1362
infarctions were associated with ipsilateral carotid ulceration, vs 32% of patients with a normal CT scan, p < 0-05). Substantial ipsilateral (70% or more) carotid artery stenosis was seen in equal proportions in patients with lacunar or cortical infarctions, and in those with normal CT scans (67% and 79%, respectively, not significant). Histological analysis of the carotid plaques revealed fresh mural thrombus in 39% of lacunar infarctions (vs 19% of plaques associated with a normal scan, p=005). Fibrous plaques were not found in this subgroup. These correlations provide evidence for a possible extracranial cause of some lacunar infarctions. Dr Hankey and Professor Warlow (Feb 9, p 335) conclude that lacunar infarctions rarely (only 6%) result from extracranial carotid artery disease. But the relevance of any pathogenetic theory based on clinical observations alone (there was no CT-scan evidence of lacunar infarction) should be discussed, since it is well known that many suggestive symptoms are difficult to ascertain from patients’ history, which is often imprecise. Penetrating branch occlusion has been proposed as the underlying cause of almost all deep lacunar infarctions.2 In a few cases (2/11), FischerZ showed that the feeding artery of a lacunar infarct was normal and assumed that a small embolic particle of thrombus from the heart or from the neck vessels caused a transient blocking of the implicated penetrating artery. Olsen et al3 observed substantial stenosis of the internal carotid artery in 7% of lacunar infarctions revealed by CT scan. This is probably an underestimation of the role of extracranial carotid atherosclerosis in the pathogenesis of lacunar infarctions, since they did not consider moderate and non-stenosing carotid atheromatous lesions as a possible cause of stroke. On the other hand, Gorsselink et al4 found a probably causative carotid embolism in some lacunar infarctions (6 of 20 patients with lacunar infarction had a pronounced stenosis of the ipsilateral internal carotid artery). Sise et al,s analysing plaque morphology in patients with preoperative lacunar infarction, also showed a high frequency of ulceration (71 %), but only half these carotid lesions were on the appropriate side of the small cerebral infarctions. These and our observations of unstable complicated plaques in patients with CT-confirmed lacunar infarction indicate that artery-to-artery embolism or hypoperfusion are rare but possible causal factors in lacunar infarction. Nevertheless, we agree that coexistent small-vessel disease (atheromatosis or lipohyalinosis) in these hypertensive patients with carotid atheroma cannot be excluded as two parallel
independent events. We have reservations about Kappelle and colleagues’ (Feb 9 and ref 2) assertion that patients with a history suggestive of transient lacunar ischaemia do not need carotid artery investigation or consideration for endarterectomy.
University Hospital Sart-Tilman, Liège, Belgium
400
H. VAN DAMME J. C. DEMOULIN R. LIMET
Kappelle LJ, Vanhatum JC, Koudstaal PL, et al. Carotid angiography in patients with lacunar infarction: a prospective study. Stroke 1988; 19: 1093-96. 2. Fischer CM Capsular infarcts: the underlying vascular lesions. Arch Neurol 1979; 36: 1.
65-68. 3. Olsen TS, SknverEB, Herning M. Cause of cerebral infarction in the carotid territory: its relation to the size and the location of the infarct and to the underlying vascular lesion. Stroke 1985; 16: 459-65. 4. Gorsselink EL, Peeters HP, Lodder J. Causes of small deep infarctions detected by CT. Clin Neurol Neurosurg 1984; 86: 271-73. 5. Sise MJ, Sedwitz MM, Rowley WR, Shackford SR. Prospective analysis of carotid endarterectomy and silent cerebral infarction in 97 patients. Stroke 1989; 20: 329-32.
MMS test scores and response to question "Who is the Prime Minister?".
admitted acutely to hospital during a one-week period a month after Mrs Thatcher resigned. They were asked the name of the Prime Minister, and their answers were classed as Mr John Major (JM), not Mrs Thatcher (Not MT), Mrs Thatcher (MT), or other (0). The mini mental state (MMS) test,3 a simple reproducible screen of higher mental function, was also administered in a standardised way by a single observer. Results were compared by Mann-Whitney U test.
Patients who knew the
of the Prime Minister has frequently been used as part of bedside testing of higher function. However, after five years in office Mrs Thatcher was found to be significantly more memorable than her predecessors,l rendering the test less useful. After her resignation, after eleven years, Le Fanu suggested that the test could be reintroduced.22 We studied 40 patients over 70 years (mean age 80, range 70-98)
SIR,-Asking the
of the
new
Prime Minister had
did not. Previous studies found that MMS scores of less than 23 are associated with dementia.3 The name of the Prime Minister, having been redundant during much of Mrs Thatcher’s term of office, seems to have re-emerged as a simple, powerful tool in screening for dementia. Department of Neurology, Charing Cross Hospital, London W6 8RF, UK
1.
G. N. FULLER K. MEERAN
Deary IJ, Wessley S, Farrell M. Dementia and Mrs Thatcher. Br Med J 1985; 291:
1786. 2. Le Fanu J. Medicine man. 3.
The Prime Minister, Mrs Thatcher, and dementia
name
significantly higher MMS scores than any of the other three groups Those who knew it (JM>NotMT,pMT,p 0 p < 0001). Only 1 patient with an MMS score below 23 knew John Major was the Prime Minister and only 1 patient with a score above this
Sunday Telegraph Review Dec 23, 1990: vii. Dick JPR, Guiloff RJ, Stewart A, et al. Mini mental state examination in neurological patients. J Neurol Neurosurg Psychiatry 1984; 47: 496-99.
CORRECTION
name
Experience with the first 250 endometrial resections for menorrhagia.-In this article by Mr A. L. Magos and colleagues (May 4, p 1074), 91 % (not 91) patients asked for total TCRE. Also, of the 7 patients with fluid overload, 5 were treated with intravenous frusemide, 2 (not 5, as might have been implied) of these because they had signs of acute left heart failure.
infarctions were associated with ipsilateral carotid ulceration, vs 32% of patients with a normal CT scan, p < 0-05). Substantial ipsilateral (70% or more) carotid artery stenosis was seen in equal proportions in patients with lacunar or cortical infarctions, and in those with normal CT scans (67% and 79%, respectively, not significant). Histological analysis of the carotid plaques revealed fresh mural thrombus in 39% of lacunar infarctions (vs 19% of plaques associated with a normal scan, p=005). Fibrous plaques were not found in this subgroup. These correlations provide evidence for a possible extracranial cause of some lacunar infarctions. Dr Hankey and Professor Warlow (Feb 9, p 335) conclude that lacunar infarctions rarely (only 6%) result from extracranial carotid artery disease. But the relevance of any pathogenetic theory based on clinical observations alone (there was no CT-scan evidence of lacunar infarction) should be discussed, since it is well known that many suggestive symptoms are difficult to ascertain from patients’ history, which is often imprecise. Penetrating branch occlusion has been proposed as the underlying cause of almost all deep lacunar infarctions.2 In a few cases (2/11), FischerZ showed that the feeding artery of a lacunar infarct was normal and assumed that a small embolic particle of thrombus from the heart or from the neck vessels caused a transient blocking of the implicated penetrating artery. Olsen et al3 observed substantial stenosis of the internal carotid artery in 7% of lacunar infarctions revealed by CT scan. This is probably an underestimation of the role of extracranial carotid atherosclerosis in the pathogenesis of lacunar infarctions, since they did not consider moderate and non-stenosing carotid atheromatous lesions as a possible cause of stroke. On the other hand, Gorsselink et al4 found a probably causative carotid embolism in some lacunar infarctions (6 of 20 patients with lacunar infarction had a pronounced stenosis of the ipsilateral internal carotid artery). Sise et al,s analysing plaque morphology in patients with preoperative lacunar infarction, also showed a high frequency of ulceration (71 %), but only half these carotid lesions were on the appropriate side of the small cerebral infarctions. These and our observations of unstable complicated plaques in patients with CT-confirmed lacunar infarction indicate that artery-to-artery embolism or hypoperfusion are rare but possible causal factors in lacunar infarction. Nevertheless, we agree that coexistent small-vessel disease (atheromatosis or lipohyalinosis) in these hypertensive patients with carotid atheroma cannot be excluded as two parallel
independent events. We have reservations about Kappelle and colleagues’ (Feb 9 and ref 2) assertion that patients with a history suggestive of transient lacunar ischaemia do not need carotid artery investigation or consideration for endarterectomy.
University Hospital Sart-Tilman, Liège, Belgium
400
H. VAN DAMME J. C. DEMOULIN R. LIMET
Kappelle LJ, Vanhatum JC, Koudstaal PL, et al. Carotid angiography in patients with lacunar infarction: a prospective study. Stroke 1988; 19: 1093-96. 2. Fischer CM Capsular infarcts: the underlying vascular lesions. Arch Neurol 1979; 36: 1.
65-68. 3. Olsen TS, SknverEB, Herning M. Cause of cerebral infarction in the carotid territory: its relation to the size and the location of the infarct and to the underlying vascular lesion. Stroke 1985; 16: 459-65. 4. Gorsselink EL, Peeters HP, Lodder J. Causes of small deep infarctions detected by CT. Clin Neurol Neurosurg 1984; 86: 271-73. 5. Sise MJ, Sedwitz MM, Rowley WR, Shackford SR. Prospective analysis of carotid endarterectomy and silent cerebral infarction in 97 patients. Stroke 1989; 20: 329-32.
MMS test scores and response to question "Who is the Prime Minister?".
admitted acutely to hospital during a one-week period a month after Mrs Thatcher resigned. They were asked the name of the Prime Minister, and their answers were classed as Mr John Major (JM), not Mrs Thatcher (Not MT), Mrs Thatcher (MT), or other (0). The mini mental state (MMS) test,3 a simple reproducible screen of higher mental function, was also administered in a standardised way by a single observer. Results were compared by Mann-Whitney U test.
Patients who knew the
of the Prime Minister has frequently been used as part of bedside testing of higher function. However, after five years in office Mrs Thatcher was found to be significantly more memorable than her predecessors,l rendering the test less useful. After her resignation, after eleven years, Le Fanu suggested that the test could be reintroduced.22 We studied 40 patients over 70 years (mean age 80, range 70-98)
SIR,-Asking the
of the
new
Prime Minister had
did not. Previous studies found that MMS scores of less than 23 are associated with dementia.3 The name of the Prime Minister, having been redundant during much of Mrs Thatcher’s term of office, seems to have re-emerged as a simple, powerful tool in screening for dementia. Department of Neurology, Charing Cross Hospital, London W6 8RF, UK
1.
G. N. FULLER K. MEERAN
Deary IJ, Wessley S, Farrell M. Dementia and Mrs Thatcher. Br Med J 1985; 291:
1786. 2. Le Fanu J. Medicine man. 3.
The Prime Minister, Mrs Thatcher, and dementia
name
significantly higher MMS scores than any of the other three groups Those who knew it (JM>NotMT,pMT,p 0 p < 0001). Only 1 patient with an MMS score below 23 knew John Major was the Prime Minister and only 1 patient with a score above this
Sunday Telegraph Review Dec 23, 1990: vii. Dick JPR, Guiloff RJ, Stewart A, et al. Mini mental state examination in neurological patients. J Neurol Neurosurg Psychiatry 1984; 47: 496-99.
CORRECTION
name
Experience with the first 250 endometrial resections for menorrhagia.-In this article by Mr A. L. Magos and colleagues (May 4, p 1074), 91 % (not 91) patients asked for total TCRE. Also, of the 7 patients with fluid overload, 5 were treated with intravenous frusemide, 2 (not 5, as might have been implied) of these because they had signs of acute left heart failure.
