Archivo de la categoria ‘Nystagmus’

MEDICOS POR NATURALEZA

Viernes, julio 15th, 2011

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Ocular motor signs in dizzy patients.

Miércoles, abril 28th, 2010

The clinical evaluation of a patient whose symptoms suggest vestibular dysfunction requires a systematic examination of each functional class of eye movements .Vestibular syndromes to be accurate indicators for a topographic diagnosis.

Nystagmus is a common finding in patients with vestibular diseases

Vestibular syndromes are commonly characterised by a combination of phenomena involving perceptual, ocular motor , postural and vegetative manifestations. These four manifestations correlate with different aspects of vestibular function and arise from different sites within vestibular structures

The Vestibular pathways run from the eighth nerve and the vestibular nuclei through the medial fasciculus to the oculomotor nuclei and the supranuclear integration centers in the rostral midbrain. From there ,they reach several vestibular cortex areas through the thalamic projection. The bilateral vestibular input invent the central vestibular tone , which stabilizes eyes, head, and body in a normal upright position. A vestibular tone imbalance may reveal itself in one of the three major planes of action of the vestibulo-ocular reflex(VOR) horizontal – Yaw -,vertical- Pitch – or Roll.

Unilateral lesion of these graviceptive pathways affects function in Roll, whereas bilateral lesions affects function in Pitch.

Diseases affecting central vestibular connections cause vertical upbeat or downbeat nystagmus, less commonly horizontal or torsional nystagmus can result. The patients with central vestibular syndrome complaints oscillopsia ,diplopia, postural imbalance, poor visual acuity and less common vertigo. Most of these patients have paramedian infratentorial lesion from ponto-medullary tegmentum involving the vestibular nuclei connections to vestibulo-cerebellar structures.

Down beat nystagmus is a sign of vestibular tone imbalance in Pitch plane , the patients present blurred vision,oscillopsia, and gait ataxia. Examination reveals vertical nystagmus ,in primary position of gaze, with the fast phase downward .The nystagmus is accentuated if the patient holds the gaze 30 degrees in the horizontal plane.

Looking downward from the primary position usually increases the magnitude of the nystagmus ,it doesn’t disappear with visual fixation.In many patients may be apparent only with positional maneuvers or by ophtalmoscopy (2-4-5-7-8-9-11-15)

Downbeat nystagmus is associated with a variety of clinical disorders, most commonly lesions near the cervico-medullary junction ,for example the A-Chiari malformation ,or in other conditions such as MS, olivoponto cerebellar atrophy , cerebellar ectopia , Wernicke’s encephalophathy ,even it may be yielded ingestion of drugs such as phenytoin and lithium.

Up beat nystagmus is another type of central vestibular syndrome , as a sign of vestibular tone imbalance in Pitch plane , it can be due to lesion of the pontomedullary or pontomesencephalic tegmentum or of the dorsal cerebellar vermis close to peri-hypoglosinuclei (2-4-5-7-11).

Up beating nystagmus is frequently found with MS, vascular diseases, malformation of cervico-medullary junction, Wernicke’s encephalophathy and posterior fossa tumours.

The examination shows , vertical nystagmus in the primary position of gaze, with the fast phase beating upward , some times it becomes apparent with a caloric test. The convergence increases the nystagmus. A vestibular tone imbalance in Roll plane due to a lesion should result in a syndrome consisting of a perceptual tilt ,head and body tilt, skew desviation and ocular torsion.

Skew deviation (4-10)presumably emerges when otolith inputs become unbalanced in a non physiological way. Cerebellar lesions may induce skew deviation .Patients with skew deviation complain of vertical and sometimes torsional (one image tilt with respect to the other) diplopia Cyclorotation of both eyes associated with an illusion of tilt visual world may appear .The head tilt may also be tilted usually towards the side of the lower eye .Together ,skew deviation ,ocular counterrolling and head tilt constitute the ocular tilt reaction (OTR).

OTR is principally a labyrinthine reflex, it results from lesions that involve in the otolith-ocular pathways at the level of peripheral labyrinth ,vestibular nerve, vestibular nucleus or caudal midbrain or the interstitial nucleus of Cajal. The patients present ipsilateral head tilt ,skew deviation with the ipsilateral eye lower than the contralateral eye and ocular torsion ,upper pole, the eye rotated towards the side of the lesion that is associated with the deviation of the subjective visual-vertical axes in the direction of the head tilt. With peripheral and vestibular nuclei lesions the lower eye is on the side of the lesion .The otolith-ocular pathway crosses at the level of the vestibular nuclei ,so with lesions above the decussation the higher eye is on the side of the lesion. The OTR has been seen in patients with peripheral labyrinthine lesions due to ishaemia at the level of the lateral medulla ( eg. Wallenberg’s syndrome) , focal brainstem abscess, haemorrhage , lesion of the rostral midbrain or patients with MS (6-4-7-11).

The main aetiologies in the torsional nystagmus (TN) are demyelination ,vascular disease and posterior fossa tumours .The TN could be predominant and present in primary gaze or be elicited by head positioning or gaze deviation .The TN was more frequently and consistently modulated by vertical canal stimuli (head oscillation in roll) than by otolith stimuli(static tilt).Statistical analysis of the MRI showed significant overlap of the abnormal MRI signals in the area of the vestibular nuclei on the opposite side to the beat direction of the TN in primary gaze .These results suggest that TN originates in a central imbalance of vertical semicircular canal function ( 5-12).

Ipsilateral cerebellar system lesions may produce ipsilateral vestibular nuclei desinhibition and elicit TN tigger by head positioning or gaze deviation.

Pure syndromes in Yaw plane are rare , because the area of the lesion that can cause a tone imbalance in Yaw is small in contrast the area of the lesion that can cause vestibular tone imbalance s in Roll or Pitch. Second the area of a lesion that theoretically can cause a pure imbalance in the Yaw plane adjoins and overlaps areas subserving vestibular function in Roll and Pitch .A lesion frequently results in mixed nystagmus.

Horizontal benign positional vertigo is one of the few vestibular disorders restricted to the Yaw plane. Here the positional nystagmus is horizontal according to the stimulation of one horizontal semicircular canal only.

Vertigo ,postural imbalance ,oscillopsia and vomiting are common in peripheral vestibular diseases, with spontaneous horizontal- torsional nystagmus. The direction of the fast phase is beating away from the damaged vestibular. This type of nystagmus is unidirectional ,it is supressed by visual fixation, it is greater when the eyes are turned in the direction of the quick phase( Alexander’s law) and increased or becomes apparent when the fixation is eliminated using the ophtalmoscope or Frenzel’s goggles. The aetiology most often is viral neuritis ,less frequently can be due to bacterial or ischemia labyrinthine or autoimmune inner ear disease (3-4-7).

Vestibular nystagmus is often influenced by head movements or a change in head position. Some times the nystagmus can be induced by a vigorous head shaking in the horizontal plane ,this type of nystagmus could show a peripheral or central pattern with a vertical nystagmus. After head-shaking transient nystagmus indicates a persistent vestibular imbalance.

Positional test could increase the spontaneous nystagmus or induce the vertical or paroxysmal positional nystagmus.

The paroxysmal positional nystagmus result from vestibular end organ disease or from brainstem and cerebellar lesions. These type of nystagmus are induced by a rapid change from erect sitting to the supine head hanging left, centre or right position .The most common variety (so called benign paroxysmal positional nystagmus-BPPN) has a 3-10 seconds latency before onset the torsional nystagmus (these nystagmus has combined torsional and linear components) beating to the ear down only in one head -hanging position ,and a burst of nystagmus occurs in the reverse direction when the patients moves back to the sitting position .The nystagmus rarely lasts longer than 30 seconds. The patient feels vertigo with the initial positioning but with repeating the maneuvers vertigo and nystagmus disappear (1). The BPPN is common after head injury , viral labyrinthitis or other causes .Infrequent bilateral cases have been reported. Positional nystagmus without vertigo is always central vestibular and the direction of the nystagmus varies This central type can be the initial sign of a posterior fossa tumour, the nystagmus does not decrease in amplitude or duration with repeated positioning, does not have a clear latency and usually lasts longer than 30 seconds .The direction is unpredictable , it may beat towards the uppermost or undermost ear, is bilateral and direction-changing when the head is tilted towards the right or left side .The frequency of central positional nystagmus is low (1-4-7-11).

The gaze -evoked nystagmus appears if there is a failure for maintaining stable the gaze in excentrical position ,the eyes drift back towards the centre .Symmetric gaze -evoked nystagmus is always in the direction of gaze, is commonly produced by ingestion of drugs such as Phenobarbital , phenytoin , diazepam alcohol or can also result from MS and cerebellar atrophy. Asymmetric gaze evoked nystagmus always indicates a structural brainstem lesion (7-11).

Lesions in the medial longitudinal fasciculus (MLF) , so called internuclear ophthalmoplegia ( ION), produces dissociated or disconjugate gaze- evoked nystagmus .The abducting eye on the side opposite the MLF lesion develops a nystagmus in the direction of the gaze .Bilateral MLF lesions are frequently seen in demyelinating diseases , but unilateral MLF lesion accompanies vascular disease of the brainstem (11). In acquired diseases the Pendular Nystagmus (PN) signals structural pathology in the brainstem, mainly in the pons , but also in the midbrain and the medulla., the most frequent associated aetiologies being demyelination ,strokes, and tumours .The PN an involuntary eye movement like a sinusoidal oscillation of the globe The trajectory of the nystagmus may be predominantly horizontal ,vertical ,torsional or a combinations of these .In some cases ,the eyes can follow a complex path with different amplitudes ,or more rarely frequencies of oscillation in horizontal and vertical planes as if the eyes were following complex trajectories as if they were following motion around a loop or figure of eight. .The frequency of oscillation is 2.5-6 Hz .The PN could be conjugate and disconjugate in amplitude or direction .The Pendular nystagmus is a significant clinical entity because it causes distressing oscillopsia and lowers visual acuity .The impaired acuity results from the slipping of retinal image because of the continuous motion of the eyes ,additional optic neuropathy ,or a combination of these (5-13-14).

In the majors of the patients the ocular oscillation develop from months to years after the onset of their disease ,this delay and rhythm of the PN supports a dysfunction of the cholinergic system (hypersensitivity to acetylcholine )associated with deafferentation of the inferior olive. It is possible that multiple or large lesions predominately involving the central tegment tract ,red nucleus and the inferior olivary nuclei may be required to elicit PN. The patients with conjugate PN have a higher incidence of symmetrical mirror image lesions on MRI that the patients with disconjugate nystagmus. The disconjugancy of PN is independent of the presence of internuclear ophtalmoplegia or asymmetrical visual acuity .It is not clear how disconjugate or monocular oscillations can occur but they tend to be associated with asymmetrical disposition of abnormal MRI signals.

Convergence- retraction nystagmus is a saccadic disorder rather than nystagmus .It is characterised by a quick phase that converge or retract the ocular globe .It is caused by lesions of the mesenceplalon that involve the region of the posterior commissure(pineal tumours) (4-11).The saccadic oscillation signals a loss of gabaergic inhibition in the superior coliculo .This type oscillation include square wave jerks, macro square wave jerks, ocular flutter and opsoclonus .They are prominent in cerebellar lesions ,progressive supranuclear palsy ,MS ,and olivopontocerebellar atrophy (11) .

REFERENCES:

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  6. Brand ,T and Dietrich ,M:pathological eye-head coordination in roll: tonic ocular tilt reaction in mesencephalic and medullary lesions.Brain 110:649-666,1987.
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  12. Lopez,L, Bronstein AM ,Gresty MA, Rudge P , DU BOULAY EPG: Torsional Nystagmus: A Neuro-otological and MRI Study of Thirty-Five cases. Brain (1992) ,115, 1107-1124.
  13. Lopez,L,Gresty MA,Bronstein AM, DU BOULAY EPG,:Acquired Pendular Nystagmus:Oculomotor and MRI Findings.Acta Otolaryngol(Stockh) 1995,Suppl 520: 285-287.
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  15. Yee RD,:Downbeat Nystagmus:Characteristics and Localization of Lesion.Transactions of the American Ophathalmology Society 87: 984-1032,1989.

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