- Email: [email protected]
Carotid and Vertebral Artery Transluminal Angioplasty Study
THE LANCET
The first study2 compared laparoscopic with minicholecystectomy and showed that the former was much more expensive than the latter. When reusable instruments were used this difference was £93 (95% CI £25–162), based on an increase in theatre costs caused by the extra time required for laparoscopic cholecystectomy (14 min). I would point out that this difference is academic, since undertaking a laparoscopic cholecystectomy, or indeed several procedures, did not result in any change in the number of patients placed on our operating list or an over-run in operating time during the study period. In my experience, operating time for laparoscopic cholecystectomy has dropped substantially since that time, from a median of 65 (46–70) to 50 (40–66) min (p=0·004).3 This fall is principally due to the fact that the learning curve for laparoscopic cholecystectomy is much longer than had been anticipated when the randomised trial was set up.2 The second study is the Medical Research Council trial funded to evaluate laparoscopic hernia repair. This trial does not compare laparoscopic hernia repair with many diffuse open methods, as Johnson suggests. The laparoscopic group is almost exclusively the totally extraperitoneal approach to hernia repair, which is not different from its open preperitoneal equivalent. Over 90% of patients in the open group have had a tension-free repair hernioplasty and a few have had other open procedures when use of mesh was considered unnecessary, eg, in a Nyhus type 1 hernia in a young adult. P J O’Dwyer Department of Surgery, Western Infirmary, Glasgow G11 6NT, UK
1 2
3
Johnson A. Laparoscopic surgery. Lancet 1997; 349: 631–35. McMahon AJ, Russell IT, Baxter JN. Laparoscopic versus minilaparotomy cholecystectomy: a randomised trial. Lancet 1994; 343: 135–38. Wallace DH, O’Dwyer PJ. Effect of a no-conversion policy on patient outcome following laparoscopic cholecystectomy. Br J Surg (in press).
SIR—Johnson1 provides data of concern regarding a question that I have previously posed but have yet to see adequately addressed.2 As I read figure 1, from 1992 to 1995 a total of roughly 3400 cholecystectomies were done in Lothian health district, of which about 600 were open procedures—ie, about 18%. In 1995 these numbers were around 840 total cholecystectomies, of which 120 were open, for a 14% rate. If this trend continues will the number of open cholecystectomies in the future
1324
be sufficient to (a) teach surgical trainees how to do this procedure, and (b) maintain previously acquired skills at a satisfactory level to allow safe conversion of the laparoscopic procedure to an open one.2 Robert Matz Mount Sinai Medical Center, Mount Sinai School of Medicine, New York, NY 10029, USA
1 2
Johnson A. Laparoscopic surgery. Lancet 1997; 349: 631–35. Matz R. The learning curve. JAMA 1994; 271: 824–25.
Carotid and Vertebral Artery Transluminal Angioplasty Study SIR—We would like to respond to the comments by Warlow and Sandercock1 and Brown and colleagues2 (March 22, p 880) concerning our essay on carotid endarterectomy versus carotid angioplasty.3 Their criticisms relate to the best method for enrolment of patients into randomised trials, the grey-area of uncertainty principle, and the denial that interim data from the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS) is being published and affecting case selection. They conclude that a consecutive study of all patients with symptoms and a carotid stenosis of greater than 70% is unethical and impractical. Warlow and Sandercock go further by saying that trial investigators need only “describe the patients they studied and not waste resources trying to describe the patients they did not”. In fact, we did recognise that a consecutive study might be impractical, but that if this was not feasible the CAVATAS investigators must standardise their selection criteria so that the results can be interpreted and applied to similarly defined groups in the future. Thus, our opinion remains unchanged on the need for a description of exclusion criteria; indeed, this approach accords with the CONSORT statement on the reporting of randomised trials.4 The grey-area principle used in the European Carotid Surgery Trial was entirely appropriate then, but we remain uneasy about its application in CAVATAS. In our essay, we noted that many clinical factors were taken into account in the recruitment of patients, but the most important consideration was the degree of carotid stenosis—something that was centrally and independently standardised within the study from the outset. No attempt was made to correlate outcome with other
angiographic variables because it was widely accepted that angiography was unable to do this reliably. However, in CAVATAS, a patient need only have a carotid stenosis of greater than 30% to be considered for randomisation—ie, standardised—but thereafter one of the main exclusion criteria in the protocol is a subjective assessment of the possibility of luminal thrombus on angiography, which is something that cannot be standardised. We therefore accept that CAVATAS will be able to make predictions of relative risk of stroke according to the degree of stenosis but not according to the many subjective assessments of plaque morphology from the contributing centres. Brown and colleagues dismiss our criticism that repeated presentations and publications from the major participating centres is inappropriate and inadvertently affects selection for CAVATAS, by stating that the trial allows for each centre to present its angioplasty data, provided that the identity of CAVATAS patients remains anonymous. However, Sivaguru and colleagues5 not only disclose the number of patients entered into CAVATAS at the time (n=193), but also that Sheffield had contributed 90 of these patients and that the rate of disabling stroke in the Sheffield patients randomised to angioplasty was 5·6%. This information is neither anonymous nor merely “the early experience”. We are also critical that the combined angioplasty experience from Sheffield and St George’s Hospital (n=85) was submitted to the 1996 European Vascular Society. The abstract published a death and anystroke rate of 8%, a figure that was made available to over 700 European vascular surgeons, many of whom were contributors to CAVATAS. Brown and colleagues refute this criticism by saying that the abstract was withdrawn. But the abstract was published in full and the paper called for presentation at the meeting. We wish to emphasise that our criticisms are not directed at any individual, but collectively Sheffield and St George’s have a responsibility because they have the greatest UK experience in carotid angioplasty and have contributed the most patients to CAVATAS. Thus, any data presented or published by them are respected and interpreted accordingly. Consequently, many surgeons have commented that if these two respected centres have an angioplasty stroke rate of 6–8%, this finding must be fairly close to the overall CAVATAS results; so is it appropriate for them to randomise patients if their own operative morbidity is lower? Whether Brown and colleagues like it or not,
Vol 349 • May 3, 1997
THE LANCET
awareness of their data invariably influences recruitment in other centres. *A R Naylor, N J M London, P R F Bell Faculty of Medicine, University of Leicester, Leicester Royal Infirmary, Leicester LE2 7LX , UK
1
2
3
4
5
Warlow C, Sandercock P. Carotid endarterectomy vs carotid angioplasty. Lancet 1997; 349: 880. Brown MM, Venebles G, Clifton A, Gaines P, Taylor RS. Carotid endarterectomy vs carotid angioplasty. Lancet 1997; 349: 880–81. Naylor AR, London NJM, Bell PRF. Carotid endarterectomy versus carotid angioplasty. Lancet 1997; 349: 203–04. Begg C, Cho M, Eastwood S, et al. Improving the quality of reporting of randomised controlled trials: the CONSORT statement. JAMA 1996; 276: 637–39. Sivaguru A, Venables GS, Beard JD, Gaines PA. European Carotid Angioplasty Trial. J Endovasc Surg 1996; 3: 16–20.
Randomised controlled trial of hydroquinine in muscle cramps SIR—Jansen and colleagues (Feb 22, p 528)1 report a randomised controlled trial of hydroquinine in muscle cramps that demonstrates the efficacy of the drug in the 2-week trial period. Hydroquinine was used because it was the only quinine derivative available to the researchers in the Netherlands for use in the prevention of muscle cramps; quinine is used in the UK. Quinine and its derivatives have potentially very serious side-effects and these must be balanced against the indiscriminate use of quinine and derivatives for an essentially benign condition such as muscle cramps.2 It is extensively metabolised by the liver but small amounts of unchanged quinine and its metabolites are excreted in the urine. The proportion of unchanged quinine excreted in the urine has been variously reported as less than 5% but up to 20%, and excretion is increased in acid urine.3 It would seem possible therefore that patients with reduced rates of glomerular filtration (including the elderly population) might be at risk from accumulation and toxicity after administration of quinine and its derivatives. Consequently, Jansen and colleagues’ suggestion that hydroquinine should be given on a regular (and presumably longer term) basis rather than as needed is perhaps premature, and potentially hazardous for patients. Muscle cramps are common in patients with chronic renal failure and in the elderly, and these two groups might be particularly vulnerable to quinine toxicity. Any study of the longer term use of
Vol 349 • May 3, 1997
quinine and its derivatives in the prevention of muscle cramps should involve very close monitoring of patients for early evidence of sideeffects, especially in those with a reduced rate of glomerular filtration. The glomerular-filtration rate should be assessed in individuals before longer term treatment is started. J R Curtis ‘Brocklea’, Westcott Street, Westcott, Dorking, Surrey RH4 3NU, UK
1
2
3
Jansen PHP, Veenhuizen KCW, Wesseling AJM, de Boo Th, Verbeck ALM. Randomised controlled trial of hydroquinine in muscle cramps. Lancet 1997; 349: 528–32. Man-Son-Hing M, Wells G. Meta-analysis of efficacy of quinine for treatment of nocturnal leg cramps in elderly people. BMJ 1995; 310: 13–17. Quinine. Martindale: the extra pharmacopoiea. 31st edn. London: Royal Pharmaceutical Society, 1996: 474–77.
SIR—Many patients might be inclined to dissent from the conclusions drawn by Jansen and colleagues1 in their comparison of the effect of hydroquinine with placebo on the frequency of leg cramps. In the active treatment group the median number of leg cramps fell from 17 during the 2-week pretreatment observation period to seven during 2 weeks of hydroquinine therapy, and continued at a low frequency of nine per 2 weeks over a 2-week washout period after discontinuation of the drug. They conclude, first, that hydroquinine greatly reduces leg cramps, and, second, that there is a carryover effect into and possibly beyond the washout period for both active treatment and placebo. Although we agree that the halving of cramp frequency is a therapeutic success, this treatment is associated with side-effects. Placebo looks like a better option. Here cramps fell from 17 per 2 weeks during pretreatment observation to 13 per 2 weeks during active placebo therapy and eight per 2 weeks during the washout period. Patients in the placebo group apparently reap the benefits of treatment without its troublesome side-effects. There is, however, another altogether more likely explanation. Although there is undoubtedly a substantial therapeutic effect of hydroquinine during the 2 weeks of active treatment, the observation of a reduction in cramps during the total 6-week period of observation almost certainly results from regression towards the mean. In studies in which patients volunteer they are more likely to show interest when the symptoms are especially troublesome, which means that, given time, they would get better anyway. A blinded review of data from our double-
blind crossover study (unpublished data) comparing the effect of magnesium citrate with placebo shows a similar trend. Ten patients reported fewer cramps during the first treatment period, one was unchanged, and 37 had fewer cramps during the second treatment period. 3–6 months after the trial, over 70% of patients had fewer cramps than before trial entry. Although this reduction might be entirely attributed to a therapeutic effect of magnesium, it is likely that here too is also an element of regression towards the mean. Since the treatment periods in our study are longer (6 weeks in each group) than those reported by Jansen et al, it will be possible to quantify the effect of time on cramp frequency and separate that from a possible treatment effect. We conclude that there is no convincing evidence of a carryover effect of hydroquinine and feel that Jansen and colleagues’ suggestion that regular use of hydroquinine is preferable to “as-required” medication is not supported by their data. *C Roffe, S Sills, P Crome Department of Geriatric Medicine, Keele University School of Postgraduate Medicine, Stoke-on-Trent ST4 7QB, UK
1
Jansen PHP, Veenhuizen KCW, Wesseling AIM, de Boo Th, Verbeek ALM. Randomised controlled trial of hydroquinine in muscle cramps. Lancet 1997; 349: 528–32.
S IR —The findings in the trial of hydroquinine in muscle cramps from the Netherlands 1 accords with the meta-analysis reported by Man-SonHing and Wells,2 which revealed that although quinine may substantially reduce the number of attacks it does not affect the severity of the attacks. So we are still left with the difficulty of how to deal with nocturnal cramp when it occurs. Moreover, in a condition that may affect 70% of elderly patients we clearly need something better than long-term treatment with a potentially toxic drug. The fact that nocturnal cramp is confined to the lower limbs suggests that it has a circulatory basis, and, as pointed out by Rivlin,3 raising the foot off the bed at least 23 cm may prevent nocturnal cramps. Although this recommendation is difficult to implement with modern bedsteads, it is surely worth trying in severe cases. With respect to the management of the acute attack, we are all familiar with the reciprocal inhibition reflex by which a muscle will relax when the antagonist contracts. Why do we not exploit this reflex in clinical practice? From personal experience I know that nocturnal calf cramp can be aborted by sustained active dorsiflexion of the
1325
The first study2 compared laparoscopic with minicholecystectomy and showed that the former was much more expensive than the latter. When reusable instruments were used this difference was £93 (95% CI £25–162), based on an increase in theatre costs caused by the extra time required for laparoscopic cholecystectomy (14 min). I would point out that this difference is academic, since undertaking a laparoscopic cholecystectomy, or indeed several procedures, did not result in any change in the number of patients placed on our operating list or an over-run in operating time during the study period. In my experience, operating time for laparoscopic cholecystectomy has dropped substantially since that time, from a median of 65 (46–70) to 50 (40–66) min (p=0·004).3 This fall is principally due to the fact that the learning curve for laparoscopic cholecystectomy is much longer than had been anticipated when the randomised trial was set up.2 The second study is the Medical Research Council trial funded to evaluate laparoscopic hernia repair. This trial does not compare laparoscopic hernia repair with many diffuse open methods, as Johnson suggests. The laparoscopic group is almost exclusively the totally extraperitoneal approach to hernia repair, which is not different from its open preperitoneal equivalent. Over 90% of patients in the open group have had a tension-free repair hernioplasty and a few have had other open procedures when use of mesh was considered unnecessary, eg, in a Nyhus type 1 hernia in a young adult. P J O’Dwyer Department of Surgery, Western Infirmary, Glasgow G11 6NT, UK
1 2
3
Johnson A. Laparoscopic surgery. Lancet 1997; 349: 631–35. McMahon AJ, Russell IT, Baxter JN. Laparoscopic versus minilaparotomy cholecystectomy: a randomised trial. Lancet 1994; 343: 135–38. Wallace DH, O’Dwyer PJ. Effect of a no-conversion policy on patient outcome following laparoscopic cholecystectomy. Br J Surg (in press).
SIR—Johnson1 provides data of concern regarding a question that I have previously posed but have yet to see adequately addressed.2 As I read figure 1, from 1992 to 1995 a total of roughly 3400 cholecystectomies were done in Lothian health district, of which about 600 were open procedures—ie, about 18%. In 1995 these numbers were around 840 total cholecystectomies, of which 120 were open, for a 14% rate. If this trend continues will the number of open cholecystectomies in the future
1324
be sufficient to (a) teach surgical trainees how to do this procedure, and (b) maintain previously acquired skills at a satisfactory level to allow safe conversion of the laparoscopic procedure to an open one.2 Robert Matz Mount Sinai Medical Center, Mount Sinai School of Medicine, New York, NY 10029, USA
1 2
Johnson A. Laparoscopic surgery. Lancet 1997; 349: 631–35. Matz R. The learning curve. JAMA 1994; 271: 824–25.
Carotid and Vertebral Artery Transluminal Angioplasty Study SIR—We would like to respond to the comments by Warlow and Sandercock1 and Brown and colleagues2 (March 22, p 880) concerning our essay on carotid endarterectomy versus carotid angioplasty.3 Their criticisms relate to the best method for enrolment of patients into randomised trials, the grey-area of uncertainty principle, and the denial that interim data from the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS) is being published and affecting case selection. They conclude that a consecutive study of all patients with symptoms and a carotid stenosis of greater than 70% is unethical and impractical. Warlow and Sandercock go further by saying that trial investigators need only “describe the patients they studied and not waste resources trying to describe the patients they did not”. In fact, we did recognise that a consecutive study might be impractical, but that if this was not feasible the CAVATAS investigators must standardise their selection criteria so that the results can be interpreted and applied to similarly defined groups in the future. Thus, our opinion remains unchanged on the need for a description of exclusion criteria; indeed, this approach accords with the CONSORT statement on the reporting of randomised trials.4 The grey-area principle used in the European Carotid Surgery Trial was entirely appropriate then, but we remain uneasy about its application in CAVATAS. In our essay, we noted that many clinical factors were taken into account in the recruitment of patients, but the most important consideration was the degree of carotid stenosis—something that was centrally and independently standardised within the study from the outset. No attempt was made to correlate outcome with other
angiographic variables because it was widely accepted that angiography was unable to do this reliably. However, in CAVATAS, a patient need only have a carotid stenosis of greater than 30% to be considered for randomisation—ie, standardised—but thereafter one of the main exclusion criteria in the protocol is a subjective assessment of the possibility of luminal thrombus on angiography, which is something that cannot be standardised. We therefore accept that CAVATAS will be able to make predictions of relative risk of stroke according to the degree of stenosis but not according to the many subjective assessments of plaque morphology from the contributing centres. Brown and colleagues dismiss our criticism that repeated presentations and publications from the major participating centres is inappropriate and inadvertently affects selection for CAVATAS, by stating that the trial allows for each centre to present its angioplasty data, provided that the identity of CAVATAS patients remains anonymous. However, Sivaguru and colleagues5 not only disclose the number of patients entered into CAVATAS at the time (n=193), but also that Sheffield had contributed 90 of these patients and that the rate of disabling stroke in the Sheffield patients randomised to angioplasty was 5·6%. This information is neither anonymous nor merely “the early experience”. We are also critical that the combined angioplasty experience from Sheffield and St George’s Hospital (n=85) was submitted to the 1996 European Vascular Society. The abstract published a death and anystroke rate of 8%, a figure that was made available to over 700 European vascular surgeons, many of whom were contributors to CAVATAS. Brown and colleagues refute this criticism by saying that the abstract was withdrawn. But the abstract was published in full and the paper called for presentation at the meeting. We wish to emphasise that our criticisms are not directed at any individual, but collectively Sheffield and St George’s have a responsibility because they have the greatest UK experience in carotid angioplasty and have contributed the most patients to CAVATAS. Thus, any data presented or published by them are respected and interpreted accordingly. Consequently, many surgeons have commented that if these two respected centres have an angioplasty stroke rate of 6–8%, this finding must be fairly close to the overall CAVATAS results; so is it appropriate for them to randomise patients if their own operative morbidity is lower? Whether Brown and colleagues like it or not,
Vol 349 • May 3, 1997
THE LANCET
awareness of their data invariably influences recruitment in other centres. *A R Naylor, N J M London, P R F Bell Faculty of Medicine, University of Leicester, Leicester Royal Infirmary, Leicester LE2 7LX , UK
1
2
3
4
5
Warlow C, Sandercock P. Carotid endarterectomy vs carotid angioplasty. Lancet 1997; 349: 880. Brown MM, Venebles G, Clifton A, Gaines P, Taylor RS. Carotid endarterectomy vs carotid angioplasty. Lancet 1997; 349: 880–81. Naylor AR, London NJM, Bell PRF. Carotid endarterectomy versus carotid angioplasty. Lancet 1997; 349: 203–04. Begg C, Cho M, Eastwood S, et al. Improving the quality of reporting of randomised controlled trials: the CONSORT statement. JAMA 1996; 276: 637–39. Sivaguru A, Venables GS, Beard JD, Gaines PA. European Carotid Angioplasty Trial. J Endovasc Surg 1996; 3: 16–20.
Randomised controlled trial of hydroquinine in muscle cramps SIR—Jansen and colleagues (Feb 22, p 528)1 report a randomised controlled trial of hydroquinine in muscle cramps that demonstrates the efficacy of the drug in the 2-week trial period. Hydroquinine was used because it was the only quinine derivative available to the researchers in the Netherlands for use in the prevention of muscle cramps; quinine is used in the UK. Quinine and its derivatives have potentially very serious side-effects and these must be balanced against the indiscriminate use of quinine and derivatives for an essentially benign condition such as muscle cramps.2 It is extensively metabolised by the liver but small amounts of unchanged quinine and its metabolites are excreted in the urine. The proportion of unchanged quinine excreted in the urine has been variously reported as less than 5% but up to 20%, and excretion is increased in acid urine.3 It would seem possible therefore that patients with reduced rates of glomerular filtration (including the elderly population) might be at risk from accumulation and toxicity after administration of quinine and its derivatives. Consequently, Jansen and colleagues’ suggestion that hydroquinine should be given on a regular (and presumably longer term) basis rather than as needed is perhaps premature, and potentially hazardous for patients. Muscle cramps are common in patients with chronic renal failure and in the elderly, and these two groups might be particularly vulnerable to quinine toxicity. Any study of the longer term use of
Vol 349 • May 3, 1997
quinine and its derivatives in the prevention of muscle cramps should involve very close monitoring of patients for early evidence of sideeffects, especially in those with a reduced rate of glomerular filtration. The glomerular-filtration rate should be assessed in individuals before longer term treatment is started. J R Curtis ‘Brocklea’, Westcott Street, Westcott, Dorking, Surrey RH4 3NU, UK
1
2
3
Jansen PHP, Veenhuizen KCW, Wesseling AJM, de Boo Th, Verbeck ALM. Randomised controlled trial of hydroquinine in muscle cramps. Lancet 1997; 349: 528–32. Man-Son-Hing M, Wells G. Meta-analysis of efficacy of quinine for treatment of nocturnal leg cramps in elderly people. BMJ 1995; 310: 13–17. Quinine. Martindale: the extra pharmacopoiea. 31st edn. London: Royal Pharmaceutical Society, 1996: 474–77.
SIR—Many patients might be inclined to dissent from the conclusions drawn by Jansen and colleagues1 in their comparison of the effect of hydroquinine with placebo on the frequency of leg cramps. In the active treatment group the median number of leg cramps fell from 17 during the 2-week pretreatment observation period to seven during 2 weeks of hydroquinine therapy, and continued at a low frequency of nine per 2 weeks over a 2-week washout period after discontinuation of the drug. They conclude, first, that hydroquinine greatly reduces leg cramps, and, second, that there is a carryover effect into and possibly beyond the washout period for both active treatment and placebo. Although we agree that the halving of cramp frequency is a therapeutic success, this treatment is associated with side-effects. Placebo looks like a better option. Here cramps fell from 17 per 2 weeks during pretreatment observation to 13 per 2 weeks during active placebo therapy and eight per 2 weeks during the washout period. Patients in the placebo group apparently reap the benefits of treatment without its troublesome side-effects. There is, however, another altogether more likely explanation. Although there is undoubtedly a substantial therapeutic effect of hydroquinine during the 2 weeks of active treatment, the observation of a reduction in cramps during the total 6-week period of observation almost certainly results from regression towards the mean. In studies in which patients volunteer they are more likely to show interest when the symptoms are especially troublesome, which means that, given time, they would get better anyway. A blinded review of data from our double-
blind crossover study (unpublished data) comparing the effect of magnesium citrate with placebo shows a similar trend. Ten patients reported fewer cramps during the first treatment period, one was unchanged, and 37 had fewer cramps during the second treatment period. 3–6 months after the trial, over 70% of patients had fewer cramps than before trial entry. Although this reduction might be entirely attributed to a therapeutic effect of magnesium, it is likely that here too is also an element of regression towards the mean. Since the treatment periods in our study are longer (6 weeks in each group) than those reported by Jansen et al, it will be possible to quantify the effect of time on cramp frequency and separate that from a possible treatment effect. We conclude that there is no convincing evidence of a carryover effect of hydroquinine and feel that Jansen and colleagues’ suggestion that regular use of hydroquinine is preferable to “as-required” medication is not supported by their data. *C Roffe, S Sills, P Crome Department of Geriatric Medicine, Keele University School of Postgraduate Medicine, Stoke-on-Trent ST4 7QB, UK
1
Jansen PHP, Veenhuizen KCW, Wesseling AIM, de Boo Th, Verbeek ALM. Randomised controlled trial of hydroquinine in muscle cramps. Lancet 1997; 349: 528–32.
S IR —The findings in the trial of hydroquinine in muscle cramps from the Netherlands 1 accords with the meta-analysis reported by Man-SonHing and Wells,2 which revealed that although quinine may substantially reduce the number of attacks it does not affect the severity of the attacks. So we are still left with the difficulty of how to deal with nocturnal cramp when it occurs. Moreover, in a condition that may affect 70% of elderly patients we clearly need something better than long-term treatment with a potentially toxic drug. The fact that nocturnal cramp is confined to the lower limbs suggests that it has a circulatory basis, and, as pointed out by Rivlin,3 raising the foot off the bed at least 23 cm may prevent nocturnal cramps. Although this recommendation is difficult to implement with modern bedsteads, it is surely worth trying in severe cases. With respect to the management of the acute attack, we are all familiar with the reciprocal inhibition reflex by which a muscle will relax when the antagonist contracts. Why do we not exploit this reflex in clinical practice? From personal experience I know that nocturnal calf cramp can be aborted by sustained active dorsiflexion of the
1325