1198
in patients with coronary heart disease and left ventricular impairment.9 Rather, the J phenomenon represents the association of low blood pressure with more severe left ventricular impairment, which is the primary determinant of risk. 10 What are the possible mechanisms of prevention of recurrent myocardial infarction and unstable angina with ACE inhibition? Blood pressure reduction and reduced myocardial oxygen demand through preload and afterload reduction may be relevant. In the long term, prevention of chronic ventricular dilatation and myocardial hypertrophy will likewise reduce myocardial oxygen demand. Blockade of the potential coronary vasoconstrictor and inotropic effects of angiotensin II11,12 may be important. Experimental studies indicate an additional vascular protective and possible antiatherosclerotic role for ACE inhibitors. Endothelial function may be preserved or restored with converting enzyme inhibition, possibly through bradykinin accumulation.13 Inhibition of angiotensin II and other growth factors could reduce progression of atherosclerosis. 14,15 In the context of accelerated atherosclerosis due to arterial injury, the remarkable effects of converting enzyme inhibition on intimal/medial proliferation in laboratory animals16,17 have not been replicated in patients after angioplasty.18 Possible reasons for this discrepancy are species differences in injury and treatment responses, different doses, and the lack of treatment before angioplasty. Studies in Watanabe heritable hyperlipidaemic rabbits19 and cholesterolfed cynomolgus monkeys20 showed a striking protective effect of ACE inhibition on spontaneous atherosclerosis. By contrast, beta-blockade and calcium-channel blockade were ineffective in preventing atherosclerosis in similar animal models, despite blood pressure reduction.21,22 Clinical studies are now being conducted to assess the protective effects of ACE inhibitors on progression of atherosclerosis and related clinical ischaemic events in high-risk groups. There are probably several mechanisms of action and there may well be useful primary or adjunctive vascular protective effects from converting enzyme inhibition when the drugs are used for established indications. The next few years should bring into perspective the overall value of vascular protection with these agents.
Scandinavian Enalapril Survival Study II (CONSENSUS II).
mortality
JM, Pfeffer MA, Braunwald E. Influence of chronic captopril therapy on the infarcted left ventricle of the rat. Circ Res 1985; 57:
1. Pfeffer
84-95.
Sharpe N, Murphy J, Smith H, Hannan S. Treatment of patients with symptomless left ventricular dysfunction after myocardial infarction. Lancet 1988; i: 255-59. 3. Pfeffer MA, Lamas GA, Vaughan DE, Parisi AF, Braunwald E. Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. N Engl J Med 1988; 319: 80-86. 4. Sharpe N, Smith H, Murphy J, Greaves S, Hart H, Gamble G. Early prevention of left ventricular dysfunction after myocardial infarction with angiotensin-converting-enzyme inhibition. Lancet 1991; 337: 2.
872-76. 5.
Swedberg K, Held P, Kjekshus J, Rasmussen K, Ryden L, Wedel H. Effects of the early administration of enalapril on mortality in patients with acute myocardial infarction: results of the Cooperative New
N Engl
J Med 1992; 327: 678-84. Investigators. Effect of enalapnl on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med 1992, 327: 685-91. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopnl on mortality and morbidity in patients with left ventricular dysfunction
6. The SOLVD
7.
myocardial infarction: results of the Survival and Ventricular Enlargement Trial. N Engl J Med 1992; 327: 669-77. 8. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium: fibrosis and renin-angiotensin-aldosterone system. after
Circulation 1991; 83: 1849-65. 9.
D’Agostino RB, Belanger AJ, Kannel WB, Cruickshank JM. Relation of
low diastolic blood pressure to coronary heart disease death in presence of myocardial infarction: the Framingham Study. BMJ 1991; 303: 385-89. 10. MacMahon S, Sharpe N. The J curve phenomenon in the treatment of hypertension. JAMA 1991; 266: 64-65. 11. Gavras H, Brown JJ, Lever AF, Macadam RF, Robertson JIS. Acute renal failure, tubular necrosis, and myocardial infarction induced in the rabbit by intravenous angiotensin II. Lancet 1971; ii: 19-22. 12. Kiowski W, Zuber M, Elsasser S, Eme P, Pfisterer M, Burkart F. Coronary vasodilatation and improved myocardial lactate metabolism after angiotensin converting enzyme inhibition with enalapril in patients with congestive heart failure. Am Heart J 1991; 122: 1382-88. 13. Becker RHA, Wiemer G, Linz W. Preservation of endothelial function by ramipril in rabbits on a long-term atherogenic diet. J Cardiovasc Pharmacol 1991; 18 (suppl): S110-15. 14. Daemen MJAP, Lombardi DM, Bosman FT, Schwartz SM. Angiotensin II induces smooth muscle cell proliferation in the normal and injured rat arterial wall. Circ Res 1991; 68: 450-56. 15. Naftilan AJ, Pratt RE, Dzau VJ. Induction of platelet-derived growth factor A-chain and c-myc gene expressions by angiotensin II in cultured rat vascular smooth muscle cells. J Clin Invest 1989; 83: 1419-24. 16. Powell JS, Clozel JP, Muller RKM, et al. Inhibitors of angiotensinconverting enzyme prevent myointimal proliferation after vascular injury. Science 1989; 245: 186-88. 17. Plissonnier D, Amichot G, Duriez M, Legagneux J, Levy BI, Michel JB. Effect of converting enzyme inhibition on allograft-induced arterial wall injury and response. Hypertension 1991; 18 (suppl II): 47-54. 18. MERCATOR Study Group. Does the new angiotensin converting enzyme inhibitor cliazapril prevent restenosis after percutaneous transluminal coronary angioplasty? Circulation 1992; 86: 100-10. 19. Chobanian AV, Haudenschild CC, Nickerson C, Drago R. Antiatherogenic effect of captopril in the Watanabe heritable hyperlipidemic rabbit. Hypertension 1990; 15: 327-31. 20. Aberg G, Ferrer P. Effects of captopril on atherosclerosis in cynomolgus monkeys. J Cardiovasc Pharmacol 1990; 15 (suppl 5): S65-72. 21. Lichenstein AH, Drago R, Nickerson C, Prescott MF, Lee SQ. Chobanian AV. The effect of propranolol on atherogenesis in the Watanabe heritable hyperlipidemic rabbit. J Vasc Med Biol 1989; 1: 248-54. 22. Ferrer P, Aberg G. Progression of atherosclerosis in cholesterol-fed cynomolgus monkeys during treatment with nifedipine. FASEBJ 1990; 4: A1151.
Shaving the head:
reason or
ritual?
Since the days of Harvey Cushing, shaving of the entire skull before cranial surgery has been a
approved of by many neurosurgeons, dreaded by most patients. Advocates of the policy mention the tendency of hair to harbour bacteria, the difficulty of planning incisions on a hairy scalp, the need to disclose all scalp injuries widely
accepted
practice,
after trauma, and the convenience of wound suture and application (and removal) of dressings. Older surgeons will even recall the loving care with which their chief applied a whole-head dressing and bandage
after In
craniotomy. 1948, Rowbotham1 emphasised the need
shave the whole head in
to
of head trauma in 1952, made the same cases
requiring operation. Oliver,2 recommendation for patients requiring operation for
1199
brain tumour. At the same time, it was emphasised that the eyebrows should never be shaved off, even when surgical incisions were required in that zone. After the advent of the operating microscope in the late 1960s, the size of craniotomy opening of the skull decreased, scalp incisions became smaller, sutures gave way to stapling for skin closure, the full-head bandage yielded to smaller transparent medicated adhesive dressings, and many neurosurgeons stopped shaving the entire scalp for elective craniotomy.33 Some believed that it was necessary only to clip, rather than shave, the hair at the wound site; this approach allowed faster regrowth of hair. In 1981, Court-Brown4 reported a comparison between skin shaving, depilation by skin cream, and no removal of hair before abdominal surgery. Skin depilation was shown not to decrease the postoperative infection rate; shaving the skin seemed to increase the risk of infection. Tenney and his colleagues5 found a very wide range of postoperative wound infection with an eleven-fold variation in infection rate following craniotomy for different neurosurgical conditions. Thus it is very hard to tell whether any particular regimen significantly reduces the infection rate. For 10 years or more, plastic surgeons have been recommending that all hair be left in patients with scalp lacerations.6 Most neurosurgeons, however, still prefer to shave all or part of the scalp before craniotomy. Winstonnow goes further and questions the need to remove any hair at all before cranial surgery. Patients were asked to shampoo with chlorhexidine the night before surgery. The entire operative region was scrubbed for eight minutes after anaesthetic induction, irrigated with alcohol, and the hair parted at the proposed incision site and tied back. Surgical drapes were stapled to the scalp. By use of this regimen, combined with prophylactic antibiotics, low postoperative infection rates were achieved that compare favourably with other series in which "conventional" head shaving was used (this was not a controlled study). What can one conclude from this evidence? Provided careful attention is paid to preoperative scalp and hair preparation, omission of head shaving does not seem to increase the postoperative infection rate. Nevertheless, the intensive skin preparation is timeconsuming, and many neurosurgeons would fmd it a nuisance to have long hairs entering the operative field. Application of the wound dressing is likewise less convenient. For the many patients whose cranial surgical approach today is by a small pterional craniotomy, with the skin incision just within the hairline, the very limited amount of hair removed is unobtrusive and usually accepted without demur.
The same applies to patients having retrosigmoid approaches to the posterior cranial fossa, in whom
only the small area of scalp behind the ear needs to be clipped. However, in the comatose head injured patient in whom there may be multiple areas of scalp
obvious and others less will so, neurosurgeons surely continue to advocate removal of all scalp hair, by clipping at least, to permit thorough examination before surgical treatment. Failure to disclose and treat a small compound head wound that proceeds to intracranial infection is too high a price to pay for the cosmetic benefits of retention of all scalp hair. laceration and bruising,
some
most
1. Rowbotham GF. Acute injuries of the head. Edinburgh: Livingstone, 1949: 210. 2. Oliver LC. Essentials of neurosurgery. London: Lewis, 1952: 26. 3. Wilkins RH, Odom GL. General operative technique. In: Youmans J, ed. Neurological surgery. 2nd ed. Philadelphia: Saunders, 1982: 1136
(vol 2). 4. Court-Brown CM.
5.
Preoperative skin depilation and its effect on post-operative wound infections. J R Coll Surg Edin 1981; 26: 238-41. Tenney JW, Vlahov D, Salcman M, Ducker TB. Wide variation in risk of wound infection following clean neurosurgery. J Neurosurg 1985; 62:
243-47. 6. Baker DC, Kaplan HY. In: Cooper PR, ed. Head injury. 2nd ed. Baltimore: Williams & Williams, 1987: 356. 7. Winston KR. Hair and neurosurgery. Neurosurgery 1992; 31: 320-29.
Changing case-definition
for AIDS
The Centers for Disease Control (CDC), in a public letter to the Council of State and Territorial Epidemiologists, state they anticipate publication of an expanded AIDS surveillance case-definition for the United States in December, with implementation from January, 1993 (see Lancet Nov 7, p 1151).1 In the short term this change in the US means that many more persons infected with human immunodeficiency virus (HIV) will meet the AIDS case-definition. 3 more diseases in HIV-infected individualspulmonary tuberculosis, recurrent pneumonia, and invasive cervical cancer-may be added to the existing list of 23 AID S-defming conditions. In addition, all HIV-infected adolescents and adults in the US without any of the expanded list of 26 conditions but who have less than 200 CD4 T lymphocytes/µl (or CD4 percentage less than 14) will be defined as having AIDS. A consistently applied case-definition is essential to the surveillance of any disease. The earliest AIDS case-definition included conditions at least moderately indicative of cellular immune dysfunction to characterise aspects of what was, in 1981, a newly recognised disease.3Major revisions to this initial case definition incorporating extra knowledge were made in 1985 and 1987.3,4 Conditions were added in 1987 which, combined with laboratory evidence of HIV infection and in the absence of other causes of cellular immune dysfunction, had sufficient positive predictive value to be of use for surveillance. The current World Health Organisation/CDC definition for AID S5 has been the standard in developed countries, but elsewhere other definitions that are less dependent on technical support are more appropriate. With more widespread use of prophylaxis and antiretroviral therapy for those known to be HIV infected, AIDS is perceived by many clinicians as a
in patients with coronary heart disease and left ventricular impairment.9 Rather, the J phenomenon represents the association of low blood pressure with more severe left ventricular impairment, which is the primary determinant of risk. 10 What are the possible mechanisms of prevention of recurrent myocardial infarction and unstable angina with ACE inhibition? Blood pressure reduction and reduced myocardial oxygen demand through preload and afterload reduction may be relevant. In the long term, prevention of chronic ventricular dilatation and myocardial hypertrophy will likewise reduce myocardial oxygen demand. Blockade of the potential coronary vasoconstrictor and inotropic effects of angiotensin II11,12 may be important. Experimental studies indicate an additional vascular protective and possible antiatherosclerotic role for ACE inhibitors. Endothelial function may be preserved or restored with converting enzyme inhibition, possibly through bradykinin accumulation.13 Inhibition of angiotensin II and other growth factors could reduce progression of atherosclerosis. 14,15 In the context of accelerated atherosclerosis due to arterial injury, the remarkable effects of converting enzyme inhibition on intimal/medial proliferation in laboratory animals16,17 have not been replicated in patients after angioplasty.18 Possible reasons for this discrepancy are species differences in injury and treatment responses, different doses, and the lack of treatment before angioplasty. Studies in Watanabe heritable hyperlipidaemic rabbits19 and cholesterolfed cynomolgus monkeys20 showed a striking protective effect of ACE inhibition on spontaneous atherosclerosis. By contrast, beta-blockade and calcium-channel blockade were ineffective in preventing atherosclerosis in similar animal models, despite blood pressure reduction.21,22 Clinical studies are now being conducted to assess the protective effects of ACE inhibitors on progression of atherosclerosis and related clinical ischaemic events in high-risk groups. There are probably several mechanisms of action and there may well be useful primary or adjunctive vascular protective effects from converting enzyme inhibition when the drugs are used for established indications. The next few years should bring into perspective the overall value of vascular protection with these agents.
Scandinavian Enalapril Survival Study II (CONSENSUS II).
mortality
JM, Pfeffer MA, Braunwald E. Influence of chronic captopril therapy on the infarcted left ventricle of the rat. Circ Res 1985; 57:
1. Pfeffer
84-95.
Sharpe N, Murphy J, Smith H, Hannan S. Treatment of patients with symptomless left ventricular dysfunction after myocardial infarction. Lancet 1988; i: 255-59. 3. Pfeffer MA, Lamas GA, Vaughan DE, Parisi AF, Braunwald E. Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. N Engl J Med 1988; 319: 80-86. 4. Sharpe N, Smith H, Murphy J, Greaves S, Hart H, Gamble G. Early prevention of left ventricular dysfunction after myocardial infarction with angiotensin-converting-enzyme inhibition. Lancet 1991; 337: 2.
872-76. 5.
Swedberg K, Held P, Kjekshus J, Rasmussen K, Ryden L, Wedel H. Effects of the early administration of enalapril on mortality in patients with acute myocardial infarction: results of the Cooperative New
N Engl
J Med 1992; 327: 678-84. Investigators. Effect of enalapnl on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med 1992, 327: 685-91. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopnl on mortality and morbidity in patients with left ventricular dysfunction
6. The SOLVD
7.
myocardial infarction: results of the Survival and Ventricular Enlargement Trial. N Engl J Med 1992; 327: 669-77. 8. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium: fibrosis and renin-angiotensin-aldosterone system. after
Circulation 1991; 83: 1849-65. 9.
D’Agostino RB, Belanger AJ, Kannel WB, Cruickshank JM. Relation of
low diastolic blood pressure to coronary heart disease death in presence of myocardial infarction: the Framingham Study. BMJ 1991; 303: 385-89. 10. MacMahon S, Sharpe N. The J curve phenomenon in the treatment of hypertension. JAMA 1991; 266: 64-65. 11. Gavras H, Brown JJ, Lever AF, Macadam RF, Robertson JIS. Acute renal failure, tubular necrosis, and myocardial infarction induced in the rabbit by intravenous angiotensin II. Lancet 1971; ii: 19-22. 12. Kiowski W, Zuber M, Elsasser S, Eme P, Pfisterer M, Burkart F. Coronary vasodilatation and improved myocardial lactate metabolism after angiotensin converting enzyme inhibition with enalapril in patients with congestive heart failure. Am Heart J 1991; 122: 1382-88. 13. Becker RHA, Wiemer G, Linz W. Preservation of endothelial function by ramipril in rabbits on a long-term atherogenic diet. J Cardiovasc Pharmacol 1991; 18 (suppl): S110-15. 14. Daemen MJAP, Lombardi DM, Bosman FT, Schwartz SM. Angiotensin II induces smooth muscle cell proliferation in the normal and injured rat arterial wall. Circ Res 1991; 68: 450-56. 15. Naftilan AJ, Pratt RE, Dzau VJ. Induction of platelet-derived growth factor A-chain and c-myc gene expressions by angiotensin II in cultured rat vascular smooth muscle cells. J Clin Invest 1989; 83: 1419-24. 16. Powell JS, Clozel JP, Muller RKM, et al. Inhibitors of angiotensinconverting enzyme prevent myointimal proliferation after vascular injury. Science 1989; 245: 186-88. 17. Plissonnier D, Amichot G, Duriez M, Legagneux J, Levy BI, Michel JB. Effect of converting enzyme inhibition on allograft-induced arterial wall injury and response. Hypertension 1991; 18 (suppl II): 47-54. 18. MERCATOR Study Group. Does the new angiotensin converting enzyme inhibitor cliazapril prevent restenosis after percutaneous transluminal coronary angioplasty? Circulation 1992; 86: 100-10. 19. Chobanian AV, Haudenschild CC, Nickerson C, Drago R. Antiatherogenic effect of captopril in the Watanabe heritable hyperlipidemic rabbit. Hypertension 1990; 15: 327-31. 20. Aberg G, Ferrer P. Effects of captopril on atherosclerosis in cynomolgus monkeys. J Cardiovasc Pharmacol 1990; 15 (suppl 5): S65-72. 21. Lichenstein AH, Drago R, Nickerson C, Prescott MF, Lee SQ. Chobanian AV. The effect of propranolol on atherogenesis in the Watanabe heritable hyperlipidemic rabbit. J Vasc Med Biol 1989; 1: 248-54. 22. Ferrer P, Aberg G. Progression of atherosclerosis in cholesterol-fed cynomolgus monkeys during treatment with nifedipine. FASEBJ 1990; 4: A1151.
Shaving the head:
reason or
ritual?
Since the days of Harvey Cushing, shaving of the entire skull before cranial surgery has been a
approved of by many neurosurgeons, dreaded by most patients. Advocates of the policy mention the tendency of hair to harbour bacteria, the difficulty of planning incisions on a hairy scalp, the need to disclose all scalp injuries widely
accepted
practice,
after trauma, and the convenience of wound suture and application (and removal) of dressings. Older surgeons will even recall the loving care with which their chief applied a whole-head dressing and bandage
after In
craniotomy. 1948, Rowbotham1 emphasised the need
shave the whole head in
to
of head trauma in 1952, made the same cases
requiring operation. Oliver,2 recommendation for patients requiring operation for
1199
brain tumour. At the same time, it was emphasised that the eyebrows should never be shaved off, even when surgical incisions were required in that zone. After the advent of the operating microscope in the late 1960s, the size of craniotomy opening of the skull decreased, scalp incisions became smaller, sutures gave way to stapling for skin closure, the full-head bandage yielded to smaller transparent medicated adhesive dressings, and many neurosurgeons stopped shaving the entire scalp for elective craniotomy.33 Some believed that it was necessary only to clip, rather than shave, the hair at the wound site; this approach allowed faster regrowth of hair. In 1981, Court-Brown4 reported a comparison between skin shaving, depilation by skin cream, and no removal of hair before abdominal surgery. Skin depilation was shown not to decrease the postoperative infection rate; shaving the skin seemed to increase the risk of infection. Tenney and his colleagues5 found a very wide range of postoperative wound infection with an eleven-fold variation in infection rate following craniotomy for different neurosurgical conditions. Thus it is very hard to tell whether any particular regimen significantly reduces the infection rate. For 10 years or more, plastic surgeons have been recommending that all hair be left in patients with scalp lacerations.6 Most neurosurgeons, however, still prefer to shave all or part of the scalp before craniotomy. Winstonnow goes further and questions the need to remove any hair at all before cranial surgery. Patients were asked to shampoo with chlorhexidine the night before surgery. The entire operative region was scrubbed for eight minutes after anaesthetic induction, irrigated with alcohol, and the hair parted at the proposed incision site and tied back. Surgical drapes were stapled to the scalp. By use of this regimen, combined with prophylactic antibiotics, low postoperative infection rates were achieved that compare favourably with other series in which "conventional" head shaving was used (this was not a controlled study). What can one conclude from this evidence? Provided careful attention is paid to preoperative scalp and hair preparation, omission of head shaving does not seem to increase the postoperative infection rate. Nevertheless, the intensive skin preparation is timeconsuming, and many neurosurgeons would fmd it a nuisance to have long hairs entering the operative field. Application of the wound dressing is likewise less convenient. For the many patients whose cranial surgical approach today is by a small pterional craniotomy, with the skin incision just within the hairline, the very limited amount of hair removed is unobtrusive and usually accepted without demur.
The same applies to patients having retrosigmoid approaches to the posterior cranial fossa, in whom
only the small area of scalp behind the ear needs to be clipped. However, in the comatose head injured patient in whom there may be multiple areas of scalp
obvious and others less will so, neurosurgeons surely continue to advocate removal of all scalp hair, by clipping at least, to permit thorough examination before surgical treatment. Failure to disclose and treat a small compound head wound that proceeds to intracranial infection is too high a price to pay for the cosmetic benefits of retention of all scalp hair. laceration and bruising,
some
most
1. Rowbotham GF. Acute injuries of the head. Edinburgh: Livingstone, 1949: 210. 2. Oliver LC. Essentials of neurosurgery. London: Lewis, 1952: 26. 3. Wilkins RH, Odom GL. General operative technique. In: Youmans J, ed. Neurological surgery. 2nd ed. Philadelphia: Saunders, 1982: 1136
(vol 2). 4. Court-Brown CM.
5.
Preoperative skin depilation and its effect on post-operative wound infections. J R Coll Surg Edin 1981; 26: 238-41. Tenney JW, Vlahov D, Salcman M, Ducker TB. Wide variation in risk of wound infection following clean neurosurgery. J Neurosurg 1985; 62:
243-47. 6. Baker DC, Kaplan HY. In: Cooper PR, ed. Head injury. 2nd ed. Baltimore: Williams & Williams, 1987: 356. 7. Winston KR. Hair and neurosurgery. Neurosurgery 1992; 31: 320-29.
Changing case-definition
for AIDS
The Centers for Disease Control (CDC), in a public letter to the Council of State and Territorial Epidemiologists, state they anticipate publication of an expanded AIDS surveillance case-definition for the United States in December, with implementation from January, 1993 (see Lancet Nov 7, p 1151).1 In the short term this change in the US means that many more persons infected with human immunodeficiency virus (HIV) will meet the AIDS case-definition. 3 more diseases in HIV-infected individualspulmonary tuberculosis, recurrent pneumonia, and invasive cervical cancer-may be added to the existing list of 23 AID S-defming conditions. In addition, all HIV-infected adolescents and adults in the US without any of the expanded list of 26 conditions but who have less than 200 CD4 T lymphocytes/µl (or CD4 percentage less than 14) will be defined as having AIDS. A consistently applied case-definition is essential to the surveillance of any disease. The earliest AIDS case-definition included conditions at least moderately indicative of cellular immune dysfunction to characterise aspects of what was, in 1981, a newly recognised disease.3Major revisions to this initial case definition incorporating extra knowledge were made in 1985 and 1987.3,4 Conditions were added in 1987 which, combined with laboratory evidence of HIV infection and in the absence of other causes of cellular immune dysfunction, had sufficient positive predictive value to be of use for surveillance. The current World Health Organisation/CDC definition for AID S5 has been the standard in developed countries, but elsewhere other definitions that are less dependent on technical support are more appropriate. With more widespread use of prophylaxis and antiretroviral therapy for those known to be HIV infected, AIDS is perceived by many clinicians as a
