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Traumatic Ocular Motor Neuropathies After Mild Head Injury
Letter to the Editor Traumatic Ocular Motor Neuropathies After Mild Head Injury
LETTER: entitled “Ocular Movement Nerve Palsy After T heMildarticle Head Trauma” by Li et al., published recently in WORLD 1
NEUROSURGERY, was read with great interest. The authors conducted a retrospective analysis of 6 of their own cases of ocular motor nerve palsies combined with a literature review. The inclusion criteria were Glasgow Coma Scale score of 14e15 and no definite skull fracture/intracranial traumatic lesions (hemorrhage, cerebral contusion, and laceration) on computed tomography (CT) scan. Thirty-one patients were identified and analyzed. The mean age was 39.1 years (range, 5e75 years). Cranial nerves (CNs) III, IV, and VI were involved in 54.8%, 3.2%, and 45.2% of cases, respectively. The CN palsies were unilateral in 22 (71%) patients, bilateral in 9 (20.9%) cases, whereas only 1 patient had multiple CN involvement. The time interval from head trauma to onset of ocular motor nerve palsy (OMNP) ranged from 0 to 6 days, and approximately 25% presented in a delayed period. Except those with associated intracranial lesions that were managed surgically, most were managed conservatively, and a few also received steroid therapy. All patients in their own series experienced complete resolution (CR), but overall, only 54.6% experienced CR between 10 days and 13 months, and 60% had CR by 3 months. Additional intracranial findings that might predispose to OMNP after mild head trauma were identified in 25.8% of cases, and 4 out of these 8 patients (50%) experienced CR after surgical intervention. On comparing the patients with CN III palsy and CN VI palsy, the following differences were noted: the mean age was slightly lower in the CN VI group, only 50% of the CN VI group presented immediately after trauma compared with 82% in the CN III group, there was a significantly higher proportion of bilateral involvement in the CN VI group, and there were slightly higher rates of CR noted in the CN VI group. OMNP after minor head trauma is rare and most commonly noted after severe head injury.2-4 Regarding the article by Li et al., I would like to address a few points that might be useful to the readers. The authors need to be appreciated for having performed such an extensive study on this rare topic. However, I would like to differ from the authors’ claim that a total of only 31 cases of palsies of CNs III, IV, and VI have been reported in the literature after mild head trauma. This appears more likely to be a reporting bias than the true numbers because many cases might be included in the bigger series and not highlighted individually. Also, many physicians may have thought it to be of relative insignificance to have them published in the literature. One such case managed at our institute recently has been subsequently presented. A 75-year-old woman was brought to our casualty services after a fall from a standing bus 2 hours prior. She had no loss of consciousness, seizures, or ear/nasal bleed. On admission, she was E4V4M6 (eye opening (E)-4, verbal response (V)-4, motor response (M)-6) (Glasgow Coma Scale score 14 out of 15), with dilated, nonreacting left pupil, left ptosis, and external ophthalmoplegia, suggestive of a complete CN III palsy (Figure 1AeD). She had a left frontal scalp laceration that was
WORLD NEUROSURGERY 98: 853-855, FEBRUARY 2017
sutured. CT scan showed no evidence of hematoma, skull fracture, or any other intracranial lesion (Figure 2A and B). She had a fracture of the fifth and sixth ribs with lung contusion and hence was electively ventilated and extubated later. She was managed conservatively with supportive treatment and had no recovery of her CN III palsy at discharge. Lin et al.3 retrospectively analyzed 26 cases of traumatic third nerve palsy in mild head injury (HI). None had any parenchymal abnormalities on CT scan, and only 6 had associated sphenoid bone fracture. All had presented immediately. Taking into consideration only those 20 cases with no fractures, all 20 (100%) had internal ophthalmoplegia, 14 (70%) had ptosis, and 13 (65%) had extraocular palsy. For this group, the recovery rates of ptosis, external ophthalmoplegia, and internal ophthalmoplegia were 92% (13 of 14 patients), 77% (10 of 13 patients), and 45% (9 of 20 patients), respectively. Kuo et al.2 analyzed 10 cases of isolated oculomotor nerve palsy after mild head trauma. All had dilated pupil at examination, 8 patients (80%) had ptosis, 9 patients had complete loss of extraocular movements, and 1 patient had isolated inferior rectus palsy. At the end of follow-up, only 3 patients (30%) had experienced complete recovery of oculomotor palsy. Nagaseki et al.5 reported on 6 cases of internal ophthalmoplegia caused by minor HI, wherein only 2 had partial extraocular palsies or ptosis, and partial anisocoria still persisted in 4 of them at a mean followup of 22 months. The pathophysiologic mechanism of the internal ophthalmoplegia was thought to be slight injury of the pupillomotor fibers on the ventromedial surface of the third nerve at the posterior petroclinoid ligament, which acts as the fulcrum because of the downward displacement of the brainstem at the time of impact. Similar case reports have been reported in isolation elsewhere.6-8 In their analysis of cranial nerve injury after minor head trauma, Coello et al.9 noted a total of 22 ocular motor palsies (CNs III, IV, and VI). However, after excluding cases with skull base fractures and hematoma/contusion, a total of 7 cases of OMNP with no CT abnormalities were identified (CN IV: n ¼ 3; CN VI: n ¼ 4). In this subset, all showed CR of their nerve palsies. The CN IV palsies recovered within 3 months, and all cases of CN VI dysfunction showed recovery within 1 year. Advani et al.10 reported a case of complete bilateral sixth nerve palsy after minor head trauma with normal imaging findings. Another case of bilateral abducens nerve palsy was reported by Dobbs et al.11 A few other authors have also reported such cases after minor HI.12,13 Traumatic oculomotor palsy can be caused by direct or indirect injury to the oculomotor nerve. Indirect injury occurs when a lesion, such as a posterior communicating aneurysm or uncal herniation or rarely a neoplasm, results in third nerve compression, whereas rootlet avulsion, ischemia, or distal fascicular damage from differential movements between the brainstem and supratentorial structures results in a direct injury.2,4,14 In indirect-type injuries, the underlying pathology can often be diagnosed with relative ease on imaging studies. However, in direct-type oculomotor injuries, only subtle findings may be noted on magnetic resonance imaging, including hemorrhage at the midbrain exit site of the oculomotor nerve, bending of the
www.WORLDNEUROSURGERY.org
853
LETTER TO THE EDITOR
Figure 1. Complete ptosis of left eye is noted (A). The left-sided cranial nerve III innervated extraocular muscle palsy is evident on right, left, and superior
ipsilateral oculomotor nerve at the posterior petroclinoid ligament, parenchymal lesion at the ventral midbrain, and enhancement of the cisternal portion of the oculomotor nerve.2,8,15,16 3There is no specific treatment for OMNP, and treatment is often challenging because of the multiple extraocular muscle involvement.3,4 If there is evidence of bony compression, surgical treatment is beneficial in most cases.3 Steroid usage has been reported in a few cases of direct injury with varying results.1,3 Botulinum toxin injection has been found to be beneficial in selected patients in the treatment of strabismus, blepharospasm, and torticollis by producing temporary muscle
gaze, whereas lateral rectus is functional (BeD). Features suggestive of leftsided third nerve palsy.
weakness. A few patients have also been managed with occluding cosmetic contact lenses to prevent diplopia as a temporary measure until recovery. Strabismus surgery is proposed when there is no further improvement but is usually delayed up to 6e12 months after the trauma.2-4 Many studies have proven the negative impact of oculomotor palsy on the functional outcome of patients with HI.2 The prognosis of traumatic oculomotor palsy is usually poor, and full recovery is rarely seen.2,17 No definitive prognostic factor has been identified; however, some studies have shown the initial deviation angle to be the only factor associated with complete recovery.18 However, it has been consistently noted by multiple
Figure 2. Noncontrast computed tomography (CT) scan showing no evidence of hematoma or contusion (A). Bone window CT showing no skull fracture (B).
854
www.SCIENCEDIRECT.com
98: 853-855, FEBRUARY 2017 WORLD NEUROSURGERY
LETTER TO THE EDITOR
authors that recovery rate of ptosis is higher than that of external ophthalmoplegia and anisocoria.2,3,6
8. Berti AF, Ramirez PM, Tran HP. MRI findings of oculomotor nerve palsy in mild traumatic brain injury: case report and review of literature. J Neurol Res. 2013;3: 163-165.
G. Lakshmi Prasad Department of Neurosurgery, Kasturba Medical College, Manipal University, Manipal, India To whom correspondence should be addressed: G. Lakshmi Prasad, M.Ch. [E-mail: [email protected]]
9. Coello AF, Canals AG, Gonzalez JM, Martín JJ. Cranial nerve injury after minor head trauma. Clinical article. J Neurosurg. 2010;113:547-555.
http://dx.doi.org/10.1016/j.wneu.2016.09.050.
REFERENCES 1. Li G, Zhu X, Gu X, Sun Y, Gao X, Zhang Y, et al. Ocular movement nerve palsy after mild head trauma. World Neurosurg. 2016;94:296-302. 2. Kuo LT, Huang AP, Yang CC, Tsai SY, Tu YK, Huang SJ. Clinical outcome of mild head injury with isolated oculomotor nerve palsy. J Neurotrauma. 2010;27: 1959-1964. 3. Lin C, Dong Y, Lv L, Yu M, Hou L. Clinical features and functional recovery of traumatic isolated oculomotor nerve palsy in mild head injury with sphenoid fracture. J Neurosurg. 2013;118:364-369. 4. Muthu P, Pritty P. Mild head injury with isolated third nerve palsy. Emerg Med J. 2001;18:310-311. 5. Nagaseki Y, Shimizu T, Kakizawa T, Fukamachi A, Nukui H. Primary internal ophthalmoplegia due to head injury. Acta Neurochir (Wien). 1989;97:117-122. 6. Liu YT, Lee YC, Liu HC. Isolated oculomotor nerve palsy due to head injury. J Chin Med Assoc. 2004;67:149-151. 7. Takeuchi S, Takasato Y, Masaoka H, Hayakawa T, Otani N, Yoshino Y, et al. Isolated traumatic oculomotor nerve palsy caused by minor head trauma. Brain Nerve. 2008;60:555-558 [in Japanese].
WORLD NEUROSURGERY 98: 853-855, FEBRUARY 2017
10. Advani RM, Baumann MR. Bilateral sixth nerve palsy after head trauma. Ann Emerg Med. 2003;41:27-31. 11. Dobbs M, Fakhoury T. Bilateral abducens nerve palsy from mild trauma with force applied at an oblique angle: a case report and review of the literature. J Ky Med Assoc. 2003;101:507-510. 12. Chrousos GA, Dipaolo F, Kattah JC, Laws ER Jr. Paresis of the abducens nerve after trivial head injury. Am J Ophthalmol. 1993;116:387-388. 13. Lahbabi M, Levy JD, Laxenaire A, Scheffer P. Bilateral paralysis of the 6th cranial nerve pair and minor head injury. Apropos of a case. Review of the literature. Rev Stomatol Chir Maxillofac. 1997;98:295-298 [in French]. 14. Eyster EF, Hoyt WF, Wilson CB. Oculomotor palsy from minor head trauma. An initial sign of basal intracranial tumor. JAMA. 1972;220:1083-1086. 15. Balcer LJ, Galetta SL, Bagley LJ, Pakola SJ. Localization of traumatic oculomotor nerve palsy to the midbrain exit site by magnetic resonance imaging. Am J Ophthalmol. 1996;122:437-439. 16. Kaido T, Tanaka Y, Kanemoto Y, Katsuragi Y, Okura H. Traumatic oculomotor nerve palsy. J Clin Neurosci. 2006;13:852-855. 17. Chen CC, Pai YM, Wang RF, Wang TL, Chong CF. Isolated oculomotor nerve palsy from minor head trauma. Br J Sports Med. 2005;39:e34. 18. Park UC, Kim SJ, Hwang JM, Yu YS. Clinical features and natural history of acquired third, fourth, and sixth cranial nerve palsy. Eye. 2008;22:691-696.
www.WORLDNEUROSURGERY.org
855
LETTER: entitled “Ocular Movement Nerve Palsy After T heMildarticle Head Trauma” by Li et al., published recently in WORLD 1
NEUROSURGERY, was read with great interest. The authors conducted a retrospective analysis of 6 of their own cases of ocular motor nerve palsies combined with a literature review. The inclusion criteria were Glasgow Coma Scale score of 14e15 and no definite skull fracture/intracranial traumatic lesions (hemorrhage, cerebral contusion, and laceration) on computed tomography (CT) scan. Thirty-one patients were identified and analyzed. The mean age was 39.1 years (range, 5e75 years). Cranial nerves (CNs) III, IV, and VI were involved in 54.8%, 3.2%, and 45.2% of cases, respectively. The CN palsies were unilateral in 22 (71%) patients, bilateral in 9 (20.9%) cases, whereas only 1 patient had multiple CN involvement. The time interval from head trauma to onset of ocular motor nerve palsy (OMNP) ranged from 0 to 6 days, and approximately 25% presented in a delayed period. Except those with associated intracranial lesions that were managed surgically, most were managed conservatively, and a few also received steroid therapy. All patients in their own series experienced complete resolution (CR), but overall, only 54.6% experienced CR between 10 days and 13 months, and 60% had CR by 3 months. Additional intracranial findings that might predispose to OMNP after mild head trauma were identified in 25.8% of cases, and 4 out of these 8 patients (50%) experienced CR after surgical intervention. On comparing the patients with CN III palsy and CN VI palsy, the following differences were noted: the mean age was slightly lower in the CN VI group, only 50% of the CN VI group presented immediately after trauma compared with 82% in the CN III group, there was a significantly higher proportion of bilateral involvement in the CN VI group, and there were slightly higher rates of CR noted in the CN VI group. OMNP after minor head trauma is rare and most commonly noted after severe head injury.2-4 Regarding the article by Li et al., I would like to address a few points that might be useful to the readers. The authors need to be appreciated for having performed such an extensive study on this rare topic. However, I would like to differ from the authors’ claim that a total of only 31 cases of palsies of CNs III, IV, and VI have been reported in the literature after mild head trauma. This appears more likely to be a reporting bias than the true numbers because many cases might be included in the bigger series and not highlighted individually. Also, many physicians may have thought it to be of relative insignificance to have them published in the literature. One such case managed at our institute recently has been subsequently presented. A 75-year-old woman was brought to our casualty services after a fall from a standing bus 2 hours prior. She had no loss of consciousness, seizures, or ear/nasal bleed. On admission, she was E4V4M6 (eye opening (E)-4, verbal response (V)-4, motor response (M)-6) (Glasgow Coma Scale score 14 out of 15), with dilated, nonreacting left pupil, left ptosis, and external ophthalmoplegia, suggestive of a complete CN III palsy (Figure 1AeD). She had a left frontal scalp laceration that was
WORLD NEUROSURGERY 98: 853-855, FEBRUARY 2017
sutured. CT scan showed no evidence of hematoma, skull fracture, or any other intracranial lesion (Figure 2A and B). She had a fracture of the fifth and sixth ribs with lung contusion and hence was electively ventilated and extubated later. She was managed conservatively with supportive treatment and had no recovery of her CN III palsy at discharge. Lin et al.3 retrospectively analyzed 26 cases of traumatic third nerve palsy in mild head injury (HI). None had any parenchymal abnormalities on CT scan, and only 6 had associated sphenoid bone fracture. All had presented immediately. Taking into consideration only those 20 cases with no fractures, all 20 (100%) had internal ophthalmoplegia, 14 (70%) had ptosis, and 13 (65%) had extraocular palsy. For this group, the recovery rates of ptosis, external ophthalmoplegia, and internal ophthalmoplegia were 92% (13 of 14 patients), 77% (10 of 13 patients), and 45% (9 of 20 patients), respectively. Kuo et al.2 analyzed 10 cases of isolated oculomotor nerve palsy after mild head trauma. All had dilated pupil at examination, 8 patients (80%) had ptosis, 9 patients had complete loss of extraocular movements, and 1 patient had isolated inferior rectus palsy. At the end of follow-up, only 3 patients (30%) had experienced complete recovery of oculomotor palsy. Nagaseki et al.5 reported on 6 cases of internal ophthalmoplegia caused by minor HI, wherein only 2 had partial extraocular palsies or ptosis, and partial anisocoria still persisted in 4 of them at a mean followup of 22 months. The pathophysiologic mechanism of the internal ophthalmoplegia was thought to be slight injury of the pupillomotor fibers on the ventromedial surface of the third nerve at the posterior petroclinoid ligament, which acts as the fulcrum because of the downward displacement of the brainstem at the time of impact. Similar case reports have been reported in isolation elsewhere.6-8 In their analysis of cranial nerve injury after minor head trauma, Coello et al.9 noted a total of 22 ocular motor palsies (CNs III, IV, and VI). However, after excluding cases with skull base fractures and hematoma/contusion, a total of 7 cases of OMNP with no CT abnormalities were identified (CN IV: n ¼ 3; CN VI: n ¼ 4). In this subset, all showed CR of their nerve palsies. The CN IV palsies recovered within 3 months, and all cases of CN VI dysfunction showed recovery within 1 year. Advani et al.10 reported a case of complete bilateral sixth nerve palsy after minor head trauma with normal imaging findings. Another case of bilateral abducens nerve palsy was reported by Dobbs et al.11 A few other authors have also reported such cases after minor HI.12,13 Traumatic oculomotor palsy can be caused by direct or indirect injury to the oculomotor nerve. Indirect injury occurs when a lesion, such as a posterior communicating aneurysm or uncal herniation or rarely a neoplasm, results in third nerve compression, whereas rootlet avulsion, ischemia, or distal fascicular damage from differential movements between the brainstem and supratentorial structures results in a direct injury.2,4,14 In indirect-type injuries, the underlying pathology can often be diagnosed with relative ease on imaging studies. However, in direct-type oculomotor injuries, only subtle findings may be noted on magnetic resonance imaging, including hemorrhage at the midbrain exit site of the oculomotor nerve, bending of the
www.WORLDNEUROSURGERY.org
853
LETTER TO THE EDITOR
Figure 1. Complete ptosis of left eye is noted (A). The left-sided cranial nerve III innervated extraocular muscle palsy is evident on right, left, and superior
ipsilateral oculomotor nerve at the posterior petroclinoid ligament, parenchymal lesion at the ventral midbrain, and enhancement of the cisternal portion of the oculomotor nerve.2,8,15,16 3There is no specific treatment for OMNP, and treatment is often challenging because of the multiple extraocular muscle involvement.3,4 If there is evidence of bony compression, surgical treatment is beneficial in most cases.3 Steroid usage has been reported in a few cases of direct injury with varying results.1,3 Botulinum toxin injection has been found to be beneficial in selected patients in the treatment of strabismus, blepharospasm, and torticollis by producing temporary muscle
gaze, whereas lateral rectus is functional (BeD). Features suggestive of leftsided third nerve palsy.
weakness. A few patients have also been managed with occluding cosmetic contact lenses to prevent diplopia as a temporary measure until recovery. Strabismus surgery is proposed when there is no further improvement but is usually delayed up to 6e12 months after the trauma.2-4 Many studies have proven the negative impact of oculomotor palsy on the functional outcome of patients with HI.2 The prognosis of traumatic oculomotor palsy is usually poor, and full recovery is rarely seen.2,17 No definitive prognostic factor has been identified; however, some studies have shown the initial deviation angle to be the only factor associated with complete recovery.18 However, it has been consistently noted by multiple
Figure 2. Noncontrast computed tomography (CT) scan showing no evidence of hematoma or contusion (A). Bone window CT showing no skull fracture (B).
854
www.SCIENCEDIRECT.com
98: 853-855, FEBRUARY 2017 WORLD NEUROSURGERY
LETTER TO THE EDITOR
authors that recovery rate of ptosis is higher than that of external ophthalmoplegia and anisocoria.2,3,6
8. Berti AF, Ramirez PM, Tran HP. MRI findings of oculomotor nerve palsy in mild traumatic brain injury: case report and review of literature. J Neurol Res. 2013;3: 163-165.
G. Lakshmi Prasad Department of Neurosurgery, Kasturba Medical College, Manipal University, Manipal, India To whom correspondence should be addressed: G. Lakshmi Prasad, M.Ch. [E-mail: [email protected]]
9. Coello AF, Canals AG, Gonzalez JM, Martín JJ. Cranial nerve injury after minor head trauma. Clinical article. J Neurosurg. 2010;113:547-555.
http://dx.doi.org/10.1016/j.wneu.2016.09.050.
REFERENCES 1. Li G, Zhu X, Gu X, Sun Y, Gao X, Zhang Y, et al. Ocular movement nerve palsy after mild head trauma. World Neurosurg. 2016;94:296-302. 2. Kuo LT, Huang AP, Yang CC, Tsai SY, Tu YK, Huang SJ. Clinical outcome of mild head injury with isolated oculomotor nerve palsy. J Neurotrauma. 2010;27: 1959-1964. 3. Lin C, Dong Y, Lv L, Yu M, Hou L. Clinical features and functional recovery of traumatic isolated oculomotor nerve palsy in mild head injury with sphenoid fracture. J Neurosurg. 2013;118:364-369. 4. Muthu P, Pritty P. Mild head injury with isolated third nerve palsy. Emerg Med J. 2001;18:310-311. 5. Nagaseki Y, Shimizu T, Kakizawa T, Fukamachi A, Nukui H. Primary internal ophthalmoplegia due to head injury. Acta Neurochir (Wien). 1989;97:117-122. 6. Liu YT, Lee YC, Liu HC. Isolated oculomotor nerve palsy due to head injury. J Chin Med Assoc. 2004;67:149-151. 7. Takeuchi S, Takasato Y, Masaoka H, Hayakawa T, Otani N, Yoshino Y, et al. Isolated traumatic oculomotor nerve palsy caused by minor head trauma. Brain Nerve. 2008;60:555-558 [in Japanese].
WORLD NEUROSURGERY 98: 853-855, FEBRUARY 2017
10. Advani RM, Baumann MR. Bilateral sixth nerve palsy after head trauma. Ann Emerg Med. 2003;41:27-31. 11. Dobbs M, Fakhoury T. Bilateral abducens nerve palsy from mild trauma with force applied at an oblique angle: a case report and review of the literature. J Ky Med Assoc. 2003;101:507-510. 12. Chrousos GA, Dipaolo F, Kattah JC, Laws ER Jr. Paresis of the abducens nerve after trivial head injury. Am J Ophthalmol. 1993;116:387-388. 13. Lahbabi M, Levy JD, Laxenaire A, Scheffer P. Bilateral paralysis of the 6th cranial nerve pair and minor head injury. Apropos of a case. Review of the literature. Rev Stomatol Chir Maxillofac. 1997;98:295-298 [in French]. 14. Eyster EF, Hoyt WF, Wilson CB. Oculomotor palsy from minor head trauma. An initial sign of basal intracranial tumor. JAMA. 1972;220:1083-1086. 15. Balcer LJ, Galetta SL, Bagley LJ, Pakola SJ. Localization of traumatic oculomotor nerve palsy to the midbrain exit site by magnetic resonance imaging. Am J Ophthalmol. 1996;122:437-439. 16. Kaido T, Tanaka Y, Kanemoto Y, Katsuragi Y, Okura H. Traumatic oculomotor nerve palsy. J Clin Neurosci. 2006;13:852-855. 17. Chen CC, Pai YM, Wang RF, Wang TL, Chong CF. Isolated oculomotor nerve palsy from minor head trauma. Br J Sports Med. 2005;39:e34. 18. Park UC, Kim SJ, Hwang JM, Yu YS. Clinical features and natural history of acquired third, fourth, and sixth cranial nerve palsy. Eye. 2008;22:691-696.
www.WORLDNEUROSURGERY.org
855