- Email: [email protected]
Transient partial ophthalmoplegia and Horner’s syndrome after intraoral local anesthesia
696 Dogan and Dora
13. Oishi NS, Luce EA. The difficult scalp and skull wound. Clin Plast Surg 1995; 22: 51–59. 14. Cuneyt O, Naci C, Ufuk B, Taner A, Ozgur E, Arman C. Marjolin’s ulcer of the scalp: report of 5 cases and review of literature. J Burn Care Rehabil 2001; 22: 65–69. 15. Darzi MA, Iqbal S, Chowdri NA, Hafiz A. Trapezius myocutaneous flap for reconstruction of a large scalp defect following excision of postburn scar carcinoma. Burns 1992; 18: 429–431. 16. Khanna NN. Management of scalp defects. Am Surg 1971; 37: 363–365.
molar had been planned for dental caries. Her symptoms occurred a few seconds after intraoral injection of prilocaine 5 mg. On examination she had slight deviation of the left eye inwards and downwards at primary position, eye abduction was completely paralysed and downward gaze was slightly affected on the left. She had ptosis and miosis of the same eye. No radiological studies were done. The symptoms recovered completely within 6 hours without any treatment.
Transient partial ophthalmoplegia and Horner’s syndrome after intraoral local anesthesia
DISCUSSION
Ebru Apaydın Dogan
MD,
Babur Dora
MD
Department of Neurology, Akdeniz University, Medical School, Antalya, Turkey
Summary Local neurological symptoms and signs are infrequent after intraoral anesthesia for dental procedures, thus diagnosis may be challenging for a neurologist unfamiliar with this benign phenomenon. Unnecessary diagnostic procedures may be performed and can be associated with complications. We present a 19-year old woman with transient diplopia, miosis, partial enophthalmia and lacrimation on the side of injection after intraoral anesthesia with prilocaine. ª 2005 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2005) 12(6), 696–697 0967-5868/$ - see front matter ª 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2004.08.029
Keywords: ophthalmoplegia, local anesthesia, prilocaine Received 15 June 2004 Accepted 10 August 2004 Correspondence to: Babur Dora, Akdeniz University, Medical School, Department of Neurology, 07030 Antalya, Turkey. Tel.: +90 242 227 4343/66243; E-mail: [email protected]
INTRODUCTION Although intraoral anesthesia is very commonly used for dental surgery, local neurological complications are rarely seen.1,2 If the neurologist who encounters such a patient is unaware of the prior anesthesia and this benign phenomenon, diagnosis may be difficult and diagnostic procedures, including angiography, may be unneccessarily performed. Clinical manifestations appear immediately after application of the anesthetic and always are transient, lasting only as long as the anesthetic drug effect.1 The most common local complication of intraoral anesthesia is paralysis of the extraocular muscles.1,3–5 Manifestations include diplopia, loss of synchronous eye movements, blindness and midriasis. Horner’s syndrome and lacrimation have also been reported.1,3,4,6 We present a patient with partial temporary ophthalmoplegia due to injection of prilocaine. CASE REPORT A 19-year old woman was referred by a dentist with diplopia, miosis, partial enophthalmia, and lacrimation on the left. She had consulted the dentist for tooth pain and removal of the left upper third Journal of Clinical Neuroscience (2005) 12(6)
Local anesthetics are frequently administered prior to dental surgery and thus can be expected to be a major source of drug related complications in the dental office. The most frequently observed complications due to local anesthesia are dizziness, headache, psychomotor reactions, tachycardia, agitation, nausea and tremor.7 Local neurological complications are extremely rare and can usually be attributed to faulty technique.1 These complication are usually transient and last between 1 minute to 6 weeks without treatment.1,3–5,8,9 Several hypotheses may explain how local anesthetic applied to the alveolar region may reach and affect the ocular muscles. After accidental arterial injection the anesthetic agent may reach ocular muscles via arterial anastomotic connections linking the alveolar artery to the ophthalmic artery. Such an anastomotic network has been described by Rood. Vasoconstrictive agents mixed with the local anesthetic could also reach the arterial network of the eye muscles and lead to local ischemia.10 This mechanism may explain the partial ophthalmoplegia in the case presented. The Horner’s syndrome in our patient may have been caused by a sympathetic block at the ciliary ganglion with subsequent dominance of parasympathetic tone. Another possible explanation is that the anesthetic agent enters the venous circulation and reaches the cavernous sinus, bathing the oculomotor nerves. This could also serve as an explanation for the findings in our patient. The Horner’s syndrome in this case would be caused by paralysis of the sympathetic plexus around the internal carotid artery. Direct involvement of orbital structures via the venous route could also occur through communication of the cavernous sinus with the pterygoid venous plexus and the ophthalmic vein.4,9 The ophthalmic artery may also have anastamoses with this plexus.5 Another theory is that the anesthetic solution may reach the orbit by local diffusion along vascular, lymphatic and nervous networks between the pterygomaxillary fossa and the orbit.1 Direct extension through a bony defect in the maxillary sinus has also been proposed.3 The exact anatomopathological mechanism of this phenomenon is still to be elucidated. Although neurological complications after intraoral anesthesia are rare, both dentist and neurologist should be aware of this transient benign phenomenon and avoid unnecessary investigations.
REFERENCES 1. Penarrocha-Diago M, Sanchis-Bielsa JM. Ophthalmologic complications after intraoral local anesthesia with articaine. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000; 90: 21–24. 2. Hidding J, Khoury F. General complications in dental local anesthesia. Dtsch Zahnarztl Z 1991; 46: 834–836. 3. Petrelli EA, Steller RE. Medial rectus muscle palsy after dental anesthesia. Am J Ophthalmol 1980; 90: 422–424. 4. Marinho RO. Abducent nerve palsy following dental local analgesia. Br Dent J 1995; 179: 69–70. 5. Goldenberg AS. Transient diplopia from a posterior alveolar injection. J Endod 1990; 16: 550–551. 6. Ing E, Ing HC, Ing M, Fusco D, Ing TGE. Diagnosing oral disease that affects the eyes. J Am Dent Assoc 1994; 125: 608–616.
ª 2005 Elsevier Ltd. All rights reserved.
Cerebral and meningeal metastatic ovarian carcinoma 697
7. Daublender M, Muller R, Lipp MD. The incidence of complications associated with local anesthesia in dentistry. Anesth Prog 1997; 44: 132–141. 8. Goldenberg AS. Transient diplopia as a result of block injections. Mandibular and posterior superior alveolar. N Y State Dent J 1997; 63: 29–31. 9. Hyams SW. Oculomotor palsy following dental anesthesia. Arch Ophthalmol 1976; 94: 1281–1282. 10. Rood JP. Ocular complications of inferior dental nerve block. Br Dent J 1972; 132: 23–24.
unusual for ovarian carcinoma to present with multiple CNS involvement. ª 2005 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2005) 12(6), 697–699 0967-5868/$ - see front matter ª 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2004.08.021
Keywords: brain metastases, multimodal treatment, outcome, ovarian carcinoma
Multiple cerebral and leptomeningeal metastases from ovarian carcinoma: unusual early presentation Mohammed al Barbarawi1 MBBS CHAM (JORDAN), 2 Sarah F Smith1 BSc BSc MPH (Hons), Suhair Qudsieh 1 Lali HS Sekhon MBBS (HONS) PhD PhD (Syd) FRACS
MBBS,
1
Department of Neurosurgery, Royal North Shore Hospital, St. Leonards, 2 Department of Foeto-Maternal Medicine, Liverpool Hospital, Liverpool; NSW, Australia
Summary Although virtually any systemic malignancy is capable of metastasizing to the brain, ovarian carcinoma, one of the more common female genital malignancies, is one of the rarer forms of brain metastases. In general, the outcome for ovarian carcinoma with brain metastases is extremely poor as most of these patients have widespread lesions elsewhere. This report describes the first known case of multiple cerebral and leptomeningeal metastases as the initial manifestation of ovarian carcinoma in a 41-year old woman who presented with a one-week history of headache, vomiting and confusion. CT scan of the brain was unremarkable, but lumbar puncture revealed atypical cells in the CSF. MRI scan of the brain showed multiple small enhancing lesions. Craniotomy for excision of one of these lesions demonstrated metastatic adenocarcinoma. A large ovarian tumour identified on pelvic CT scan was resected and the patient subsequently received chemotherapy and radiotherapy. Unfortunately she continued to decline and died within six months. Unlike primary tumours such as malignant melanoma, ovarian carcinoma does not have a predilection for the central nervous system (CNS), but the rare instances with CNS involvement occur at an advanced stage of the disease. Once the CNS is involved, the outcome is abysmal, even with multimodality therapy. It is extremely
Received 12 May 2004 Accepted 17 August 2004 Correspondence to: Sarah F. Smith, Department of Neurosurgery Level 7, Royal North Shore Hospital, St. Leonards NSW 2065, Australia. Tel.: +61 2 9926 8756; Fax: +61 2 9437 5172; E-mail: [email protected]
INTRODUCTION Metastatic involvement of the brain is one of the most feared complications of cancer because even small metastases may cause incapacitating neurological symptoms. In recent years important advances have been made in diagnosis and management of brain metastases. As a result, most patients receive effective systemic therapy leading to longer survival.1,2 Stereotactic radiosurgery, once a diagnosis has been established, has also been more recently shown to have some added efficacy.3 However, results with some tumours remain poor regardless of treatment. This group includes ovarian carcinoma. The outcome of patients with ovarian carcinoma will be dramatically affected by CNS involvement. CASE PRESENTATION A previously healthy 41-year old woman was admitted to our institution in September 2002 with a one-week history of headache, vomiting and blurred vision. On the day of admission she acutely developed delirium and a falling level of consciousness which required intubation. Unenhanced CT scan of the brain showed no abnormalities although with double-dosing of intravenous contrast, enhancing cortical lesions were visualised (Fig. 1). A lumbar puncture to rule out encephalopathy showed malignant (atypical) cells. MRI of the brain with gadolinium revealed multiple punctate enhancing lesions within the cerebral hemispheres and right cerebellar hemisphere (Fig. 2). Twelve hours after admission she underwent a right posterior parietal stereotactic craniotomy for excision of the largest lesion. Microscopy revealed metastatic
Fig. 1 Axial contrast enhanced CT scan of the brain showing several small cortical lesions (arrowed). The larger subcortical left parietal lesion was resected.
ª 2005 Elsevier Ltd. All rights reserved.
Journal of Clinical Neuroscience (2005) 12(6)
13. Oishi NS, Luce EA. The difficult scalp and skull wound. Clin Plast Surg 1995; 22: 51–59. 14. Cuneyt O, Naci C, Ufuk B, Taner A, Ozgur E, Arman C. Marjolin’s ulcer of the scalp: report of 5 cases and review of literature. J Burn Care Rehabil 2001; 22: 65–69. 15. Darzi MA, Iqbal S, Chowdri NA, Hafiz A. Trapezius myocutaneous flap for reconstruction of a large scalp defect following excision of postburn scar carcinoma. Burns 1992; 18: 429–431. 16. Khanna NN. Management of scalp defects. Am Surg 1971; 37: 363–365.
molar had been planned for dental caries. Her symptoms occurred a few seconds after intraoral injection of prilocaine 5 mg. On examination she had slight deviation of the left eye inwards and downwards at primary position, eye abduction was completely paralysed and downward gaze was slightly affected on the left. She had ptosis and miosis of the same eye. No radiological studies were done. The symptoms recovered completely within 6 hours without any treatment.
Transient partial ophthalmoplegia and Horner’s syndrome after intraoral local anesthesia
DISCUSSION
Ebru Apaydın Dogan
MD,
Babur Dora
MD
Department of Neurology, Akdeniz University, Medical School, Antalya, Turkey
Summary Local neurological symptoms and signs are infrequent after intraoral anesthesia for dental procedures, thus diagnosis may be challenging for a neurologist unfamiliar with this benign phenomenon. Unnecessary diagnostic procedures may be performed and can be associated with complications. We present a 19-year old woman with transient diplopia, miosis, partial enophthalmia and lacrimation on the side of injection after intraoral anesthesia with prilocaine. ª 2005 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2005) 12(6), 696–697 0967-5868/$ - see front matter ª 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2004.08.029
Keywords: ophthalmoplegia, local anesthesia, prilocaine Received 15 June 2004 Accepted 10 August 2004 Correspondence to: Babur Dora, Akdeniz University, Medical School, Department of Neurology, 07030 Antalya, Turkey. Tel.: +90 242 227 4343/66243; E-mail: [email protected]
INTRODUCTION Although intraoral anesthesia is very commonly used for dental surgery, local neurological complications are rarely seen.1,2 If the neurologist who encounters such a patient is unaware of the prior anesthesia and this benign phenomenon, diagnosis may be difficult and diagnostic procedures, including angiography, may be unneccessarily performed. Clinical manifestations appear immediately after application of the anesthetic and always are transient, lasting only as long as the anesthetic drug effect.1 The most common local complication of intraoral anesthesia is paralysis of the extraocular muscles.1,3–5 Manifestations include diplopia, loss of synchronous eye movements, blindness and midriasis. Horner’s syndrome and lacrimation have also been reported.1,3,4,6 We present a patient with partial temporary ophthalmoplegia due to injection of prilocaine. CASE REPORT A 19-year old woman was referred by a dentist with diplopia, miosis, partial enophthalmia, and lacrimation on the left. She had consulted the dentist for tooth pain and removal of the left upper third Journal of Clinical Neuroscience (2005) 12(6)
Local anesthetics are frequently administered prior to dental surgery and thus can be expected to be a major source of drug related complications in the dental office. The most frequently observed complications due to local anesthesia are dizziness, headache, psychomotor reactions, tachycardia, agitation, nausea and tremor.7 Local neurological complications are extremely rare and can usually be attributed to faulty technique.1 These complication are usually transient and last between 1 minute to 6 weeks without treatment.1,3–5,8,9 Several hypotheses may explain how local anesthetic applied to the alveolar region may reach and affect the ocular muscles. After accidental arterial injection the anesthetic agent may reach ocular muscles via arterial anastomotic connections linking the alveolar artery to the ophthalmic artery. Such an anastomotic network has been described by Rood. Vasoconstrictive agents mixed with the local anesthetic could also reach the arterial network of the eye muscles and lead to local ischemia.10 This mechanism may explain the partial ophthalmoplegia in the case presented. The Horner’s syndrome in our patient may have been caused by a sympathetic block at the ciliary ganglion with subsequent dominance of parasympathetic tone. Another possible explanation is that the anesthetic agent enters the venous circulation and reaches the cavernous sinus, bathing the oculomotor nerves. This could also serve as an explanation for the findings in our patient. The Horner’s syndrome in this case would be caused by paralysis of the sympathetic plexus around the internal carotid artery. Direct involvement of orbital structures via the venous route could also occur through communication of the cavernous sinus with the pterygoid venous plexus and the ophthalmic vein.4,9 The ophthalmic artery may also have anastamoses with this plexus.5 Another theory is that the anesthetic solution may reach the orbit by local diffusion along vascular, lymphatic and nervous networks between the pterygomaxillary fossa and the orbit.1 Direct extension through a bony defect in the maxillary sinus has also been proposed.3 The exact anatomopathological mechanism of this phenomenon is still to be elucidated. Although neurological complications after intraoral anesthesia are rare, both dentist and neurologist should be aware of this transient benign phenomenon and avoid unnecessary investigations.
REFERENCES 1. Penarrocha-Diago M, Sanchis-Bielsa JM. Ophthalmologic complications after intraoral local anesthesia with articaine. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000; 90: 21–24. 2. Hidding J, Khoury F. General complications in dental local anesthesia. Dtsch Zahnarztl Z 1991; 46: 834–836. 3. Petrelli EA, Steller RE. Medial rectus muscle palsy after dental anesthesia. Am J Ophthalmol 1980; 90: 422–424. 4. Marinho RO. Abducent nerve palsy following dental local analgesia. Br Dent J 1995; 179: 69–70. 5. Goldenberg AS. Transient diplopia from a posterior alveolar injection. J Endod 1990; 16: 550–551. 6. Ing E, Ing HC, Ing M, Fusco D, Ing TGE. Diagnosing oral disease that affects the eyes. J Am Dent Assoc 1994; 125: 608–616.
ª 2005 Elsevier Ltd. All rights reserved.
Cerebral and meningeal metastatic ovarian carcinoma 697
7. Daublender M, Muller R, Lipp MD. The incidence of complications associated with local anesthesia in dentistry. Anesth Prog 1997; 44: 132–141. 8. Goldenberg AS. Transient diplopia as a result of block injections. Mandibular and posterior superior alveolar. N Y State Dent J 1997; 63: 29–31. 9. Hyams SW. Oculomotor palsy following dental anesthesia. Arch Ophthalmol 1976; 94: 1281–1282. 10. Rood JP. Ocular complications of inferior dental nerve block. Br Dent J 1972; 132: 23–24.
unusual for ovarian carcinoma to present with multiple CNS involvement. ª 2005 Elsevier Ltd. All rights reserved. Journal of Clinical Neuroscience (2005) 12(6), 697–699 0967-5868/$ - see front matter ª 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2004.08.021
Keywords: brain metastases, multimodal treatment, outcome, ovarian carcinoma
Multiple cerebral and leptomeningeal metastases from ovarian carcinoma: unusual early presentation Mohammed al Barbarawi1 MBBS CHAM (JORDAN), 2 Sarah F Smith1 BSc BSc MPH (Hons), Suhair Qudsieh 1 Lali HS Sekhon MBBS (HONS) PhD PhD (Syd) FRACS
MBBS,
1
Department of Neurosurgery, Royal North Shore Hospital, St. Leonards, 2 Department of Foeto-Maternal Medicine, Liverpool Hospital, Liverpool; NSW, Australia
Summary Although virtually any systemic malignancy is capable of metastasizing to the brain, ovarian carcinoma, one of the more common female genital malignancies, is one of the rarer forms of brain metastases. In general, the outcome for ovarian carcinoma with brain metastases is extremely poor as most of these patients have widespread lesions elsewhere. This report describes the first known case of multiple cerebral and leptomeningeal metastases as the initial manifestation of ovarian carcinoma in a 41-year old woman who presented with a one-week history of headache, vomiting and confusion. CT scan of the brain was unremarkable, but lumbar puncture revealed atypical cells in the CSF. MRI scan of the brain showed multiple small enhancing lesions. Craniotomy for excision of one of these lesions demonstrated metastatic adenocarcinoma. A large ovarian tumour identified on pelvic CT scan was resected and the patient subsequently received chemotherapy and radiotherapy. Unfortunately she continued to decline and died within six months. Unlike primary tumours such as malignant melanoma, ovarian carcinoma does not have a predilection for the central nervous system (CNS), but the rare instances with CNS involvement occur at an advanced stage of the disease. Once the CNS is involved, the outcome is abysmal, even with multimodality therapy. It is extremely
Received 12 May 2004 Accepted 17 August 2004 Correspondence to: Sarah F. Smith, Department of Neurosurgery Level 7, Royal North Shore Hospital, St. Leonards NSW 2065, Australia. Tel.: +61 2 9926 8756; Fax: +61 2 9437 5172; E-mail: [email protected]
INTRODUCTION Metastatic involvement of the brain is one of the most feared complications of cancer because even small metastases may cause incapacitating neurological symptoms. In recent years important advances have been made in diagnosis and management of brain metastases. As a result, most patients receive effective systemic therapy leading to longer survival.1,2 Stereotactic radiosurgery, once a diagnosis has been established, has also been more recently shown to have some added efficacy.3 However, results with some tumours remain poor regardless of treatment. This group includes ovarian carcinoma. The outcome of patients with ovarian carcinoma will be dramatically affected by CNS involvement. CASE PRESENTATION A previously healthy 41-year old woman was admitted to our institution in September 2002 with a one-week history of headache, vomiting and blurred vision. On the day of admission she acutely developed delirium and a falling level of consciousness which required intubation. Unenhanced CT scan of the brain showed no abnormalities although with double-dosing of intravenous contrast, enhancing cortical lesions were visualised (Fig. 1). A lumbar puncture to rule out encephalopathy showed malignant (atypical) cells. MRI of the brain with gadolinium revealed multiple punctate enhancing lesions within the cerebral hemispheres and right cerebellar hemisphere (Fig. 2). Twelve hours after admission she underwent a right posterior parietal stereotactic craniotomy for excision of the largest lesion. Microscopy revealed metastatic
Fig. 1 Axial contrast enhanced CT scan of the brain showing several small cortical lesions (arrowed). The larger subcortical left parietal lesion was resected.
ª 2005 Elsevier Ltd. All rights reserved.
Journal of Clinical Neuroscience (2005) 12(6)