Upbeat nystagmus and the ventral tegmental pathway of the upward vestibulo‐ocular reflex

Ranalli, Paul J.; Sharpe, James

doi:10.1212/wnl.38.8.1329

Cited by 64 publications

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“…Indeed, the previously reported cases of pontine lesions with UBN involved extensive bilateral damage to the ventral tegmentum and the posterior part of the basis pontis [3][4][5] . Thus, the location of this lesion would appear to support the hypothesis that the CVTT, transmitting upward vestibular signals to the third nucleus, also exists in humans [6] . The medial longitudinal fasciculus (MLF) and the brachium conjunctivum (BC), which are also involved in upward slow eye movement transmission [1,2] , were not affected here since they are located in the paramedian and lateral parts, respectively, of the posterior pontine tegmentum, and thus at a distance from the lesion.…”

Section: Discussionsupporting

confidence: 63%

“…In the pons, the lesions were large and bilateral [3][4][5] , resulting in a coarse UBN of about 10° amplitude in the primary position [5] . It has been hypothesized that these pontine lesions interrupt the excitatory 'crossing ventral tegmental tract' (CVTT) connecting the superior vestibular nucleus, involved in the transmission of anterior canal inputs, to the superior rectus and inferior oblique motoneurons in the third nerve nucleus [6] . We report a case of UBN resulting from a small unilateral pontine lesion, which supports the above hypothesis and improves our knowledge of the brainstem upward vestibular pathways.…”

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confidence: 99%

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Upbeat Nystagmus due to a Small Pontine Lesion: Evidence for the Existence of a Crossing Ventral Tegmental Tract

Pierrot‐Deseilligny

Miléa

Sirmai³

et al. 2005

Eur Neurol

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We report a patient with an isolated large upbeat nystagmus (UBN) in the primary position of gaze. Eye movements were filmed and recorded using electro-oculography. The upward vestibulo-ocular reflex gain, evaluated by pitching the head forward, was markedly reduced compared to when pitching the head back. The lesion was a probable lacunar infarction located in the paramedian and posterior part of the basis pontis, at the upper pons level. This UBN case, with one of the smallest brainstem lesions reported so far, supports the existence in humans of the crossing ventral tegmental tract, described in the cat and transmitting excitatory upward vestibular signals to the third nerve nucleus. It is also suggested that the decussation of this tract lies at the same upper pons level as in the cat but in a slightly more ventral location, i.e. in the posterior basis pontis.

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Section: Discussionsupporting

confidence: 63%

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confidence: 99%

Upbeat Nystagmus due to a Small Pontine Lesion: Evidence for the Existence of a Crossing Ventral Tegmental Tract

Pierrot‐Deseilligny

Miléa

Sirmai³

et al. 2005

Eur Neurol

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“…It is also a fixation-induced nystagmus that beats upward in primary gaze position, and is combined with a disorder of the vertical smooth pursuit eye movements, a visual and vestibulospinal ataxia with a tendency to fall backward, and pastpointing downward [2,4,13,19]. On the one hand, the pathoanatomical location of most acute lesions is near the median plane in the medulla oblongata in neurons of the paramedian tract (PMT), close to the caudal part of the perihypoglossal nucleus [15,19,20], which are responsible for vertical gaze-holding [21] (Fig. 2).…”

Section: Vestibular Syndromes In the Sagittal (Pitch) Planementioning

confidence: 99%

Central vestibular disorders

Dieterich

2007

J Neurol

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Dizziness or vertigo is an erroneous perception of selfmotion or object-motion as well as an unpleasant distortion of static gravitational orientation. It is caused by a mismatch between the vestibular, visual, and somatosensory systems. Thanks to their functional overlap, the three systems are able to compensate, in part, for each other's deficiencies. Thus, vertigo is not a well-defined disease entity, but rather a multisensory syndrome that results when there is a pathological dysfunction of any of the stabilizing sensory systems (e.g., central vestibular disorders, peripheral vestibular diseases with asymmetric input into the vestibular nuclei). This article provides an overview of the most important and frequent forms of central vestibular vertigo syndromes, including basilar/vestibular migraine, which are characterized by ocular motor, postural, and perceptual signs. In a simple clinical classification they can be separated according to the three major planes of action of the vestibulo-ocular reflex: yaw, roll, and pitch. A tonic imbalance in yaw is characterized by horizontal nystagmus, lateropulsion of the eyes, past-pointing, rotational and lateral body falls, and lateral deviation of the perceived straight-ahead. A tonic imbalance in roll is defined by torsional nystagmus, skew deviation, ocular torsion, tilts of head, body, and the perceived vertical. Finally, a tonic imbalance in pitch can be characterized by some forms of upbeat or downbeat nystagmus, fore-aft tilts and falls, and vertical deviation of the perceived straight ahead. The thus defined syndromes allow for a precise topographic diagnosis as regards their level and side.

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“…Wray and colleagues [7] suggest imbalance of central otolithic projections from autoimmune attack on the nodulus and ventral uvula, based on the fact that their patient's nystagmus was "strongly dependent on head position," meaning that the upbeat nystagmus was absent in the supine position, and supine positional testing on either side provoked apogeotropic nystagmus. In our case this positional dependence was absent, so we are inclined towards Pierrot-Deseilligny and colleagues' hypothesis [9] that upbeat nystagmus results from dysfunction of the crossing ventral tegmental tract [10]. Paraneoplastic diseases involving the central nervous system are thought to affect surface neuronal antigens [11] but why the crossing ventral tegmental tract should exhibit selective vulnerability to paraneoplastic antibodies in this case is unknown.…”

Section: Discussionmentioning

confidence: 51%

Paraneoplastic Upbeat Nystagmus in Renal Cell Carcinoma

2015

J Neurol Neurophysiol

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CaseA 72 year-old man with a longstanding past medical history of hypertension and restless legs syndrome presented with a chief complaint of unsteadiness and oscillopsia that he reported as starting abruptly three months previously, with rapid deterioration. As the unsteadiness progressed, it also became associated with nausea, to which he attributed an unintentional 10-pound weight loss over 1 month. He denied any other symptoms, including other stigmata of malignancy (new cough, bleeding in the urine or stool). He did not drink alcohol, but smoked 1 pack of cigarettes per day. His only medications were lisinopril and gabapentin. He reported no family medical history.Some of his workup had been completed before he presented to our clinic. Audiometry showed presbycusis. MRI of the brain and internal auditory canals without and with contrast was normal; specifically, there were no abnormalities in the cerebellum. Lumbar puncture reported cerebrospinal fluid protein elevated at 70 (normal 15 -45), IgG elevated at 4.38 (normal 0.00 -3.40), albumin elevated at 47.50 (normal 0.00 -34.99). Lyme disease antibody screen was negative and myelin basic protein was <2.0 (normal 0 -4.0). Serum antibodies to Hu, Yo and Ri were negative. He came to clinic in a wheelchair because he was unable to ambulate or transfer independently. On physical examination he had spontaneous upbeat nystagmus on primary position of gaze (16 deg/sec in the dark, diminished to 6 deg/sec with fixation; see Figure 1 and Video), which also intruded into smooth pursuit. The upbeat nystagmus did not change at the extremes of lateral gaze, nor did it depend on position with respect to gravity. The remainder of his examination, including appendicular cerebellar function, was normal.Having examined him in clinic, we referred him immediately for CT of the chest, abdomen and pelvis without and with oral and intravenous contrast, which revealed a 2 cm solid focal partially exophytic mass in the left kidney.Subsequent workup included MRI of the abdomen that demonstrated the same renal mass. An F18 FDG PET scan showed increased uptake in this renal mass, as well as mildly increased uptake in a precarinal lymph node. Transbronchial needle biopsy of a right paratracheal lymph node was negative for carcinoma and lymphoma. A separate FDGPET/CT study showed increased uptake in a right abdominal precaval mesenteric lymph node; needle biopsy found this to be inflammatory, without evidence of malignancy. A second lumbar puncture had an opening pressure of 120 mm H2O. Cerebrospinal fluid had a protein of 112 and a lymphocytic pleocytosis of 16 and no red cells; IgG index and synthesis were normal; oligoclonal bands were negative; cytology was negative. Cerebrospinal fluid infectious studies were negative, including VDRL, Blastomyces, Coccidioides, Cryptococcus, yeast, fungi, adenovirus, LaCrosse encephalitis virus, cytomegalovirus, Epstein-Barr virus, Herpes simplex virus 1/2, HHV6, JC virus, St. Louis enephalitus virus, Varicella zoster virus, Eastern and Western equi...

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Upbeat nystagmus and the ventral tegmental pathway of the upward vestibulo‐ocular reflex

Cited by 64 publications

References 0 publications

Upbeat Nystagmus due to a Small Pontine Lesion: Evidence for the Existence of a Crossing Ventral Tegmental Tract

Upbeat Nystagmus due to a Small Pontine Lesion: Evidence for the Existence of a Crossing Ventral Tegmental Tract

Central vestibular disorders

Paraneoplastic Upbeat Nystagmus in Renal Cell Carcinoma

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