persist inde®nitely in permanent infarcts. Here, we report on two patients in whom we found the surprising and intriguing observation that the T2 of the region of infarction returned to normal, or near normal, about 12 days after the onset of stroke but then became abnormal again a few days later.

High quality stroke management is based on doing the simple things well and may greatly improve long-term patient outcome. This article provides a straightforward approach to managing stroke patients.

Background and Purpose— Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS) patients with carotid stenosis were randomized between endovascular treatment and endarterectomy. The rates of residual severe stenosis and restenosis and their contribution to recurrent symptoms was unclear. Methods— Endovascular patients were treated by balloon angioplasty alone (88%) or stenting (22%). Patches were used in 63% of endarterectomy patients. Carotid stenosis was categorized as mild (0% to 49%), moderate (50% to 69%), severe (70% to 99%), or occluded, using standardized Doppler ultrasound criteria at the examination closest to 1 month (n=283) and 1 year (n=347) after treatment. Recurrent cerebrovascular symptoms during follow-up were analyzed. Results— More patients had ≥70% stenosis of the ipsilateral carotid artery 1 year after endovascular treatment than after endarterectomy (18.5% versus 5.2%, P =0.0001). Residual severe stenosis was present in 6.5% of patients at 1 month after endovascular treatment. Between 1 month and 1 year, restenosis to ≥70% stenosis occurred in 10.5% of the endovascular group. After endarterectomy, 1.7% had residual severe stenosis at 1 month, and 2.5% developed severe restenosis. The results were significantly better after stenting compared with angioplasty alone at 1 month ( P P =0.02), but most were transient ischemic attacks and none were disabling or fatal strokes. There were no recurrent symptoms in the 9 endarterectomy patients with ≥70% stenosis at 1 year. Conclusions— Carotid stenosis 1 year after endovascular treatment is partly explained by poor initial anatomical results and partly by restenosis. The majority of patients were treated by angioplasty without stenting. Further randomized studies are required to determine whether newer carotid stenting techniques are associated with a lower risk of restenosis. The low rate of recurrent stroke in both endovascular and endarterectomy patients suggests that treatment of restenosis should be limited to patients with recurrent symptoms, but long term follow up data are required.

Coeliac disease has been associated with a variety of neurological conditions, most frequently cerebellar ataxia and peripheral neuropathy. To date, chorea has not been associated with coeliac disease. We present the case histories of 4 individuals with coeliac disease and chorea (4 women, average age of onset of chorea 61 years). Unexpectedly, most of these patients showed a notable improvement in their motor symptoms after the introduction of a gluten-free diet.

The primary deficit in acute ischaemic stroke is one of impaired blood flow. Part of the cerebral circulation is occluded either by in situ thrombosis, or embolism from the heart or a more proximal artery (for example, the ipsilateral internal carotid artery). Angiographic studies of the cerebral circulation in acute stroke demonstrate occluding thrombus in up to 80% of patients.1 The aim of thrombolytic therapy therefore is to lyse an occluding thrombus or embolus and reduce the volume of cerebral tissue irreversibly damaged. Such an approach is of course successfully employed in the treatment of acute myocardial infarction.2 However a major complication of thrombolysis in stroke is cerebral haemorrhage which could offset any beneficial effects. Here we review the available evidence for thrombolysis in acute stroke and suggest imaging methods that could be used to aid future selection of patients who are most likely to benefit from such treatment. Data from animal stroke models confirm that cerebral blood flow can be restored to near normal levels after administration of recombinant tissue plasminogen activator (rtPA)3 and that thrombolysis results in smaller infarcts and improved neurological function.4-6 Comparison of streptokinase with rtPA suggested that, although their effectiveness in producing thrombolysis was comparable, streptokinase was less clot specific and animals treated with it had increased frequency and severity of cerebral haemorrhage.7 Animals treated with rtPA had the same frequency of cerebral haemorrhages as those treated with saline but the proportion of large haematomas was increased.6 In humans, thrombolytic therapy was first tried over 40 years ago but was largely abandoned due to excess mortality from major haemorrhagic complications.8 When computed tomography became widely available interest in the use of thrombolysis returned, leading to several larger randomised controlled trials. A dose escalation study using rtPA reported that …

Stroke is defined as rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 h or longer or leading to earlier death, with no apparent cause other than of vascular origin. Transient ischaemic attack (TIA) is defined identically except that the symptoms and signs resolve within 24h [1]. There is no fundamental difference between a TIA and a stroke except for the duration. Stroke is therefore a syndrome with numerous symptoms and signs; it has different aetiologies and the prognosis can vary enormously. Disability may be considered by some to be a worse outcome than death since stroke can affect every aspect of normal life, from higher mental functions such as intelligence, personality and expression to more mundane tasks such as toileting, dressing and feeding. The extremely wide definition of stroke and the enormous variety of outcomes has made the conduct of clinical trials in stroke and the choice of outcome measures problematic. In spite of this, there is more information available from clinical trials to facilitate evidence-based practice in stroke than in any other neurological discipline. In this chapter, we discuss the major issues, problems and solutions derived from the most important multicentre trials of cerebrovascular disease.

Acute stroke treatment using aspirin and/or heparin was studied in the International Stroke Trial (IST) and Chinese Acute Stroke Trial (CAST) which randomised over 40,000 patients altogether. Combining the results demonstrated that aspirin (150-300 mg) given within 48 h of the onset of stroke produced a small but significant improvement in outcome (death or dependency) 4 weeks to 6 months after stroke of about 1 patient per 100 treated. There was a significant reduction in recurrent ischaemic stroke of similar degree, which was not associated with significant increase in cerebral haemorrhage. Therefore, aspirin should be used as early secondary prevention against recurrent stroke, after excluding cerebral haemorrhage by scanning the patient. Heparin does not improve clinical outcome after stroke even in patients in atrial fibrillation. It decreased recurrent ischaemic stroke significantly in IST, but at the cost of a significant increase in cerebral haemorrhage. Low molecular weight heparins and heparinoids have not proved any more beneficial. Therefore, heparin does not appear to be a useful routine therapy in acute stroke. The use of heparin should, therefore, be limited to patients at high risk of deep vein thrombosis or early recurrence.

Background and Purpose — 1 H MR spectroscopy can be used to study biochemical changes occurring in the brain in stroke. We used it to examine the relationship between metabolite concentration ( N -acetyl aspartate [NAA], lactate, cholines and creatines), size of infarct, clinical deficit, and 3-month clinical outcome in patients with middle cerebral artery (MCA) territory infarction. Methods —Thirty-one patients with acute MCA territory infarction were recruited within 72 hours of the onset of symptoms. Single-voxel short echo time stimulated echo acquistion mode spectroscopy was used to obtain metabolite data from the infarct core. Metabolite concentrations were determined with use of variable projection time domain-fitting analysis. Infarct size was determined with T2-weighted images. Patient outcome groups at 3 months were “independent,” “dependent,” or “dead.” Results —All patients (100%; 95% CI 75% to 100%) who had an infarct >70 mL did poorly. Eighteen of 20 patients (90%; 95% CI 68% to 99%) with a core NAA concentration 7 mmol/L did well. Combining these results showed that all patients who had an initial infarct volume >70 mL did poorly, irrespective of the NAA concentration. Of those patients with infarcts 7 mmol/L did well (88%; 95% CI 47% to 100%), whereas those with a lower NAA concentration did poorly (80%; 95% CI 44% to 97%). There was no association between other metabolite concentrations and outcome. Conclusions —Infarct volume and NAA concentration can together predict clinical outcome in MCA infarction in humans.

Cerebral fat embolism can complicate long bone fractures and orthopaedic surgery. We present two patients with this syndrome who developed coma following long bone fracture or hip replacement surgery. Patient 1 was a 71 year old previously independent lady who was admitted following a fall and underwent total hip replacement surgery for a left neck of femur fracture. Immediately after cementing the shaft, she developed marked hypoxia, tachycardia, hypotension and pyrexia and remained intubated and sedated after surgery. Following withdrawal of sedation, she remained unconscious. Neurological examination revealed a GCS of 3/15, roving eye movements, intact brainstem reflexes, increased tone on the left side and up–going plantars. Over the next few days her GCS remained low at 5/15, with flexor motor response to pain. EEG was diffusely slow and compatible with an encephalopathic process. MRI showed innumerable small emboli on DWI (“star–field pattern”), and multiple, hyper–intense lesions on T2 and FLAIR. Bubble echo was positive and suggestive of a patent foramen ovale. Over the next four weeks, she made a dramatic recovery and one month after surgery was obeying commands, verbally communicating, oriented in time but disoriented in place. Patient 2 was a 66 year old, previously independent lady who was admitted with a femoral shaft fracture. The day following her admission, her GCS dropped to 7/15 and she developed hypoxia, tachycardia and pyrexia. Neurological examination initially did not reveal a focal deficit. During a transient improvement in GCS to 14/15, she was noted to have a right sided face and arm weakness. MRI DWI again showed the characteristic “star–field pattern”. Clinically she deteriorated again with a drop in her GCS, development of thrombocytopaenia, pulmonary emboli and nephrogenic diabetes insipidus and remained on ITU at the time of writing this abstract. Cerebral fat embolism syndrome may be under–diagnosed in clinical practice. It should be considered in the differential of coma following orthopaedic surgery and fractures. Neurological outcome has been reported to be generally good.

A 24-year-old female Punjabi student came to the UK in 2010. A right hilar mass on routine CXR and respiratory physicians performed mediastinoscopy. Right paratracheal lymph node histology demonstrated non-caseating granulomatous lymphadenitis with central necrosis. TB culture was negative. She was well and followed up with presumed quiescent sarcoidosis or TB. In September 2011, she reported 2 months of headache, 5 weeks of right eye swelling and a persistent cough. She had a right exopthalmos with left-sided weakness especially the arm. MRI brain demonstrated six enhancing intra-axial masses within the right hemisphere, six in the cerebellum and one lesion extending into the medulla. Abnormal tissue expanded into the right orbit causing exopthalmos. HIV status was negative and she was not diabetic. She was commenced on steroids and empirical quadruple therapy for TB. The presumed differentials were sarcoidosis, TB or possible malignancy Bone marrow trephine was normal (no evidence of lymphoma or organisms). Biopsy of the orbital lesion contained numerous, well preserved, fungal hyphae within the granulomas. IgE was 2000 kU/L (0–81), aspergillus precipitins >200 (0–40). Culture was positive for aspergillus flavus. Histological re-examination of the original chest lesion also confirmed aspergillus hyphae. This is a case of disseminated aspergillus infection. The patient responded well to antifungal treatment with ambisome, andulifungin IV, voroconizole and dexamethsone with resolution clinically and radiologically.

A 23-year-old left-handed female developed progressive right arm weakness and expressive dysphasia. She had papilloedema and right-sided UMN facial palsy, arm weakness and positive Babinski reflex. MRI brain demonstrated a 7.7 cm diameter heterogeneously enhancing mass lesion with surrounding vasogenic oedema lying within the left posterior frontal lobe with associated midline shift. CSF contained unmatched oligoclonal bands, consistent with a diagnosis of tumefactive multiple sclerosis. She was treated with IV methylprednisolone with complete recovery. Three years later she presented with dizziness, visual disturbance and cognitive deficits. On examination, she had a left homonymous hemianopia and a Gerstmann-like syndrome. She rapidly deteriorated with left-sided weakness, neglect, hemisensory loss, aphasia and dysphagia. MRI demonstrated an acute, demyelinating plaque of 7.2 cm involving the right parieto-occipital white matter and posterior frontal white matter with mass effect. Repeat CSF examination showed unmatched oligoclonal bands. She was treated with intravenous methylprednisolone and plasma exchange and dramatically improved. She is continuing her inpatient rehabilitation. Tumefactive lesions in MS usually convert to typical relapsing-remitting disease on recurrence. Here we present a rare case of relapsing-remitting tumefactive disease which has only previously been reported once in the literature. We have demonstrated a good response to immunosuppressive and immunomodulatory therapy.

Stroke has become a major NHS priority. Daniel Davies and colleagues look at a career in the area

We enjoyed A practical approach to acute vertigo by Seemungal and Bronstein in the August issue. However, we disagree that the head impulse test “will only be positive in patients with vestibular neuritis”1 and so …