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Box 1.  

Complete ophthalmoplegia:[55]
  • Bilateral ptosis, loss of all extraocular movements, including voluntary and reflex eye movements, dilated and unreactive pupils to light
  • Rare finding associated with bilateral infarcts or hemorrhages at the level of thalamomesencephalic junction
Peering at the tip of the nose:[56]
  • Vergence disorder and lesion of down-gaze pathways
  • Characterized by a tonic inward and downward deviation of the eyes
  • Alternating esotropia may occur
  • Observed in midbrain infarcts and thalamic hemorrhages compressing or extending to the mesencephalon
Pseudo-abducens palsy:[57]
  • Unilateral or bilateral, often due to paramedian thalamic infarcts involving the riMLF and the INC
  • Disruption of supranuclear projections to midbrain vergence neurons
Convergence–retraction nystagmus:[57,61,62]
  • Quick phases of adductive movements that converge and retract the eyes
  • Often associated with pseudo-abducens palsy
  • Paramedian thalamic infarcts extending to the midbrain and involvement of NPC or INC
INO disorders:
  • INO as isolated finding or associated with ataxia or dysarthria, due to small caudal midbrain infarction or pontomesencephalic junction[71]
  • Bilateral INO is composed of rare, paramedian midbrain tegmentum infarcts[72–74]
  • Associated with down-beat nystagmus and impairment of convergence[71,73]and ataxia[74,75]
  • Usually, convergence is spared in bilateral INO
SD:[76]
  • Isolated finding or as part of OTR (head tilt, ocular torsion and vertical skew)
  • Alternating SD (one eye is hypertrophic in one field of gaze and the fellow eye becomes hypertrophic in a different field of gaze)
  • Due to bilateral pretectal lesion, other elements of Parinaud’s syndrome are usual
  • SD may be associated with INO, with the ipsilateral eyes deviated upward in most cases[72]
OTR:[77,78]
  • Unilateral small pretectal hemorrhage
  • In the acute stage, downward-gaze palsy, upward-gaze paresis, vergence intact
  • Chronic-stage OTR explained by unilateral INC lesion
Parinaud’s syndrome:[79]
  • Stroke accounts for 25% of all causes
  • Thalamic hemorrhages extending downward to the pretectal region leading etiology, less often primary pretectal hemorrhage or infarction
  • Complete or partial
  • All forms of upward gaze affected, and downward saccades often slowed
  • Paralysis of convergence or convergence spasm
  • Convergence retraction nystagmus on attempted upward gaze
  • Bilateral eyelid retraction (Collier’s sign), sometimes with moderate bilateral ptosis
  • Light-near pupillary dissociation
  • Dilated and either fixed or poorly responsive pupils to light
  • Vertical SD usual found
Nuclear third-nerve palsy:[31,84]
  • Ipsilateral third-nerve palsy, bilateral ptosis and contralateral superior rectus palsy
  • Middle paramedian infarcts and hematomas
Fascicular third-nerve palsy:[31,90,92,93,96]
  • Small midbrain hemorrhage or intermediolateral infarcts
  • Distinct patterns of intramesencephalic nerve-segment involvement, rarely as isolated neurological finding:[96]
    • Isolated inferior rectus palsy[90,92,95]
    • Isolated superior rectus palsy[36,88]
    • Isolated medial rectus palsy[31]
    • Third-nerve palsy with pupil sparing[96]
    • Bilateral ptosis[36,92]
Claude’s syndrome:
  • Ipsilateral oculomotor nerve palsy and contralateral hemiataxia
  • Unusual finding[97]
  • A variant: ipsilateral third-nerve palsy and ipsilateral hemiataxia, due to small anterior midbrain infarct impairing the dento–rubro–thalamo pathway before the decussation[98]
Benedikt’s syndrome:
  • Ipsilateral oculomotor nerve palsy, contralateral hemiparesis, involuntary movements or contralateral tremor[99]
Weber’s syndrome:
  • Classic brainstem syndrome, ipsilateral third-nerve palsy and contralateral hemiparesis
  • Rarely reported in infarcts[83]

Uncommon Eye Movement Disorders in Midbrain and Thalamic Stroke

INC = Interstitial nucleus of Cajal; INO = Internuclear ophthalmoplegia; NPC = Nucleus of the posterior commissure; OTR = Ocular-tilt reaction; riMLF = Rostral interstitial nucleus of the medial longitudinal fasciculus; SD = Skew deviation.

Box 2.  

Fast and slow vergence paresis:[138]
  • Paresis of fast and slow vergence
  • Saccades are normal
  • SPMs affected in horizontal and vertical plane
  • Partial involvement of NRTP by infarct
  • MLF and midbrain spared
Isolated palsy of lateral rectus muscle:[148]
  • Initially, conjugate-gaze paralysis followed by isolated palsy or lateral rectus
  • This implies initial involvement of the AN and/or PPRF, rather than just the abducens fascicles
  • Small hemorrhage at origin of sixth cranial nerve
Raymond–Cestan syndrome:[150]
  • Ipsilesional sixth-nerve palsy and contralateral hemiparesis
  • Infarct medial and intermediolateral involving the middle and rostral pontine tegmentum and the pontine basis
Millard–Gubler syndrome:[151]
  • Rare crossed brainstem syndrome
  • Ventromedial infarct
  • Ipsilateral abducens and facial nerve paresis and contralateral hemiparesis
Gasperini syndrome:[152]
  • Uncommon pattern of pontine infarct
  • Ipsilateral abducens palsy, lateral-gaze palsy and peripheral facial palsy, facial hypalgesia
  • Contralateral hemihypalgesia and deafness
INO disorders
INO and cheiro-oral syndrome
:[155]
  • Rare association
  • Small infarct involving ipsilateral MLF, PPRF, sixth-nerve nucleus and medial lemniscus
INO and jerk see-saw nystagmus:[156]
  • Exceedingly rare finding
  • Minute dorsomedial pontine tegmentum lesion (MLF level)
  • Mechanism no clear, vertical nystagmus may depend on the patterns involving pathways from contralateral vertical semicircular canals
WEMINO syndrome:[157,157]
  • INO plus ipsilateral exotropia
  • Small ischemia paramedian pontine tegmentum involving MLF
Eight-and-a-half syndrome:[165]
  • One-and-a-half syndrome plus a seventh cranial-nerve palsy
  • Small pontine tegmentum infarct abutting the anterior aspect of the fourth ventricle
Typical ocular bobbing:[172]
  • Intermittent, spontaneous, usually conjugate downward jerk of both eyes followed after a few seconds by a slow return to the mid position
  • Uncommon, associated with large pontine ischemia or hemorrhage
Paretic ocular bobbing:[169]
  • Rare form of ocular bobbing
  • Pontomesencephalic infarct
  • Quick downward movement of one eye and intorsion or no movement in the fellow eye
  • Fascicular third-nerve lesion may alter appearance of vertical movement

Unusual Eye Movement Disorders in Pontine Stroke

AN = Abducens nucleus; INO = Internuclear ophthalmoplegia; MLF = Medial longitudinal fasciculus; NRTP = Nucleus reticularis tegmenti pontis; PPRF = Paramedian pontine reticular formation; SPM = Smooth-pursuit movement; WEMINO = Wall-eyed monocular internuclear ophthalmoplegia.

Box 3.  

Gaze-evoked horizontal nystagmus:[197]
  • Common in PICA infarction sparing the medulla
  • In SCA infarcts restricted to cerebellum, nystagmus is found in 50% of cases
  • Commonly beats toward the lesion
Downbeat nystagmus:[203]
  • Etiology diverse
  • 12% due to cerebellar infarct in a series of 117 patients
  • Damage of floccular and parafloccular lobes
PAN:[216]
  • Uvulonodular damage or connections with vestibular nuclei
  • PAN, perverted HSN and impaired tilt suppression of the postrotatory nystagmus due to circumscribed nodular ischemia
Unilateral rebound nystagmus:[219]
  • Involvement of flocculus and paraflocculus
  • A patient with cerebellar hemorrhage (multiple foci), nystagmus was contralateral with respect to the lesioned side
Contrapulsion saccades:[197]
  • Rare in infarct of lateral branch of the SCA
  • Often as a result of lesions of the superior cerebellar peduncle
Upside-down vision:[222]
  • Transient visual illusion, most frequent in LMI
  • Nodulus and flocculus rarely have a common arterial supply
  • Infarct restricted to medial branch of the PICA
Abnormal OT:[223]
  • 75% of patients with cerebellar infarct in the AICA territory
  • Often overlooked at bedside examination
  • Ipsiversive ocular tilt of both eyes in half of patients
  • SD present in all patients with ipsiversive ocular tilt
  • Direction of SVV tilt correspond to direction of OT
  • Audiovestibular loss common finding

Uncommon Eye Movement Disorders in Cerebellar Stroke

AICA = Anterior inferior cerebellar artery; HSN = Head-shaking nystagmus; LMI = Lateral medullary infarct; OT = Ocular torsion; PAN = Periodic alternating nystagmus; PICA = Posterior inferior cerebellar artery; SCA = Superior cerebellar artery; SD = Skew deviation; SVV = Subjective visual vertical.

Box 4.  

Spontaneous downbeat nystagmus:[231]
  • Very uncommon in hemimedullary infarction
Rebound nystagmus:[249]
  • Nystagmus observed when the eyes return from lateral gaze
Gaze-evoked horizontal nystagmus:[254]
  • Associated with vertigo; truncal ataxia (contralateral or bilateral falls) suggest infarction of NPH at the medullary level
Positional nystagmus:[255]
  • Uncommon finding in LMI
  • Damage of the cerebello–vestibular pathways from the nodulus and uvula
Ipsilesional head-shaking nystagmus:[256]
  • Provoked jerk nystagmus that follows a prolonged sinusoidal head oscillation
  • Found in patients with LMI, mainly in infarcts of the caudal or middle portion of medulla
  • Probably due to asymmetric nodulo-uvular inhibition of the velocity storage
Upbeat and bowtie nystagmus:[231,257]
  • Oblique upbeat nystagmus with horizontal quick phases that alternate from one side to the other side
  • Reported in bilateral MMI
Hemi see-saw nystagmus:[231]
  • Very rare in MMI
Popper-type of lid nystagmus:[258]
  • Very rare in LMI
  • Palpebral nystagmus synchronous with fast phase of horizontal
Ocular contrapulsion:[231]
  • Observed in 25% of patients with MMI
  • Damage of uncrossed climbing fibers in the upper part of the ION in the rostral medulla
  • Pattern contrary to LMI (ocular ipsipulsion)
Smooth pursuit movements:[231]
  • Impaired to the side of the lesion in MMI
Contralesional OTR:[231]
  • Very rare finding in MMI
  • Unilateral damage of graviceptive brainstem pathways from VN after decussation (at level of pontomedullary junction)

Infrequent Oculomotor Abnormalities in Medullary Stroke

ION = Inferior olivary nucleus; LMI = Lateral medullary infarct; MMI = Medial medullary infarct; NPH = Nucleus prepositus hypoglossi; OTR = Ocular-tilt reaction; VN = Vestibular nucleus.

CME

Oculomotor Disorders in Vertebrobasilar Stroke

  • Authors: Jorge Moncayo, MD; Julien Bogousslavsky, MD
  • CME Released: 6/4/2009
  • THIS ACTIVITY HAS EXPIRED
  • Valid for credit through: 6/4/2010
Start Activity


Target Audience and Goal Statement

This activity is intended for ophthalmologists, primary care clinicians, neurologists, vascular surgeons, cardiologists, and other specialists who care for patients with stroke or suspected stroke.

The goal of this activity is to review anatomic pathways associated with eye movements in the territory of the vertebrobasilar system arteries and identify clinical presentations and patterns associated with different types of stroke.

Upon completion of this activity, participants will be able to:

  1. Describe the most likely cause of stroke in the vertebrobasilar territory
  2. Identify the prevalence and consequences of midbrain infarcts
  3. Describe characteristics of the vertical one-and-a-half syndrome
  4. Identify patterns of nystagmus associated with cerebellar stroke
  5. Describe the most common abnormalities seen in lateral medullary infarction


Disclosures

As an organization accredited by the ACCME, MedscapeCME requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest.

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Author(s)

  • Jorge Moncayo, MD

    Department of Neurology, Eugenio Espejo Hospital, International University of Ecuador, Quito, Ecuador

    Disclosures

    Disclosure: Jorge Moncayo, MD, has disclosed no relevant financial relationships.

  • Julien Bogousslavsky, MD

    Department of Neurology and Neurorehabilitation, Swiss Medical Network, Montreux, Switzerland

    Disclosures

    Disclosure: Julien Bogousslavsky, MD, has disclosed no relevant financial relationships.

CME Author(s)

  • Désirée Lie, MD, MSEd

    Clinical Professor, Family Medicine, University of California, Orange; Director, Division of Faculty Development, UCI Medical Center, Orange, California

    Disclosures

    Disclosure: Désirée Lie, MD, MSEd, has disclosed no relevant financial relationships.

Editor(s)

  • Elisa Manzotti

    Editorial Director, Future Science Group, London, United Kingdom

    Disclosures

    Disclosure: Elisa Manzotti has disclosed no relevant financial relationships.


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CME

Oculomotor Disorders in Vertebrobasilar Stroke: Eye Movement Disorders Occurring in Midbrain Stroke

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Eye Movement Disorders Occurring in Midbrain Stroke

Anatomical Basis of Eye Motor Control at the Mesencephalon

The neural substrate subserving vertical- and horizontal-gaze subsystems is organized differently. A detailed description of all complex pathways underlying generation and control of the functional classes of human eye movements is beyond the scope of this review.

The mesodiencephalic junction is the critical site of prenuclear (supranuclear) vertical and torsional eye motion control.[9-12] At this level, the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF – the vertical-gaze center), the interstitial nucleus of Cajal (INC), the posterior commissure (PC) and the nucleus of Darkschewitsch – all clustered around the Sylvian aqueduct – are the anatomical structures mediating vertical-gaze inputs to the oculomotor nuclei.[13-17] The riMLF is located rostrally to the oculomotor nucleus, dorsomedially to the anterior pole of the red nucleus and ventrally to the periaqueductal gray matter.[15] It houses essential neurons for the generation of fast eye movements in vertical directions and torsional saccades.[15,18] At this level, the neurons for upward saccades are placed more laterally than those for downgaze.[10,11,15-17] The riMLF burst neurons fire at high frequencies, beginning just before the saccadic movement; otherwise, they are silent.[14] Moreover, the omnipause neurons located in the nucleus raphe interpositus cease firing during vertical and torsional saccades.[12] Inputs to each riMLF come from the superior colliculus, the nucleus of the PC, the contralateral riMLF, the fastigial nucleus of the cerebellum and the cerebral hemispheres.[12,13,18,19] From each riMLF, impulses traveling ventrally to the Sylvian aqueduct pass to the subnuclei of the eye muscles controlling upward and downward movements in both eyes, whereas impulses are uncrossed for torsional saccades.[20-22] Moreover, motoneurons for eye elevator muscles receive bilateral signals from the riMLF crossing through the oculomotor nuclear complex, while afferent signals for depressor muscles are only ipsilateral.[12,21]

The INC (lying just below the riMLF) is important for integration of premotor signals (eccentric gaze holding or neural integrator) of the saccadic and torsional movements in vertical plane and head posture.[23-25] The neural integrator is defined as a neural circuit required for gaze maintenance, where the velocity-encoded motor command must be integrated to produce an appropriate eye position command or the gaze-holding mechanism.[12] The INC projects by way of the PC to motoneurons of the contralateral nuclei of the third and fourth cranial nerves and the contralateral INC.[12,26,27] Inputs to the INC come from the riMLF and caudal brainstem structures (i.e., the pons, medulla and the anterior semicircular canal) mainly by way of the MLF, the INC participates in vertical smooth-pursuit and vertical vestibular eye movements.[28] Finally, the PC contains fibers crossing from the INC to the contralateral structures involved in vertical gaze, while nuclei of the PC coordinate lid and eye movements occurring in saccade and pursuit movements in the vertical plane (Figure 1).[29,30]

Figure 1.

Enlarge

Main cortical and brainstem structures involved in generation and control of saccadic and smooth-pursuit movements in horizontal and vertical axes. Dotted lines indicate saccadic pathways. Solid lines indicate smooth-pursuit pathways.
DLPC = Dorsolateral pontine cortex; DLPN = Dorsolateral pontine nucleus; EBN = Excitatory premotor burst neuron; FEF = Frontal eye field; FL = Flocculus; FN = Fastigial nucleus; IBN = Inhibitory premotor burst neuron; INC = Interstitial nucleus of Cajal; LIP = Lateral intraparietal area; MLF = Medial longitudinal fasciculus; MST = Medial superior temporal; MT = Middle temporal; MVN = Medial vestibular nucleus; NPH = Nucleus prepositus hypoglossi; NRTP = Nucleus reticularis tegmenti pontis; OCV = Oculomotor cerebellar vermis; OPN = Omnipause neuron; PC = Posterior commissure; PEF = Parietal eye field; PPRF =Paramedian pontine reticular formation; riMLF = Rostral interstitial nucleus of the medial longitudinal fasciculus; SC = Superior colliculus; SEF = Supplementary eye field; UV = Uvula; III = Oculomotor nucleus; IV = Trochlear nucleus; VI = Abducens nucleus.

Midbrain Vascular Supply

Although the midbrain is a small anatomic structure, the blood supply is quite complex. An overlap between arterial territories of the basilar artery (BA), posterior cerebral artery (PCA) and superior cerebellar artery (SCA) can occur, and the degree of arterial contribution will depend on the midbrain level. The BA gives off direct perforators supplying the paramedian region (anteromedial territory), that is, short circumferential branches of the SCA that loop around the mesencephalon and feed the caudal two-thirds of the latero-dorsal region.[31,32] At the upper half of the midbrain, the proximal segment of the PCA branches into the thalamo–subthalamic and mesencephalic arteries. The former irrigate the riMLF, among other subthalamic structures.[33] Peduncular arteries, directed to the lateral upper midbrain stem, from the postcommunicating-PCA or P2 segment.[34]

Midbrain Stroke

Midbrain ischemia accounts for anywhere from 3 to 9.5% of all infarcts in the posterior circulation and often coexists with larger infarcts involving other brainstem arterial territories, mostly the neighboring pons and the thalamus.[31,32,35,36] Less often, midbrain ischemia may be exclusively restricted to the midbrain.[31,32,36] Up to 70% of patients with mesencephalic infarcts, commonly covering the middle and upper thirds, may exhibit a broad variety of neuro-ophthalmologic signs, sometimes in a complex pattern, which are usually observed with additional clinical features reflecting midbrain or brainstem involvement, but can also (less commonly) be isolated clinical findings.[31,32,35,36] Spontaneous hemorrhages rarely occur in the midbrain.[37-41]

Supranuclear Eye Movement Abnormalities in Midbrain Stroke

Supranuclear (prenuclear) vertical-gaze palsy, occurring in midbrain stroke, may be conjugate or disconjugate. Conjugate prenuclear palsy most commonly affects upgaze and downgaze together, but selective upgaze palsy or, more rarely, selective downgaze palsy may occur. Supranuclear vertical-gaze palsy is often due to ischemia in the most caudal territory of the thalamo–subthalamic artery and, less often, of the anterior choroidal artery, when this artery feeds the midbrain.[10] Vertical-gaze palsy may be due to midbrain hemorrhages, although this is far from common.[11,37,39,41]

Combined upgaze and downgaze palsy often arises from upper-midbrain bilateral tegmental lesions, involving the riMLF, the INC, the PC or the periaqueductal gray matter due to either occlusion of midbrain–thalamic perforating arteries or because both paramedian arteries stem from one side or from a single pedicle, as occurs in a third of all brains.[15,16,42-45] A similar combined gaze deficit may occasionally result from unilateral lesions damaging the same areas as those produced by bilateral lesions.[15,17,33,46,47] Thus, unilateral lesions may affect the ipsilateral riMLF, as well as the contralateral riMLF fibers after their decussation, owing to damage of excitatory burst neurons of the riMLF.[17,33,46,47] Rapidity of all types of upward or downward eye movements may be affected or these movements may be lost altogether.[17,47] When a lesion is restricted to the riMLF, both vertical vestibulo–ocular reflex response and smooth-pursuit movements (SPMs) may be spared or impaired in only one direction.[15,16,45,48]

Isolated upgaze palsy results from bilateral or unilateral lesions that involve the riMLF and the PC region and, thus, affect the INC or riMLF efferents traveling to the oculomotor neurons on both sides.[11,46,48,49] Unilateral infarcts may give rise to a functionally bilateral lesion of fibers at the PC level.[46] Small bilateral periaqueductal gray matter hemorrhages that spare the riMLF and the PC may produce this type of selective gaze palsy, although infrequently.[50] Although combined upgaze and downgaze palsy and isolated upgaze palsy have more frequently been reported with paramedian thalamic–subthalamic infarcts, purely midbrain infarcts may also produce these conjugate vertical-gaze palsies.[31]

Selective downgaze palsy requires bilateral infarcts in the territory of the thalamo–subthalamic paramedian artery affecting the mediocaudal region of the riMLF,[10,16,46,51-53] although it may very rarely also be caused by small bilateral hemorrhages in the periaqueductal gray matter.[54] Other eye movement disorders [55-57]observed in midbrain or thalamo–mesencephalic infarcts are summarized in Box 1 .

Disconjugate supranuclear eye movement disorders attributed to midbrain vascular lesions include monocular elevation palsy, crossed paralysis, the vertical one-and-a-half syndrome, skew deviation (SD), see-saw nystagmus (SSN) and V-pattern pseudobobbing.[10,11,46]

Monocular elevation palsy (MEP; also known as double-elevator palsy) is a combined palsy of the elevator muscles reported in rostral midbrain infarcts. Ipsilateral MEP is due to interruption of efferents just after they leave the riMLF toward the oculomotor nuclear complex and before crossing. MEP can occasionally be accompanied by unilateral internuclear ophthalmoplegia (INO).[46,58] In contralateral MEP, ischemia affects riMLF fibers after decussating and before they reach the oculomotor nuclear complex.[46,59] Crossed vertical-gaze paresis is a very peculiar finding attributed to a unilateral mesodiencephalic junction infarct that impaired ipsilateral downgaze (monocular depressor paresis) and contralateral upgaze fibers (monocular elevator paresis) arising from the riMLF.[60] Moreover, a mild bilateral ptosis was found.[60]

Nystagmus, which may also occur in midbrain stroke, mainly with lesions located at the mesodiencephalic junction, has a high localizing significance. Convergence-retraction nystagmus, associated with selective upgaze paresis and ipsilateral hypotropia, may, in rare cases, be the outstanding clinical finding as the result of a minute infarct strategically involving the periaqueductal region, the PC and the INC.[61,62]

See-saw nystagmus is characterized by alternate elevation and depression of one eye accompanied by a similar movement in the other eye (but in the opposite direction). While one eye goes up and intorts, the other goes down and extorts. Although rare, jerk SSN (hemi-SSN) has also been reported with upper brainstem infarcts or hemorrhages, in which case the torsional component of the nystagmus fast phases rotates the upper poles of the eyes toward the side of the lesion.[63,64]

A central disturbance of otholitic input has been identified as a pathogenic mechanism.[11,65] A dissociated vertical nystagmus (up- and down-beating) plus INO has been reported in a single patient with a tiny periaqueductal caudal midbrain infarct in the MLF region.[66] The vertical nystagmus was more prominent on the INO side.[66] Pendular SSN has been described in patients with unilateral mesodiencephalic infarcts or hemorrhages involving the INC.[17,65,67] Upbeat nystagmus may be observed after small midbrain ischemia located along the course of the ventral tegmental tract (Figure 2).

Figure 2.

Enlarge

39-year-old male patient with an upbeat nystagmus and a midline tegmental midbrain infarction. (A) Eye movements are normal in all directions of gaze. (B) Axial, sagittal MRI T2 sequences, sagittal T1 sequences and axial diffusion weighted images show a tegmental caudal midbrain infarction.

In certain rare cases, a vertical impairment sparing a single direction in one eye may occur in bilateral or unilateral thalamo–mesencephalic infarctions.[68] The so-called vertical one-and-a-half syndrome is characterized by bilateral supranuclear impairment of all fast and slow downward eye movements on one side, combined with monocular paresis of elevation due to bilateral infarction.[68] The opposite may also occur: vertical upgaze palsy along with monocular depressor paresis on the side of the lesion,[46,69] or contralateral to the lesion,[46,69] has been described with thalamo–mesencephalic infarction, best explained by selective upward-gaze fibers at the PC level.[46] For downward-gaze palsy, a clear explanation has not been provided; nevertheless, an impairment before or after decussation in contralateral or ipsilateral lesions has been postulated.[46] Coexisting vertical and horizontal one-and-a-half syndromes have rarely been associated with ischemia involving the medial thalamus and the upper midbrain.[70] INO,[71-75] skew deviation[76] and ocular tilt reaction (OTR)[77,78] can be observed in midbrain infarcts, along with supranuclear gaze abnormalities Box 1 .[79]

Nuclear or Fascicular Dysfunction of the Oculomotor & Trochlear Nerves in Midbrain Stroke

Oculomotor palsies are a common finding in middle midbrain infarcts; up to 90% of patients with ischemia affecting either the ventral or ventrolateral territories may have nuclear or fascicular third-nerve dysfunction.[31] These palsies result from occlusion of the small paramedian arteries of the BA when ischemia is the etiology, and may be the best indication of a midbrain stroke or be associated with other clinical signs of brainstem involvement.[10,31,36,80,81] Oculomotor nuclear complex lesions may have a constellation of clinical signs reflecting the particular topographical arrangement of the subnucleus and the selective vascular supply. They essentially present as complete homolateral oculomotor palsy together with contralateral superior rectus palsy (due to decussation of the fibers for superior rectus within the nuclear complex) and partial bilateral ptosis.[82,83] A nuclear lesion can have other forms of presentation.[11,84,85]

Fascicular third-nerve lesions may have a form of presentation very similar to that found in peripheral etiologies; in both situations, signs of central neurological dysfunction are usually absent. Involvement may be partial or complete, depending on fascicular arrangement in the ventral midbrain.[31,86,87] Mostly, intra-axial lesions are attributed to infarcts or, much less commonly, to hemorrhages Box 1.[85-96] Contralesional hemiparesis, ataxia and involuntary movements along with ipsilesional intra-axial third nerve lesions constitute the different classic eponymous midbrain syndromes Box 1.[83,97-99]

Nuclear or fascicular trochlear involvement is exceptional for two reasons: first, the dorsal position of the nucleus in the brain stem and, second, the fascicle’s short intra-axial course. A superior oblique palsy contralateral to the lesion and a central Claude Bernard Horner syndrome on the side of the lesion may be characteristic and have a high localizing value.[11,100] Contralateral fourth-nerve palsy with a homolateral INO due to a small infarct in the caudal midbrain tegmentum has also been reported.[101]