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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 1  |  Issue : 1  |  Page : 148-150

Torsipulsion, a useful diagnostic sign in lateral medullary infarction: A report of three cases


Department of Neuroophthalmology, The Eye Foundation, Coimbatore, Tamil Nadu, India

Date of Submission18-Jan-2020
Date of Acceptance16-Jul-2020
Date of Web Publication31-Dec-2020

Correspondence Address:
Dr. R Muralidhar
Department of Pediatric Ophthalmology, 582 A DB Road, R.S. Puram, Coimbatore, Tamil Nadu - 641 002
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijo.IJO_64_20

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  Abstract 


A number of ocular motility disturbances such as skew deviation, saccadic/smooth pursuit abnormalities, Horner's syndrome, and nystagmus have been reported in lateral medullary infarction. We report 3 patients who had torsipulsion as the main ocular movement abnormality directly attributable to lateral medullary infarction. Patients 1 and 2 had a clockwise torsional movement that was diagnosed on slit lamp. The movement was elicited on asking the patients to make a horizontal saccade. Both patients were noted to have dorsolateral medullary infarction on MRI of the brain. Neither patient had symptoms directly attributable to torsipulsion. Patient No. 3 was referred for non-resolving left 6th nerve palsy. He had infarcts in the left pons, cerebellum and dorsolateral medulla. Torsipulsion was the only ocular motility disorder caused by medullary infarction. Different pathways in the dorsolateral medulla have been implicated in the various ocular motility and neurological abnormalities seen in lateral medullary syndrome. It is possible that sparing of some and involvement of others could result in varied clinical presentations reported in literature. It is important for the ophthalmologist to be aware of torsipulsion as a diagnostic sign of lateral medullary infarction.

Keywords: Lateral medullary infarction, ocular movement abnormalities, torsipulsion


How to cite this article:
Muralidhar R, Vidhya N, Ramamurthy D. Torsipulsion, a useful diagnostic sign in lateral medullary infarction: A report of three cases. Indian J Ophthalmol Case Rep 2021;1:148-50

How to cite this URL:
Muralidhar R, Vidhya N, Ramamurthy D. Torsipulsion, a useful diagnostic sign in lateral medullary infarction: A report of three cases. Indian J Ophthalmol Case Rep [serial online] 2021 [cited 2021 Feb 25];1:148-50. Available from: https://www.ijoreports.in/text.asp?2021/1/1/148/305532



A number of ocular motility abnormalities can occur in Wallenberg lateral medullary infarction. Lateral medullary infarction may occur as an isolated event or in combination with cerebellar and pontine infarction. Patients may complain of bizarre environmental tilt and may report the entire room to be tilted to one side or even upside down. These complaints may be mistakenly interpreted as having a psychogenic basis. Other neurologic features of Wallenberg lateral medullary infarction include ipsilateral facial hypalgesia and hypalgesia of contralateral trunk and extremities, ipsilateral cerebellar signs, ipsilateral Horner's syndrome, ipsilateral vocal cord, pharyngeal and palatal paralysis causing dysphagia, vertigo, nausea and vomiting.[1],[2]

We report on 3 patients with torsipulsion. In 2 patients, the identification aided the diagnosis of lateral medullary infarction.


  Case Reports Top


Case 1

A 62-year-old female patient was referred to us from her neurologist with the diagnosis of a suspected brainstem infarction and a “funny eye movement”. She had complaints of vertigo, tilting of surroundings towards the left and a feeling of being pulled towards the left side for the past four days. There were no ocular complaints. The patient had poorly controlled diabetes and hypertension. She had a vision of 20/20 OU and a review of the anterior and posterior segment was normal. The eyes were orthophoric and the ocular motility was full. Attempted gaze to the left elicited a conjugate clockwise torsional eye movement (torsipulsion) that was recorded on slit lamp [Video 1]. Saccades to the left side were slightly hypometric and the saccades to the right were normal. The patient had no complaints on looking towards objects on either side. The smooth pursuit was normal. The remainder of the ocular exam was unremarkable. She had impairment of pain on the left side of the face and on the right upper limb and trunk. Remainder of her systemic neurologic examination was normal. Wallenberg syndrome was suspected and MRI of the brain showed infarction of the dorsolateral medulla on the left side [Figure 1]. She was referred back to the neurologist.
Figure 1: T2 weighted axial MRI image of patient 1 showing hyperintensity in posterolateral medulla on the left side suggested of an infarct (arrow)

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Case 2

A 75-year-old male patient presented to us with a vague disturbance in vision for the past 1 week. On examination, the patient had a best corrected vision of 20/20 OU. A review of the anterior and posterior segment was normal. The ocular motility was full. Attempted saccades to either side elicited a clockwise torsional eye movement (torsipulsion) that could be detected on slit lamp only. He had impairment of pain and temperature sensation on the left side of the face and on the right upper limb and trunk. MRI of the brain showed infarction of the dorsolateral medulla on the left side [Figure 2]. He was referred to a neurologist.
Figure 2: T2 weighted axial MRI image of patient 2 showing hyperintensity in posterolateral medulla on the left side suggested of an infarct (arrow)

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Case 3

A 55-year-old male patient with poorly controlled diabetes and hypertension diagnosed elsewhere as brainstem stroke 6 months back was referred to our neuro-ophthalmology clinic for diplopia. On examination, the patient had left esotropia with abduction restriction due to left 6th nerve palsy [Figure 3]. The adduction saccades of the right eye and the abduction saccades of the left eye were slow. The patient mentioned that he was not able to move his eyes leftward in the beginning. Over the next 3-4 months, the right eye movements recovered but his left eye movements did not. The old records also mentioned left gaze palsy. Attempted horizontal saccades to the right revealed a subtle counter clockwise movement in both eyes that could be recorded on the slit lamp (torsipulsion - Video 2). He also had left 7th nerve palsy, right hemiplegia and ataxia towards the left side, impairment of pain and temperature sensation on the left side of face and the right upper limb. MRI of the brain revealed infarcts in the cerebellum, dorsolateral medulla and medial pons on the left side [Figure 4]. He was advised strabismus surgery after systemic clearance. The patient was however lost to follow-up.
Figure 3: Cardinal gaze photograph of Patient 3 showing left esotropia and left abduction restriction (due to 6th nerve palsy). There is no ptosis or anisocoria suggestive of Horner's syndrome or skew deviation

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Figure 4: T2 weighted axial MRI image of patient 3 showing hyperintensities in posterolateral medulla, cerebellum and pons on the left side suggestive of infarction (arrows)

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  Discussion Top


A number of ocular motility disorders have been described in patients with infarctions of the dorsolateral medulla and are often unappreciated. Torsipulsion refers to an inappropriate torsional saccade that occurs during attempted horizontal or vertical saccades. It is often associated with torsional nystagmus. Torsipulsion may be the result of a central imbalance of the anterior and posterior semi-circular canals pathways probably resulting from damage to the vestibular nuclei.[1],[3],[4]

Other reported ocular motility abnormalities include disturbance of ocular alignment (skew deviation, ocular tilt reaction), nystagmus (horizontal, vertical, torsional, mixed with the fast phase away from the side of the lesion, but may be towards the side of the lesion or may change direction), smooth pursuit abnormalities (impaired contralateral smooth pursuit) and saccadic abnormalities (ipsipulsion, lateropulsion, torsipulsion and oblique saccadic trajectories on attempted vertical gaze).[1],[2]

Utricular projections cross the midline and ascend in the medial longitudinal fasciculus to connect to the third and fourth nerve nuclei. Lesions of these otolithic pathways may result in imbalance of the otolithic input causing skew deviation. Damage to the otolithic central projections that mediate ocular counter roll is thought to cause torsional/see-saw nystagmus. A subjective sense of tilting of surroundings (as reported by patient 1) also is attributed to damage to vestibular-otolith central connections. The cerebellum is involved in modulating the amplitude of fast eye movements. Interruption of the cerebellar connections that traverse the lateral medulla may explain the abnormalities in saccades and smooth pursuit. Damage to the juxtarestiform body, which carries signals from the fastigial nucleus to the brainstem reticular formation, is thought to be responsible for lateropulsion.[2] Damage to the ocular sympathetic pathway that traverses in the dorsolateral medulla results in Horner's syndrome.[5] It is thus clear that the clinical features of lateral medullary infarction is caused by damage to multiple distinct pathways that are clustered in the dorsolateral medulla. Involvement of some pathways/structures and sparing of the others could explain the difference in clinical features reported by different authors.

Kommerell et al. reported on a 52-year-old female with lateropulsion of saccadic movements and left lateral medullary infarction. Saccades to the left overshot the target and saccades to the right were small and fell short of the target. When the patient was asked to sit in front of a contour free screen, the eyes deviated to the left. The same finding was noted when the patient tried to close her eyes. Vertical saccades tended to deflect leftward. Other ocular findings included left Horner's syndrome, impaired left smooth pursuit movements, difficulty in maintaining steady fixation, and abnormalities in optokinetic nystagmus. The patient had dissociated analgesia with preserved tactile sensations[6] Morrow et al. also reported on torsional saccades (torsipulsion) directed away from the side of infarction during attempted vertical and contralateral saccades in two of their patients. Other ocular movement abnormalities noted in their series of three patients include vertical & torsional nystagmus, skew deviation, Horner's syndrome, and lateropulsion of saccades.[3]

It may be noted that our patients did not have any complaints pertaining to torsipulsion. Conscious information about gaze direction is derived from internal reference to the ocular motor input called the corollary discharge. It is believed that in lateral medullary infarction, this system is biased. This bias is added to the ocular motor system before prenuclear gaze mechanism. So the patient believes that he is looking straight ahead even when there is a saccadic abnormality.[6] (torsipulsion in our case) This may explain why our patients did not have a subjective perception of rotation of the surroundings when their eyes turned in torsipulsion.

Our case series is unique in that torsipulsion was the only ocular motility disorder directly attributable to the medullary infarct. Patient 1 did have mild hypometric saccades to the left that was not in line with the left medullary infarction (which should have saccades that overshoot the target on the side of infarction and should be hypometric towards the contralateral side). Saccades to the right were normal and the patient did not have any complaints fixing either to the right or left. It is difficult to comment if this was a true saccadic dysmetria. In 2 patients, the disorder was subtle and could be recorded on slit lamp examination only (Patients 2 and 3). Recognition of this entity aided the diagnosis in two patients (Patients 1 and 2). The direction of torsional eye movement and the gaze that evoked the movement was towards the side of the lesion in patient 1 and 2 and away from the side of the lesion in patient 3. In patient 3, torsipulsion had persisted for over 6 months. The other patients were lost to follow-up and the persistence or resolution of torsipulsion could not be ascertained. The commonest etiology of lateral medullary syndrome is occlusion of the ipsilateral vertebral artery. Rarely the posterior inferior cerebellar artery is selectively involved. Other uncommon causes include dissection of the vertebral artery and demyelination.[1] An ischemic etiology was suspected in all our patients. Patients 1 & 2 had infarction of the dorsolateral medulla only and the symptoms and signs were of Wallenberg's lateral medullary syndrome. Patient 3 also had left medial pontine syndrome and cerebellar infarction in addition to lateral medullary syndrome [Figure 4] due to a more extensive posterior circulation stroke. This caused the ipsilateral ataxia in our patient. Medial pontine syndrome is characterized by involvement of the 6th nerve nucleus (which could explain the gaze palsy that later recovered partially leaving behind slow adducting saccades of the right eye and left abduction deficit), and contralateral hemiplegia. Ipsilateral internuclear ophthalmoplegia has also been reported in medial pontine syndrome but was not seen in our patient. The 7th nerve nucleus is spared but the fibres that wind around the 6th nerve nucleus can be involved.[5] Patients with lateral medullary syndrome should therefore be carefully examined for other neurological deficits. Most patients have good functional recovery after lateral medullary infarction,[7] but there is no literature on the recovery of ocular movement abnormalities to the best of our knowledge.


  Conclusion Top


To sum up, torsipulsion is a valuable clinical sign to aid the diagnosis of lateral medullary infarction. The abnormality can be subtle and may require careful slit lamp exam for diagnosis. The movement is elicited only on asking the patient to make a saccade. It is possible that the patient may have vague disturbances of vision, giddiness or tilting of the surroundings and may present to the ophthalmologist first. Long-term follow-up is needed to ascertain the course and recovery of torsipulsion in lateral medullary infarction.

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

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Milller NR, Newman NJ. Supranuclear and infranuclear ocular motility disorders. In: Miller NR, Newman NJ, editors. Walsh & Hoyt's Clinical Neuro Ophthalmology. Williams & Wilkins; 1999. p. 562-613.  Back to cited text no. 1
    
2.
Brazis PW. Ocular motor abnormalities in Wallenberg's lateral medullary syndrome. Mayo Clin Proc 1992;67:365-8.  Back to cited text no. 2
    
3.
Morrow MJ, Sharpe JA. Torsional nystagmus in the lateral medullary syndrome. Ann Neurol 1988;24:390-8.  Back to cited text no. 3
    
4.
Beh SC, Frohman TC, Frohman EM. Neuro-ophthalmic manifestations of cerebellar disease. Neurol Clin 2014;32:1009-80.  Back to cited text no. 4
    
5.
Cuoco JA, Hitscherich K, Hoehmann CL. Brainstem vascular syndromes: A practical guide for medical students. Edorium J Neurol 2016;3:4-16.  Back to cited text no. 5
    
6.
Kommerell G, Hoyt WF. Lateropulsion of saccadic eye movements. Electro-oculographic studies in a patient with Wallenberg's syndrome. Arch Neurol 1973;28:313-8.  Back to cited text no. 6
    
7.
Nelles G, Contois KA, Valente SL, Higgins JL, Jacobs DH, Kaplan JD, et al. Recovery following lateral medullary infarction. Neurology 1998;50:1418-22.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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