I read with interest the article by Gautam, et al. [1]. I agree
that brainstem tuberculoma can cause nuclear gaze palsy and fascinating
neuro-ophthalmological findings. However, I think further clarification
regarding pathophysiological mechanism of the gaze palsy may be
interesting for the readers. Particularly, two points I want to raise
are: difficulty in differentiating pathological lesions located in VI
nerve nucleus and parapontine reticular formation (PPRF), and less
usefulness of vestibule-ocular reflex to differentiate between lesions
present in these two anatomical regions.
Gaze palsies – limited movement of two eyes in one
direction – are caused by malfunction of one of the gaze centers located
either in the cortical (premotor frontal cortex) or in PPRF located in
the brainstem. Nuclear gaze palsy is caused by a lesion in the brainstem
gaze center, whereas supranuclear gaze palsy is caused by a lesion in
the cortical gaze center. Horizontal eye movements are initiated by the
stimulation of PPRF from the contralateral premotor frontal cortex.
PPRF, then, activates the ipsilateral lateral rectus muscle via VI
nucleus and contralateral medial rectus muscle via contralateral medial
longitudinal fasciculus (MLF). PPRF doesn’t have a defined anatomical
location but located anterior and lateral to the MLF and anterior to the
VI nucleus. Excitatory burst neurons (EBNs) in the PPRF generate the
"pulse" movement that initiates a horizontal saccade by providing input
to the VI nucleus via axonal fibers.
Though lesions of the VI nucleus can produce
paralysis of both the ipsilateral lateral rectus and contralateral
medial rectus for all conjugate eye movements, clinical lesions that
affect only the nucleus are rare, and there is usually involvement of
adjacent structures such as PPRF as well. Because of proximity of
location, right VI nucleus lesion likely associated with right PPRF
lesion in this patient, causing right lateral rectus and left medial
rectus weakness, appreciated as right lateral gaze palsy.
Doll’s eye maneuver has been suggested as useful in
differentiating among different types of horizontal gaze palsy as
passive horizontal rotation of the head directly stimulates the sixth
nerve nucleus via the vestibule-ocular reflex. In all practical purpose,
it is more helpful to characterize gaze palsy between frontal lobe
lesion versus nuclear and infranuclear lesion: gaze palsies induced by
frontal lobe lesions will be corrected but gaze palsies caused by
pontine nuclear and infranuclear lesions will persist during the
maneuver. Though theoretically sixth nerve nucleus and PPRF lesion can
be differentiated with this maneuver, controversy exists regarding
clinical utility in this scenario [2], and in most situations combined
lesions are seen due to close association of these areas with no defined
boundary described for PPRF.
References