1.

FUNCTIONS OF THE SYMPATHETIC NERVOUS SYSTEM: The sympathetic nervous system is responsible for up- and down-regulating many homeostatic mechanisms in living organisms. Fibers from the SNS innervate tissues in almost every organ system, providing at least some regulatory function to things as diverse as pupil diameter, gut motility, and urinary output. It is perhaps best known for mediating the neuronal and hormonal stress response commonly known as the fight-or-flight response. This response is also known as sympatho-adrenal response of the body, as the preganglionic sympathetic fibers that end in the adrenal medulla (but also all other sympathetic fibers) secrete acetylcholine, which activates the great secretion of adrenaline (epinephrine) and to a lesser extent noradrenaline (norepinephrine) from it. Therefore, this response that acts primarily on the cardiovascular system is mediated directly via impulses transmitted through the sympathetic nervous system and indirectly via catecholamines secreted from the adrenal medulla. Some evolutionary theorists suggest that the sympathetic nervous system operated in early organisms to maintain survival as the sympathetic nervous system is responsible for priming the body for action.[6] One example of this priming is in the moments before waking, in which sympathetic outflow spontaneously increases in preparation for action.

The sympathetic nervous system innervates all the smooth muscles and the various glands of the body, and the striated muscle of the heart. The efferent sympathetic fibers which leave the central nervous system in connection with certain of the cranial and spinal nerves all end in sympathetic ganglia and are known as preganglionic fibers. From these ganglia postganglionic fibers arise and conduct impulses to the different organs. In addition, afferent or sensory fibers connect many of these structures with the central nervous system. The peripheral portion of the sympathetic nervous system is characterized by the presence of numerous ganglia and complicated plexuses. These ganglia are connected with the central nervous system by three groups of sympathetic efferent or preganglionic fibers, i. e., the cranial, the thoracolumbar, and the sacral. These outflows of sympathetic fibers are separated by intervals where no connections exist. The cranial and sacral sympathetic are often grouped together owing to the resemblance between the reactions produced by stimulating them and by the effects of certain drugs. Acetylcholine, for example, when injected intravenously in very small doses, produces the same effect as the stimulation of the cranial or sacral sympathetics, while the introduction of adrenalin produces the same effect as the stimulation of the thoracolumbar sympathetic. Much of our present knowledge of the sympathetic nervous system has been acquired through the application of various drugs, especially nicotine which paralyzes the connections or synapses between the preganglionic and postganglionic fibers of the sympathetic nerves. When it is injected into the general circulation all such synapses are paralyzed; when it is applied locally on a ganglion only the synapses occurring in that particular ganglion are paralyzed. Langley, who has contributed greatly to our knowledge, adopted a terminology somewhat different from that used here and still different from that used by the pharmacologists. This has

led to considerable confusion, as shown by the arrangement of the terms in the following columns. Gaskell has used the term involuntary nervous system. GRAY. LANGLEY. MEYER AND GOTTLIEB.

Sympathetic nervous system. - Autonomic nervous system -. Vegetative nervous system. Cranio-sacral sympathetics. - Parasympathetics. Oculomotor sympathetics. Facial Fsympathetics. Glossopharyngeal sympathetics. Vagal sympathetics. Sacral sympathetics. Sacral autonomics. Thoracic autonomic. Enteric. Enteric. Enteric. Sacral autonomics. Sympathetic. Thoracolumbar sympathetics. - Sympathetic. Bulbar autonomics. Tectal autonomics. Autonomic. Cranial autonomics.

2. SYMPATHETIC NERVOUS SYSTEM ALSO CALLED AS THORAACO-LUMBAR DIVISION: the sympathetic (or thoracolumbar) division in which the preganglionic cells are located in the thoracic and first two lumbar segments of the spinal cord. SYMPATHETIC (THORACOLUMBAR) DIVISION : Sympathetic nerves originate from the thoracic and lumbar regions . The term thoracolumbar control is often used in reference to the sympathetic division. All preganglionic fibers of the sympathetic enter the sympathetic trunk . Many of these fibers form synapses with ganglionic neurons in the sympathetic trunk ganglia. (you may Come across the term paravertebral ganglion, which means the same thing as sympathetic Trunk ganglion.) Some preganglionic fibers pass through the sympathetic trunk via nerves Called splanchnic nerves to make synapses with ganglionic neurons in other ganglia, such as the Prevertebral (or collateral) ganglia. Preganglionic fibers that send sympathetic commands to The adrenal medulla travel directly to the adrenal medulla. These preganglionic fibers do not Synapse with ganglionic neurons. Rather, they stimulate the adrenal gland directly and both Norepinephrine and epinephrine are released directly into the blood. What is the significance of Releasing these chemicals into the blood? Most sympathetic ganglia (e.g., the sympathetic trunk ganglia and the prevertebral ganglia) are Located near the spinal cord; therefore the preganglionic fibers are generally short and the Postganglionic fibers are generally long.

SYMPATHETIC DIVISION: A. The myelinated sympathetic preganglionic axons leave the lateral gray horns of all thoracic and the first 2 or 3 lumbar segments of the spinal cord; they leave along with somatic motor fibers via the anterior root of a spinal nerve. B. After exiting through the intervertebral foramina, the preganglionic axons enter a short pathway called a white ramus before entering the nearest sympathetic trunk ganglion on the same side; collectively, the white rami are called white rami communicantes. The preganglionic axons synapse with the cell bodies of ganglionic neurons in the ganglion. The axons of ganglionic neurons are unmyelinated and exit the ganglion via the gray rami communicantes. C. The paired sympathetic trunk ganglia are located anterior and lateral to the spine, one on either side; although the sympathetic trunks extend along the entire length of the spine, the ganglia receive preganglionic axons only from the thoracic and lumbar segments of the spinal cord. D. Sympathetic preganglionic fibers also extend to the adrenal medullae which are modified sympathetic ganglia that secrete the hormones epinephrine and norepinephrine into the blood; this is the one exception to the usual pattern of two efferent neurons in an autonomic motor pathway. 3. LOCATIONS OF GANGLIA : Anantomic features

Ganglia that contain cell bodies of sensory neurons; these are not synaptic stations.

Dorsal root ganglia of all spinal nerves Sensory ganglia of cranial nerves

Trigeminal (semilunar, Gasserian) ganglion of trigeminal (V) nerve Geniculate ganglion of facial (VII) nerve Spiral ganglion (contains bipolar neurons) of vestibulocochlear (VIII) nerve Vestibular ganglion (contains bipolar neurons) of vestibulocochlear (VIII) nerve Superior and inferior ganglia of glossopharyngeal (IX) nerve Superior and inferior ganglia of vagus (X) nerve

Ganglia that contain cell bodies of autonomic (postsynaptic) neurons; these are synaptic stations.

Sympathetic ganglia

Sympathetic trunk (paravertebral or vertebral chain) ganglia Prevertebral ganglia (adjacent to origins of large branches of abdominal aorta), including celiac, superior mesenteric, inferior mesenteric, and aorticorenal ganglia The adrenal medulla

Parasympathetic ganglia HEAD GANGLIA

Ciliary ganglion of oculomotor (III) nerve Geniculate ganglion of facial (VII) nerve Submandibular ganglion of facial (VII) nerve Pterygopalatine (sphenopalatine) ganglion of facial (VII) nerve Otic ganglion of glossopharyngeal (IX) nerve Terminal (intramural) ganglia (near or in wall of organs) including ganglia of submucosal (Meissner's) and myenteric (Auerbach's) plexuses of the intestine and isolated ganglion cells in variety of organs. SPINAL GANGLIA

Location: on the dorsal (posterior) root of the spinal nerve. Each segment of the spinal cord has two ganglia, one on each side in the posterolateral position. Function: afferent component of the peripheral nervous system, the site of sensory cell bodies that conduct impulses to the central nervous system Composition:

connective tissue capsule and trabeculae pseudounipolar neurons capsule cells (amphycytes) and satellite cells - neuroglia nerve fibers AUTONOMIC GANGLIA

Location: paravertebral, prevertebral, and terminal locations Function: the site of efferent cell bodies and synaptic stations of autonomic nervous system (sympathetic and parasympathetic) Composition:

connective tissue capsule and trabeculae multipolar neurons capsule cells and satellite cells - neuroglia nerve fibers synapses

4. DIFFERENCE IN THE LOCATION OF SYMPATHETIC AND PARA-SYMPATHETIC GANGLIA: A. Sympathetic division The sympathetic division (thoracolumbar outflow) consists of cell bodies in the lateral horn of spinal cord (intermediolateral cell columns) of the spinal cord from T1 to L2. These cell bodies are GVE

(general visceral efferent) neurons and are the preganglionic neurons. There are several locations upon which preganglionic neurons can synapse for their postganglionic neurons:

Paravertebral ganglia (3) of the sympathetic chain (these run on either side of the vertebral bodies) 1. Cervical Ganglia (3) 2. Thoracic Ganglia (11) and Rostral Lumbar Ganglia (2 or 3) 3. Caudal Lumbar Ganglia and Pelvic Ganglia

Prevertebral ganglia (celiac ganglia, superior mesenteric ganglia, inferior mesenteric ganglia). Chromaffin cells of adrenal medulla (this is the one exception to the two-neuron pathway rule: synapse is direct onto the target cell bodies)

These ganglia provide the postganglionic neurons from which innervation of target organs follows. Examples of splanchnic (visceral) nerves are:

Cervical cardiac nerves & thoracic visceral nerves which synapse in the sympathetic chain Thoracic splanchnic nerves (greater, lesser, least) which synapse in the prevertebral ganglion Lumbar splanchnic nerves which synapse in the prevertebral ganglion Sacral splanchnic nerves which synapse in the inferior hypogastric plexus

These all contain afferent (sensory) nerves as well, known as GVA (general visceral afferent) neurons.

Location of Preganglionic neurons: T1 - L2 in the lateral horns of the gray matter of the spinal cord. Preganglionic neurons send fibers out the ventral root. They leave the spinal nerves through the white rami (myelin) and enter the sympathetic trunk. Ganglionic neurons are located within the sympathetic chain ganglia or in collateral ganglia outside of the sympathetic trunk. Postganglionic fibers leave the sympathetic trunk through the gray rami and pass through the spinal nerve again before terminating on the effector organ. Preganglionic fibers are short and myelinated. Postganglionic fibers are long and unmyelinated. Preganglionic fibers may: Synapse with one or more neurons in the sympathetic trunk directly across from them; Ascend or descend in the trunk before synapsing; Pass through the sympathetic trunk and synapse with a collateral ganglion outside the sympathetic trunk. Directly stimulate the release of epinephrine and norepinephrine from the adrenal medulla. The sympathetic division is responsible for vasomotor (sympathetic) tone.

PARASYMPATHETIC DIVISION The parasympathetic division (craniosacral outflow) consists of cell bodies from one of two locations: brainstem (Cranial Nerves III, VII, IX, X) or sacral spinal cord (S2, S3, S4). These are the preganglionic neurons, which synapse with postganglionic neurons in these locations:

 Parasympathetic ganglia of the head (Ciliary (CN III), Submandibular (CN VII), Pterygopalatine (CN VII), Otic (CN IX)). In or near wall of organ innervated by Vagus (CN X), Sacral nerves (S2, S3, S4)) These ganglia provide the postganglionic neurons from which innervations of target organs follows. Examples are: The preganglionic parasympathetic splanchnic (visceral) nerves. Vagus nerve, which wanders through the thorax and abdominal regions innervating, among other organs, the heart, lungs, liver and stomach.

A. Location of preganglionic neurons: Brain stem and S2, S3, and S4. B. Preganglionic fibers travel through cranial nerves III, VII, IX, and X, and spinal nerves S2-S4, and synapse with peripheral ganglia located very near or directly on the effector organ. C. Ganglionic neurons are located within peripheral ganglia. D. Preganglionic fibers are long and myelinated. E. Postganglionic fibers are short and not myelinated. F. Parasympathetic fibers do not control the diameter of the systemic arterioles but ARE responsible for peristalsis.

5.SYMPATHETIC NERVE FIBRES SYNAPSE : Axons of these nerves leave the spinal cord in the ventral branches (rami) of the spinal nerves, and then separate out as 'white rami' (so called from the shiny white sheaths of myelin around each axon) which connect to two chain ganglia extending alongside the vertebral column on the left and right. These elongated ganglia are also known as paravertebral ganglia or sympathetic trunks. In these hubs, connections (synapses) are made which then distribute the nerves to major organs, glands, and other parts of the body. 6. DIFFERENCE BETWEEN SYMPATHETIC AND PARA SYMPATHETIC SYNAPSES:

The Sympathetic Nervous System The preganglionic motor neurons of the sympathetic system (shown in black) arise in the spinal cord. They pass into sympathetic ganglia which are organized into two chains that run parallel to and on either side of the spinal cord. The preganglionic neuron may do one of three things in the sympathetic ganglion:

synapse with postganglionic neurons (shown in white) which then reenter the spinal nerve and ultimately pass out to the sweat glands and the walls of blood vessels near the surface of the body. pass up or down the sympathetic chain and finally synapse with postganglionic neurons in a higher or lower ganglion leave the ganglion by way of a cord leading to special ganglia (e.g. the solar plexus) in the viscera. Here it may synapse with postganglionic sympathetic neurons running to the smooth muscular walls of the viscera. However, some of these preganglionic neurons pass right on through this second ganglion and into the adrenal medulla. Here they synapse with the highlymodified postganglionic cells that make up the secretory portion of the adrenal medulla.

THE PARASYMPATHETIC NERVOUS SYSTEM The main nerves of the parasympathetic system are the tenth cranial nerves, the vagus nerves. They originate in the medulla oblongata. Other preganglionic parasympathetic neurons also extend from the brain as well as from the lower tip of the spinal cord. Each preganglionic parasympathetic neuron synapses with just a few postganglionic neurons, which are located near or in the effector organ, a muscle or gland. Acetylcholine (ACh) is the neurotransmitter at all the pre- and many of the postganglionic neurons of the parasympathetic system. However, some of the postganglionic neurons release nitric oxide (NO) as their neurotransmitter. The Nobel Prize winning physiologist Otto Loewi discovered (in 1920) that the effect of both sympathetic and parasympathetic stimulation is mediated by released chemicals. He removed the living heart from a frog with its sympathetic and parasympathetic nerve supply intact. As expected, stimulation of the first speeded up the heart while stimulation of the second slowed it down. Loewi found that these two responses would occur in a second frog heart supplied with a salt solution taken from the stimulated heart. Electrical stimulation of the vagus nerve leading to the first heart not only slowed its beat but, a short time later, slowed that of the second heart also. The substance responsible was later shown to be acetylcholine. During sympathetic stimulation, adrenaline (in the frog) is released.

Parasympathetic stimulation causes

slowing down of the heartbeat (as Loewi demonstrated) lowering of blood pressure constriction of the pupils increased blood flow to the skin and viscera peristalsis of the GI tract

In short, the parasympathetic system returns the body functions to normal after they have been altered by sympathetic stimulation. In times of danger, the sympathetic system prepares the body for violent activity. The parasympathetic system reverses these changes when the danger is over. The vagus nerves also help keep inflammation under control. Inflammation stimulates nearby sensory neurons of the vagus. When these nerve impulses reach the medulla oblongata, they are relayed back along motor fibers to the inflamed area. The acetylcholine from the motor neurons suppresses the release of inflammatory cytokines, e.g., tumor necrosis factor (TNF), from macrophages in the inflamed tissue. Although the autonomic nervous system is considered to be involuntary, this is not entirely true. A certain amount of conscious control can be exerted over it as has long been demonstrated by practitioners of Yoga and Zen Buddhism. During their periods of meditation, these people are clearly able to alter a number of autonomic functions including heart rate and the rate of oxygen consumption. These changes are not simply a reflection of decreased physical activity because they exceed the amount of change occurring during sleep or hypnosis.

7. NEUROTRANSMITTERS RELEASED BY PREGANGLIONIC FIBRES OF SYMPATHETIC NERVOUS SYSTEM: The neurotransmitter of the preganglionic sympathetic neurons is acetylcholine (ACh). It stimulates action potentials in the postganglionic neurons. The neurotransmitter released by the postganglionic neurons is noradrenaline (also called norepinephrine). The action of noradrenaline on a particular gland or muscle is excitatory is some cases, inhibitory in others. (At excitatory terminals, ATP may be released along with noradrenaline.) The release of noradrenaline

Stimulates heartbeat Raises blood pressure Dilates the pupils Dilates the trachea and bronchi Stimulates glycogenolysis the conversion of liver glycogen into glucose Shunts blood away from the skin and viscera to the skeletal muscles, brain, and heart Inhibits peristalsis in the gastrointestinal (gi) tract Inhibits contraction of the bladder and rectum

And, at least in rats and mice, increases the number of ampa receptors in the hippocampus and thus increases long-term potentiation (ltp).

In short, stimulation of the sympathetic branch of the autonomic nervous system prepares the body for emergencies: for "fight or flight" (and, perhaps, enhances the memory of the event that triggered the response). Activation of the sympathetic system is quite general because

A single preganglionic neuron usually synapses with many postganglionic neurons; The release of adrenaline from the adrenal medulla into the blood ensures that all the cells of the body will be exposed to sympathetic stimulation even if no postganglionic neurons reach them directly.

8. NEUROTRANSMITTERS RELEASED BY POST-GANGLIONIC FIBRES OF SYMPATHETIC NERVOUS SYSTEM: The neurotransmitter released by the postganglionic neurons is noradrenaline (also called norepinephrine). The action of noradrenaline on a particular gland or muscle is excitatory is some cases, inhibitory in others. (At excitatory terminals, ATP may be released along with noradrenaline.) The release of noradrenaline

stimulates heartbeat raises blood pressure dilates the pupils dilates the trachea and bronchi stimulates glycogenolysis the conversion of liver glycogen into glucose shunts blood away from the skin and viscera to the skeletal muscles, brain, and heart inhibits peristalsis in the gastrointestinal (GI) tract inhibits contraction of the bladder and rectum and, at least in rats and mice, increases the number of AMPA receptors in the hippocampus and thus increases long-term potentiation (LTP).

In short, stimulation of the sympathetic branch of the autonomic nervous system prepares the body for emergencies: for "fight or flight" (and, perhaps, enhances the memory of the event that triggered the response). Activation of the sympathetic system is quite general because

a single preganglionic neuron usually synapses with many postganglionic neurons; the release of adrenaline from the adrenal medulla into the blood ensures that all the cells of the body will be exposed to sympathetic stimulation even if no postganglionic neurons reach them directly.

11.DESCRIBE THE STRUCTURES: a.Sclera The sclera is commonly known as "the white of the eye." It is the tough, opaque tissue that serves as the eye's protective outer coat. Six tiny muscles connect to it around the eye and control the eye's movements. The optic nerve is attached to the sclera at the very back of the eye. In children, the sclera is thinner and more translucent, allowing the underlying tissue to show through and giving it a bluish cast. As we age, the sclera tends to become more yellow. b.Iris The iris (plural: irides or irises) is a thin, circular structure in the eye, responsible for controlling the diameter and size of the pupils and thus the amount of light reaching the retina. "Eye color" is the color of the iris, which can be green, blue, or brown. In some cases it can be hazel (a combination of light brown, green and gold), grey, violet, or even pink. In response to the amount of light entering the eye, muscles attached to the iris expand or contract the aperture at the center of the iris, known as the pupil. The larger the pupil, the more light can enter. c.Pupils The pupil is a hole located in the center of the iris of the eye that allows light to enter the retina.[1] It appears black because most of the light entering the pupil is absorbed by the tissues inside the eye. In humans the pupil is round, but other species, such as some cats, have slit pupils.[2] In optical terms, the anatomical pupil is the eye's aperture and the iris is the aperture stop. The image of the pupil as seen from outside the eye is the entrance pupil, which does not exactly correspond to the location and size of the physical pupil because it is magnified by the cornea. On the inner edge lies a prominent structure, the collarette, marking the junction of the embryonic pupillary membrane covering the embryonic pupil. d.Fovea The fovea (arrow) is the center most part of themacula. This tiny area is responsible for our central, sharpest vision. A healthy fovea is key for reading, watching television, driving, and other activities that require the ability to see detail. Unlike the peripheral retina, it has no blood vessels. Instead, it has a very high concentration of cones (photoreceptors responsible for color vision), allowing us to appreciate color.

12. THE CRANIAL NERVES CONTROLLING EYE MUSCLES: There are three right cranial nerves (III, IV, and VI) involved in innervating the right eye muscles and three left cranial nerves (III, IV, and VI) involved in innervating the left eye muscles. Cranial nerve III innervate four muscles (medial rectus muscle, superior rectus muscle, inferior rectus muscle, and inferior oblique muscle). Cranial nerve IV innervates the superior oblique muscle. Cranial nerve VI innervates the lateral rectus muscle.

Cranial Nerve III Cranial Nerve IV Cranial Nerve VI

medial rectus muscle, superior rectus muscle, inferior rectus muscle, inferior oblique muscle superior oblique muscle lateral rectus muscle

A damaged cranial nerve will produce the same symptoms that would occur if the associated eye muscle is damaged. For example if cranial nerve VI is damaged, the eye will have the same motion as when the lateral rectus muscle is damaged. If cranial nerve III is damaged, the symptoms will be the same as if the four eye muscles controlled by CN III is damaged. A damaged cranial nerve III has an additional characteristic that affects the eye. The parasympathetic nerve innervating the pupillary sphincter travels with CN III. If CN III is damaged, the eye pupil will dilate.

13.LINKS BETWEEN THE EYES AND VISUAL CORTEX: Visual information travels in separate pathways for each half of the visual field. Light entering the eye from the right hemifield hits the left half of the retina, on the rear surface of each eye. The inputs from each eye are combined at the optic chiasm, and travel to the left lateral geniculate nucleus (LGN) of the thalamus, then to the primary visual cortex (also called V1, visual area 1, striate cortex, or Brodmann area 17) of the left hemisphere. Light entering the eye from the left hemifield strikes the right half of each retina, which send signals to the right LGN and then to the right half of V1.

Very similar structures are present in other mammals, including such well-studied laboratory animals as monkeys, cats, and rats. For each species, light entering the eye is detected by the retina, an array of photoreceptors on the inside of the rear surface of the eye. The photoreceptors and related circuitry in the retina encode light levels as electrical signals. These signals leave the eye through nerve cells called retinal ganglion cells. From there, they travel to the lateral geniculate nucleus (LGN) of the thalamus, at the base of each side of the brain. From the LGN, the signals travel to the primary visual cortex (V1) at the rear of the brain, the first stage of cortical processing of vision.

14.a. STRABISMUS: DEFINITION Strabismus is a misalignment of the eyes in which the visual axes deviate from bifoveal fixation. CLASSIFICATION The classification of strabismus may be based on a number of features including the relative position of the eyes, whether the deviation is latent or manifest, intermittent or constant, concomitant or otherwise and according to the age of onset and the relevance of any associated refractive error. The type of strabismus is established by a detailed history and orthoptic examination.

Infantile esotropia (syn: congenital or essential esotropia) is an idiopathic syndrome in which an esodeviation is present before the age of six months. It is variably associated with other clinical features including dissociated vertical deviation, inferior oblique overaction, latent nystagmus, crossed fixation, asymmetrical monocular optokinetic responses (OKN) and, usually, no refractive error. (36) Acquired strabismus includes fully and partially accommodative refractive esotropia, convergence excess esotropia, cyclic esotropia, occlusion esotropia and various forms of paretic squint.(31) Exotropla may also occur in congenital and acquired forms, both concomitant and incomitant. Vertical strabismus includes dissociated deviations, cyclovertical muscle anomalies and restrictive conditions (e.g. Brown's syndrome) as well as rarities such as double elevator palsy.

These broad categories of strabismus are distinguished by having various aetiologies and usually differ in prognosis with and without treatment. PRESENTATION AND REFERRAL Intermittent deviation of the eyes is a quite common finding in healthy neonates and should not cause undue concern. Normal binocular coordination becomes evident at about three months and strabismus after this age is significant. Constant squint is generally recognised early by the family, health visitor or general practitioner. A positive family history of squint or amblyopia should alert those in primary care when carrying out routine checks or immunisations.

Strabismus is often found in association with neurological disease such as in cerebral palsy and in craniofacial developmental anomalies. Strabismus, amblyopia and refractive error are much more common in children with treated or regressed retinopathy of prematurity (ROP).Premature infants with a history of stage III ROP or worse should be followed up after the neonatal period to screen for these complications. If squint or amblyopia is suspected in the primary care setting, it is appropriate for local protocols to provide for direct referral to an optometrist or an orthoptist to exclude refractive error and strabismus. If no abnormality is detected, such patients may be discharged. Cases with intermittent or constant manifest squint should be referred to an ophthalmologist without delay. In all children referred with strabismus or amblyopia the possibility must be considered that this is the presenting feature of a serious ophthalmic or systemic disease requiring urgent management. STRABISMUS MANAGEMENT a.Infantile esotropia There are five broad considerations in planning management.

b.CATARACT: A cataract is a clouding of the eye's natural lens, which lies behind the iris and the pupil. Cataracts are the most common cause of vision loss in people over age 40 and are the principal cause of blindness in the world. In fact, there are more cases of cataracts worldwide than there are of glaucoma, macular degeneration and retinopathy combined, according to Prevent Blindness America (PBA). Today, cataracts affect more than 22 million Americans age 40 and older. And as the U.S. population ages, more than 30 million Americans are expected to have cataracts by the year 2020, PBA says. Types of cataracts include:

A subcapsular cataract occurs at the back of the lens. People with diabetes, high farsightedness or retinitis pigmentosa, or those taking high doses of steroid medications have a greater risk of developing a subcapsular cataract. A nuclear cataract forms deep in the central zone (nucleus) of the lens. Nuclear cataracts usually are associated with aging. A cortical cataract is characterized by white, wedge-like opacities that start in the periphery of the lens and work their way to the center in a spoke-like fashion. This type of cataract occurs in the lens cortex, which is the part of the lens that surrounds the central nucleus. Cataract Symptoms and Signs A cataract starts out small and at first has little effect on your vision. You may notice that your vision is blurred a little, like looking through a cloudy piece of glass or viewing an impressionist painting.

A cataract may make light from the sun or a lamp seem too bright or glaring. Or you may notice when you drive at night that the oncoming headlights cause more glare than before. Colors may not appear as bright as they once did. The type of cataract you have will affect exactly which symptoms you experience and how soon they will occur. When a nuclear cataract first develops, it can bring about a temporary improvement in your near vision, called "second sight." Unfortunately, the improved vision is short-lived and will disappear as the cataract worsens. On the other hand, a subcapsular cataract may not produce any symptoms until it's well-developed.

c.EXPLAIN GLAUCOMA:
GLAUCOMA Glaucoma is a disease of the major nerve of vision, called the optic nerve. The optic nerve receives lightgenerated nerve impulses from the retina and transmits these to the brain, where we recognize those electrical signals as vision. Glaucoma is characterized by a particular pattern of progressive damage to the optic nerve that generally begins with a subtle loss of side vision (peripheral vision). If glaucoma is not diagnosed and treated, it can progress to loss of central vision and blindness. Glaucoma is usually, but not always, associated with elevated pressure in the eye (intraocular pressure). Generally, it is this elevated eye pressure that leads to damage of the eye (optic) nerve. In some cases, glaucoma may occur in the presence of normal eye pressure. This form of glaucoma is believed to be caused by poor regulation of blood flow to the optic nerve.

Causes of glaucoma: Elevated pressure in the eye is the main factor leading to glaucomatous damage to the eye (optic) nerve. Glaucoma with normal intraocular pressure is discussed below in the section on the different types of glaucoma. The optic nerve, which is located in back of the eye, is the main visual nerve for the eye. This nerve transmits the images we see back to the brain for interpretation. The eye is firm and round, like a basketball. Its tone and shape are maintained by a pressure within the eye (the intraocular pressure), which normally ranges between 8 mm and 22 mm (millimeters) of mercury. When the pressure is too low, the eye becomes softer, while an elevated pressure causes the eye to become harder. The optic nerve is the most susceptible part of the eye to high pressure because the delicate fibers in this nerve are easily damaged. The front of the eye is filled with a clear fluid called the aqueous humor, which provides nourishment to the structures in the front of the eye. This fluid is produced constantly by the ciliary body, which surrounds the lens of the eye. The aqueous humor then flows through the pupil and leaves the eye through tiny channels called the trabecular meshwork. These channels are located at what is called the drainage angle of the eye. This angle is where the clear cornea, which covers the front of the eye, attaches to the

base (root or periphery) of the iris, which is the colored part of the eye. The cornea covers the iris and the pupil, which are in front of the lens. The pupil is the small, round, black-appearing opening in the center of the iris. Light passes through the pupil, on through the lens, and to the retina at the back of the eye. Please see the figure, which is a diagram that shows the drainage angle of the eye.

The diagram of the front part of the eye is in cross section to show the filtering, or drainage, angle. This angle is between the cornea and the iris, which join each other right where the drainage channels (trabecular meshwork) are located. The arrow shows the flow of the aqueous fluid from the ciliary body, through the pupil, and into the drainage channels. This figure is recreated from Understanding and Treating Glaucoma, a human anatomy board book by Tim Peters and Company Inc., Gladstone N.J. In most people, the drainage angles are wide open, although in some individuals, they can be narrow. For example, the usual angle is about 45 degrees, whereas a narrow angle is about 25 degrees or less. After exiting through the trabecular meshwork in the drainage angle, the aqueous fluid then drains into tiny blood vessels (capillaries) into the main bloodstream. The aqueous humor should not be confused with tears, which are produced by a gland outside of the eyeball itself. This process of producing and removing the fluid from the eye is similar to that of a sink with the faucet always turned on, producing and draining the water. If the sink's drain becomes clogged, the water may overflow. If this sink were a closed system, as is the eye, and unable to overflow, the pressure in the sink would rise. Likewise, if the eye's trabecular meshwork becomes clogged or blocked, the intraocular pressure may become elevated. Also, if the sink's faucet is on too high, the water may overflow. Again, if this sink were a closed system, the pressure within the sink would increase. Likewise, if too much fluid is being produced within the eye, the intraocular pressure may become too high. In either event, since the

eye is a closed system, if it cannot remove the increased fluid, the pressure builds up and optic-nerve damage may result. GLAUCOMA RISK FACTORS: Glaucoma is often called "the sneak thief of sight." This is because, as already mentioned, in most cases, the intraocular pressure can build up and destroy sight without causing obvious symptoms. Thus, awareness and early detection of glaucoma are extremely important because this disease can be successfully treated when diagnosed early. While everyone is at risk for glaucoma, certain people are at a much higher risk and need to be checked more frequently by their eye doctor. The major risk factors for glaucoma include the following:

Age over 45 years Family history of glaucoma Black racial ancestry Diabetes History of elevated intraocular pressure Nearsightedness (high degree of myopia), which is the inability to see distant objects clearly History of injury to the eye Use of cortisone (steroids), either in the eye or systemically (orally or injected) Farsightedness (hyperopia), which is seeing distant objects better than close ones (Farsighted people may have narrow drainage angles, which predispose them to acute [sudden] attacks of angle-closure glaucoma.)

TYPES OF GLAUCOMA: There are many different types of glaucoma. Most, however, can be classified as either open-angle glaucomas, which are usually conditions of long duration (chronic), or angle-closure (closed angle) glaucomas, which include conditions occurring both suddenly (acute) and over a long period of time (chronic). The glaucomas usually affect both eyes, but the disease can progress more rapidly in one eye than in the other. Involvement of just one eye occurs only when the glaucoma is brought on by factors such as a prior injury, inflammation, or the use of steroids only in that eye. OPEN-ANGLE GLAUCOMA: PRIMARY CHRONIC OPEN-ANGLE GLAUCOMA (COAG) is by far the most common type of glaucoma. Moreover, its frequency increases greatly with age. This increase occurs because the drainage mechanism gradually may become clogged with aging, even though the drainage angle is open. As a consequence, the aqueous fluid does not drain from the eye properly. The pressure within the eye, therefore, builds up painlessly and without symptoms. Furthermore, as mentioned previously, since the resulting loss of vision starts on the side (peripherally), people are usually not aware of the problem until the loss encroaches on their central visual area. NORMAL TENSION (PRESSURE) GLAUCOMA OR LOW TENSION GLAUCOMA are variants of primary chronic open-angle glaucoma that are being recognized more frequently than in the past. This

type of glaucoma is thought to be due to decreased blood flow to the optic nerve. This condition is characterized by progressive optic-nerve damage and loss of peripheral vision (visual field) despite intraocular pressures in the normal range or even below normal. This type of glaucoma can be diagnosed by repeated examinations by the eye doctor to detect the nerve damage or the visual field loss. CONGENITAL (INFANTILE) GLAUCOMA is a relatively rare, inherited type of open-angle glaucoma. In this condition, the drainage area is not properly developed before birth. This results in increased pressure in the eye that can lead to the loss of vision from optic-nerve damage and also to an enlarged eye. The eye of a young child enlarges in response to increased intraocular pressure because it is more pliable than the eye of an adult. Early diagnosis and treatment with medicine and/or surgery are critical in these infants and children to preserve their sight. SECONDARY OPEN-ANGLE GLAUCOMA is another type of open-angle glaucoma. It can result from an eye (ocular) injury, even one that occurred many years ago. Other causes of secondary glaucoma are inflammation in the iris of the eye (iritis), diabetes, cataracts, or in steroid-susceptible individuals, the use of topical (drops) or systemic (oral or injected) steroids (cortisone). It can also be associated with a retinal detachment or retinal vein occlusion or blockage. (The retina is the layer that lines the inside of the back of the eye.) The treatments for the secondary open-angle glaucomas vary, depending on the cause. PIGMENTARY GLAUCOMA is a type of secondary glaucoma that is more common in younger men. In this condition, for reasons not yet understood, granules of pigment detach from the iris, which is the colored part of the eye. These granules then may block the trabecular meshwork, which, as noted above, is a key element in the drainage system of the eye. Finally, the blocked drainage system leads to elevated intraocular pressure, which results in damage to the optic nerve. EXFOLIATIVE GLAUCOMA (pseudoexfoliation) is another type of glaucoma that can occur with either open or closed angles. This type of glaucoma is characterized by deposits of flaky material on the front surface of the lens (anterior capsule) and in the angle of the eye. The accumulation of this material in the angle is believed to block the drainage system of the eye and raise the eye pressure. While this type of glaucoma can occur in any population, it is more prevalent in older people and people of Scandinavian descent. It is recently been shown to often be associated with hearing loss in older people. ANGLE-CLOSURE GLAUCOMA Angle-closure glaucoma is a less common form of glaucoma in the Western world but is extremely common in Asia. Angle-closure glaucoma may be acute or chronic. The common element in both is that a portion or all of the drainage angle becomes anatomically closed, so that the aqueous fluid within the eye cannot even reach all or part of the trabecular meshwork. In acute angle-closure glaucoma, the patient's intraocular pressure, which ordinarily is normal, can go up very suddenly (acutely). This sudden pressure increase occurs because the drainage angle becomes closed and blocks off all the drainage channels. This type of glaucoma can occur when the pupil dilates (widens or enlarges). As a result, the peripheral edge of the iris can become bunched up against its corneal attachment, thereby causing the drainage angle to close. Thus, the problem in angle-closure glaucoma is the difficulty with access of the eye fluid to the drainage system (trabecular meshwork). In contrast, remember that the problem in open-angle glaucoma is clogging within the drainage system itself. In chronic open-angle glaucoma, portions of the drainage

angle become closed over a long period of time. As more and more areas become closed, the pressure within the eye rises, often over a period of months or years. People with small eyes are predisposed to developing angle-closure glaucoma because they tend to have narrow drainage angles. Small eyes are not obvious from their appearance, but they can be measured by an eye doctor. Thus, individuals who are farsighted or of Asian descent may have small eyes, narrow drainage angles, and an increased risk of developing angle-closure glaucoma. Furthermore, this condition may be acutely triggered by medications that can dilate the pupils. These agents can be found in certain eyedrops, cold remedies, citalopram (Celexa), topiramate(Topamax), or patches used to prevent seasickness. This condition can also occur spontaneously in a darkened room or a movie theater, when the pupil automatically dilates to let in more light. Sometimes, therefore, people with narrow angles are given eyedrops to keep their pupils small. (See the section below on parasympathomimetic agents.) An attack of acute angle-closure glaucoma may be associated with severe eye pain and headache, a red (inflamed) eye, nausea, vomiting, and blurry vision. In addition, the high intraocular pressure leads to corneal swelling (edema), which causes the patient to see haloes around lights. Sometimes, acute glaucoma is treated with oral carbonic anhydrase inhibitors. (See the section below on these medications.) An attack of acute glaucoma, however, is usually relieved by eye surgery. In this operation, the doctor makes a small hole in the iris with a laser (laser iridotomy) to allow the fluid to resume draining into its normal outflow channels. GLAUCOMA SYMPTOMS AND SIGNS: Patients with open-angle glaucoma and chronic angle-closure glaucoma in general have no symptoms early in the course of the disease. Visual field loss (side vision loss) is not a symptom until late in the course of the disease. Rarely patients with fluctuating levels of intra-ocular pressure may have haziness of vision and see haloes around lights, especially in the morning. On the other hand, the symptoms of acute angle-closure are often extremely dramatic with the rapid onset of severe eye pain,headache, nausea and vomiting, and visual blurring. Occasionally, the nausea and vomiting exceed the ocular symptoms to the extent that an ocular cause is not contemplated. The eyes of patients with open-angle glaucoma or chronic angle-closure glaucoma may appear normal in the mirror or to family or friends. Some patients get slightly red eyes from the chronic use of eyedrops. The ophthalmologist, on examining the patient, may find elevated intraocular pressure, optic-nerve abnormalities, or visual field loss in addition to other less common signs. The eyes of patients with acute angle-closure glaucoma will appear red, and the pupil of the eye may be large and nonreactive to light. The cornea may appear cloudy to the naked eye. The ophthalmologist will typically find decreased visual acuity, corneal swelling, highly elevated intraocular pressure, and a closed drainage angle.

TREATMENT FOR GLAUCOMA: GENERAL APPROACH: Although nerve damage and visual loss from glaucoma cannot usually be reversed, glaucoma is a disease that can generally be controlled. That is, treatment can make the intraocular pressure normal and, therefore, prevent or retard further nerve damage and visual loss. Treatment may involve the use of eyedrops, pills (rarely), laser ,or surgery. In the United States, eyedrops are usually used first in treating most types of open-angle glaucoma. In contrast, in Europe, laser or surgery is sometimes the first choice of treatment. One or more types of eyedrops may have to be taken up to several times a day to lower intraocular pressure. These drops work either by reducing the production of the aqueous fluid (shutting the faucet) or by increasing the drainage of the fluid out of the eye. Each type of therapy has its benefits and potential complications.