The main goal of this study is to examine the effect of intramuscular bupivacaine in oculomotor paresis, analyzing whether it is possible to obtain a stronger muscle contraction due to the muscle hypertrophy caused by the drug. An injection of 4.5 mL of a 0.50% solution of bupivacaine was administered in the paretic muscle of three patients. Magnetic resonance imaging was performed before and 3 months after injection to compare muscle cross-sectional areas. The symptoms of two patients improved and an increase of muscle cross-sectional area was observed. However, it is necessary to be prudent when employing intramuscular bupivacaine in oculomotor paresis treatment until there are more and larger studies.
From Gregorio Marañon University Hospital, Madrid, Spain.
Presented at the 19th “Sociedad Española de Estrabologia” Congress, April 18 to 19, 2008, Alacant, Spain.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Olga Seijas, MD, Calle de la Infanta Maria Teresa, 18 5º A. 28016 Madrid, Spain.
Received: April 12, 2008
Accepted: November 12, 2008
Posted Online: May 21, 2010
Bupivacaine, a local anesthetic drug, seems to induce muscle hypertrophy when it is injected into eye muscles under experimental conditions.1–3 Scott et al.4 recently used this drug to treat strabismus, with the goal of obtaining stronger muscle contraction.
Intramuscular bupivacaine was used in three patients with oculomotor paresis and diplopia. Informed consent for an experimental injection was obtained in each case, according to the tenets of the Declaration of Helsinki. Bupivacaine, 4.5 mL of a 0.50% solution, was injected into the muscle in every patient (3 months after diagnosis), using the recording of muscle electrical activity from the needle tip to guide the location of the injection. Immediately after injection, findings were similar in all patients: total ptosis, with mild proptosis and almost complete ophthalmoplegia, according to the high volume and nature of the anesthetic drug injected. None of the patients felt pain, and there was no change in visual acuity.
A 72-year-old man had right incomplete third cranial nerve paresis (mild ptosis, exotropia of 35 prism diopters [PD], and adduction limitation of grade -2). Thirty days postinjection, recovery of adduction was observed and horizontal strabismus had decreased to 6 PD.
Magnetic resonance imaging was performed before and 3 months after injection. The cross-sectional area of the medial rectus muscle was 27.74 mm2 before bupivacaine injection and increased to 46.56 mm2 after injection. Measures were always obtained 16 mm anterior to the orbital apex and in primary gaze. The cross-sectional area of the muscle increased by 67.8%.
Dynamic magnetic resonance imaging was performed to determine whether the increase in the cross-sectional area of the muscle indicates higher contractile function or fibrosis. To determine the contractile functional index, the cross-sectional area of the right medial rectus muscle (pathologic) was compared with the cross-sectional area of the left medial rectus muscle (not pathologic), in both positions (contracted and relaxed). Measurements were taken 16 mm anterior to the orbital apex.
On right gaze, it was 26.90 mm2 (relaxed) for the right medial rectus muscle, increasing to 49.76 mm2 (contracted) on left gaze. The increase observed from the relaxed position to the contracted position shows muscle contractile function. The cross-sectional area of the medial rectus muscle of the other eye also should be measured as a control (32.27 mm2 [relaxed] and 56.48 mm2 [contracted]). The muscle area is slightly smaller in the pathologic eye in both positions.
Six months after injection, diplopia was resolved and exotropia was 2 PD in primary gaze (final follow-up = 12 months).
An 81-year-old woman had right sixth cranial nerve paresis. The patient was lost to follow-up.
A 66-year-old man had right sixth cranial nerve paresis (esotropia of 18 PD, with abduction in the right eye reduced to grade -1). Esotropia decreased to 16 PD by 21 days after treatment and to 6 PD by 42 days after treatment. Two months after treatment, the patient had orthotropia without duction limitation and without diplopia (final follow-up = 10 months). It was not possible to perform magnetic resonance imaging.
Bupivacaine was recently used for the first time in the treatment of strabismus.4 The current study shows its effects in the treatment of oculomotor paresis. Two of the three patients studied showed improvement in their symptoms. In case 1, the improvement in muscle contraction was measured with magnetic resonance imaging. All observed side effects were promptly reversed.
Nevertheless, there are still many questions. The first is concerning the dosage; the great volume employed could have an effect on other muscles or could even damage the optic nerve. Another question is whether the muscular hypertrophy could become fibrosis in time, causing inversion in the clinical pattern of the patient. Finally, an important point to consider is the natural evolution of oculomotor paresis without treatment; most cases tend to resolve.5 Is the good result caused by the drug treatment, or is it the result of time? Could bupivacaine offer an advantage over botulinum toxin? Bupivacaine acts directly on the paretic muscle, with slow, progressive improvement in muscle function, and is less costly than botulinum toxin. It is necessary to be prudent with this use of bupivacaine.
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