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Vertebrobasilar transient ischemic attacks in internal carotid artery occlusion or tight stenosis
68
Surv Ophthalmol
30( 1) July-August
CURRENT
1985
OPHTHALMOLOGY
Because the study population was composed ofvolunteers, without adequate randomization or controls, the caution stated by the authors that this data should not be extrapolated beyond the group actually studied is appropriate. Hopefully, the authors will continue their work in a controlled study and correlate the answers on the questionnaires with physical measurements of the ergonomics, lighting, VDT screen clarity and readability, and keyboard design and layout with their conclusions. PALIt_ F. VINGER, M.D. LEXINGTON, MASSACHUSETTS
Vertebrobasilar Transient Ischemic Attacks in Internal Carotid Artery Occlusion Tight Stenosis, by J. Bogousslavsky and F. Regli. Arch Neural 42: 64-68, 1985
or
The pathogenic role of atherosclerotic carotid artery diseases in vertebrobasilar insufficiency has been suggested but also strongly contested. The authors studied 12 patients with internal carotid artery occlusion or tight stenosis but without vertebrobasilar and subclavian atherosclerosis who suffered vertebrobasilar insufficiency. The patients with internal carotid artery occlusion were compared with a sex- and age-matched control group that had internal carotid artery occlusion but no vertebrobasilar insufficiency. Visible infarct on computed tomographic scan, greater size ofvisible infarct, weak collateral circulation and bilateral atherosclerosis of the internal carotid artery significantly correlated with the occurrence of vertebrobasilar insufficiency. No significant difference was demonstrated for emboligenic lesions but posterior to anterior flow through the posterior communicating arteries was demonstrated only in the patients with vertebrobasilar insufficiency. These facts suggested hemodynamic disturbance with “steal vertebrobasilar insufficiency.” In internal carotid artery tight stenosis, vertebrobasilar insufficiency symptoms disappeared after endarterectomy but persisted in patients with more than 50% stenosis. Vertebrobasilar insufficiency had a prognostic significance, being associated with an increased occurrence of delayed stroke. (Author address: Dr. Bogousslavsky,
Service de Neurologie,
Centre
Hospitalier
Universitaire
Vaudois,
1011 Lausanne,
Switzerland.)
Comment This article addresses the pathogenic role of atherosclerotic internal carotid artery disease in vertebrobasilar insuficiency. The authors studied a specific subgroup of patients with vertebrobasilar insufficiency, namely those with angiographic evidence of internal carotid artery occlusion of high degree stenosis without vertebral artery or subclavian artery atherosclerosis. The study was retrospective in nature and contained a small number of patients, nine with internal carotid artery occlusion and three with internal carotid artery stenosis (two 70-80%; one > 90%). Of the twelve patients, eight had had four-vessel angiography with visualization of the basilar artery and four had had arch studies and carotid angiography. All nine patients with internal carotid artery occlusion and vertebrobasilar insufficiency were referred because of carotid strokes. Compared to the controls, the patients with internal carotid artery disease and vertebrobasilar insufficiency were more likely to have a visible infarction on CT, a larger.infarct on CT, weaker collateral circulation, and bilateral internal carotid artery atherosclerosis. In six of nine patients with both conditions, the basilar artery was angiographically studied. Five of six had evidence of posterior to anterior flow via the posterior communicating artery of the circle of Willis. In seven of nine patients in the control group where the basilar artery was angiographically visualized, no posterior to anterior flow was noted. In the three patients with high-degree internal carotid artery stenosis and vertebrobasilar insufflciency, the basilar artery was angiographically studied in two. Posterior to anterior flow was noted in one. In a control group of three patients with internal carotid artery stenosis without vertebrobasilar insufficiency, the basilar artery was angiographically visualized in two patients, neither of which showed evidence of posterior to anterior flow. All three patients with high-degree internal carotid artery stenosis and vertebrobasilar insufflciency underwent endarterectomy. Postoperatively, all three ceased to exhibit the latter condition. This study of a limited number of patients supports the importance of hemodynamic factors in the pathogenesis of vertebrobasilar insufficiency in patients with internal carotid artery occlusion or stenosis. Specifically because of inadequate carotid blood flow, blood is shunted anteriorly from the vertebrobasilar system through the circle of Willis via the posterior communicating arteries. This phenomena is referred to as “steal vertebrobasilar insufficiency.”
CURRENT
OPHTHALMOLOGY
69
From a management point of view, the critical question is the value of carotid endarterectomy in patients with vertebrobasilar insuficiency. This is a controversial area with conflicting data in previous articles on this topic. The present paper presents arguments which favor surgery, but because ofthe small number ofpatients in this study, no definitive conclusions can be drawn. WALTER
M. JAY, M.D.
AUGUSTA,
GEORGIA
Oral and Topical Beta Receptor Blockers in Glaucoma Treatment. A Multicenter Study, by A. Ohrstrijm, 0. KSttstrGm, W. Polland, J. Mortensen and B. Stenstrijm. Acta Ophthalmol 62681-695, 1984 The usefulness of beta blockers given topically or systemically to lower intraocular pressure is now well established. This study was undertaken to clarify the therapeutic value as well as the possible problems and side effects of oral propranolol in the treatment of glaucoma. In a longterm multicenter open randomized study of 103 patients with glaucoma or intraocular hypertension, oral propranolol combined with 2% pilocarpine was compared with 0.5% topical timolol also combined with 2% pilocarpine with respect to the effects on intraocular pressure and other signs of glaucoma. The results showed that the hypotensive effects were highly significant and equal for both treatments. There were no significant differences between the two groups in the amount of cupping of the nerve head or the visual field defects developing during treatment. An additive hypotensive effect was recorded when both propranolol and timolol were combined with pilocarpine, which indicates the development of tolerance to both beta blockers. Pulse rate and blood pressure were moderately reduced in both groups, both significantly more so in the propranolol group. The investigation indicates that when combined with pilocarpine, the two adrenergic beta receptor blockers are equally effective. The authors suggest that oral propranolol can improve drug compliance in the treatment of glaucoma. (Author address: Dr. Arne ~hrstrikn, Eye Clinic, &ebro Medical Center Hospital, S-701 85 &ebro, Sweden.)
Comment Dr. Ohrstrom and colleagues have had extensive experience with beta blocking agents in the therapy of glaucoma and new contributions from this group deserve particular study. The intent of the current investigation was to compare the use of topical timolol eyedrops with systemic propranolol given orally for glaucoma therapy. Surprisingly, the authors did not choose to treat one group with oral propranolol alone and another with timolol eyedrops alone, but rather they chose to treat one group with 5% timolol b.d. plus 2% pilocarpine t.d.s. and the other group with systemic propranolol plus 2% pilocarpine t.d.s. Perhaps it was in the interest of longterm study that pilocarpine was included from the beginning. The protocol for the study is complex. In the planning stages the authors calculated that to detect a 20% difference in efficacy between the two treatments, at least 112 patients would be necessary to demonstrate a significant difference (p < 0.05). A total of 115 patients were admitted to the study. Twelve had to be excluded subsequently, including one patient in the propranolol group who apparently died (no further details given). Of the remaining 103 patients, only 18 completed the first treatment period of58 weeks without any change in therapy. Eleven of the 18 patients finishing the 58-week course used timolol and pilocarpine; seven had used “The main reason for change of treatment period was insufficient IOP control propranolol and pilocarpine. (IOP > 20 mm Hg).” A total of 64 patients entered a second treatment period consisting of topical pilocarpine plus topical timolol plus systemic propranolol. This meant that systemic propranolol was added to the regimen of patients who had not achieved IOP < 20 mm Hg with topical pilocarpine and topical timolol and, similarly, that topical timolol was added to the regimen of those patients who had not achieved TOP < 20 mm Hg with systemic propranolol and topical pilocarpine. The authors suggest that the results of this section indicate that “the timolol patients may already be receiving maximal beta receptor blockade and that the addition of propranolo1 did not have a great additional effect, whereas the prppranolol patients were on too low a dose of propranolol and the addition of timolol could thus increase the effectiveness of the beta blockade.”
Surv Ophthalmol
30( 1) July-August
CURRENT
1985
OPHTHALMOLOGY
Because the study population was composed ofvolunteers, without adequate randomization or controls, the caution stated by the authors that this data should not be extrapolated beyond the group actually studied is appropriate. Hopefully, the authors will continue their work in a controlled study and correlate the answers on the questionnaires with physical measurements of the ergonomics, lighting, VDT screen clarity and readability, and keyboard design and layout with their conclusions. PALIt_ F. VINGER, M.D. LEXINGTON, MASSACHUSETTS
Vertebrobasilar Transient Ischemic Attacks in Internal Carotid Artery Occlusion Tight Stenosis, by J. Bogousslavsky and F. Regli. Arch Neural 42: 64-68, 1985
or
The pathogenic role of atherosclerotic carotid artery diseases in vertebrobasilar insufficiency has been suggested but also strongly contested. The authors studied 12 patients with internal carotid artery occlusion or tight stenosis but without vertebrobasilar and subclavian atherosclerosis who suffered vertebrobasilar insufficiency. The patients with internal carotid artery occlusion were compared with a sex- and age-matched control group that had internal carotid artery occlusion but no vertebrobasilar insufficiency. Visible infarct on computed tomographic scan, greater size ofvisible infarct, weak collateral circulation and bilateral atherosclerosis of the internal carotid artery significantly correlated with the occurrence of vertebrobasilar insufficiency. No significant difference was demonstrated for emboligenic lesions but posterior to anterior flow through the posterior communicating arteries was demonstrated only in the patients with vertebrobasilar insufficiency. These facts suggested hemodynamic disturbance with “steal vertebrobasilar insufficiency.” In internal carotid artery tight stenosis, vertebrobasilar insufficiency symptoms disappeared after endarterectomy but persisted in patients with more than 50% stenosis. Vertebrobasilar insufficiency had a prognostic significance, being associated with an increased occurrence of delayed stroke. (Author address: Dr. Bogousslavsky,
Service de Neurologie,
Centre
Hospitalier
Universitaire
Vaudois,
1011 Lausanne,
Switzerland.)
Comment This article addresses the pathogenic role of atherosclerotic internal carotid artery disease in vertebrobasilar insuficiency. The authors studied a specific subgroup of patients with vertebrobasilar insufficiency, namely those with angiographic evidence of internal carotid artery occlusion of high degree stenosis without vertebral artery or subclavian artery atherosclerosis. The study was retrospective in nature and contained a small number of patients, nine with internal carotid artery occlusion and three with internal carotid artery stenosis (two 70-80%; one > 90%). Of the twelve patients, eight had had four-vessel angiography with visualization of the basilar artery and four had had arch studies and carotid angiography. All nine patients with internal carotid artery occlusion and vertebrobasilar insufficiency were referred because of carotid strokes. Compared to the controls, the patients with internal carotid artery disease and vertebrobasilar insufficiency were more likely to have a visible infarction on CT, a larger.infarct on CT, weaker collateral circulation, and bilateral internal carotid artery atherosclerosis. In six of nine patients with both conditions, the basilar artery was angiographically studied. Five of six had evidence of posterior to anterior flow via the posterior communicating artery of the circle of Willis. In seven of nine patients in the control group where the basilar artery was angiographically visualized, no posterior to anterior flow was noted. In the three patients with high-degree internal carotid artery stenosis and vertebrobasilar insufflciency, the basilar artery was angiographically studied in two. Posterior to anterior flow was noted in one. In a control group of three patients with internal carotid artery stenosis without vertebrobasilar insufficiency, the basilar artery was angiographically visualized in two patients, neither of which showed evidence of posterior to anterior flow. All three patients with high-degree internal carotid artery stenosis and vertebrobasilar insufflciency underwent endarterectomy. Postoperatively, all three ceased to exhibit the latter condition. This study of a limited number of patients supports the importance of hemodynamic factors in the pathogenesis of vertebrobasilar insufficiency in patients with internal carotid artery occlusion or stenosis. Specifically because of inadequate carotid blood flow, blood is shunted anteriorly from the vertebrobasilar system through the circle of Willis via the posterior communicating arteries. This phenomena is referred to as “steal vertebrobasilar insufficiency.”
CURRENT
OPHTHALMOLOGY
69
From a management point of view, the critical question is the value of carotid endarterectomy in patients with vertebrobasilar insuficiency. This is a controversial area with conflicting data in previous articles on this topic. The present paper presents arguments which favor surgery, but because ofthe small number ofpatients in this study, no definitive conclusions can be drawn. WALTER
M. JAY, M.D.
AUGUSTA,
GEORGIA
Oral and Topical Beta Receptor Blockers in Glaucoma Treatment. A Multicenter Study, by A. Ohrstrijm, 0. KSttstrGm, W. Polland, J. Mortensen and B. Stenstrijm. Acta Ophthalmol 62681-695, 1984 The usefulness of beta blockers given topically or systemically to lower intraocular pressure is now well established. This study was undertaken to clarify the therapeutic value as well as the possible problems and side effects of oral propranolol in the treatment of glaucoma. In a longterm multicenter open randomized study of 103 patients with glaucoma or intraocular hypertension, oral propranolol combined with 2% pilocarpine was compared with 0.5% topical timolol also combined with 2% pilocarpine with respect to the effects on intraocular pressure and other signs of glaucoma. The results showed that the hypotensive effects were highly significant and equal for both treatments. There were no significant differences between the two groups in the amount of cupping of the nerve head or the visual field defects developing during treatment. An additive hypotensive effect was recorded when both propranolol and timolol were combined with pilocarpine, which indicates the development of tolerance to both beta blockers. Pulse rate and blood pressure were moderately reduced in both groups, both significantly more so in the propranolol group. The investigation indicates that when combined with pilocarpine, the two adrenergic beta receptor blockers are equally effective. The authors suggest that oral propranolol can improve drug compliance in the treatment of glaucoma. (Author address: Dr. Arne ~hrstrikn, Eye Clinic, &ebro Medical Center Hospital, S-701 85 &ebro, Sweden.)
Comment Dr. Ohrstrom and colleagues have had extensive experience with beta blocking agents in the therapy of glaucoma and new contributions from this group deserve particular study. The intent of the current investigation was to compare the use of topical timolol eyedrops with systemic propranolol given orally for glaucoma therapy. Surprisingly, the authors did not choose to treat one group with oral propranolol alone and another with timolol eyedrops alone, but rather they chose to treat one group with 5% timolol b.d. plus 2% pilocarpine t.d.s. and the other group with systemic propranolol plus 2% pilocarpine t.d.s. Perhaps it was in the interest of longterm study that pilocarpine was included from the beginning. The protocol for the study is complex. In the planning stages the authors calculated that to detect a 20% difference in efficacy between the two treatments, at least 112 patients would be necessary to demonstrate a significant difference (p < 0.05). A total of 115 patients were admitted to the study. Twelve had to be excluded subsequently, including one patient in the propranolol group who apparently died (no further details given). Of the remaining 103 patients, only 18 completed the first treatment period of58 weeks without any change in therapy. Eleven of the 18 patients finishing the 58-week course used timolol and pilocarpine; seven had used “The main reason for change of treatment period was insufficient IOP control propranolol and pilocarpine. (IOP > 20 mm Hg).” A total of 64 patients entered a second treatment period consisting of topical pilocarpine plus topical timolol plus systemic propranolol. This meant that systemic propranolol was added to the regimen of patients who had not achieved IOP < 20 mm Hg with topical pilocarpine and topical timolol and, similarly, that topical timolol was added to the regimen of those patients who had not achieved TOP < 20 mm Hg with systemic propranolol and topical pilocarpine. The authors suggest that the results of this section indicate that “the timolol patients may already be receiving maximal beta receptor blockade and that the addition of propranolo1 did not have a great additional effect, whereas the prppranolol patients were on too low a dose of propranolol and the addition of timolol could thus increase the effectiveness of the beta blockade.”