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The neuronal basis for diplopia following local anesthetic injections
The neuronal basis for diplopia following local anesthetic injections J. H. Kronman, D.D.S., Ph.D.,* and S. Kabani, D.M.D., M.S.,*+ Boston, Mass. TUFTS
UNIVERSITY
SCHOOL
OF DENTAL
MEDICINE
The case report presented here describes a situation in which diplopia resulted as an effect secondary to maxillary infiltration anesthesia. Prior casesand theories regarding the mechanisms involved are reviewed, and a new theory explaining this phenomenon is proposed. The autonomic nervous system is presented as the logical basis for the untoward systems, rather than simple circulation of anesthetic solution in the vascular tree. (ORAL SURG. S&533-534, 1984)
A
healthy 37-year-old female patient presented for routine dental care. She required endodontic treatment for a nonvital maxillary left canine, and a maxillary infiltration of Carbocaine was administered in the mucobuccal fold above the tooth to be treated. After a few minutes, accesswith a handpiece was attempted. The patient complained of pain. A supplementary injection of a few drops of anesthetic solution was delivered palatally. An additional % Carpule of anesthetic was also administered at the original injection site. The patient, who was lying supine, then complained of double vision approximately 3 to 4 minutes after administration of the supplemental injections. The double vision disappeared when the patient was placed in an upright position and reappeared when placed in a supine position. All signs of double vision disappeared after 45 to 50 minutes. DISCUSSION
The description of double vision following inferior alveolar anesthesia appears several times in the literature.le4 The most generally accepted explanation for this phenomenon is that anesthetic solution was inadvertently injected directly into the inferior alveolar artery and, becauseof the speedof injection, a retrograde flow of anesthetic solution resulted. The proposed flow passedthrough the first division of the maxillary artery and then further superiorly into the middle meningeal artery and into the skull. The connection between the middle meningeal artery and *Professor of Orthodontics. **Assistant Clinical Professor of Oral Health Services.
the lacrimal artery, through the superior orbital fissure by way of a recurrent lacrimal branch, is commonly accepted. The proposed mechanism of the double vision, therefore, is related to vasoconstriction of muscular branches to the lateral rectus muscle. In addition, rich anastomatic branching between the recurrent lacrimal branch and branches of the ophthalmic artery is also well established. Other orbital symptoms reported previously were generally related to this vascular phenomenon. In only one of these prior citations was any involvement of the autonomic nervous system advanced as a possible explanation.4 The internal cartoid plexus was assumed to be involved in the symptoms described. These included myosis, ptosis, and a suggestion of enophthalmos. Impaired hearing and dizziness, which were also reported in the previous case, were ascribed to sympathetic nerves of the internal carotid plexus. Only one report in the literature describes a case of diplopia as a result of a maxillary infiltration procedure.5 The condition reappeared in this same patient on two subsequent visits. The author postulated that the anesthetic might have penetrated the orbit through a bony defect in the wall of the maxillary sinus. Although this is possible, it would require the flow of anesthetic over a rather long course and would have the solution passing upward against gravity to reach the orbit. Since the use of aspiration syringes is commonplace, but the occurrence of casesof diplopia following dental injections persists, we propose a different mechanism which may help to explain many of the untoward symptoms secondary to dental local anesthetic injections. 533
534
Kronman and Kabani
We proposethat trauma to the sympathetic plexus of nerves which surround the common carotid, the external and internal carotids, and all their branches occurs when the anesthetic needle inadvertently scrapes the wall of an artery. In the case of inferior alveolar anesthesia, the inferior alveolar artery would be involved. In the caseof a maxillary infiltration, the anterior, middle, or posterior superior alveolar arteries would be involved. In both instances the trauma could set up an impulse which would travel along the maxillary artery into the pterygopalatine fossa. From there, the sympathetic impulse would pass along the deep petrosal nerve to the internal carotid plexus, then along the internal carotid artery, and finally the ophthalmic artery into the orbit. If the secondary response to the traumatic damage were decreasedsympathetic activity, then the usually reported sequelae,all under parasympathetic control would be enhanced. Lacrimation, salivation, and blanching of tissues would all be manifestations of an enhanced parasympathetic effect as a result of decreased sympathetic function. It would appear more reasonable to assumethat a vesselwas traumatized rather than penetrated, particularly when one considers the case in which the results were replicated three times.4 If the parasympathetic effect were enhanced, vasoconstriction would increase. This would affect the ocular muscles, as described above. When the patient was brought to an upright position, blood flow was enhanced. Increased blood flowed through the constricted vessels,and the diplopia was relieved. When the patient was again placed in a supine position, the sympathetic traumatic effect persisted, the blood flow decreased,and diplopia returned. The only support to the concept of anesthetic effects to the sympathetic system was that the diplopia persisted for a period of time that approxi-
Oral Surg. November, 1984
mated the anesthetic effectivenessof the solution. It doesnot preclude the disappearanceof the traumatic effect in that same time period. In the event that deposition of anesthetic solution caused anesthesia of the sympathetic vascular plexus, then the cases described and referred to here would be commonplace, rather than unusual. CONCLUSION
It would appear that the ocular changes observed after dental local anesthetic procedures are related to sympathetic and parasympathetic effects, rather than to anesthetic solution circulating in the vascular tree. In any event, it is of extreme importance for the clinician to understand that the effects are transitory and are unavoidable. When such casesdo occur, the patient should and must be reassured, comforted, and made to understand that the symptoms will generally disappear in an hour or less. REFERENCES I. O’Connor
2.
3. 4.
5.
M, Estate P: Tonic pupil and lateral rectus palsy following dental anaesthesia. Nemo-ophthalmol 3: 205-208. 1983. Cooper JC: Deviation of eye and transient blurring of vision after mandibular nerve anesthesia. J Oral Surg 20: 61-62. 1962. Blaxter PL. Britten MJA: Transient amaurosis after mandibular nerve block. Br Med J 1: 681, 1967. Dodds AE: Alarming sequelac of an inferior alveolar nerve block simulated Horner’s syndrome. J Dent Assoc S Afr 11: 385-386, 1956. Petrelli PA, Steller RE: Medial rectus muscle palsy after dental anesthesia. Am J Ophthalmal 90: 422-423, 1980.
Reprint request.5 to: Dr. Joseph H. Kronman Tufts University School of Dental Medicine I Kneeland St. Boston, MA 02 I I I
UNIVERSITY
SCHOOL
OF DENTAL
MEDICINE
The case report presented here describes a situation in which diplopia resulted as an effect secondary to maxillary infiltration anesthesia. Prior casesand theories regarding the mechanisms involved are reviewed, and a new theory explaining this phenomenon is proposed. The autonomic nervous system is presented as the logical basis for the untoward systems, rather than simple circulation of anesthetic solution in the vascular tree. (ORAL SURG. S&533-534, 1984)
A
healthy 37-year-old female patient presented for routine dental care. She required endodontic treatment for a nonvital maxillary left canine, and a maxillary infiltration of Carbocaine was administered in the mucobuccal fold above the tooth to be treated. After a few minutes, accesswith a handpiece was attempted. The patient complained of pain. A supplementary injection of a few drops of anesthetic solution was delivered palatally. An additional % Carpule of anesthetic was also administered at the original injection site. The patient, who was lying supine, then complained of double vision approximately 3 to 4 minutes after administration of the supplemental injections. The double vision disappeared when the patient was placed in an upright position and reappeared when placed in a supine position. All signs of double vision disappeared after 45 to 50 minutes. DISCUSSION
The description of double vision following inferior alveolar anesthesia appears several times in the literature.le4 The most generally accepted explanation for this phenomenon is that anesthetic solution was inadvertently injected directly into the inferior alveolar artery and, becauseof the speedof injection, a retrograde flow of anesthetic solution resulted. The proposed flow passedthrough the first division of the maxillary artery and then further superiorly into the middle meningeal artery and into the skull. The connection between the middle meningeal artery and *Professor of Orthodontics. **Assistant Clinical Professor of Oral Health Services.
the lacrimal artery, through the superior orbital fissure by way of a recurrent lacrimal branch, is commonly accepted. The proposed mechanism of the double vision, therefore, is related to vasoconstriction of muscular branches to the lateral rectus muscle. In addition, rich anastomatic branching between the recurrent lacrimal branch and branches of the ophthalmic artery is also well established. Other orbital symptoms reported previously were generally related to this vascular phenomenon. In only one of these prior citations was any involvement of the autonomic nervous system advanced as a possible explanation.4 The internal cartoid plexus was assumed to be involved in the symptoms described. These included myosis, ptosis, and a suggestion of enophthalmos. Impaired hearing and dizziness, which were also reported in the previous case, were ascribed to sympathetic nerves of the internal carotid plexus. Only one report in the literature describes a case of diplopia as a result of a maxillary infiltration procedure.5 The condition reappeared in this same patient on two subsequent visits. The author postulated that the anesthetic might have penetrated the orbit through a bony defect in the wall of the maxillary sinus. Although this is possible, it would require the flow of anesthetic over a rather long course and would have the solution passing upward against gravity to reach the orbit. Since the use of aspiration syringes is commonplace, but the occurrence of casesof diplopia following dental injections persists, we propose a different mechanism which may help to explain many of the untoward symptoms secondary to dental local anesthetic injections. 533
534
Kronman and Kabani
We proposethat trauma to the sympathetic plexus of nerves which surround the common carotid, the external and internal carotids, and all their branches occurs when the anesthetic needle inadvertently scrapes the wall of an artery. In the case of inferior alveolar anesthesia, the inferior alveolar artery would be involved. In the caseof a maxillary infiltration, the anterior, middle, or posterior superior alveolar arteries would be involved. In both instances the trauma could set up an impulse which would travel along the maxillary artery into the pterygopalatine fossa. From there, the sympathetic impulse would pass along the deep petrosal nerve to the internal carotid plexus, then along the internal carotid artery, and finally the ophthalmic artery into the orbit. If the secondary response to the traumatic damage were decreasedsympathetic activity, then the usually reported sequelae,all under parasympathetic control would be enhanced. Lacrimation, salivation, and blanching of tissues would all be manifestations of an enhanced parasympathetic effect as a result of decreased sympathetic function. It would appear more reasonable to assumethat a vesselwas traumatized rather than penetrated, particularly when one considers the case in which the results were replicated three times.4 If the parasympathetic effect were enhanced, vasoconstriction would increase. This would affect the ocular muscles, as described above. When the patient was brought to an upright position, blood flow was enhanced. Increased blood flowed through the constricted vessels,and the diplopia was relieved. When the patient was again placed in a supine position, the sympathetic traumatic effect persisted, the blood flow decreased,and diplopia returned. The only support to the concept of anesthetic effects to the sympathetic system was that the diplopia persisted for a period of time that approxi-
Oral Surg. November, 1984
mated the anesthetic effectivenessof the solution. It doesnot preclude the disappearanceof the traumatic effect in that same time period. In the event that deposition of anesthetic solution caused anesthesia of the sympathetic vascular plexus, then the cases described and referred to here would be commonplace, rather than unusual. CONCLUSION
It would appear that the ocular changes observed after dental local anesthetic procedures are related to sympathetic and parasympathetic effects, rather than to anesthetic solution circulating in the vascular tree. In any event, it is of extreme importance for the clinician to understand that the effects are transitory and are unavoidable. When such casesdo occur, the patient should and must be reassured, comforted, and made to understand that the symptoms will generally disappear in an hour or less. REFERENCES I. O’Connor
2.
3. 4.
5.
M, Estate P: Tonic pupil and lateral rectus palsy following dental anaesthesia. Nemo-ophthalmol 3: 205-208. 1983. Cooper JC: Deviation of eye and transient blurring of vision after mandibular nerve anesthesia. J Oral Surg 20: 61-62. 1962. Blaxter PL. Britten MJA: Transient amaurosis after mandibular nerve block. Br Med J 1: 681, 1967. Dodds AE: Alarming sequelac of an inferior alveolar nerve block simulated Horner’s syndrome. J Dent Assoc S Afr 11: 385-386, 1956. Petrelli PA, Steller RE: Medial rectus muscle palsy after dental anesthesia. Am J Ophthalmal 90: 422-423, 1980.
Reprint request.5 to: Dr. Joseph H. Kronman Tufts University School of Dental Medicine I Kneeland St. Boston, MA 02 I I I