The levator palpebrae superioris () is the muscle in the orbit that elevates the upper eyelid.
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Encyclopædia Britannica 2006 Ultimate Reference Suite DVD 2008 The tarsus has a lower and upper part making up the palpebrae.
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The superior tarsal muscle is a smooth muscle adjoining the levator palpebrae superioris muscle that helps to raise the upper eyelid.
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The superior tarsal muscle works to keep the upper eyelid raised after the levator palpebrae superioris has raised the upper eyelid.
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The superior tarsal muscle originates on the underside of levator palpebrae superioris and inserts on the superior tarsal plate of the eyelid.
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The superior tarsal muscle, a smooth muscle, is attached to the levator palpebrae superioris, and inserts on the superior tarsal plate as well.
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The superior branch of the oculomotor nerve or the superior division, the smaller, passes medially over the optic nerve. It supplies the superior rectus and levator palpebrae superioris.
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Lid-lengthening surgeries can be done on upper and lower eyelid to correct the patient's appearance and the ocular surface exposure symptoms. Marginal myotomy of levator palpebrae muscle can reduce the palpebral fissure height by 2–3 mm. When there is a more severe upper lid retraction or exposure keratitis, marginal myotomy of levator palpebrae associated with lateral tarsal canthoplasty is recommended. This procedure can lower the upper eyelid by as much as 8 mm.
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The exact cause of ALO is not yet fully understood. Despite its name, it is not a true apraxia, but thought to be due to a supranuclear origin of abnormal neuronal activity. Voluntary eyelid opening involves the simultaneous activation of the levator palpebrae superioris muscle and the inhibition of the orbicularis oculi muscle. Electromyographic studiesAramideh M, Bour LJ, Koelman JH, Speelman JD, Ongerboer de Visser BW. Abnormal eye movements in blepharospasm and involuntary levator palpebrae inhibition.
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Clinical and pathophysiological considerations. Brain. 1994 Dec. 117 (Pt 6):1457-74Esteban A, Gimenez-Roldan S. Involuntary closure of eyelids in parkinsonism. Electrophysiological evidence for prolonged inhibition of the levator palpebrae muscles.
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Tan et al. reported a 10-year-old girl with multiple superficial angiomyxoma associated with neurothekeoma palpebrae. There was no evidence of visceral involvement. The lesions were excised with no recurrence during follow up.
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Consequently, some affected individuals choose to wear sunglasses. The term "ocular myasthenia gravis" describes a subtype of MG where muscle weakness is confined to the eyes, i.e. extraocular muscles, m. levator palpebrae superioris, and m.
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The supraorbital artery branches from the ophthalmic artery after it passes through the optic canal and passes medially over the optic nerve. It travels anteriorly in the orbit by passing superior to the eye and medial to the superior rectus and levator palpebrae superioris. It then travels with the supraorbital nerve between the periosteum of the roof of the orbit and the levator palpebrae superioris to enter the supraorbital foramen. After passing through the supraorbital foramen, it bifurcates into a superficial and deep branch.
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The levator palpebrae superioris receives motor innervation from the superior division of the oculomotor nerve. The smooth muscle that originates from its undersurface, called the superior tarsal muscle is innervated by postganglionic sympathetic axons from the superior cervical ganglion.
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The supraorbital artery branches from the OA as it passes over the optic nerve. The supraorbital artery passes anteriorly along the medial border of the superior rectus and levator palpebrae and through the supraorbital foramen to supply muscles and skin of the forehead.
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The extraocular muscles are the six muscles that control movement of the eye and one muscle that controls eyelid elevation (levator palpebrae). The actions of the six muscles responsible for eye movement depend on the position of the eye at the time of muscle contraction.
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1992 May. 55(5):369-71Lepore FE, Duvoisin RC. Apraxia of eyelid opening: an involuntary levator inhibition. Neurology. 1985 Mar. 35(3):423-7 have shown that ALO may involve either involuntary levator palpebrae superioris muscle inhibition, persistent pretarsal orbicularis oculi muscle contraction, or both.
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The superior transverse ligament of the eye (also known as Whitnall's ligament) is a transverse ligament surrounding the levator palpebrae superioris muscle close to its partial implantation into the skin of the upper eyelid. The muscle also attaches to the superior tarsal plate and into orbital bone. The ligament allows for a change of the functional origin of the levator palpebrae superioris muscle, enabling the superior tarsus (eyelid) to be elevated superiorly rather than directly toward the muscle's origin on the sphenoid bone. Attaches medially to the pulley of superior oblique muscle (Trochlea of superior oblique) and laterally to the lacrimal gland 10mm above Whitnall tubercle.
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Clinical findings mainly eyeball is down and out ipsilateral lateral squint. Ptosis present. Pupil dilated and fixed as the levator palpebrae superioris nerve supply is disrupted. Contralateral hemiplegia CT scan or MRI might help in delineating the cause or the vessel or region of brain involved in stroke.
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The nasals have large foramina dorsolaterally and a midline fossa. No palpebrae are preserved. Though cervical vertebrae and caudal vertebrae have been preserved, their exact number is unknown. The femur is bowed and has an anterior trochanter slightly lower than the greater trochanter and a third as narrow as the latter.
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Abadie's sign of exophthalmic goiter is a medical sign characterized by spasm of the levator palpebrae superioris muscle with retraction of the upper lid (so that sclera is visible above cornea) seen in Graves-Basedow disease which, together with exophthalmos causes the bulging eyes appearance. It is named for Jean Marie Charles Abadie.
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The levator palpebrae superioris originates from inferior surface of the lesser wing of the sphenoid bone, just above the optic foramen. It broadens and decreases in thickness (becomes thinner) and becomes the levator aponeurosis. This portion inserts on the skin of the upper eyelid, as well as the superior tarsal plate. It is a skeletal muscle.
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It is important to distinguish between these two very different causes of ptosis. This can usually be done clinically without issue, as each type of ptosis is accompanied by other distinct clinical findings. The ptosis seen in paralysis of the levator palpebrae superioris is usually more pronounced than that seen due to paralysis of the superior tarsal muscle.
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In about two-thirds of individuals, the initial symptom of MG is related to the muscles around the eye. Eyelid drooping (ptosis may occur due to weakness of m. levator palpebrae superioris) and double vision (diplopia, due to weakness of the extraocular muscles). Eye symptoms tend to get worse when watching television, reading, or driving, particularly in bright conditions.
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Inverse Marcus Gunn phenomenon is a rare condition that causes the eyelid to fall upon opening of the mouth. In this case, trigeminal innervation to the pterygoid muscles of the jaw is associated with an inhibition of the branch of the oculomotor nerve to the levator palpebrae superioris, as opposed to stimulation in Marcus Gunn jaw-winking.
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The supratrochlear nerve branches from the frontal nerve midway between the base and apex of the orbit. It travels anteriorly above the levator palpebrae superioris and exits the orbit through the supratrochlear notch in the superomedial margin of the orbit. It then ascends onto the forehead beneath the corrugator supercilii and frontalis muscles. It then divides into sensory branches.
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The levator palpebrae superioris, which is supplied by a branch of the oculomotor nerve, also elevates the upper eyelid. Eyelid elevation is therefore under both voluntary and involuntary control. Interruption of either pathway will result in eyelid droop (ptosis). The other two eye muscles with sympathetic supply (the inferior tarsal muscle and the orbitalis) are vestigial in humans.
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An eyelid is a thin fold of skin that covers and protects the eye. The levator palpebrae superioris muscle helps in the movement of eyelid. The human eyelid features a row of eyelashes along the eyelid margin, which helps in protection of the eye from dust and foreign debris. The main function of eyelid is to keep the cornea moist and clean.
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Eyelashes are hairs attached to the upper and lower eyelids that create a line of defense against dust and other elements to the eye. The eyelashes catch most of these irritants before they reach the eyeball. There are multiple muscles that control reflexes of blinking. The main muscles, in the upper eyelid, that control the opening and closing are the orbicularis oculi and levator palpebrae superioris muscle.
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Blepharochalasis results from recurrent bouts of painless eyelid swelling, each lasting for several days. This is thought to be a form of localized angioedema, or rapid accumulation of fluid in the tissues. Recurrent episodes lead to thin and atrophic skin. Damage to the levator palpebrae superioris muscle causes ptosis, or drooping of the eyelid, when the muscle can no longer hold the eyelid up.
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The oculomotor nerve passes through the lateral wall of the cavernous sinus and enters the orbit through the superior orbital fissure. It divides into branches that innervate the levator palpebrae superioris and four of the six extraocular muscles. Parasympathetic fibers initially run in the inferior division of the oculomotor nerve. They exit as one or two short “motor roots” that synapse in the ciliary ganglion.
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The supraorbital nerve branches from the frontal nerve midway between the base and apex of the orbit. It travels anteriorly above the levator palpebrae superioris and exits the orbit through the supraorbital foramen (or notch) in the superior margin orbit. It exits the orbit lateral to the supratrochlear nerve. It then ascends onto the forehead beneath the corrugator supercilii and frontalis muscles and divides into a medial branch and lateral branch.
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An eyelid is a thin fold of skin that covers and protects an eye. The levator palpebrae superioris muscle retracts the eyelid, exposing the cornea to the outside, giving vision. This can be either voluntarily or involuntarily. The human eyelid features a row of eyelashes along the eyelid margin, which serve to heighten the protection of the eye from dust and foreign debris, as well as from perspiration.
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The frontal nerve branches from the ophthalmic nerve immediately before entering the superior orbital fissure. In then travels superolateral to the annulus of Zinn between the lacrimal nerve and inferior ophthalmic vein. After entering the orbit it travels anteriorly between the roof periosteum and the levator palpebrae superioris. Midway between the apex and base of the orbit it divides into two branches, the supratrochlear nerve and supraorbital nerve.
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Damage to this muscle or its innervation can cause ptosis, which is drooping of the eyelid. Lesions in CN III can cause ptosis, because without stimulation from the oculomotor nerve the levator palpebrae cannot oppose the force of gravity, and the eyelid droops. Ptosis can also result from damage to the adjoining superior tarsal muscle or its sympathetic innervation. Such damage to the sympathetic supply occurs in Horner's syndrome and presents as a partial ptosis.
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To perform Bienfang’s test, the examiner should ensure that the patient is seated comfortably with head and eyes in primary gaze. The examiner is positioned 2–3 feet in front of the patient’s face to allow for clear observation of the patient’s eyes. The patient is instructed to tightly squeeze his or her eyelids shut for five to ten seconds. This not only relaxes the levator palpebrae superioris but actively inhibits it.
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Though one may think that the stimulus triggering blinking is dry or irritated eyes, it is most likely that it is controlled by a "blinking center" of the globus pallidus of the lenticular nucleus—a body of nerve cells between the base and outer surface of the brain. Nevertheless, external stimuli can contribute. The orbicularis oculi is a facial muscle; therefore its actions are translated by the facial nerve root. The levator palpebrae superioris’ action is sent through the oculomotor nerve.
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Oculomotor nerve palsy is an eye condition resulting from damage to the third cranial nerve or a branch thereof. As the name suggests, the oculomotor nerve supplies the majority of the muscles controlling eye movements. Thus, damage to this nerve will result in the affected individual being unable to move their eye normally. In addition, the nerve also supplies the upper eyelid muscle (levator palpebrae superioris) and It is accompanied by parasympathetic fibers innervating the muscles responsible for pupil constriction (sphincter pupillae) .
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The orbicularis oculi closes the eye, while the contraction of the levator palpebrae muscle opens the eye. The Müller’s muscle, or the superior tarsal muscle, in the upper eyelid and the inferior palpebral muscle in the lower 3 eyelid are responsible for widening the eyes. These muscles are not only imperative in blinking, but they are also important in many other functions such as squinting and winking. The inferior palpebral muscle is coordinated with the inferior rectus to pull down the lower lid when one looks down.
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It can sometimes be difficult to distinguish between eye symptoms due to hyperthyroidism and those due to Graves' antibodies, not in the least because the two often occur coincidentally. What can make things particularly difficult, is that many patients with hyperthyroidism have lid retraction, which leads to stare and lid lag (due to contraction of the levator palpebrae muscles of the eyelids). This stare may then give the appearance of protruding eyeballs (proptosis), when none in fact exists. This subsides when the hyperthyroidism is treated.
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In the upper eyelid, the orbital septum blends with the tendon of the levator palpebrae superioris, and in the lower eyelid with the tarsal plate. When the eyes are closed, the whole orbital opening is covered by the septum and tarsi. Medially it is thin, and, becoming separated from the medial palpebral ligament, attaches to the lacrimal bone at its posterior crest. The medial ligament and its much weaker lateral counterpart, attached to the septum and orbit, keep the lids stable as the eye moves.
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Myasthenia gravis is an autoimmune disease involving the neuromuscular junction leading to skeletal muscle weakness and fatigability. In ocular myasthenia gravis (OMG), the symptoms are confined to the extraocular and eyelid muscles. Patients most commonly experience ptosis caused by fatigue of levator palpebrae superioris and/or diplopia due to weakness of extraocular muscles. These symptoms are generally characterized by diurnal fluctuation, worsening with increased use of the eyes and improving with rest. Bienfang’s test is indicated for patients who are suspected of having OMG.
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The oculomotor nerve include axons of type GSE, general somatic efferent, which innervate skeletal muscle of the levator palpebrae superioris, superior rectus, medial rectus, inferior rectus, and inferior oblique muscles.(innervates all the extrinsic muscles except superior oblique and lateral rectus.) The nerve also includes axons of type GVE, general visceral efferent, which provide preganglionic parasympathetics to the ciliary ganglion. From the ciliary ganglion post ganglionic fibers pass through the short ciliary nerve to the constrictor pupillae of the iris and the cilliary muscles.
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In addition, it is possible that inflammation of the cavernous sinus will result in compression of the optic chiasm (resulting in vision problems) and/or the pituitary gland. Failure of CN III will result in loss of function of the following muscles: medial rectus, superior rectus, inferior rectus, and inferior oblique as well as muscles that are responsible for opening the eyelid: levator palpebrae superioris muscle and the superior tarsal muscle (Muller's muscle). CN III damage also results in loss of parasympathetic innervation of the eye (loss of pupillary constriction and lens accommodation).
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Kearns–Sayre syndrome (KSS), Oculocraniosomatic disorder or Oculocranionsomatic neuromuscular disorder with ragged red fibers, is a mitochondrial myopathy with a typical onset before 20 years of age. KSS is a more severe syndromic variant of chronic progressive external ophthalmoplegia (abbreviated CPEO), a syndrome that is characterized by isolated involvement of the muscles controlling movement of the eyelid (levator palpebrae, orbicularis oculi) and eye (extra-ocular muscles). This results in ptosis and ophthalmoplegia respectively. KSS involves a combination of the already described CPEO as well as pigmentary retinopathy in both eyes and cardiac conduction abnormalities.
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Abnormalities of visual movement may also be seen on examination, such as jittering (nystagmus). Damage to the oculomotor nerve (III) can cause double vision and inability to coordinate the movements of both eyes (strabismus), also eyelid drooping (ptosis) and pupil dilation (mydriasis). Lesions may also lead to inability to open the eye due to paralysis of the levator palpebrae muscle. Individuals suffering from a lesion to the oculomotor nerve may compensate by tilting their heads to alleviate symptoms due to paralysis of one or more of the eye muscles it controls.
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A slow-motion example of a blinking human eye Blinking is a bodily function; it is a semi-autonomic rapid closing of the eyelid. A single blink is determined by the forceful closing of the eyelid or inactivation of the levator palpebrae superioris and the activation of the palpebral portion of the orbicularis oculi, not the full open and close. It is an essential function of the eye that helps spread tears across and remove irritants from the surface of the cornea and conjunctiva. Blinking may have other functions since it occurs more often than necessary just to keep the eye lubricated.
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Although these blocking antibodies may be confined to one of the larger muscles responsible for moving the face or appendages or for breathing, about 90% of MG patients eventually have eye involvement. The most common symptoms are double vision (diplopia) and eyelid drooping (ptosis), whereas the pupil is always spared. Diplopia occurs when MG affects a single extraocular muscle in one eye, limiting eye movement and leading to double vision when the eye is turned toward the affected muscle. Ptosis occurs when the levator palpebrae superioris (the muscle responsible for eyelid elevation) is affected on one or both sides, leading to eyelid drooping.
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Cranial nerves III, IV, and VI are usually tested together as part of the cranial nerve examination. The examiner typically instructs the patient to hold his head still and follow only with the eyes a finger or penlight that circumscribes a large "H" in front of the patient. By observing the eye movement and eyelids, the examiner is able to obtain more information about the extraocular muscles, the levator palpebrae superioris muscle, and cranial nerves III, IV, and VI. Loss of function of any of the eye muscles results in ophthalmoparesis. Since the oculomotor nerve controls most of the eye muscles, it may be easier to detect damage to it.
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The Indian white-eye was described by the Dutch zoologist Coenraad Jacob Temminck in 1824 from a specimen collected in Bengal. He coined the binomial name Sylvia palpebrosa. The 5 volumes were originally issued in 102 parts, 1820-1839 The English and scientific names refer to the conspicuous ring of white feathers round the eyes, palpebrosus being New Latin for "having prominent eyelids", from the Latin palpebrae "eylids". The English name of this species was changed from "Oriental white-eye" to "Indian white-eye" to more accurately reflect the geographic range following the reorganisation of the taxa with the introduction of Hume's white-eye (Zosterops auriventer), the warbling white-eye (Zosterops japonicus) and Swinhoe's white-eye (Zosterops simplex).
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Hair gel or baby oil is applied to style short hair; while hairspray is applied to style long hair. Powders (especially baby powder) are applied to the body to eliminate odors, and it is also applied to the face to achieve a matte and fresh effect to prevent oiliness of the corpse. Mortuary cosmeticizing is not done for the same reason as make-up for living people; rather, it is designed to add depth and dimension to a person's features that lack of blood circulation has removed. Warm areas – where blood vessels in living people are superficial, such as the cheeks, chin, and knuckles – have subtle reds added to recreate this effect, while browns are added to the palpebrae (eyelids) to add depth, especially important as viewing in a coffin creates an unusual perspective rarely seen in everyday life.
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