High resolution SPECT, small deep infarcts and ... - Europe PMC

142

Journal of the Royal Society of Medicine Volume 85 March 1992

High resolution SPECT, small deep infarcts and diaschisis

J V Bowler BSc MRCP' J P H Wade MD MRCP'

D C Costa MD PhD2 B E Jones MSc' T J Steiner MB PhD' 'Regional Neurosciences Department, and 2Department of Nuclear Medicine,

Charing Cross Hospital, Fuiham Palace Road, London W6 8RF Keywords: SPECT; diaschisis; lacunar stroke; pure motor syndrome

Summary Eighteen cases of lacunar infarction are presented. Six of these cases had a purely motor clinical deficit. All the cases were studied by serial high resolution SPECT (single photon emission computerized tomography) using 99Tcm HMPAO. The degree and extent of the changes in cerebral perfusion consistent with diaschisis were noted and these compared with the severity of the clinical deficit at presentation and over time. No significant correlation between diaschisis and the clinical state was found at any stage. The nature, aetiology and importance of diaschisis are discussed and it is suggested that caution should be exercised in attributing clinical features to diaschisis simply because it may be present. Introduction The term diaschisis is used to refer to areas of functional cerebral deactivation occurring remotely from the responsible structural lesionl"2. Originally inferred as a functional change' it was subsequently used to describe electroencephalographic changes remote from the causative lesion3 and has been used most recently in functional imaging to describe disturbances in cerebral blood flow or metabolism remote from the primary lesion. In normal brain local blood flow and metabolism are closely coupled. Blood flow can therefore be used as a metabolic

marker4. Diaschisis has been extensively reported in association with stroke5rl-. It is most often seen in the cerebellum contralateral to supratentorial lesions and is also well described in the cortex overlying small deep lesions, especially those of the thalamus12-14. It has been suggested that resolution of diaschisis may be important in recovery from stroke 2. Several reports11,12,14,15 have suggested a correlation between diaschisis and deficit but they have been unable to establish whether the association is causal, or whether it is simply the case that appropriately sited lesions may produce both the clinical deficit and diaschisis, without the diaschisis adding to the deficit. It is difficult to apportion the clinical deficit between the primary lesion and diaschisis because of the difficulty in separating the two. These difficulties are compounded by the natural tendency for both diaschisis and clinical deficit to recover which could lead to incorrect assumptions of a causal relationship. However, if diaschisis made a substantial contribution to the clinical deficit and if recovery from diaschisis contributed significantly to recovery from stroke, then it should be possible, if clinical deficit and diaschisis were quantified, to establish a close correlation between deficit and diaschisis which would be a

necessary first step towards demonstrating causality. Paper read to The best prospect for establishing this would be the Section of serial study of patients with small discrete lesions. Neurology, We report 18 cases of lacunar infarction, six of 6 December 1990 which caused a pure motor syndrome, which were investigated with high resolution SPECT.

Patients and methods All patients admitted to Charing Cross Hospital with first stroke were eligible for the study. Exclusions to entry were previous stroke, cranial neurosurgery, primary intracerebral haemorrhage, non English speakers, current psychiatric illness, epilepsy, dementia and alcohol abuse. Of the 60 consecutive cases recruited, 18 had small deep lesions and six of these had purely motor clinical deficits16. Clinical examination and SPECT were carried out as soon as possible, at about one week and 3 months post ictus. X-ray CT scanning was done at 5 days. A detailed neuropsychological evaluation was carried out, usually on the same day as the second and third SPECT studies. Echocardiography, carotid duplex doppler studies and full haematological investigations were also done. SPECT scanning began 15-30 min after the injection of 20 mCi of 99Tcm HMPAO (hexamethylpropyleneamine oxime, Ceretec, Amersham International) and was done using the NOVO 810 scanner which is a dedicated multidetector tomographic head scanner with a resolution of 9 mm at full width half maximum (FWHM) in the plane of the scan. Scans were independently inspected by two of us in full knowledge of the X-ray CT scan result. One of us (DCC) was blind to the clinical picture. Features leading to disagreement were reviewed until agreement was established. Areas of decreased HMPAO uptake affecting cerebral or cerebellar cortex detected on inspection were then confirmed and quantifiled by placing regions of interest (ROIs) over the affected cortex and the equivalent contralateral site. These ROIs were twice the resolution of the scanner (full width at half maximum) in diameter, ie 18 mm. The counts from the ROIs in each area were summed and the percentage deviation from the normal side calculated. The volume measured was also recorded. Normal data is taken from a series of 11 cases of tension headache analysed in a similar way. Contiguous ROTs were placed in each predetermined region (the cortex of each lobe, the cerebellar cortex, thalamus and lentiform nucleus) and the counts and total volume measured recorded. For each of these predetermined regions the counts were totalled and the ratio right/left calculated. The 95% intervals

0141-0768/92/

030142-05/$02.00/0 © 1992 The Royal Society of Medicine

Journal of the Royal Society of Medicine Volume 85 March 1992

Table 1. Details ofpatients studied with pure motor stroke

Days to Seen on Stroke SPECT SPECT score

Volume

(cm3)

Sex/age Site

1

M/57

Corona radiata

6

F/66

High internal capsle

3

M/55

Corona radiata

1

M/731

Lenticular nucleus

3

F/68

Internal capsule

2

F/67

Internal capsule

N N N; -v Y-..

1.2 12.2 X 1.9

6 4 2 6

, 8t'-".' * 49

"'' 6 tY 5;''"

95 11.9

Y Y

2 4

181, Y 0.6 -Y

1 10

6.5 99 1.2 5.2 67 0.8 3.8 118

10 7 10 9 2 5 0 0

Y y Y Y N N N N

Diaschisis

None

10.3

CCD Thalamus Cortex Lentiform Parietal CCD Thalamus Cortex Cortex Lentiform Parietal

10.2 6.5*

7.9* 9.1 11.1 23.3 0.9* 10.0 11.0 8.1 5.8 18.7 6.3

11.8 -4.7 2.8* 0.8* 1.7*

6.8* 15.4 2.4* 15.1 0.9* 2.7* 13.5 4.1* 1.9* 4.8* 0.8*

5.4

2.4*

0.7*

None Cortex

Figures for diaschisis are given as the percentage difference from the normal side. Figures marked * lie within the 95% intervals. CCD, crossed cerebellar diaschisis. ¶ cerebellum inadequately seen

Table 2. Details of the patients with small deep infarcts who did not have a purely motor clinical deficit

Volume Sex] No (cm3) age Sidet Site of infarct 7 1

F/76 R

Possibly thalamus

9

F/76 X

Not identified

10 7 12 1

M/63 R F/41 P

Lentiform nucleus Paramedian pons

13 4

M/83 P

Central pons

28 3

F/77 L

Head of caudate

Barthel Time to Canaidian SPECT neurological scale Index Diaschisis 1.0 6.0 93.0 1.0 7.2 91.0 0:8 3.8 101.0 4.2 136.0 1.3 5.3 95.0 0.8

6.843 1

F/75 L

Internal capsule

45 2

M/84 R

Corona radiata

46 5 49 56 1 59 3

F/69 R F/84 X

F/83 R F/82 R

Corona radiata Not identified

Internal capsule Internal capsule

tX means not seen on any imaging investigation *Figures lie within the 95% intervals

94.0 0.3 7.0 1.2 6.1 98.0 1.7 6.7

92.0 4.0 10.2 4.0 1.1 9.1 92.0

10.0 10.0 10.0 7.5 8.5 10.0 9.5 9.5 10.0 9.0 9.5 8.0 9.5 9.5 5.0 6.5 8.5 7.5 10.0 7.5 8.5 9.0 8.5 8.0 9.0 4.5 7.0 5.0 5.5 5.5 8.0

20 20

None

-

CCD

7.0*

3.0*

8.0

17 17 -

20 20 -

20 19 20 -

8 20 19 -

Parietal OVC

CCD

19.3 7.3

7.0 12.7

7.6 -

3.5* 19.4 14.8

None

CCD Parietal OVC None

11.1 7.8 8.0

16.7 8.6 5.6

8.8

10.6

10.6 5.1 8.7

None

17 20 -

CCD

4.5*

7 20 -

18 -

7 10

None Thalamus Parietal Thalamus Temporal OVC

11.7 7.9 7.1 9.2* 11.7 7.5* 5.0* 4.1* 0.3*

2.3* 1.0* 8.6 4.4

143

144

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Journal of the Royal Society of Medicine Volume 85 March 1992

(1.96 standard deviations) were then calculated. In the study, data ratios falling outside this interval were considered to be consistent with diaschisis. In the scans from the patients in this study a further subjective area was defined consisting of an area of cortex often seen superficial to the lesion which did not correspond exactly with a predefmeable area. This was also measured as described above. Normal data for the parietal cortex was used as the bulk of these volumes were parietal. Where significant diaschisis was detected on one scan in the series from a patient, the remaining scans, for that patient were analysed for that region and the data used, even if within the 95% confidence interval, to give information on the evolution of diaschisis. Infarct volume was measured by planimetry from the CT scans. In the cases with a purely motor deficit clinical severity was measured according to the National Institutes of Health Stroke Scale'7 as this has a relatively detailed section for motor deficit. Only the elements for dysarthria, facial, arm and leg weakness and the plantar response were applicable in these cases, giving a worst case score of 14. In the remaining 12 cases both the Canadian Neurological Scale18 and the Barthel Index'9 were used (there is no Barthel Index score for the first exination as the period available for assessment is too short). Informed consent was obtained from all patients or their relatives and the study was approved by the Ethics Committee of Charing Cross Hospital. Results The standard deviations in the control cases were, in the lentiform nucleus 4.56%, cerebellum 3,75%, parietal cortex 2.15% and thalamus 5.46%. Details of the cases with a pure motor syndrome are given in Table 1, and of the remaining small deep infarcts the details are given in Table 2 with a brief clinical description in Table 3. The volumes analysed were from 10 to 25 cm3 in the cerebellum, 3-5 cm3 in the thalamus and basal ganglia, 21-61 cm3 in the cortex overlying the lesion and 15-43 cm3 in the parietal cortex. In the cases with a pure motor syndrome diaschisis was not identified in the frontal or temporal lobes. It was most often evident in the overlying cortex (5 of 17 scans) but also in the thalamus (3 of 17), lentiform nucleus (5 of 17), parietal cortex (2 of 17) and contralateral cerebellum in 3 of 15 adequate scans. Diaschisis followed a similar distribution in

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