The National High Blood Pressure Education Program presents the complete Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Like its predecessors, the purpose is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are these: in those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease (CVD) risk factor than diastolic BP; beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg; those who are normotensive at 55 years of age will have a 90% lifetime risk of developing hypertension; prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg) require health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD; for uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes; this report delineates specific high-risk conditions that are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg) for patients with diabetes and chronic kidney disease; for patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of which usually will be a thiazide diuretic, should be considered; regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan. Positive experiences, trust in the clinician, and empathy improve patient motivation and satisfaction. This report serves as a guide, and the committee continues to recognize that the responsible physician's judgment remains paramount.

Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

Co-Planar Stereotaxic Atlas of the Human Brain—3-Dimensional Proportional System: An Approach to Cerebral Imaging, J. Talairach, P. Tournoux. Georg Thieme Verlag, New York (1988), 122 pp., 130 figs. DM 268

New evidence and consensus has led to further revision of the McDonald Criteria for diagnosis of multiple sclerosis. The use of imaging for demonstration of dissemination of central nervous system lesions in space and time has been simplified, and in some circumstances dissemination in space and time can be established by a single scan. These revisions simplify the Criteria, preserve their diagnostic sensitivity and specificity, address their applicability across populations, and may allow earlier diagnosis and more uniform and widespread use.

/pdf/diagnostic-criteria-for-multiple-sclerosis-2010-revisions-to-24iph50480.pdf

Diagnostic criteria for multiple sclerosis: 2010 Revisions to the McDonald criteria

Background and Purpose—The authors present an overview of the current evidence and management recommendations for evaluation and treatment of adults with acute ischemic stroke. The intended audienc...

/pdf/guidelines-for-the-early-management-of-patients-with-acute-19udbft6e7.pdf

Guidelines for the Early Management of Patients With Acute Ischemic Stroke A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association

The International Panel on MS Diagnosis presents revised diagnostic criteria for multiple sclerosis (MS). The focus remains on the objective demonstration of dissemination of lesions in both time and space. Magnetic resonance imaging is integrated with dinical and other paraclinical diagnostic methods. The revised criteria facilitate the diagnosis of MS in patients with a variety of presentations, including "monosymptomatic" disease suggestive of MS, disease with a typical relapsing-remitting course, and disease with insidious progression, without clear attacks and remissions. Previously used terms such as "clinically definite" and "probable MS" are no longer recommended. The outcome of a diagnostic evaluation is either MS, "possible MS" (for those at risk for MS, but for whom diagnostic evaluation is equivocal), or "not MS."

https://www.onlinelibrary.wiley.com/doi/epdf/10.1002/ana.1032

Recommended diagnostic criteria for multiple sclerosis: Guidelines from the International Panel on the Diagnosis of Multiple Sclerosis

The Austrian Stroke Prevention Study: Serum fibrinogen predicts carotid atherosclerosis and white matter disease in neurologically asymptomatic individuals

This article prepared by members of International Panel working on new diagnostic criteria of multiple sclerosis (MS) presents and discusses these criteria, which pay special attention to MRI as a method of confirmation of dissemination in space and in time, necessary for MS diagnosis. Also main problems of MS differential diagnosis are discussed as well as significance of other laboratory methods like evoked potentials and cerebrospinal fluid studies. Nevertheless the significance of clinical signs in MS diagnosis are decisive.

Diagnosis of multiple sclerosis

In the international neurological literature, neuroimaging research plays an important role. Neuroimaging techniques are also of steadily increasing importance for clinical diagnosis and treatment monitoring. Therefore, neuroimaging research activities were surveyed by a questionnaire, which was completed by 100 neurological centres across Europe. It showed that most groups use magnetic resonance imaging (MRI), fMRI, computerized tomography (CT) and single photon emission computerized tomography (SPECT). Positron emission tomography (PET) and ultrasound are also employed by nearly half of the centres. Neuroimaging research involves co-operation amongst typically five to 10 disciplines. Cerebrovascular disease, dementia, cognitive disorders, epilepsy, movement disorders, brain tumours and multiple sclerosis are frequently being studied. Many groups rely on small budgets, have few full-time scientists and limited access to expensive resources. There is little exchange of scientists amongst laboratories. It was felt that funding and co-operation needed improvement in order to maintain a high standard in neuroimaging research.

A survey of neuroimaging research in European neurological departments.

Sirs: Terpentine oil, also called Venetian terpentine, is a dye diluent derived from Pinus species used by professional and hobby painters. It contains a mixture of the etheric oils αand β-pines and 3-caren. To our knowledge, there are no previous reports on the cerebral consequences of ingestion of terpentine oil in humans. We identified terpentine oil ingestion as a possible cause of transient cerebral white matter changes and intracortical ecchymosis probably due to toxically increased vascular permeability. A 56 year old female presented in a comatose state (Glasgow Coma Scale 6), with ketoacidosis, hyperglycaemia, renal insufficiency and aspiration pneumonia. From the accompanying persons it became apparent that she had ingested about 200 ml of Venetian terpentine which she used for her painting. Whether terpentine ingestion occurred accidentially or in a suicidal attempt could not be fully determined. The patient’s history also revealed alcohol abuse and depression. Following admission, intensive care and artificial ventilation were needed to improve the patient’s cardiopulmonary function and to treat septic shock. When the patient was weaned from the respirator on day 18 following admission she had regained consciousness but was still severely confused and tetraparetic. CT of the brain on day 21 following admission showed widespread white matter hypodensity. MRI on day 26 confirmed extensive abnormality of predominantly the frontolateral and parietotemporal deep and subcortical white matter of both hemispheres (Fig. A). Gradient echo T2*-weighted images showed rims of hypointensity outlining the cerebral surface especially over the convexity but also in selected gyri of the frontotemporal lobes. At that time the patient was still mildly confused with a general slowing of her cognitive functions and some weakness especially of the lower extremities. Over the next weeks the patient continued to improve to her premorbid condition and follow-up neurological examination revealed no focal neurological deficits. Follow-up MRI on day 48 revealed almost complete remission of the signal abnormalities in the white matter (Fig. B) while the cortical rims of hypointensity appeared to be unchanged (Figs. C, D). The constituents of terpentine oil are lipophilic substances which are easily absorbed from the gastrointestinal tract and then distributed to lipid-rich compartments of the body. The cerebral consequences of terpentine intoxication in our patient were extensive MR signal abnormalities of the white matter and rims of cortical hypointensity on gradient echo T2*weighted images. It could be speculated that central nervous system myelin might be prone to accumulate terpentine oil constituents which in turn could lead to a breakdown of myelin. While such a mechanism cannot be excluded the rapid and almost complete resolution of white matter signal changes appears to favour oedema as the cause for these abnormalities. Rapid resolution of extensive white matter hyperintensity is also known to occur in the posterior reversible encephalopathy syndrome. However, the distribution of signal abnormalities throughout the brain of our patient and the absence of factors known to provoke this syndrome argue against such an explanation [1, 2]. It could also be speculated that terpentine intoxication might have caused a sort of fat embolism with concomitant ischaemic changes and oedema preferentially in the periphery of the arterial border zones. While the distribution of signal hyperintensities would fit, the absence of significant cortical signal changes appears to argue against such hypotheses. For the same reasons global hypoxia which might have occurred during the acute phase of the illness appears an unlikely cause of the observed white matter changes. It cannot be completely excluded, however, that cortical changes have been missed because of the long time interval between MRI and the acute event although the almost complete resolution of hyperintense signal changes also rules against more pronounced ischaemic tissue damage. Rims of cortical hypointensity were the second striking observation in this patient. Such regions of signal loss on gradient echo T2*weighted images are highly suggestive of haemosiderin deposition indicating earlier extravasation of blood. In hypertensive encephalopathy only petechial haemorrhages have been reported [3]. Calcification as another possibility can be excluded on the basis of CT which showed white matter hypodensity only. The rims of hypointensity were not only seen at the cortical surface such as in superficial haemosiderosis [4] but directly involved the cortical ribbon and even the subcortical white matter LETTER TO THE EDITORS

Franz Fazekas

Papers

The Austrian Stroke Prevention Study: Serum fibrinogen predicts carotid atherosclerosis and white matter disease in neurologically asymptomatic individuals

Diagnosis of multiple sclerosis

A survey of neuroimaging research in European neurological departments.

MR brain changes following terpentine oil ingestion.

Quantitative magnetization transfer imaging in human brain by means of a PACE technique.