It has been demonstrated that a relatively low-cost resistive NMR imager can be installed in a normal hospital environment without many major or expensive modifications. The magnet can be adjusted to give adequate uniformity and there is sufficient RF shielding to give good quality clinical images (Fig. 3). The fringe field of the magnet of this system, which operates at the lowest field strength of any commercial NMR imager, does not present a problem to imaging unit staff (NRPB, 1984). The long term reliability and detailed specifications with regard to image quality have yet to be determined. These will be determined whilst the imager is being used for clinical studies as part of the national clinical evaluation of NMR imaging supported by the Medical Research Council.
Magnetic resonance imaging of the brain in 69 detoxified alcoholics revealed that relaxation time (T1) in whole brain and in grey matter and parietal white matter was greater than in age‐matched controls. In 48 patients, data on cognitive function and lifetime alcohol consumption were available. With age‐controlled, lifetime consumption, and impairment on performance in the cognitive test (a Category Sorting Test) correlated positively withT1in whole brain and in selected regions. Impairment in the cognitive test correlated with increasedT1in whole brain and white matter independently of cerebral atrophy. Alcohol consumption patterns in the following 6 months were unrelated to changes inT1. The excess water implied by the elevatedT1values may be intra‐ or extracellular. It is uncertain whether or notT1elevation in alcoholics is a marker of neuronal damage.T1elevation appears to be a marker of one type of alcohol‐related cognitive impairment.
Twenty-seven patients had a first Magnetic Resonance Imaging (MRI) scan 1–3 days after stopping drinking and a second approximately 2 weeks later with no change in whole brain T1 or T1 in selected brain areas. Six patients whose first scan was over 36 h after the last drink underwent an increase in whole brain T1 in the interval to the second scan. The later the first scan was performed the greater was the increase in T1. These results are compatible with a very early fall in brain water immediately on cessation of drinking (perhaps due to a rebound increase of vasopressin activity) with a return to ‘baseline’ after two weeks. A third scan after discharge from hospital in 23 individuals who had abstained from alcohol or drank very little did not reveal any further significant change in brain T1.
Myocardial involvement in systemic lupus erythematosus is commonly found at autopsy but seldom recognized clinically or by routine cardiological investigations. As the magnetic resonance relaxation parameter, T1, is altered by changes in tissue cellularity, we carried out magnetic resonance imaging in 10 patients with systemic lupus erythematosus. Five had active systemic lupus erythematosus when assessed using the lupus activity criteria count. The mean (+/- SD) T1 was 319 +/- 12 in normal volunteers and 321 +/- 10 in a second control group with hypertrophic cardiomyopathy. In the group with systemic lupus erythematosus, there was a higher mean value of 336 ms with a wider scatter of individual results (SD +/- 22 ms). In the subgroup of patients with active disease, T1 was significantly higher (349 +/- 24) than in either of the two control groups. In addition, there was an inverse correlation between serum complement and myocardial T1 in patients with systemic lupus erythematosus. Myocardial abnormalities in systemic lupus erythematosus were demonstrated by magnetic resonance imaging even where other non-invasive cardiac investigations were negative. We conclude that T1 calculated from magnetic resonance imaging is often abnormal in systemic lupus erythematosus and probably indicates myocardial involvement.
A low field resistive nuclear magnetic resonance imaging system (0.08 Tesla) was used to study the in vivo changes in the relaxation parameter T1 of the left ventricular myocardium from the first day to six months after acute myocardial infarction in 41 consecutive patients admitted to a coronary care unit. T1 maps were constructed from transverse and coronal images at various times after infarction. Thrombolytic treatment had been successful in 28 patients. Thirty three of the 34 patients studied within two weeks of infarction had a significantly increased T1 value but this developed only after the third day in four. At day 1-3 the mean (1 SD) maximum T1 was 413 (29) ms (n = 23) compared with 430 (41) ms (n = 22) at day 4-7, 433 (35) ms (n = 24) at day 8-14, 420 (34) at one month (n = 22), 388 (39) (n = 20) at three months, and 361 (24) (n = 14) at six months. The number of regions of interest with an increased T1 followed a similar time course. Although the increase in T1 measured at three months correlated with the initial maximum creatine kinase and with the left ventricular ejection fraction measured at one month, the number of regions with abnormal T1 from day 4 through to one month correlated best with left ventricular ejection fraction. There was no significant difference in T1 between patients with or without reperfusion. The rise in T1 over the first few days together with the prolonged time course of T1 increase suggests that the increase in T1 may reflect cellular infiltration as much or more than tissue oedema.
The uptake of 99mTc-MDP was studied in 73 patients after a tibial fracture. The image obtained five minutes after injection during a period between one and four weeks after fracture was found to be related to the incidence of non-union after six months. A ratio of 1.3 between the uptake at the fracture site and at normal bone adjacent to it predicted non-union in an individual patient with a sensitivity of about 70% and a specificity of 90%.
The important radiological differential diagnosis of syringomyelia is an intramedullary tumour. Magnetic resonance (MR) is now the modality of choice to image the spinal cord and canal (Han et al, 1983; Yeates et al, 1983; Norman et al, 1983). However, differentiation between the cerebrospinal fluid (CSF) contained within a syrinx and a cystic tumour is a potential problem, as there may be little difference in the relaxation parameters (T1 and T2) or in the morphology. One possible means of differentiating these conditions is to study CSF flow using a MR phase imaging technique (Ridgway & Smith, 1986; Ridgway et al, 1987), which has recently been developed to allow quantitative measurement of flow velocities, including low values found in CSF flow.
A single photon absorption imaging technique has been developed to assess the bone mass of the hand, especially in patients with rheumatoid arthritis or bronchial asthma. A modified rectilinear scanner images the hand by transmission scanning in a water bath with a 7.4 GBq 125I source. A microcomputer is used to calculate the bone mineral distribution, and the total bone mineral content (BMC) of the hand is determined from that distribution. The precision (coefficient of variation) of the measurement is 1.9%. A control population of 20 men and 58 women has been studied to determine normal variations in hand bone mineral content with age, sex, body size, hand volume and years since menopause. The normal men are found to have an average hand BMC of 25.1 g with a coefficient of variation (CV) of 22%, which is reduced to 12% by normalising for body size using span. The normal women had an average hand BMC of 18.0 g +/- 15%. The CV is reduced to 13% by normalising for span and years post-menopause.
Nuclear magnetic resonance images of the brain were obtained in fourteen patients with major depression during a course of ECT. The T1 relaxation time rose immediately after the fit, reaching a maximum 4-6 h later. The T1 values then returned to their original level; no long-term increase occurred over the course of treatment. These results are consistent with an extensive but temporary breakdown of the blood-brain barrier during ECT.
The authors show how measurements on patients over a long period of time to monitor either their bone loss as a result of disease or a change in bone calcium as a result of treatment, can be used to obtain a measurement of the long term precision of total body neutron activation analysis in vivo.
The study of pulsatile cerebrospinal-fluid (CSF) flow may be useful in diagnosis of certain forms of intracranial disease. Previous techniques used to study CSF flow either are invasive or do not allow accurate measurement. Magnetic resonance imaging (MRI) offers a non-invasive method of studying the CSF pathways. Our technique uses MR phase images and allows quantitative measurement of flow velocities and volume-flow rates. Four volunteers were studied at the level of the second cervical vertebra (C2). The MRI pulse sequence was gated from the R-wave of the subject's electrocardiogram and 12 scans were taken corresponding to different times in the cardiac cycle. The variation in flow velocity throughout the cycle was plotted, and maximum caudad and cephalad flow velocities and flow rates were calculated. Good agreement was found between three of the four volunteers. The mean maximum caudad velocity was 2.91 cm s-1 occurring at a mean time of 190 ms after the R-wave. This corresponds to a mean maximum flow rate of 4.13 ml s-1. The total imaging time for each study was about 1 h. Technical developments, allowing simultaneous acquisition of several images throughout the cardiac cycle, will reduce this time significantly.
Brain water content was measured in tissue samples taken at operation from 19 patients with intrinsic cerebral tumours imaged preoperatively by magnetic resonance. A high correlation (r = 0.94, p less than 0.0001) between white matter water content and the longitudinal relaxation time (T1) enabled water content to be estimated from T1 to within 4%. 11 patients received dexamethasone and improved clinically but their T1, and thus brain water content, was unchanged an average of 6 days later. Intravenous infusion of 20% mannitol in 11 patients significantly reduced T1 in oedematous white matter and tumour within 15 min of administration, and by 30 min the T1 of oedematous white matter had fallen to a mean of 32.4 (SEM 7.1) ms, corresponding to a reduction in water content of 1.4 (0.3)%.
Bone mass has previously been shown to be reduced at peripheral bone sites in patients with bronchial asthma receiving corticosteroids. To assess whether total bone mass is reduced in asthma total body calcium was measured by in vivo neutron activation analysis in patients receiving various treatments for asthma and compared with results from normal controls and patients with rheumatoid arthritis and polymyalgia rheumatica. Compared with controls total body calcium was reduced by 13.6% (p less than 0.001) in patients with asthma receiving daily oral corticosteroids but by only 9.0% (p less than 0.005) in a similar group of patients who had received oral calcium supplements at the start of their corticosteroid treatment. Total body calcium was also reduced in a group of patients receiving only inhaled corticosteroids (8.8%; p less than 0.001) but not significantly reduced in a small group of patients with asthma who had never received these drugs. When compared with controls a group of patients matched for age and for dose of corticosteroids given for rheumatoid arthritis had a similar reduction in total body calcium to the patients with asthma receiving daily oral treatment (17.7%; p less than 0.001), but no such reduction was shown in patients with polymyalgia rheumatica. These findings suggest that the risk of bone loss with low dose oral corticosteroids in similar in asthma and rheumatoid arthritis. Further work is required to assess the clinical relevance of small losses of bone associated with the use of inhaled corticosteroids.