Saturday, 21 January 2012

DIFFERENTIAL DIAGNOSIS OF LEUKOCORIA


Leukocoria is an abnormal white reflection from the retina of the eye.Leukocoria can be seen in Cataract,Retinoblastoma,Toxocariasis,Coats disease,Retinopathy of prematurity,persistence of the tunica vasculosa lentis(PHPV),Retinal detachment,Coloboma,Retinal dysplasia and Norrie´sdisease.Nontraumatic unilateral cataracts first detected after 6 months of age also present special concerns.Usually, the precise age of onset is not known.Retinoblastoma is the most common intraocular tumor of childhood, accounting for 1% of childhood cancer deaths in the United States and 5% of blindness in children.

Graves' Ophthalmopathy (Thyroid Eye Disease)


Graves' ophthalmopathy is an autoimmune inflammatory disorder affecting the orbit around the eye, characterized by eyelid retraction,exophthalmos,swelling,redness,conjunctivitis and proptosis.The autoantibodies target the fibroblasts in the eye muscles, and those fibroblasts can differentiate into fat cells. Fat cells andmuscles expand and become inflamed. Veins become compressed, and are unable to drain fluid, causing edema.
In mild disease, patients present with eyelid retraction. In fact, upper eyelid retraction is the most common ocular sign of Graves' orbitopathy. This finding is associated with lid lag on infraduction,eye globe lag on supraduction, a widened palpebral fissure during fixation and an incapacity of closing the eyelids completely (lagophthalmos). Due to the proptosis, eyelid retraction and lagophthalmos, the cornea is more prone to dryness and may present with chemosis, punctate epithelial erosions and superior limbic keratoconjunctivitis. The patients also have a dysfunction of the lacrimal gland with a decrease of the quantity and composition of tears produced.Periorbital swelling due to inflammation can also be observed.
In moderate active disease, the signs and symptoms are persistent and increasing and include myopathy. The inflammation and edema of the extraocular muscles lead to gaze abnormalities.Patient may experience vertical diplopia on upgaze and limitation of elevation of the eyes due to fibrosis of the muscle.
In more severe and active disease, mass effects and cicatricial changes occur within the orbit. With enlargement of the extraocular muscle at the orbital apex, the optic nerve is at risk of compression. The orbital fat or the stretching of the nerve due to increased orbital volume may also lead to optic nerve damage. The patient experiences a loss of visual acuity, visual field defect, afferent pupillary defect, and loss of color vision.

Glaucoma


Glaucoma is a disease in which the optic nerve is damaged, leading to progressive, irreversible loss of vision. It is often, but not always, associated with increased pressure of the fluid in the eye.
Intraocular pressure is a function of production of liquid aqueous humor by the ciliary processes of the eye and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary processes into the posterior chamber, bounded posteriorly by the lens and the zonules of Zinn and anteriorly by the iris. It then flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris and anteriorly by the cornea. From here the trabecular meshwork drains aqueous humor via Schlemm's canal into scleral plexuses and general blood circulation.
The nerve damage involves loss of retinal ganglion cells in a characteristic pattern.Raised intraocular pressure is a significant risk factor for developing glaucoma (above 21 mmHg).Glaucoma can be divided roughly into two main categories, "open angle" and "closed angle" glaucoma. In angle closure glaucoma, the iris is apposed to the lens resulting in the inability of the aqueous fluid to flow from the posterior to the anterior chamber and then out of the trebecular network.Closed angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly but the discomfort often leads patients to seek medical attention before permanent damage occurs.In open angle glaucoma there is reduced flow through the trabecular meshwork.Open angle, chronic glaucoma tends to progress at a slower rate and the patient may not notice that they have lost vision until the disease has progressed significantly.Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.

ophthalmia neonatorum


Neonatal conjunctivitis, also known as ophthalmia neonatorum, is a form of bacterial conjunctivitis contracted by newborns duringdelivery. The baby's eyes are contaminated during passage through the birth canal from a mother infected with either Neisseria gonorrhoeae or Chlamydia trachomatis.If left untreated it can cause blindness.
Many different bacteria and viruses can cause conjunctivitis in the neonate. The two most feared causes are N. gonorrheae and Chlamydia acquired from the birth canal during delivery.Other agents causing Opthalmia neonatorum include Herpes simplex virus (HSV 2),Staphylococcus aureus, Streptococcus haemolyticus, Streptococcus pneumoniae.
Ophthalmia neonatorum due to gonococci (Neisseria gonorrhoeae) typically manifests in the first five days of life and is associated with marked bilateral purulent discharge and local inflammation. In contrast, conjunctivitis secondary to infection with chlamydia (Chlamydia trachomatis) produces conjunctivitis after day three of life, but may occur up to two weeks after delivery. The discharge is usually more watery in nature (mucopurulent) and less inflamed. Babies infected with chlamydia may develop pneumonitis (chest infection) at a later stage.Infants with chlamydia pneumonitis should be treated with oral erythromycin for 10–14 days.

Monday, 16 January 2012

Teenager has eyelash transplant


Teenager has eyelash transplant

Louise Thomas suffers from trichotillomania
Hair taken from Louise Thomas's head was placed into her eyelids
A woman from Greater Manchester has become the first person in the UK to undergo an eyelash transplant, surgical teams have claimed.
Louise Thomas, 19, from Stockport, had the treatment because she suffers from trichotillomania - obsessive plucking or pulling out hair.
The procedure involves taking hair strands from the back of the head, and placing them into cuts in the eyelid.
The lashes thicken up gradually between four and six months after treatment.
Miss Thomas said: "Having suffered from trichotillomania for 17 years, I learned to accept that I'd never have real lashes again. That's quite a hard issue for a young girl to come to terms with.
"When I heard about this treatment it sounded too good to be true but the results are absolutely amazing."
The procedure was pioneered in the United States.
Shami Thomas, from Transform, which carried out the surgery, said: "We often look to America for the latest in cosmetic surgery as they are the pioneers in the industry, but not all are as successful and safe as this one."

Eyelid Retractors & PROTRACTOR


         Orbicularis oculi muscle anatomy. (A) Frontalis, (

Orbicularis oculi muscle anatomy. (A) Frontalis, (B) corrugator superciliaris, (C) procerus, (D) orbital orbicularis, (E) preseptal orbicularis, (F) pretarsal orbicularis.

Upper lid retractors

The levator palpebra superioris (LPS) arises at the orbital apex from the undersurface of the lesser wing of the sphenoid bone. The levator muscle and superior rectus muscle share a developmental origin and are connected by fibrous attachments. The LPS proceeds anteriorly for 40 mm and ends in an aponeurosis approximately 10 mm behind the orbital septum. The levator complex changes direction from a horizontal to a more vertical direction at the superior transverse ligament (Whitnall ligament).
The superior transverse ligament lies near the junction of the muscular and aponeurotic levator and represents an orbital fascial condensation spanning the anterosuperior orbit between the trochlea and the lacrimal gland fascia. Variations in thickness and adherence to the levator complex are evident. Thin fascial attachments lie between the superior transverse ligament and superior orbital rim.
The levator aponeurosis spreads laterally and medially to form lateral and medial horns. The medial horn attaches to the posterior lacrimal crest. The lateral horn divides the lacrimal gland into orbital and palpebral lobes before attaching to the lateral retinaculum at the lateral orbital tubercle. The aponeurosis fuses with the orbital septum prior to reaching the level of the superior tarsal plate border. At the inferior edge of this fusion, some aponeurotic fibers descend to insert into the lower third of the anterior surface of the tarsal plate. An anterior extension from this fusion inserts into the pretarsal orbicularis oculi muscle and overlying skin, forming the upper lid skin crease.
Kakizaki proposed that the levator aponeurosis consists of 2 layers, anterior and posterior, which also contain smooth muscle in their proximal parts.[4]The anterior layer ends in the junctional region with the orbital septum and pulls the preaponeurotic pad of fat in conjunction with the orbital septum and the submuscular fibroadipose tissue. The posterior layer is attached to the anterior inferior one-third of the tarsal plate. It thus regulates the tension of the eyelid and the ordered movement of the lid.
Müller muscle is smooth muscle innervated by the sympathetic nervous system. Fibers originate from the undersurface of the levator in the region of the aponeurotic muscle junction, travel inferiorly between the levator aponeurosis and conjunctiva, and insert into the superior margin of the tarsus. With age, fatty infiltration may occur, giving the muscle a yellowish color.
Contrary to previous understanding, the Müller muscle may also be involved in thyroid eye disease, by fibrosis and mast cell infiltration. The Müller muscle may function as a large, serial muscle spindle. The stretching of the Müller muscle by the initial eye opening action of the levator may initiate a reflex via the mesencephalic trigeminal nucleus, which subsequently is routed through the ipsilateral or bilateral levator muscle, evoking involuntary tonic contraction to maintain an adequate visual field.
The peripheral vascular arcade of the upper eyelid lies adherent to the lower border of the anterior surface of the Müller muscle, just above the upper border of the tarsus, and is apparent during blepharoptosis surgery as a plane of dissection is created between the levator aponeurosis and the Müller muscle. The action is to widen the palpebral fissure with increased sympathetic tone. About 2 mm of ptosis is observed in Horner syndrome. Sympathetically innervated smooth muscle fibers are also noted in the lower eyelid and constitute the inferior tarsal muscle.

Lower lid retractors

The lower eyelid retractor is a fascial extension from the terminal muscle fibers and tendon of the inferior rectus muscle, originating as the capsulopalpebral head. As it passes anteriorly from its origin, it splits to envelop the inferior oblique muscle and reunites as the inferior transverse ligament (Lockwood ligament). From there, the fascial tissue passes anterosuperiorly as the capsulopalpebral fascia. The bulk of the capsulopalpebral fascia inserts on the inferior border of the inferior tarsus. Fibers also pass forward, to unite with the Tenon capsule, and to the inferior fornix conjunctiva, through orbital fat to the orbital septum, and forward to the subcutaneous tissues forming the lower eyelid crease. The orbital septum fuses with the capsulopalpebral fascia approximately 5 mm below the inferior tarsal border.
The inferior tarsal muscle (Müller muscle) lies just posterior to the fascia and is intimate with its structure. The sympathetically innervated smooth muscle fibers are first noted near the origin of the capsulopalpebral head. The capsulopalpebral head splits into 2 portions to pass around the inferior oblique muscle sheath; the portion beneath the muscle is thin and devoid of smooth muscle, while the portion above is a much thicker fascial layer and contains the smooth muscle fibers. As they continue to pass forward, the smooth muscle fibers do not insert directly onto the inferior tarsal border but into the fascia several millimeters below the tarsal border.
In the Asian lower lid, the line of fusion of the orbital septum to the capsulopalpebral fascia is often higher, or indistinct, with anterior and superior orbital fat projection, and overriding of the preseptal orbicularis oculi over the pretarsal orbicularis.

Urinary Incontinence



Urinary incontinence is the inability to control urination which results in unintended urinary flow or leakage
Normal Bladder Function and Continence
Detrusor muscle: 
under simultaneous sympathetic and parasympathetic control
Filling phase: 
sympathetic tone predominates 
allows relaxation of detrusor and tightening of internal sphincter 

Voluntary voiding: 
sensation of bladder fullness mediated by proprioceptive fibers in detrusor 
reflex arc between detrusor and brainstem initiates bladder contraction via increase in parasympathetic and decrease in sympathetic stimulation
reflex under cortical inhibition 
voiding occurs with release of inhibition and voluntary relaxation of external sphincter
urethrovesicular angle changes to allow full drainage of bladder

Classification of Urinary Incontinence
6 major subtypes of urinary incontinence:
Stress
Urge (“overactive bladder”)
Overflow
Mixed
Functional
Other (deformity/lack of continuity)

Stress incontinence
Causes: 
urethral hypermobility due to pelvic floor laxity
aging
difficult or multiple vaginal deliveries
hysterectomy 
other perineal injury (e.g. radiation) 
intrinsic urethral sphincter deficiency 
autonomic neuropathy
inadequate estrogen levels 
partial denervation

Urge incontinence (overactive bladder, detrusor instability)
Cause: 
Inappropriate contraction of detrusor muscle during bladder filling
idiopathic
related to aging (unclear mechanism)
decreased cortical inhibition (CVA, Parkinson’s disease, Alzheimer’s disease, brain tumor)
bladder irritation (UTI, bladder CA, stones)

Reflex incontinence (FYI)
variant of overactive bladder caused by SCI, MS, neurosyphilis, or cord compression
loss of central control leads to detrusor spasticity and functional outlet obstruction
symptoms: 
frequent voiding without warning
moderate volumes
equal frequency day and night
decreased perineal sensation and sphincter control
sacral reflexes intact.. 

Sunday, 15 January 2012

DIFFERENCE BETWEEN BLINKING AND WINKING???

   
blink z an involuntary upper lid physiological, symmetrical, bilateral eyes phenomenon repeat it self after aset regular secs of hour


wink is a deliberate jesture or in a case pathology involving just one eye-lid movement ,dznt own a regular tym of repitation. in syndrome wink has pathophysiological assosaiation with jaw movement particularly

spasm is the twiching of upper and lower lids both purely a pathological condition not pysilogical as BLINk z 

Saturday, 14 January 2012

Ocular Trauma


A blowout fracture is a fracture of the walls or floor of the orbit. Intraorbital material may be pushed out into one of the paranasal sinuses. This is most commonly caused by blunt trauma of the head, generally personal altercations.
Orbital floor fractures can increase volume of the orbit with resultant hypoglobus and enophthalmos.The inferior rectus muscle or orbital tissue can become entrapped within the fracture, resulting in tethering and restriction of gaze and diplopia.
Significant orbital emphysema from a communication with the maxillary sinus can occur. Orbital hemorrhage is possible with risk of a compressive optic neuropathy.
The globe can be ruptured or suffer less severe forms of trauma, resulting in hyphema, retinal edema, and profound visual loss.
Periorbital ecchymosis and edema accompanied by pain are obvious external signs and symptoms, respectively. Enophthalmos is possible but initially can be obscured by surrounding tissue swelling. This swelling can restrict ocular motility, giving the impression of soft tissue or inferior rectus entrapment. Retrobulbar or peribulbar hemorrhage may be heralded by proptosis. A bony step-off of the orbital rim and point tenderness are possible during palpation.
Examination of the globe is essential, albeit difficult because of soft tissue edema. Desmarres retractors may be helpful to spread edematous eyelids.
Pupillary dysfunction coupled with decreased visual acuity should alert one to the possibility of a traumatic or compressive optic neuropathy.Ocular misalignment, hypotropia or hypertropia, and limitation of elevation ipsilateral to the fracture are possible. Forced duction testing can differentiate entrapment versus neuromyogenic etiologies of muscle underaction.The supratarsal crease may deepen, along with narrowing of the palpebral fissure stemming from enophthalmos or fibrous tissue contraction. Although the palpebral fissure may in fact narrow, the geometric shape is preserved, since dehiscence or disruption of the canthal tendons is uncommon.