|Year : 2018 | Volume
| Issue : 2 | Page : 127-130
Neurosurgical strike by a coconut “shell”: A rare case of isolated internuclear ophthalmoplegia following closed head injury due to coconut fall
Vasu Kamaladevi Lathika, Tia Sebastin, Charles Kakkuzhyil Skariah
Department of Ophthalmology, Amala Institute of Medical Sciences, Thrissur, Kerala, India
|Date of Web Publication||28-Aug-2018|
Vasu Kamaladevi Lathika
Department of Ophthalmology, Amala Institute of Medical Sciences, Amala Nagar, Thrissur - 680 555, Kerala
Source of Support: None, Conflict of Interest: None
A 24-year-old female patient presented to the casualty following coconut fall on the head a few hours back with acute-onset binocular diplopia maximum on the left gaze and also on looking to the left and downward. Clinical examination revealed no external injuries, focal neurological deficits, or features of raised intracranial pressure. Computed tomography imaging was within normal limits. Hence, she was referred to ophthalmology by the neurosurgeon as a case of suspected partial third nerve palsy. Ocular examination revealed best-corrected visual acuity of 6/6 BE. There was limitation of adduction in the right eye and nystagmus in the left eye on attempted laevoversion. Convergence was absent. Anterior segment and fundus of both eyes were normal. Diplopia charting showed crossed diplopia which was maximum on left gaze. A clinical diagnosis of right anterior internuclear ophthalmoplegia (type-1) was made. It was confirmed by magnetic resonance imaging which revealed acute infarcts in the region of superior pons near right medial longitudinal fasciculus. The patient was treated with occlusion glasses.
Keywords: Head trauma, internuclear ophthalmoplegia, medial longitudinal fasciculus
|How to cite this article:|
Lathika VK, Sebastin T, Skariah CK. Neurosurgical strike by a coconut “shell”: A rare case of isolated internuclear ophthalmoplegia following closed head injury due to coconut fall. Kerala J Ophthalmol 2018;30:127-30
|How to cite this URL:|
Lathika VK, Sebastin T, Skariah CK. Neurosurgical strike by a coconut “shell”: A rare case of isolated internuclear ophthalmoplegia following closed head injury due to coconut fall. Kerala J Ophthalmol [serial online] 2018 [cited 2019 May 26];30:127-30. Available from: http://www.kjophthal.com/text.asp?2018/30/2/127/239973
| Introduction|| |
Trauma is an unusual cause for internuclear ophthalmoplegia (INO). Dorsal head trauma presenting with isolated INO is even rare (3.9%). This is the first case report in the literature describing coconut fall on the head as a cause for traumatic INO. It is especially relevant to us because coconut fall on the head is not uncommon in Kerala. The report intends to highlight the possibility of isolated INO in patients sustaining seemingly trivial head trauma with no other external injuries or obvious signs of brain stem damage.
| Case Report|| |
A 24-year-old female presented to the casualty with history of coconut fall on the head a few hours back. She had mild giddiness following the incident. There was no loss of consciousness, headache, vomiting, nose, or ear bleeds. On reaching casualty, she complained of double vision. Her past and personal histories were uneventful. General examination revealed the patient to be conscious and oriented with stable vitals with no external injuries. Neurosurgical examination showed no other neurological/higher function deficits, abnormal reflexes, or signs of increased intracranial tension. Computed tomography (CT) imaging was normal. She was referred to ophthalmology with suspected 3rd nerve involvement. Ocular examination revealed normal head posture. There was no facial asymmetry/ptosis/proptosis. There was right exotropia on primary gaze (15° by Hirschberg test and thirty prism diopters by the prism bar cover test in primary position). Best-corrected visual acuity was 6/6 in both eyes. Anterior and posterior segment examinations were within normal limits. Ocular movements showed the limitation of adduction in the right eye and nystagmus in the abducting left eye on attempted laevoversion [Figure 1]a. There was also a limitation of laevoelevation [Figure 1]b and laevodepression [Figure 1]c. Convergence was defective. Diplopia charting showed crossed diplopia, maximum on the left gaze, suggestive of the right medial rectus involvement [Figure 2]. A clinical diagnosis of isolated type 1/anterior right INO was made. Magnetic resonance imaging (MRI) revealed acute infarcts with hemorrhagic transformation at the level of superior pons involving medial longitudinal fasciculus (MLF), thus clinching the diagnosis [Figure 3]. The patient was given occlusion glasses with which she was symptomatically better and was advised follow-up.
|Figure 1: Composite picture showing the limitation of ocular movements. ([a] limitation of adduction in the right eye on the left gaze, [b] limitation of laevo elevation, [c] limitation of laevo depression)|
Click here to view
|Figure 3: Magnetic resonance imaging showing acute infarcts at the level of superior pons|
Click here to view
| Discussion|| |
INO is an ocular movement disorder caused by a lesion of the MLF, characterized by impaired adduction of the ipsilateral eye with nystagmus of the abducting eye. INO can be bilateral if medial longitudinal fasciculi of both sides are affected. MLF is a nerve fiber tract connecting 6th nerve nucleus to the contralateral 3rd nerve nucleus. It is a paired white matter tract passing close to the midline, through the brainstem lying ventral to the cerebral aqueduct in the midbrain and the fourth ventricle in the pons and medulla. It is the final common pathway for different types of conjugate eye movements. Connections from left sixth nerve pass to the right third nerve nucleus through right MLF. On attempted left gaze, MLF normally ensures simultaneous abduction in left eye and adduction in the right eye, thus bringing about smooth laevoversion. A lesion in the right MLF (as in this case) would result in the absence of adduction on the right eye and nystagmus of the abducting left eye on attempted left gaze (right INO.).
Classification of internuclear ophthalmoplegia
Type 1/anterior INO-lesion affects rostral part of MLF near third nerve nucleus, involving convergence center. Here, convergence center is involved with signs of adductor paralysis. It has been suggested that MLF lesions very close to third nerve sub nuclei as in this case may cause spillover damage to adjacent neural elements, thus prompting the differential of partial third nerve palsy. The patient showed signs of type 1 INO including defective convergence and limitation of laevo elevation and laevo depression.
Type 2/posterior INO-caudal part of the pathways is affected, convergence is spared, the variable extent of abductor paralysis.
Type 3 INO/posterior INO of Lutz-while Cogan used the term “posterior INO” to refer to INO associated with signs of pontine damage, it was used by Lutz to refer to a motility pattern the reverse of typical INO: that is, slowness of abduction with dissociated adducting nystagmus. This abduction defect is distinguished from VI nerve palsy by orthotropia in primary position and the adducting nystagmus. Some sources find evidence of this entity sketchy.
INO is a sign of exquisite localizing value. Common causes include multiple sclerosis, brainstem infarction, brainstem tumors, nutritional disorders, metabolic disorders, drug intoxication, and degenerative brainstem diseases. In a series of 410 patients, etiological factors found were multiple sclerosis (34%), especially in young patients, infarction (38%) in older people and unusual causes (28%). Unusual causes included trauma, tentorial herniation, infection tumor, iatrogenic injury, hemorrhage, and vasculitis. Among the trauma cases in the series, blunt trauma to head as a cause of INO as in this case was extremely rare (incidence −3.9%.) Of a total 36 reported cases in medical literature of traumatic INO, 83.33% were male and 16.67% were female. The mean age was 31.7 years. About 54% of the cases were bilateral; 46% of the cases were unilateral. Most were due to motor vehicle accidents (41.79%), blunt trauma (16.42%), or fall (10.49%). The mechanism of traumatic damage to MLF may be shear injury caused by angular acceleration leading to forward displacement of posterior brainstem downward, stretching of nerve fibers of MLF or compression and tearing of its arterial supply.
Literature review suggests that MRI is superior to CT in diagnosing INO. In our case too, the initial CT imaging was normal. The pontine lesion was picked up later on MRI (protocol-T1SE Axial, T2FSE axial, coronal, sagittal, FLAIR, DWI, and HSI axial) which showed two small discrete foci of diffusion hyperintensity in the right pontine tegmentum at the level of superior pons showing blooming on a gradient.
Variable recovery patterns have been reported following INO due to presumed brainstem ischemia. Recovery rate over 2–3 months ranges from 40% in one series to 80% in another consisting of 33 patients. Another study of 30 patients with strokes producing INO noted improvement in all patients over a mean period of 15 months. Recovery was more likely if the INO was isolated., Unfortunately, our patient was lost to follow up as she had to go abroad immediately following discharge.
Comparable case reports of isolated INO following closed head trauma are there, though scant. One such is of a 40-year-old woman who had sustained minor head trauma when a car struck against the right side of her car while driving slowly. The contusion involving MLF was detected by magnetic resonance imaging. Diplopia resolved in 5 months. Another report is of bilateral INO in a 35-year-old male patient following RTA. Unlike in our case, he had a transient loss of consciousness immediately following the trauma. However as in our case, there was no evidence of neurological deficits, ocular, or periorbital trauma. CT revealed no specific finding. The patient was then referred for ophthalmologic evaluation, with the primary complaint of diplopia. MRI of the brain revealed a small focus of hemorrhage at the pontomesencephalic junction. Seven days later, his diplopia subsided and versions were completely normal.
To conclude, INO can occur even in seemingly trivial head traumas with no external injuries or gross neurological deficits. This is the first case report so far of INO due to a coconut falling on the head. Diplopia can be the only presenting symptom of isolated INO. A high index of clinical suspicion is crucial in such cases. MRI is definitely superior to CT in clinching the diagnosis
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Keane JR. Internuclear ophthalmoplegia: Unusual causes in 114 of 410 patients. Arch Neurol 2005;62:714-7.
Cogan DG. Internuclear ophthalmoplegia, typical and atypical. Arch Ophthalmol 1970;84:583-9.
Doe JW 4th
, Jay WM. Traumatic unilateral internuclear ophthalmoplegia. Semin Ophthalmol 2006;21:245-53.
Chan JW. Isolated unilateral post-traumatic internuclear ophthalmoplegia. J Neuroophthalmol 2001;21:212-3.
Awerbuch G, Brown M, Levin JR. Magnetic resonance imaging correlates of internuclear ophthalmoplegia. Int J Neurosci 1990;52:39-43.
Eggenberger E, Golnik K, Lee A, Santos R, Suntay A, Satana B, et al.
Prognosis of ischemic internuclear ophthalmoplegia. Ophthalmology 2002;109:1676-8.
Kim JS. Internuclear ophthalmoplegia as an isolated or predominant symptom of brainstem infarction. Neurology 2004;62:1491-6.
Cerovski B, Vidović T, Papa J, Cerovski J, Bojić L. Minor head trauma and isolated unilateral internuclear ophthalmoplegia. J Emerg Med 2006;31:165-7.
Chon J, Kim M. Bilateral internuclear ophthalmoplegia following head trauma. Indian J Ophthalmol 2017;65:246-7.
] [Full text]
[Figure 1], [Figure 2], [Figure 3]