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| Internuclear Ophthalmoplegia |
Internuclear ophthalmoplegia
Internuclear ophthalmoplegia is a physical finding, or sign, that is a particular form of ophthalmoparesis. It can affect either the right or left eye. It is a disorder of conjugate lateral gaze. The affected eye shows impairment of adduction. The partner eye diverges from the affected eye during abduction, producing diplopia; during extreme abduction, compensatory nystagmus can be seen in the partner eye.
The disorder is caused by injury or dysfunction in the medial longitudinal fasciculus, a crossed tract which links the pontine paramedian reticular formation to the oculomotor nucleus of the affected, contralateral eye.
Causes are manifold; brainstem demyelinating diseases such as multiple sclerosis are frequently found to be causal, and should be considered especially if no other abnormalities are discovered by examination or brain imaging.
Category:Sign (medicine) Category:Neurology Category:Ophthalmology
Ophthalmoparesis
Ophthalmoparesis is a physical finding in certain neurologic illnesses. It refers to paralysis of the extraocular muscles which are responsible for eye movements. It can refer to complete paralysis of the eyes, in which case it is synonymous with ophthalmoplegia. More usually, it refers to a partial paralysis, in contrast to the complete paralysis denoted by ophthalmoplegia.
Ophthalmoparesis can involve any or all of the extraocular muscles, which include the superior recti, inferior recti, medial recti, lateral recti, inferior oblique and superior oblique muscles. It can also be classified by the directions of affected movements, e.g. "vertical ophthalmoparesis".
Ophthalmoparesis can result from disorders of various parts of the eye and nervous system:
- The orbit (anatomy) of the eye, including mechanical restrictions of eye movement, as in Graves disease.
- The muscle, as in progressive external ophthalmoplegia.
- The neuromuscular junction, as in myasthenia gravis.
- The cranial nerves or their brainstem nuclei, including the oculomotor, trochlear, and abducens.
- White matter tracts in the brainstem, as in internuclear ophthalmoplegia, an occasional finding in multiple sclerosis.
- Injury to supranuclear structures, as in progressive supranuclear palsy.
- Very rarely, disorders of higher brain structures, including the parietal lobes of the cerebral cortex.
Thiamine deficiency can cause ophthalmoparesis in susceptible persons; this is part of the syndrome called Wernicke encephalopathy. The causal pathway by which this occurs is unknown. Intoxication with certain substances, such as phenytoin, can also cause ophthalmoparesis.
Treatment and prognosis depend on the underlying condition.
Category:NeurologyCategory:Sign (medicine)
Adduction: Anatomical terms of location
Nystagmus
Nystagmus is rapid involuntary rhythmic eye movement, with the eyes moving quickly in one direction (quick phase), and then slowly in the other (slow phase). The direction of nystagmus is defined by the direction of its quick phase (e.g., right nystagmus is due to a right moving quick phase). Nystagmus may occur in the vertical or horizontal directions, and also in a semicircular movement, and thus are called downbeat nystagmus, upbeat nystagmus, seesaw nystagmus, periodic alternating nystagmus, and pendular nystagmus. There are other similar alterations in periodic eye movements (saccadic oscillations) such as opsoclonus or ocular flutter. One can accurately think of nystagmus as the combination of a slow adjusting eye movement (slow phase) like would be seen with the vestibulo-ocular reflex, followed by a quick saccade (quick phase) when the eye has reached the limit of its rotation.
In medicine, the clinical importance of nystagmus is that it indicates that the patient's spatial sensory system perceives rotation and is rotating the eyes to adjust. Thus it depends on the coordination of activities between two major physiological systems: the vision and the vestibular apparatus (which controls posture and balance). This may be physiological (or normal) or pathological.
Physiological nystagmus
An easy way of inducing physiological nystagmus is by having the person close her or his eyes and spin around. After a few spins, there is a distinct jerking of the eyes from side to side when they are reopened: this is rotatory-induced nystagmus. The degree of physiological nystagmus varies greatly between people and even in the same person at different times.
Another type of physiological nystagmus is the optokinetic nystagmus (OKN). It can be induced by presenting a moving pattern. The eyes tend to track the pattern, but snap back regularly. Nystagmus is distinguished from normal involuntary eye activity by the rapidity and repetitive pattern of the movement.
Pathological nystagmus
Nystagmus is a relatively common clinical condition, affecting one in every 5,000 to 10,000 individuals.
The cause for pathological nystagmus may be congenital, idiopathic, secondary to a pre-existing neurological disorder or may be induced temporarily by certain drugs (alcohol and other central nervous system depressants and stimulants, such as lithium salts, dilantin and ecstasy). Nystagmus generally causes a degree of vision impairment, although the severity of such impairment varies widely.
If the pathologic nystagmus is based in the central nervous system (CNS), such as with a cerebellar problem, the nystagmus will be in any direction including horizontal.
Vestibular nystagmus is always horizontal, and may be spontaneous or positional.
Spontaneous vestibular nystagmus is nystagmus that occurs spontaneously, regardless of the position of the patient's head.
In milder cases, the patient is often asked to fixate on an object, or wear fresnel lens glasses, which blur vision, to bring out the nystagmus.
Positional nystagmus is the opposite of spontaneous nystagmus in that it occurs when the patient's head is in a specific position (e.g., benign paroxysmal positional vertigo; BPPV).
Again, in milder cases the patient is often asked to fixate on an object, or wear fresnel lens glasses, which blur vision, to bring out the nystagmus.
Horizontal nystagmus is also classified into three degrees as follows:
- First degree nystagmus is present only on lateral gaze, and has the fast phase in the direction of gaze;
- Second degree nystagmus is present in the primary (neutral) position of gaze;
- Third degree nystagmus is present in the same direction in all gaze positions
Such distinctions help to identify the anatomical source of the nystagmus. First degree nystagmus usually originates in the brainstem or cerebellum, while second and third degree nystagmus are usually vestibular in origin.
Other (extremely) rare pathologic nystagmuses are gaze paretic, rebound, fixation, congenital and dissociated nystagmus.
Diseases presenting nystagmus
Some of the diseases which present nystagmus as a pathological sign are:
- Head trauma (the most common cause in young people)
- Stroke (the most common cause in older people)
- Ménière’s disease and other balance disorders
- Multiple sclerosis
- Brain tumors
- Wernicke-Korsakoff syndrome
- Encephalopathy
- Lateral medullary syndrome
- Aniridia
- Optic nerve hypoplasia
- Albinism
- Noonan syndrome
- Pelizaeus-Merzbacher disease
Causes
Congenital nystagmus occurs more frequently than acquired nystagmus, is not associated with other disorders (such as refraction errors or diplopia) and is usually mild and non-progressive. The affected persons are not aware of their spontaneous, small-amplitude eye movements.
- Congenital
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- Infantile:
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- Idiopathic
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- Albinism
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- Aniridia
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- Leber's congenital amaurosis
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- Bilateral optic nerve hypoplasia
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- Bilateral congenital cataracts
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- Rod monochromatism
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- Optic nerve or macular disease
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- Latent nystagmus
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- Nystagmus blockage syndrome
- Acquired
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- Visual loss (e.g. dense cataract, trauma, cone dystrophy)
:
- Toxic/metabolic (e.g. alcohol intoxication, lithium, barbituates, phenytoin, salicylates, benzodiazepines, phencyclidine, other anticonvulsants or sedatives, Wernicke's encephalopathy, thiamine deficiency)
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- Central nervous system disorders (e.g. thalamic hemorrhage, tumor, stroke, trauma, multiple sclerosis)
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- Non-physiologic
Diagnosis and therapy
Nystagmus can be clinically investigated by using a number of non-invasive standard tests. The simplest one is to irrigate an external auditory meatus with warm or cold water. The temperature gradient provokes the stimulation of the vestibulocochlear nerve and the consequent nystagmus.
The resulting movement of the eyes may be recorded and quantified by a special device called electronystagmograph (ENG), which is a form of electrooculography (an electrical method of measuring eye movements using external electrodes). Special swinging chairs with electrical controls are also used in this test to induce rotatory nystagmus.
Pathological acquired nystagmus is mostly a temporary condition and stops spontaneously. When it is secondary to a neurological disorder, this must be treated accordingly. Congenital nystagmus is usually non-treatable, but several therapeutic approaches, such as contact lenses, drugs, surgery, and low vision rehabilitation can be used in order to improve visual function.
See also
- Myokymia
- Oscillopsia
- Ocular flutter
- Opsoclonus
- Vestibular paroxysmia
References
- The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease, J.B. Lippincott, 1994.
- [http://www.med.uwo.ca/UME/Diane/Year2Postings2004-2005/Trimester%202/CNS/VestibularDisordersAndTinnitusDrParnes.pdf Vestibular disorders and tinnitus] - Lecture notes from a lecture given to a second year medical school class at the [http://www.uwo.ca University of Western Ontario] on 19 November 2004 by Dr. Lorne Parnes. These notes are released under the FDL.
External links
- [http://www.nlm.nih.gov/medlineplus/ency/article/003037.htm Eyes Movements - Uncontrollable]. MedlinePlus.
- Hensil J, Gurwood AS: Understanding Nystagmus. Optometry 2000 Jul;71(7):439-48. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15326897 Medline access]
- [http://www.nystagmus.org American Nystagmus Network]
- [http://www.nystagmus.de German-Language Nystagmus Forum]
Category:Sign (medicine)
Category:Ophthalmology
Category:Neurology
Medial longitudinal fasciculusThe medial longitudinal fasciculus (MLF) is a pair of crossed fiber tracts (group of axons), one on each side of the brainstem, that carry information about the direction that the eyes should move.
It connects the cranial nerve nuclei III, IV and VI together, as well as the gaze centres and information about head movement (from cranial nerve VIII).
It also descends into the cervical spinal cord, and innervates some muscles of the neck.
The MLF arises from the Vestibular Nucleus (VN) and is thought to be involved in the maintainance of gaze. This is achived by inputs to the VN from
# the Vestibulocochlear (8th cranial) nerve about head movements,
# gain adjustments from the flocculus of the cerebellum,
# head and neck propioceptors and foot and ankle muscle spindle, via the fastigial nucleus.
Lesions of the MLF produce internuclear ophthalmoplegia.
Category:Sign (medicine)
See also :category:Symptoms
Category:Medicine
Category:Ophthalmology
Category:Medical specialties
Category:Eye
Category:Vision
WGBA-TV
WGBA is a television station in Green Bay, Wisconsin, with a transmitter in nearby rural Glenmore. The station's signal covers the area commonly called the 'Fox Valley (for the Fox River) and the Lakeshore (for Lake Michigan)', which includes Appleton, Oshkosh, Fond du Lac, Manitowoc-Two Rivers, and Sheboygan.
The station also has translator stations in Sturgeon Bay on Channel 22, W22BW, which serves the Door County area, and another in Menominee on Channel 31, W31BK, which serves the northern reaches of the Green Bay market, and the southeastern portion of Michigan's Upper Peninsula. In addition, WGBA maintains a local marketing agreement with UPN affiliate WACY (Channel 32), with both stations sharing studios located in suburban Ashwabenon.
Early History
WGBA, originally with the call letters WLRE, began as an independent station on analog channel 26 on December 31, 1980. The call letters were for station co-founder Lyle R. Evans. The station was the first commercial UHF station and the first independent station in the Green Bay-Appleton market.
In 1985, the station was bought by Family Group Broadcasting, Inc.. On October 3 of that year, the call letters were changed to WGBA[http://www.fccinfo.com/CMDProEngine.php?sCurrentService=TV&tabSearchType=Appl&sAppIDNumber=596813&PHPSESSID=27f736e089acabb7eb90d1e8778b2c6a]. The station (then known as 'TV-26') was well known in its early years for children's programming host Cuddles the Clown, who would stay with the station up until they acquired the NBC affiliation (when he would move to WACY before retiring).
However, the ownership of Family Media, led by Jerold R. Newman, a local investment agent, fell apart after Newman was convicted of fraud. The new owers were a family group, Aries Telecommunications.
Affiliation with Fox (1992-1995)
In the wake of a bankruptcy, WXGZ (the original operation on Channel 32) went off the air February 14, 1992. WGBA then became the new Fox affiliate the day after, and changed its identification to 'Fox 26'.
The station was handicapped by not having a local news operation. In 1994, the first year of Fox coverage of the NFL, the station had to contract with WBAY to do a pregame show before Packers games.
WGBA would end up relaunching Channel 32 with Ace TV, Inc. under a local marketing agreement in 1995 under the new call letters WACY. The stations share studio and office facilities in the Green Bay suburb of Ashwaubenon, Wisconsin, and WGBA provides weather warnings and staff for WACY's coverage of high school football games.
Affiliation with NBC (1995-)
WGBA became an NBC affiliate in mid-1995 in the wake of WLUK (Channel 11) changing from NBC to Fox after an ownership change and Fox's acquisition of the NFL's NFC contract, enabling WLUK to be the Green Bay Packers home station. The station then became 'NBC26' and struggled to find a constant identity to compete with Green Bay's other three stations, which were all established in the 1950s and had loyal audiences.
During NBC coverage of the 1996 Summer Olympics, WGBA began newscasts, at first only at 6 p.m. and 10 p.m. every evening. Eventually as the news department grew, the station added newscasts in other dayparts. Currently the station runs newscasts in the morning (a local version of Today), at 5 p.m, 6 p.m., and 10 p.m., all under the banner of 'NBC26 Live at [Time of Day]'.
Ownership
In October 2004, Journal Broadcast Group bought WGBA for $43.2 million after Aries Telecommunications sold the station. Journal has owned market-leading NBC affiliate WTMJ-TV (Channel 4) in Milwaukee since the beginning days of television, and had always been looking to expand into Northeastern Wisconsin. Journal continues to maintain the WACY LMA, and is looking to buy the station outright to form a true duopoly in the area.
Since the purchase, Channel 26 and Channel 4 have become close sister stations to each other, and now share the same news themes, promotions, and graphics packages. WGBA promotes its connections with Journal Broadcast Group heavily, including the opening of its newscasts. The stations also share a news director based in Milwaukee, allowing WGBA use of the stronger Milwaukee newsroom's resources for breaking news, live events, and sports coverage. There is also a more professional polish to the newscasts, and Journal's marketing is now trying to position WGBA as a strong alternative to the older station newscasts in Green Bay.
External links
- http://www.wgba.com/
- http://www.journalbroadcastgroup.com/
- http://www.greenbaypressgazette.com/news/archive/biz_15907516.shtml
Category:NBC network affiliates
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