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Year : 2016  |  Volume : 19  |  Issue : 3  |  Page : 426-428

Thalamus and vertical gaze: Arguing for an independent association

Department of Neurology, St Stephen's Hospital, New Delhi, India

Date of Submission17-Dec-2015
Date of Decision31-Dec-2015
Date of Acceptance17-Jan-2016
Date of Web Publication25-Jul-2016

Correspondence Address:
Sachin Suresh Babu
Department of Neurology, St Stephen's Hospital, New Delhi - 110 054
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-2327.179981

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How to cite this article:
Babu SS, Khanna L, Peter S, Chindrippu S, Patras E. Thalamus and vertical gaze: Arguing for an independent association. Ann Indian Acad Neurol 2016;19:426-8

How to cite this URL:
Babu SS, Khanna L, Peter S, Chindrippu S, Patras E. Thalamus and vertical gaze: Arguing for an independent association. Ann Indian Acad Neurol [serial online] 2016 [cited 2021 Oct 28];19:426-8. Available from:


We are keen to report two cases of thalamic lesions presenting with vertical gaze abnormalities in the absence of midbrain involvement on magnetic resonance imaging (MRI) despite careful scrutiny. These scenarios would serve to unleash the thalamus from the conventional thinking that its dysfunction cannot cause vertical gaze abnormalities unless accompanied by coexistent midbrain involvement. This finding, although previously reported in literature, is haunted by conflicting evidence and further proof of this legitimate association will take us a step forward in the understanding of the key players in the genesis of vertical gaze palsy.

Case 1: A 23-year-old boy presented with a history of right focal seizures, followed by double vision, and weakness of the right side of the body of 2 weeks' duration. There was a history of holocranial headache, low grade fever with evening rise of temperature and generalized malaise. At the time of admission, this patient was conscious and alert with a Glasgow Coma Scale (GCS) of E4 M6 V5 but had a skew deviation of the right eye with bilateral upgaze palsy and moderate restriction of downgaze. He had a right hemiparesis with motor power 4/5 and right extensor plantar. Routine hematology, biochemistry, and X-ray chest were normal. Cerebrospinal fluid examination was normal. (color - Clear and transparent, pressure −150 mm CSF, cells - Nil, protein −21 mg/dL, glucose −64 mg/dL, random blood sugar (RBS) −96 mg/dL, Ziehl-Neelsen (ZN) stain - Negative, gram stain - Negative, adenosine deaminase (ADA)-<1.00, polymerase chain reaction (PCR) for tuberculosis (TB) - Not detected). MRI of the brain with contrast study (1.5 Tesla) revealed a conglomerated discoid enhancing lesion in the left thalamus suggestive of tuberculoma [Figure 1]. The patient was treated with antiepileptics, cerebral decongestants, and antiTB medication. He recovered from his upgaze palsy and right hemiparesis and was discharged from the hospital.
Figure 1: MRI of the brain diffusion revealing bilateral thalamic infarcts and a contrast-enhanced study with a conglomerated discoid lesion in the left thalamus suggestive of a tuberculoma. Both patients with these lesions had bilateral upgaze palsy

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Case 2: A 34-year-old man was admitted with excess drowsiness and altered sensorium of abrupt onset. He was not a diabetic or hypertensive and he did not have fever or any chronic infections such as TB. On examination he was lethargic, drowsy with a GCS of E3 M4 V2 and he was noticed to have bilateral upgaze palsy with preserved downward gaze. His pupils were equal and reacting to light and there was no facial deviation. Soon recovered his speech and was moving on all four limbs. His routine hematology and biochemistry including blood sugars were normal. His lipid profile was deranged and he had hypercholesterolemia (serum cholesterol 218 mg/dL). Cerebrospinal fluid examination was normal (color - Transparent, pressure −140 mm CSF, cells - Nil, protein −46 mg/dL, sugar −70 mg/dL, RBS −107 mg/dL, gram stain - No organism, acid-fast bacilli (AFB) stain - Negative, PCR for Japanese encephalitis virus - Negative). Two-dimensional echocardiography (2 D Echo) - Normal left ventricular (LV) function with left ventricular ejection fraction (LVEF) 60%, carotid doppler and vertebral artery study - Normal. MRI of the brain diffusion-weighted imaging (DWI) (1.5 Tesla) revealed bilateral symmetrical foci of altered signal intensity showing restricted diffusion in the anteromedial aspect of both thalami suggestive of acute infarcts [Figure 1]. This patient was treated for stroke with aspirin, statins, and folic acid.

   Discussion Top

These two cases of vertical gaze palsy are being discussed for a cardinal finding on neuroimaging, namely thalamic involvement with the conspicuous absence of midbrain involvement. This raises a pertinent question - Can a pure thalamic lesion result in vertical gaze palsy?

However, it is not unusual to find vertical gaze palsies in thalamic lesions, especially paramedian thalamic infarctions. [1] But most authors have opined that this observation could be a consequence of an associated pathology of the thalamomesencephalic or midbrain projections. This conclusion is driven by two important rationales. The first being the traditional understanding of the neural centers responsible for vertical gaze. The burst neurons for vertical gaze are located predominantly in the rostral interstitial part of the medial longitudinal fasciculus (riMLF) and posterior commissure (upgaze), while the neural integrator that regulates the movement is the interstitial nucleus of Cajal, all of which are located in the midbrain. The second reason is the demonstration of associated midbrain lesions by imaging or autopsy in a good number of these cases. [2],[3] This is most commonly observed in vascular lesions because of the shared blood supply of these structures. [4] Nevertheless, this is not always true, because the medial thalamus is supplied by perforating arteries distinct from the paramedian mesencephalic branches.

The conjugate coordinated movement of eyes in the horizontal plane and vertical plane are termed horizontal and vertical gaze respectively. Paralysis of upward or downward gaze may be described as vertical gaze palsy. Our first patient had complete restriction of upgaze and partial impairment of downgaze, while the second one had only upgaze restriction bilaterally. Eye movements can broadly be divided into two types: Fast eye movements or saccades that move the eyes from one target to another and slow eye movements or pursuits that allow the eyes to follow a target when either the target or the head are moving.

Two integral commands are required for the smooth execution of saccades namely:

  1. Pulse (or a velocity command) that surpasses the resistance of the orbital tissues, the inertia of the globe and alters the position of the eye in the orbit, and
  2. A step command that overcomes the elasticity of the orbital tissues and keeps the eye in the new position.

For vertical gaze the pulse command is delivered from the excitatory burst neurons located in the riMLF and the posterior commissure (only for upgaze) while the step command is performed by the interstitial nucleus of Cajal. Apart from these brainstem centers, the cerebellum has been found to contribute to the smoothness of the vertical pursuit. The rest of the supranuclear pathways and the contribution of thalamus have not been established in humans. The supranuclear control of vertical gaze involves descending fibers from the cortex that travel via the medial thalamus to reach their final destination in the midbrain and vice versa according to data from primate models. So, interruption of these fibers could potentially culminate in vertical gaze impairments of varying degree. [5],[6] If one were to disregard the modest possibility of the 5 mm MRI slices failing to capture subtle midbrain lesions, there is a case to reaffirm that the alternate explanation holds good in those reports where MRI was used to document the neural structures affected.

Clark and Albers were able to establish this thalamic connection for the first time in medical literature through three cases of ischemic stroke affecting the thalami but totally sparing midbrain structures. [7] Nevertheless, this important clinico-radiological vignette has only rarely appeared in medical literature since then. We came across only few other case reports where vertical gaze palsy was observed in a unilateral thalamic infarction. [8],[9],[10] The two cases presented here are aimed to reignite the discussion on the possible role of the thalamus in a vertical gaze.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: Clinical syndromes, etiology, and prognosis. Neurology 1988;38:837-48.  Back to cited text no. 1
Gentilini M, De Renzi E, Crisi G. Bilateral paramedian thalamic artery infarcts: Report of eight cases. J Neurol Neurosurg Psychiatry 1987;50:900-9.  Back to cited text no. 2
Van der Graaff MM, Vanneste JA, Davies GA. Unilateral thalamic infarction and vertical gaze palsy: Cause or coincidence? J Neuroophthalmol 2000;20:127-9.   Back to cited text no. 3
Perren F, Clarke S, Bogousslavsky J. The syndrome of combined polar and paramedian thalamic infarction. Arch Neurol 2005;62:1212-6.  Back to cited text no. 4
Schlag J, Schlag-Rey M. Neurophysiology of eye movements. Adv Neurol 1992;57:135-47.   Back to cited text no. 5
Guberman A, Stuss D. The syndrome of bilateral paramedian thalamic infarction. Neurology 1983;33:540-6.  Back to cited text no. 6
Clark JM, Albers GW. Vertical gaze palsies from medial thalamic infarctions without midbrain involvement. Stroke 1995;26:1467-70.doi: 10.1161/01.STR.26.8.1467.  Back to cited text no. 7
Khan M, Sidiropoulos C, Mitsias P. Unilateral thalamic infarction presenting as vertical gaze palsy: A case report. J Med Case Rep 2011;5:535.  Back to cited text no. 8
Surapaneni K, Ferguson L, Altschuler EL. Why can't this patient look up? Bilateral vertical gaze palsy. PM R 2015;7:1306-8.   Back to cited text no. 9
Deleu D. Selective vertical saccadic palsy from unilateral medial thalamic infarction: Clinical, neurophysiologic and MRI correlates. Acta Neurol Scand 1997;96:332-6.  Back to cited text no. 10


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