114
(or a linked mutation) might lead to these changes by causing overexpression of apo-Cl 11.6,7 Irrespective of the molecular mechanisms, the finding of the S2 allele in a large proportion of Arab MI patients (36/79,46%) is noteworthy. Dietary excesses (eg, overconsumption of sugar and sweets8) and the high prevalence of type-II diabetes mellitus among Arabs in Kuwait (N.A. Abdella, personal communication), along with other risk factors, may have contributed to the strength of the association of the S2 allele with CHD. The relation of this allele to CHD should be studied in other populations with attention to co-existing risk factors. Department of Pathology, Kuwait University Faculty of Medicine, and Clinical Chemistry Laboratory, Mubarak Al-Kabeer Hospital, Safat 13110, Kuwait *Present address. Samur Sokak 29/12,
Pointing to objects test. SINAN TAS* Saray Apt, Kurtulus, Ankara, Turkey.
A, Stocks J, Sharpe CR, et al. Deooxyribonucleic acid polymorphism m the apolipoprotein A-1-C-III gene cluster Association with hypertriglyceridemia. J Clin Invest 1985; 76: 1090-95 Ferns GAA, Ritchie C, Stocks J, Galton DJ. Genetic polymorphisms of apolipoprotein C-III and insulin in survivors of myocardial infarction. Lancet
1. Rees
2
1985; ii 300-03. 3. Pnce WH, Moms SW, Burgon R, Donald PM, Kitchin AH. Apolipoprotein C-III polymorphism and coronary heart disease. Lancet 1986; ii: 1041. 4. Aalto-Setala K, Kontula K, Sane T, Nieminen M, Nikkila E. DNA polymorphisms of and insulin genes in familial hypertriglyceridemia and coronary heart disease. Atherosclerosis 1987, 66: 145-52. 5. Paulweber B, Friedl W, Krempler F, Humphries SE, Sandhofer F. Genetic variation in the apolipoprotein AI-CIII-AIV gene cluster and coronary heart disease. Atherosclerosis 1988, 73: 125-33. 6. Tas S. Strong association of a single nucleotide substitution in the 3’-untranslated region of the apolipoprotein-CIII gene with hypertriglyceridemia in Arabs. Clin Chem 1989, 35: 256-59. 7. Ito Y, Azrolan N, O’Connel A, Walsh A, Breslow JL. Hypertriglyceridemia as a result of human apo CIII gene expression in transgenic mice. Science 1990; 249: 790-93. 8. Kamel BS, Martinez OB. Food habits and nutrient intake of Kuwaiti males and females. Ecol Food Nutr 1985; 15: 261-72
apolipoprotein A-1/CIII
Assessing neglect
in stroke
patients
SiR,—Dr Nicklason and Dr Finacune (Dec 1, p 1380) describe a "hanging spectacles" sign of neglect in stroke. The "pointing to objects" test, with Albert’s test of line cancellation2 and signs such as "hanging spectacles", forms a 2 minute battery allowing a busy clinician to detect 90% of cases of neglect in acute stroke, using only a pencil and paper. We studied 171 consecutive patients with an acute stroke (69 right hemisphere, 102 left hemisphere). Patients 3 were examined at 2-3 days for visual neglect by a modified version3 of the behavioural inattention test battery,4 which includes line cancellation and pointing to objects. Line cancellation is fully described elsewhere.2,4In the other test1 the patient was asked to point to and/or name all the objects he or she could see on both sides scattered about the hospital room or ward. The examiner stood directly behind the patient and made sure that the distribution of objects on the left and right hand sides was roughly the same. Using a photocopy of a closed semicircle, with the position of the patient’s head marked at the centre of the base and with marks on the circumference at 45, 90, and 135°, the examiner noted which objects were situated at 0, 45, 90, 135, and 180° and used these as landmarks. When the patient pointed to or named objects in the room the examiner marked their approximate position relative to the landmarks and estimated the number of degrees omitted (figure). 98 patients (50 right, 48 left hemisphere) were found to have visual neglect on the modified battery. 59 had neglect on cancellation (31 right, 28 left hemisphere). 60 patients had neglect on pointing (35 right, 25 left). A combination of lines and pointing detected neglect in 80 patients (43 right, 37 left). Of the 18 patients whose neglect was only apparent on other tests in the modified battery’ there were 7 whose general spontaneous behaviour during examination suggested an inability to orientate to contralesional environmental stimuli. Examples of these included people approaching, noises or activity in the ward,5,6hanging spectacles,’ failure to shave the neglected sideor lack of awareness of contralesional limbs.s Thus a pocket battery of pointing to objects, line cancellation, and observation of a patient’s behaviour detected
in nearly 90% of neglect patients. Physicians should routinely apply these tests in the early assessment of stroke patients to direct occupational therapists towards the further evaluation and treatment of a perceptual disorder that might be an obstacle to
neglect
successful rehabilitation.8 Departments of Geriatrics and Neurosciences, St Bartholomew’s Hospital, London EC1A 7BE, UK
SHELDON STONE RICHARD GREENWOOD
1. Patterson A, Zangwill O. Disorders of visual space perception associated with lesions of the right cerebral hemisphere Brain 1944; 67: 331-58. 2. Albert ML. A simple test of neglect. Neurology 1973; 23: 658-64. 3. Stone SP, Wilson B, Rose FC. The development of a standard test battery to detect, measure and monitor visuo-spatial neglect in acute stroke. Int Rehab Res 1987; 10: J 110. 4 Wilson B, Cockburn J, Halligan P Development of a behavioural test of visuo-spatial neglect. Arch Phys Med 1987; 68: 98-102 5. Heilman KM, Watson RT, Valenstein E. Neglect and related disorders. In: Heilman KM, Valenstein E, eds. Clinical neuropsychology. Oxford: Oxford University Press, 1985; 243-50 6. Battersby WS, Bender MR, Pollack M, Kahn RL. Unilateral "spatial agnosia" ("inattention") in patients with cerebral lesions. Brain 1956; 79: 68-93. 7 Gordon WA, Hibbard MR, Egelko S, et al. Perceptual remediation in patients with nght brain damage: a comprehensive programme. Arch Phys Med Rehahil 1985; 66: 353-59. 8. Fullerton KJ, Mackenzie G, Stout RW. Prognostic indices in stroke Quart J Med 1988; 66: 147-62.
Endothelin, vasoconstriction, and endothelial
damage in Raynaud’s phenomenon
SiR,—Dr Zamora and colleagues (Nov 10, p 1144) report that high basal and stimulated serum endothelin concentrations might be implicated in vasoconstriction in patients with primary Raynaud’s phenomenon. However, they also emphasise that these high concentrations could be secondary to endothelial cell stimulation, since they show no association between onset of symptoms and variations from baseline endothelin values after cold stimulus. To elucidate further the importance of circulating endothelin in subjects with isolated Raynaud’s phenomenon, we investigated changes in plasma immunoreactive endothelin (irET), as well as changes in other plasma proteins known to be markers of endothelial damage, such as the von Willebrand factor (vWF) and the antigen of tissue-plasminogen activator (tPA).1,2 5 men and 10 women (mean age 43 [6]) were compared with a group of healthy controls (4 men, 6 women, mean age 38 [3]) at baseline conditions and after immersion of the hand in water at about 3°C. All patients had the characteristic microvascular abnormalities of the finger nailfold, according to Maricq’s3 classification (IID or greater); none had signs or symptoms suggesting an underlying connective tissue disorder. Raynaud’s phenomenon was seen in 4 patients after immersion in cold water but in none of the controls. Plasma irET was measured with a commercial radioimmunoassay (endothelin-1,2 [l2sl], RPA 535, Amersham, UK) with magnetic separation of the antibody-bound fraction. The patients’ irET values were 5-4 (1-3) fmol/ml at baseline and 5-7 (2-0) fmol/ml after immersion in cold water. The corresponding values for the controls were 4-2 (0-7) and 46 (12) fmol/ml. The two values within each group did not differ significantly, but there was a small difference (p < 0-01; unpaired t-test) between baseline values in the controls and the patients.
(or a linked mutation) might lead to these changes by causing overexpression of apo-Cl 11.6,7 Irrespective of the molecular mechanisms, the finding of the S2 allele in a large proportion of Arab MI patients (36/79,46%) is noteworthy. Dietary excesses (eg, overconsumption of sugar and sweets8) and the high prevalence of type-II diabetes mellitus among Arabs in Kuwait (N.A. Abdella, personal communication), along with other risk factors, may have contributed to the strength of the association of the S2 allele with CHD. The relation of this allele to CHD should be studied in other populations with attention to co-existing risk factors. Department of Pathology, Kuwait University Faculty of Medicine, and Clinical Chemistry Laboratory, Mubarak Al-Kabeer Hospital, Safat 13110, Kuwait *Present address. Samur Sokak 29/12,
Pointing to objects test. SINAN TAS* Saray Apt, Kurtulus, Ankara, Turkey.
A, Stocks J, Sharpe CR, et al. Deooxyribonucleic acid polymorphism m the apolipoprotein A-1-C-III gene cluster Association with hypertriglyceridemia. J Clin Invest 1985; 76: 1090-95 Ferns GAA, Ritchie C, Stocks J, Galton DJ. Genetic polymorphisms of apolipoprotein C-III and insulin in survivors of myocardial infarction. Lancet
1. Rees
2
1985; ii 300-03. 3. Pnce WH, Moms SW, Burgon R, Donald PM, Kitchin AH. Apolipoprotein C-III polymorphism and coronary heart disease. Lancet 1986; ii: 1041. 4. Aalto-Setala K, Kontula K, Sane T, Nieminen M, Nikkila E. DNA polymorphisms of and insulin genes in familial hypertriglyceridemia and coronary heart disease. Atherosclerosis 1987, 66: 145-52. 5. Paulweber B, Friedl W, Krempler F, Humphries SE, Sandhofer F. Genetic variation in the apolipoprotein AI-CIII-AIV gene cluster and coronary heart disease. Atherosclerosis 1988, 73: 125-33. 6. Tas S. Strong association of a single nucleotide substitution in the 3’-untranslated region of the apolipoprotein-CIII gene with hypertriglyceridemia in Arabs. Clin Chem 1989, 35: 256-59. 7. Ito Y, Azrolan N, O’Connel A, Walsh A, Breslow JL. Hypertriglyceridemia as a result of human apo CIII gene expression in transgenic mice. Science 1990; 249: 790-93. 8. Kamel BS, Martinez OB. Food habits and nutrient intake of Kuwaiti males and females. Ecol Food Nutr 1985; 15: 261-72
apolipoprotein A-1/CIII
Assessing neglect
in stroke
patients
SiR,—Dr Nicklason and Dr Finacune (Dec 1, p 1380) describe a "hanging spectacles" sign of neglect in stroke. The "pointing to objects" test, with Albert’s test of line cancellation2 and signs such as "hanging spectacles", forms a 2 minute battery allowing a busy clinician to detect 90% of cases of neglect in acute stroke, using only a pencil and paper. We studied 171 consecutive patients with an acute stroke (69 right hemisphere, 102 left hemisphere). Patients 3 were examined at 2-3 days for visual neglect by a modified version3 of the behavioural inattention test battery,4 which includes line cancellation and pointing to objects. Line cancellation is fully described elsewhere.2,4In the other test1 the patient was asked to point to and/or name all the objects he or she could see on both sides scattered about the hospital room or ward. The examiner stood directly behind the patient and made sure that the distribution of objects on the left and right hand sides was roughly the same. Using a photocopy of a closed semicircle, with the position of the patient’s head marked at the centre of the base and with marks on the circumference at 45, 90, and 135°, the examiner noted which objects were situated at 0, 45, 90, 135, and 180° and used these as landmarks. When the patient pointed to or named objects in the room the examiner marked their approximate position relative to the landmarks and estimated the number of degrees omitted (figure). 98 patients (50 right, 48 left hemisphere) were found to have visual neglect on the modified battery. 59 had neglect on cancellation (31 right, 28 left hemisphere). 60 patients had neglect on pointing (35 right, 25 left). A combination of lines and pointing detected neglect in 80 patients (43 right, 37 left). Of the 18 patients whose neglect was only apparent on other tests in the modified battery’ there were 7 whose general spontaneous behaviour during examination suggested an inability to orientate to contralesional environmental stimuli. Examples of these included people approaching, noises or activity in the ward,5,6hanging spectacles,’ failure to shave the neglected sideor lack of awareness of contralesional limbs.s Thus a pocket battery of pointing to objects, line cancellation, and observation of a patient’s behaviour detected
in nearly 90% of neglect patients. Physicians should routinely apply these tests in the early assessment of stroke patients to direct occupational therapists towards the further evaluation and treatment of a perceptual disorder that might be an obstacle to
neglect
successful rehabilitation.8 Departments of Geriatrics and Neurosciences, St Bartholomew’s Hospital, London EC1A 7BE, UK
SHELDON STONE RICHARD GREENWOOD
1. Patterson A, Zangwill O. Disorders of visual space perception associated with lesions of the right cerebral hemisphere Brain 1944; 67: 331-58. 2. Albert ML. A simple test of neglect. Neurology 1973; 23: 658-64. 3. Stone SP, Wilson B, Rose FC. The development of a standard test battery to detect, measure and monitor visuo-spatial neglect in acute stroke. Int Rehab Res 1987; 10: J 110. 4 Wilson B, Cockburn J, Halligan P Development of a behavioural test of visuo-spatial neglect. Arch Phys Med 1987; 68: 98-102 5. Heilman KM, Watson RT, Valenstein E. Neglect and related disorders. In: Heilman KM, Valenstein E, eds. Clinical neuropsychology. Oxford: Oxford University Press, 1985; 243-50 6. Battersby WS, Bender MR, Pollack M, Kahn RL. Unilateral "spatial agnosia" ("inattention") in patients with cerebral lesions. Brain 1956; 79: 68-93. 7 Gordon WA, Hibbard MR, Egelko S, et al. Perceptual remediation in patients with nght brain damage: a comprehensive programme. Arch Phys Med Rehahil 1985; 66: 353-59. 8. Fullerton KJ, Mackenzie G, Stout RW. Prognostic indices in stroke Quart J Med 1988; 66: 147-62.
Endothelin, vasoconstriction, and endothelial
damage in Raynaud’s phenomenon
SiR,—Dr Zamora and colleagues (Nov 10, p 1144) report that high basal and stimulated serum endothelin concentrations might be implicated in vasoconstriction in patients with primary Raynaud’s phenomenon. However, they also emphasise that these high concentrations could be secondary to endothelial cell stimulation, since they show no association between onset of symptoms and variations from baseline endothelin values after cold stimulus. To elucidate further the importance of circulating endothelin in subjects with isolated Raynaud’s phenomenon, we investigated changes in plasma immunoreactive endothelin (irET), as well as changes in other plasma proteins known to be markers of endothelial damage, such as the von Willebrand factor (vWF) and the antigen of tissue-plasminogen activator (tPA).1,2 5 men and 10 women (mean age 43 [6]) were compared with a group of healthy controls (4 men, 6 women, mean age 38 [3]) at baseline conditions and after immersion of the hand in water at about 3°C. All patients had the characteristic microvascular abnormalities of the finger nailfold, according to Maricq’s3 classification (IID or greater); none had signs or symptoms suggesting an underlying connective tissue disorder. Raynaud’s phenomenon was seen in 4 patients after immersion in cold water but in none of the controls. Plasma irET was measured with a commercial radioimmunoassay (endothelin-1,2 [l2sl], RPA 535, Amersham, UK) with magnetic separation of the antibody-bound fraction. The patients’ irET values were 5-4 (1-3) fmol/ml at baseline and 5-7 (2-0) fmol/ml after immersion in cold water. The corresponding values for the controls were 4-2 (0-7) and 46 (12) fmol/ml. The two values within each group did not differ significantly, but there was a small difference (p < 0-01; unpaired t-test) between baseline values in the controls and the patients.
