Meredith August, DMD, MD

• Associate Professor, Harvard School of Dental Medicine
• Visiting Oral and Maxillofacial Surgeon, Oral and
• Maxillofacial Surgery,
• Massachusetts General Hospital
• Boston Massachusetts

However blood pressure near death purchase exforge 80 mg with visa, in some cases of recalcitrant fungal ulcers an anterior chamber tap to test the hypopyon for fungal invasion followed by an anterior chamber wash with antifungals may be required blood pressure charts readings order exforge 80 mg on line. Prominent or Enlarged Corneal Nerves Prominent or enlarged corneal nerves may be asymptomatic and detected accidentally or may be associated with other local disease conditions such as keratoconus heart attack jarren benton order exforge online. Other systemic diseases associated with prominent corneal nerves include neurofibromatosis and Refsum syndrome arteria ileocolica generic exforge 80mg visa. Local ocular disorders with this clinical sign include keratoconus blood pressure medication exforge cheap exforge 80 mg otc, keratitis (most characteristically seen in acanthamoebic keratitis) arteriogram procedure order exforge amex, Fuchs endothelial dystrophy, trauma and congenital glaucoma. Hypopyon A hypopyon consists of polymorphonuclear leucocytes which accumulate in the lower angle of the anterior chamber and eventually become enmeshed in a network of fibrin. Corneal ulcers are associated with some iritis owing to the diffusion of toxins released by bacteria or invasion of organisms such as fungal hyphae into the eye. The resultant iridocyclitis is severe leading to the outpouring of leucocytes from the vessels and these cells gravitate to the bottom of the anterior chamber to form a hypopyon. The development of a hypopyon depends on two factors: (i) the virulence of the infecting organism and (ii) resistance of the tissues. Many pyogenic organisms (staphylococci, streptococci, gonococci, pneumococci, Pseudomonas pyocyanea, etc) may produce this result, but unless the organism is very virulent, some lack of resistance on the part of the tissues must be present. Hence, hypopyon ulcers are much more common in old, debilitated or alcoholic subjects. This accounts for the ease and rapidity with which the hypopyon is often absorbed. It may be so small that it is scarcely visible, being hidden behind the rim of sclera which overlaps the cornea. It may reach halfway up the iris, having a flat upper surface, determined by gravity, or it may fill the anterior chamber, wholly obscuring the iris. The hypopyon, if fluid, will be Vascularization of the Cornea the cornea is normally essentially avascular to retain its transparency. Vessels may become atrophic and regress with time or remain as empty channels called ghost vessels. Clinical Features: Symptoms, Signs and Diagnosis the cornea may be affected by infection, injury, inflammation, dystrophy, degeneration or cancerous conditions. The diseases manifest in different ways but certain common clinical features exist. Loss of transparency and decrease in vision Circumcorneal congestion Loss of smoothness of the surface Epithelial defect Vascularization Change in shape, thickness or curvature Appearance of nodules or growth on the surface. Photophobia is the term applied to the discomfort experienced on exposure to bright light. In corneal disorders, this is accompanied by blepharospasm triggered as a reflex response by corneal irritation due to stimulation of the terminal fibres of the corneal nerves which are derived from the ophthalmic division of the trigeminal nerve. The slightest attempt to separate the lids, especially if the attempt is made in bright light greatly increases the irritation. This blepharospasm is not completely abolished in the dark, but is greatly diminished by thorough anaesthetization. It is thus a reflex predominantly involving the trigeminal nerve and not triggered by direct stimulation of the optic nerve by exposure to light. Measurement of the curvature is done by keratometry (see Chapter 7) and corneal topography (see Chapter 11). The corneal thickness can be measured manually by an optical pachymeter attached to a slit-lamp, with an ultrasonic pachymeter or a slit-scanning topography system. Exogenous infections: the cornea is primarily affected by exogenous organisms, including virulent organisms already present in the conjunctival sac, gaining access to the corneal tissues and causing keratitis. Endogenous infections or inflammation: these are typically immunological in nature. The avascularity of the cornea allows immunological changes to persist for an unusually long time; examples are phlyctenular keratitis related to tuberculosis and interstitial keratitis related to syphilis and measles. Sometimes the cornea is affected by a hypersensitivity or autoimmune reaction rather than related to a specific infection. These changes are common near the limbal blood vessels close to the corneal margin and are called marginal keratitis or marginal corneal ulcers. Contiguous spread from the ocular tissues: Owing to direct anatomical continuity, diseases of the conjunctiva readily spread to the corneal epithelium (such as trachoma and vernal keratoconjunctivitis); those of the sclera to the stroma. From the clinical point of view, corneal inflammations are best divided into categories: l l Based on location: Superficial and deep Based on the nature of the aetiology: Infectious, immune-mediated, degenerative, neoplastic and traumatic (including chemical and thermal injuries). Superficial purulent keratitis includes corneal ulcers which are characterized by an epithelial defect with infiltration of the underlying and surrounding stroma. Superficial non-purulent keratitis includes a number of conditions of varied aetiology. Many of them are viral infections or parasitic (acanthamoebic, microsporidiosis, onchocerciasis) while others such as phlyctenular and rosacea keratitis are of constitutional origin. Superficial keratitis, if untreated or inappropriately treated, evolves into deep keratitis. Certain conditions begin with deep stromal involvement in which case the term deep stromal keratitis is applied. The deep forms of keratitis comprise those due to infections where organisms enter the cornea from the body through the limbus, for example, syphilis, onchocerciasis, tuberculosis; or some forms of immunological inflammation in viral infections (disciform keratitis) and lesions of indeterminate origin or due to the spread of scleral inflammations (sclerosing keratitis, see in Chapter 16). It is hypothesized that commensal organisms from periocular skin or the ocular surface gain access to the stroma via suture tracks or through compromised unhealthy corneal epithelium. Microorganisms that can produce this type of infection include alpha haemolytic streptococcus, peptostreptococcus, pseudomonas and candida and prolonged treatment with topical vancomycin, moxifloxacin or gatifloxacin eye drops with discontinuation or minimization of topical steroid use is generally required. Recurrence of infection and stromal scarring are common which may then require keratoplasty. Loss of corneal sensations is typically seen in diseases associated with damage to the corneal nerves as seen herpes simplex or herpes zoster infections or lesions affecting the ophthalmic division of the trigeminal nerve. This is tested by touching it with a wisp of cotton-wool or a Cochet Bonnet aesthesiometer and comparing the reaction with that in the fellow eye; the slightest touch is followed by a reflex closure of the lids if the cornea is sensitive and absent or dull corneal reflex indicates an anesthetic cornea. A corneal ulcer is a manifestation of infectious keratitis due to organisms that cause tissue death (necrosis) and pus formation in the corneal tissue. Investigations Before starting treatment, collecting corneal scraping specimens for preliminary microbiological investigations to identify the causative organism are mandatory. Signs: Red eye with loss of vision, conjunctival and circumcorneal congestion, hazy cornea with an epithelial defect that stains with fluorescein dye and is surrounded by corneal infiltration and oedema, necrotic slough at base of the ulcer, hypopyon, vascularization, encapsulated corneal abscess or corneal thinning and prolapse of uveal tissue with hypotony if perforated. The clinical assessment of a corneal ulcer requires careful examination with a slit-lamp. The ulcers can be graded according to size, area of infiltration and depth of involvement (superficial or deep) to indicate their severity (mild, moderate or severe), location and extent of possible threat to vision. Diagnosis: the diagnosis is made based on the clinical finding of a corneal epithelial defect that stains with fluorescein and is accompanied by surrounding infiltration with or without a purulent or necrotic slough at the base. Multiple scrapings are obtained and smeared onto slides and plated on culture media for culture and sensitivity (blood agar, chocolate agar, thioglycollate broth for bacteria, non-nutrient agar with Escherichia coli overlay for Acanthamoeba and Sabouraud dextrose agar without chlorhexidine for fungi). Smears are stained with Gram and Giemsa stains to identify the causative agent and study the morphology of the inflammatory cells. Bacterial Corneal Ulcers Causative Organisms Purulent keratitis pyogenic bacteria aureus and albus, Escherichia coli, is nearly always exogenous, due to such as Pseudomonas, Staphylococcus Pneumococcus, Neisseria gonorrhoeae, etc. Pseudomonas aeruginosa is particularly likely to have a rapid course with deep and extensive corneal necrosis Fungal Trauma with vegetative matter Viral Low immunity, recurrent attacks Parasitic Contact lens wear and exposure to contaminated water (acanthamoeba) or visit to endemic zone (onchocerciasis) Clinical features Relatively less pain and watering compared to the loss of vision and ulcerative signs. Hypopyon (if present) is thick, immobile and may even have a convex upper surface Relatively more pain and watering compared to the extent of vision loss and ulcerative signs. Recurrences are characteristic Disproportionately severe pain is a characteristic feature of acanthamoeba induced ulceration. It has been noted that the only organisms known to be able to invade normal corneal epithelium are N. Organisms such as staphylococci may lead to superficial erosions initially, which coalesce to form frank ulcers. Pathology Pathology of corneal ulcer is characterized by a breach in the continuity of the surface epithelium with a localized necrosis of the layers of the cornea. The sequestrum partly disintegrates and is cast off into the conjunctival sac, while some adheres to the surface of the ulcer. The epithelium, however, regenerates and rapidly advances towards the ulcer, grows over its edge, and sometimes over the slough or purulent infiltration which forms the floor and if complete converts the ulcer into a corneal abscess. The ulcer is usually saucer-shaped, and the walls project above the normal surface of the cornea owing to swelling caused by the fluid imbibed by the corneal lamellae. The surrounding area is packed with leucocytes and appears as a grey zone of infiltration. While these events occur in the cornea, irritative signs are always found within the eye as well. Some of the toxins produced by the bacteria diffuse through the cornea into the anterior chamber, just as topical medications do when instilled into the conjunctival sac. They exert an irritative effect upon the vessels of the iris and ciliary body, so that hyperaemia of the iris occurs with ciliary injection resulting in keratouveitis. Mode and Source of Infection the principal mode of entry of organisms is through the corneal epithelium either as a result of a break in the surface, diminished resistance of the epithelium, necrosis or desquamation. Although minute abrasions of the cornea are probably of everyday occurrence, highly virulent, pathogenic organisms are not usually present in the conjunctival sac and, if they are, the tear film and the resistance of the normal tissues suffice to deal with them. However, there are certain specific predisposing factors which increase the risk of developing corneal ulceration. These are: introduction of organisms during trauma, prolonged use of topical steroids, dry eyes, entropion with trichiasis, laophthalmos due to neuroparalysis (facial nerve), wearing of contact lenses, bullous keratopathy and poor local hygiene. Here, a wall of polymorphonuclear leucocytes forms a second line of defence while leucocytes macerate and dissolve the necrotic tissues. Initially when the necrotic material has been shed off the ulcer is somewhat larger, but as it starts healing the surrounding infiltration and swelling disappear, the floor and edges become more smooth and transparent, and the regressive stage is reached. The healing process continues with regeneration of collagen and the laying down of fibrous tissue, i. The newly formed fibres are not arranged regularly as in the normal corneal lamellae, hence they refract the light irregularly and the scar is, therefore, more or less opaque. If it is large and dense, some of the larger vessels persist while the smaller ones disappear. Here, vascularization plays a considerable part as is shown by the fact that the opacities clear first in the immediate vicinity of the vessels. The scar tissue which replaces the destroyed portions of the cornea usually fills in the gap exactly, so that the surface is level. It is quite common, however, for some deficiency to remain so that although the resultant cicatrix may be almost transparent, the surface could become flattened or even faceted. Such corneal facets can be seen only by careful examination of the corneal reflex but they may cause considerable diminution of visual acuity. Fungal Corneal Infections Mycotic or fungal keratitis is frequently seen in tropical countries, rural areas and in immunocompromised individuals. Causative organisms: It is commonly due to Aspergillus, Fusarium or Candida albicans. Mode of infection: Fungal ulcers are typically seen after injury with vegetable matter such as a thorn or wooden stick and are characterized by a relatively indolent course. Symptoms: Compared to bacterial ulcers, symptoms are much milder than the clinical signs would suggest. The hypopyon, if present, is thick and immobile, and is due to direct invasion into the anterior chamber of fungal hyphae enmeshed in thick exudates. An immune ring (Wesseley) may be visible due to deposition of immune complexes and inflammatory cells around the ulcer. There is marked ciliary and conjunctival congestion, but symptoms of pain, watering and photophobia are disproportionately less as compared to those in cases of bacterial corneal ulcers. As the cicatrix becomes consolidated the bulging may disappear, or it may remain permanently as secondary keratectasia, an ectatic cicatrix. This may persist, surrounded by a white cicatricial ring, or it may eventually rupture. Perforation: Perforation of an ulcer is usually caused by sudden exertion by the patient, such as coughing, sneezing, straining at stool or spasm of the orbicularis muscle. Any such activity causes a rise in the blood pressure, which at once manifests itself by a rise in the intraocular pressure and the weak floor of the ulcer, unable to support the sudden strain, gives way. When an ulcer perforates, the aqueous suddenly escapes and the intraocular pressure falls to the atmospheric level, the iris and lens being driven forwards into contact with the back of the cornea. The effect upon the nutrition of the cornea is good; owing to the diminution of intraocular pressure the diffusion of fluid through the cornea is facilitated, extension of the ulceration usually ceases, pain is alleviated, and cicatrization proceeds rapidly. The complications which follow a perforation are, however, of extreme danger to sight as well as preservation of the eye. Usually the perforation takes place opposite some part of the iris which is drawn into the aperture when the aqueous escapes. The blocking of the perforation with the iris allows the anterior chamber to be reformed as fresh aqueous is rapidly secreted. If the perforation is large, a portion of the iris is carried not only into the opening but through it causing a prolapse of the iris. Secondary glaucoma: If prolapse of the iris has occurred, cicatrization may still progress. The exudate which covers the prolapse becomes organized and forms a thin layer of connective tissue over which the conjunctival or corneal epithelium rapidly grows. Contraction of the bands of fibrous tissue tends to flatten the protruding prolapse. It rarely, however, becomes absolutely flat; more commonly the iris and cicatricial tissue are too weak to support the restored intraocular pressure, which is often increased owing to the development of a secondary glaucoma. Staphyloma: An ectatic cicatrix in which the iris is incarcerated is called an anterior staphyloma which, depending on its extent, may be either partial or total. The bands of scar tissue on the staphyloma vary in breadth and thickness, producing a lobulated surface often blackened with pigment; hence the name.

This appearance is pathognomonic and leads eventually to the development of cataract blood pressure chart over 60 buy exforge mastercard. The iris is also characteristically stained pulse pressure vs stroke volume purchase exforge american express, first greenish and later reddish-brown hypertension emedicine buy exforge with paypal. The vision of these eyes prehypertension during pregnancy order exforge canada, however little affected by the primary injury hypertension while pregnant generic 80mg exforge free shipping, gradually fails owing to degenerative changes in the retina and lens arteria espinal anterior exforge 80 mg low price. The retinal degeneration, associated with great attenuation of the blood vessels, eventually becomes generalized, taking the form of pigmentation resembling that of pigmentary retinal dystrophy. In early siderosis, the electroretinogram shows increased amplitude of the a-wave with a normal b-wave. As the condition progresses the b-wave diminishes and in advanced cases the electroretinogram is flat. The corneal wound of entry is seen as a leucomatous corneal opacity overlying a sphincter tear. Occasionally it pierces the coats of the eye and comes to rest in the orbital tissues, a condition known as a double perforation of the eye. If it lies in the retina, the foreign body, generally black and often with a metallic lustre, is surrounded by a white exudate and red blood-clot, but eventually it is usually encapsulated by fibrous tissue and the retina in the neighbourhood becomes heavily pigmented. Apart from its chemical nature, the lodgement of a foreign body in the posterior segment frequently leads to degenerative changes, which may damage sight considerably. These may entail a widespread degeneration, but most frequently fine pigmentary disturbances at the macula, often the result of concussion, diminish or destroy central vision. The vitreous usually turns fluid, bands of fibrous tissue may traverse it along the path of the foreign body, haemorrhage may be extensive and retinal detachment may follow. Infection As with other perforating wounds, the introduction of infection is an ever-present danger when a foreign body enters the eye. Some types of foreign bodies are more likely to be associated with infection than others. Owing to the heat generated partly on their emission and partly by their rapid transit through the air, small flying metallic particles are frequently sterile, and infections are more likely to follow the introduction of pieces of stone or wood. Such eyes should be treated with antibiotics prophylactically as in penetrating wounds. The characteristic blue pigmentation is found particularly in the corneal corpuscles, in the meshes of the trabeculae, on the inner surface of the ciliary body, and in the retina where the entire retinal vascular system is clearly marked out. The anterior layers of the iris are impregnated and, in addition to subcapsular deposits in the lens, the fibres are also stained. Copper the reaction of copper or brass (as from percussion caps) varies with the content of pure copper. Occasionally this results in the profuse formation of fibrous tissue so that the particle becomes encapsulated but, more often, a suppurative reaction follows which eventually results in shrinkage of the globe. If, however, the metal is heavily alloyed, a much milder reaction ensues-chalcosis. The copper becomes electrolytically dissociated and is deposited particularly where resistance to its migration is offered by continuous membranes. However, as there is no chemical combination with the proteins of the cells, as occurs with iron, degenerative changes do not appear and vision may remain indefinitely good. Organic Materials Organic material tends to produce a proliferative reaction characterized by the formation of granulation tissue. Vegetable matter such as leaves, fronds and thorns may introduce a fungal infection into the eye. Wood and other vegetable matter produce a proliferative reaction characterized by the formation of giant cells. Eyelashes may be carried into the anterior chamber in perforating wounds of the cornea, and proliferation of the epithelium of the root of the hair frequently leads to the formation of intraocular cysts. Caterpillar hair may penetrate the eye, exciting a severe iridocyclitis characterized by the formation of granulomatous nodules (ophthalmia nodosa). Diagnosis the diagnosis of an intraocular foreign body is extremely important, particularly as the patient is often unaware that a particle has entered the eye. In all suspicious cases, particularly those with a history of having used a hammer and chisel, a careful search must be made for a wound of entry, which may be very minute and difficult to find. If the particle has passed through the cornea, however, the most mnute scar can always be seen on careful examination with the slit-lamp, but its detection in the sclera may be much more difficult or sometimes even impossible. The anterior segment of the eye must be thoroughly explored with the slit-lamp and the angle of the anterior chamber with the gonioscope. These tracks, together with the position of the wound of entrance, are often valuable clues in localizing the foreign body. If the media are clear, the entire fundus must be similarly searched under full mydriasis. Radiography is indispensable for the discovery and location of foreign bodies, which are radio-opaque. Fortunately, these particles are usually metallic and many-although by no means all-can thus be demonstrated. One of the most useful methods involves the suturing of a metal ring at the limbus or the use of a contact lens which contains a radioactive ring, and taking X-ray photographs in the anteroposterior and lateral axes. The foreign body can then be located in terms of the meridian and the number of millimetres behind the limbus or corneal apex. The thinnest slices are used to localize a small foreign body with great accuracy. Ultrasonography allows the detection of most foreign bodies, as well as associated intraocular conditions such as retinal detachment, suprachoroidal haemorrhage and a perforating injury of the eye. A useful method of detection and localization in the operating theatre is to utilize the alterations in a secondary induced current produced by a metallic particle in its vicinity. This principle has been incorporated in instruments (locators) in which the searching element is a pointed probe and alterations in the current in the neighbourhood of the particle are revealed by the deflections of a needle on a dial or changes in the pitch of an audible signal amplified and transmitted to a loudspeaker. Treatment A foreign body should be removed unless: (i) it is inert and probably sterile; (ii) little damage has been done to vision and (iii) the process of removal will almost inevitably destroy sight. If the foreign body lies within the lens, it is better to treat such particles as if they were non-magnetic or remove the lens as a whole. If a magnetic foreign body is in the vitreous or retina, an intravitreal magnet or intravitreal forceps are necessary for its removal. Extraction is undertaken by the posterior route together with vitreoretinal surgery, whereby the particle is extracted directly. After excising any surrounding fibrous tissue and vitreous traction bands, areas of retinal breaks are treated at the same sitting. Subretinal foreign bodies are removed externally through an overlying scleral incision or internally by retinotomy as part of a vitreoretinal surgical procedure. The immediate effect of extraction of foreign bodies is often good, but prognosis should be guarded. The tracks through the vitreous may become filled with fibrous tissue, and as this organizes and contracts, the retina may be pulled upon and its total detachment destroys vision. Modern sophisticated vitrectomy instruments have helped greatly in the better management of cases of penetrating wounds due to intraocular foreign bodies. Lens opacities and vitreous haemorrhage, bands and membranes can be removed at the time of initial surgery. Unfortunately, in these cases there is a tendency for the macula to pucker and for proliferative retinopathy to develop, which adversely affect the quality of post-operative vision. The extraction of a non-magnetic foreign body from the anterior segment of the eye is often easy. If the foreign body lies upon the iris it can usually be picked out by an iris forceps through a suitably placed keratome incision. If it lies in the angle of the anterior chamber, it is impossible to grasp it with forceps through an ordinary incision immediately over it. The incision should be made 3 mm inside the limbus in the quadrant of the cornea lying over the foreign body, the point of the keratome being directed straight at it. The foreign body can then be lifted out with toothless forceps to minimize the risk of prolapse of the iris. If the foreign body is in the lens, a few days should be allowed to elapse for the aqueous to act upon the lens fibres. An aspiration is then performed and the foreign body will probably be evacuated with the lens matter. If a non-magnetizable foreign body lies on the retina, and if accurate localization has been attained, it may be removed directly by intra-vitreal forceps as part of a vitreoretinal procedure which includes a complete vitrectomy. Laser photocoagulation of the surrounding retina should be performed to prevent a late retinal detachment. A foreign body retained in the eye has a serious prognosis, even if little mechanical damage has been done at the time of injury. If the foreign body is allowed to remain and is inert, it may be retained indefinitely without affecting vision, although an iridocyclitis (sometimes appearing after many years) may be anticipated. If the foreign body has been removed from the anterior chamber, the prognosis is usually good provided the lens was not injured. An injury of the lens adds to therapeutic problems owing to the immediate difficulties of its evacuation, the subsequent irritant reaction, and the tendency for the development of secondary glaucoma. Even if the foreign body has been successfully extracted from the posterior segment of the globe, a long-term follow-up is essential. Sympathetic ophthalmitis or ophthalmia almost always results from a penetrating wound, occurring in 0. Wounds involving the ciliary body and leading to its incarceration in the scar, have always been considered particularly dangerous. Incarceration of the iris or lens capsule are also more likely to set up sympathetic ophthalmitis than others. Sympathetic ophthalmitis very rarely occurs if actual suppuration has taken place in the exciting eye. The onset has been reported to occur as early as 9 days after the accident and may be delayed for many months or even years, with 80% occurring within 3 months of the injury. Aetiology the aetiology of the condition is unknown but is considered to be an autoimmune, T cell-mediated disease. Uveal pigment can act as an allergen and those who suffer from sympathetic diseases show a skin sensitivity to it. Pathology Pathologically, the microscopic features in both the exciting and the sympathizing eyes are the same. In the earliest stages, examination shows nodular aggregations of lymphocytes and plasma cells scattered throughout the uveal tract. The retina is also heavily infiltrated, especially in the neighbourhood of the vessels. In the later stages the infiltrate becomes diffuse and giant cells appear; in fact, the condition is scarcely distinguishable from tuberculosis of the uveal tract, although caseation is never present. In sympathetic ophthalmitis, the plastic iridocyclitis differs clinically in no respect from this form of irido-cyclitis due to other causes. Prodromal symptoms are sensitivity to light and transient indistinctness of near objects due to weakness of accommodation. The prodromal symptoms may occur in intermittent attacks, spread over a considerable period of time. In other cases, the patient first seeks advice for photophobia and lacrimation, or defective vision in the uninjured eye (sympathetic irritation). In cases which are prone to develop this condition, the first sign may be the presence of keratic precipitates on the back of the cornea or the presence of retrolenticular flare and cells, which are noticed at this early stage because they have been anticipated. On examination at this stage, there may be lacrimation, slight ciliary injection, tenderness of the eyeball, as shown by the patient shrinking from an attempt at examination, precipitates on the back of the cornea and vitreous opacities; occasionally there is some oedema of the optic disc. When fully developed, all the signs and symptoms of granulomatous uveitis are present, varying in degree according to the severity of the case. The prognosis as to vision is always doubtful, but if there is extensive deposition of plastic exudates in the pupillary area it becomes extremely grave. Cases showing little exudation but a deep anterior chamber and keratic precipitates have a more favourable prognosis, but they may at any moment develop into the severe plastic type. In every case of penetrating injury, with or without the retention of a foreign body, prophylactic and long-term treatment, including the topical and systemic administration of steroids, may be adopted for a time. If the eye quietens down quickly it is unlikely to set up sympathetic inflammation. The chief causes which prolong irritation are entanglement of the iris or ciliary body or lens capsule in the wound. It must be remembered that children are more susceptible to the disease than adults. Sympathetic ophthalmitis rarely occurs after the excision of an injured eye unless it has already commenced at the time of operation. Usually it is a plastic iridocyclitis which has been set up by injury and has not subsided in the course of 3 or 4 weeks. Instead of quietening down, the ciliary injection remains, there is lacrimation and the eye is tender. Special attention should be directed to the presence or absence of keratic precipitates on the back of the cornea. In the rarer cases of delayed sympathetic ophthalmitis, the exciting eye may have passed into a quiescent state. The exciting eye, while showing evident traces of old iridocyclitis, may still possess useful vision. The treatment of sympathetic iridocyclitis is that of iridocyclitis in general with the proviso that steroid preparations have a more dramatic effect than in most other ocular inflammations. At the earliest suggestion of inflammation, steroids should be given systemically in large doses-intravenous methylprednisolone 1 g followed by 100 mg of prednisone orally tapered off slowly.

Eczema may occur in association with a discharging conjunctivitis or where there is excess lacrimation blood pressure chart during exercise discount exforge 80 mg amex. The ordinary coccal infections cause boils and abscesses pulse blood pressure chart discount exforge 80 mg line, while specific infections such as anthrax or zoster may occur pulse pressure by age 80mg exforge free shipping. Erysipelas is dangerous as it may spread to the orbit heart attack man exforge 80mg amex, leading to cellulitis blood pressure numbers for seniors purchase exforge in india, thrombosis of the cavernous sinus or meningitis pulse pressure readings generic exforge 80mg on line. Blepharitis this is a chronic inflammation of the margins of the lids, appearing as a simple hyperaemia or as a true inflammation, which may occur in two forms: anterior and posterior. The condition may follow chronic conjunctivitis due to staphylococci carried to the lid margins by infected fingers. Occasionally, parasites cause blepharitis-blepharitis acarica, due to Demodex folliculorum, and phthiriasis palpebrarum, due to the crab louse, very rarely to the head louse. The lower lid shows a loss of lashes in areas and an ulcer with surrounding mucopurulent discharge at the lash line. Anterior Blepharitis Seborrhoeic or Squamous Blepharitis In this condition, small white scales accumulate among the lashes which readily fall out, but are replaced without distortion. If the scales are removed the underlying surface is found to be hyperaemic, but not ulcerated. The condition is often essentially metabolic and similar to seborrhoea associated frequently with dandruff of the scalp. Infections need to be treated when they supervene Staphylococcal or Ulcerative Blepharitis this is an infective condition commonly due to staphylococcus. The symptoms are redness of the edges of the lids, itching, soreness, lacrimation and photophobia. This distinguishes the condition from a conjunctival discharge, which causes matting together of the lashes, but removal of the crusts reveals normal lid margins. This is most easily done by thorough bathing of the eyes with 1:4 baby shampoo or with warm 3% bicarbonate of soda lotion. The application softens the deposits, so that they can be picked or rubbed off with a pledget of cotton-wool. When the crusts have been removed entirely, antibiotic drops, depending on the sensitivity of the organism, are prescribed. When the infection has been eliminated a simple daily habit of swabbing the lid margins with a warm bland lotion must be established. Rubbing of the eyes or fingering the lids with unwashed hands must be completely avoided. If not treated energetically and with perseverance, the disease is extremely chronic, causing or being accompanied by chronic conjunctivitis. The ulceration is liable to extend deeply, destroying the hair follicles so that the lashes that fall out are either not replaced (madarosis) or only by a few small, scattered, distorted cilia. Neighbouring hair follicles are drawn out of place and a false direction given to the remaining cilia so that they may rub against the cornea (trichiasis). Occasionally the development of cicatricial tissue may be extreme so that the edge of the lid becomes hypertrophied and droops as a consequence of its weight (tylosis). The lower lid is particularly liable to be displaced by prolonged ulcerative blepharitis. The contraction of the scar tissue drags the conjunctiva over the margin, and the posterior lip of the intermarginal strip, instead of being acuteangled, becomes rounded, so that its capillarity is impaired. Tears then tend to spill over (epiphora), a condition which is accentuated if the punctum becomes everted and ceases to lie in accurate contact with the bulbar conjunctiva. The continuous wetting of the skin with tears leads to eczema, which is followed by contraction. The condition is made worse by perpetually wiping the eyes, so that eventually ectropion develops, thus aggravating the epiphora and setting up a vicious circle. Meibomian seborrhoea: Oil droplets may be seen at the Meibomian gland openings which can be expressed out like foam. Meibomianitis: Patients present with a diffuse rounded posterior lid margin and thickening around Meibomian gland openings. Treatment is again by warm compresses and lid massage, together with doxycycline or minocycline for 6 weeks. Molluscum Contagiosum this is a small, white, umbilicated swelling, generally multiple, due to a large poxvirus from which a substance resembling sebum can be expressed. Histologically, large intracytoplasmic inclusion bodies occur within the acanthotic epidermis. It produces a severe conjunctivitis and occasionally a keratitis which are intractable to treatment unless the primary nodules on the lid margin are dealt with. If the infection spreads posterior to the orbital septum it can lead to visual disturbances, proptosis and even meningitis. It is imperative to treat this with broad spectrum oral antibiotics such as amoxycillin and a non-steroidal anti-inflammatory drug to contain the infection. In the early stages the gland becomes swollen, hard and painful, and usually the whole edge of the lid is oedematous. Styes often occur in crops, or may alternate with boils on the neck, carbuncles, or acne, usually indicating a deficient resistance to staphylococci. It is commonest in Pre-septal Cellulitis Pre-septal cellulitis is a bacterial infection of the eyelid anterior to the orbital septum, and is due to trauma, or spread of infection from surrounding structures. Treatment: Antibiotics orally and the use of hot compresses are advocated for a few days. When the abscess points it may often be evacuated by pulling out the affected lash. If the infection spreads to form a pre-septal cellulitis, oral antibiotics may be required. If crops of styes occur, conditions such as diabetes must be excluded and rubbing of the eye prevented. Hordeolum Internum this is a suppurative inflammation of a meibomian gland, and may be due to secondary infection of a chalazion. It is less common but the inflammatory symptoms are more violent than in an external stye, because the gland is larger and embedded in dense fibrous tissue. The pus appears as a yellow spot shining through the conjunctiva when the lid is everted. Treatment: It is the same as for the external type, except that the incision should be made exactly as for a chalazion. The patient often notices a hard, painless swelling in either lid, increasing very gradually in size and without inflammatory symptoms. The smaller chalazia are difficult to see, but are readily appreciated by passing the finger over the skin. If the lid is everted the conjunctiva is red or purple over the nodule, in later stages is often grey, or rarely, if infection has occurred, yellow (hordeolum internum). The grey appearance is due to alteration in the granulation tissue, which becomes converted into a jelly-like mass. Chalazia become smaller over months, but complete spontaneous resolution rarely occurs. The contents may be extruded through the conjunctiva, in which case a fungating mass of granulation tissue often sprouts through the opening, causing the conjunctival discharge and irritation to continue. Sometimes the granulation tissue is formed in the duct of the gland, from which it projects as a reddish-grey nodule on the intermarginal strip (marginal chalazion). Treatment Intralesional injection: An intralesional injection of triamcinolone acetonide may help in the resolution of smaller chalazia. If the chalazion does not resolve, or there is a large chalazion, it should be incised and curetted. Surgical management (I&C): the conjunctival sac and the lid are well anaesthetized by a submuscular injection of 2% lignocaine locally deep to the orbicularis and a topical anaesthetic. A chalazion clamp is applied around the nodule to help keep the lid everted and to provide a bloodless field for the surgery. The lid is everted and at the point of greatest discoloration a vertical incision made through the palpebral conjunctiva with a sharp scalpel to avoid damage to the adjacent meibomian glands. Any semifluid contents which may be present escape and the walls of the cavity are thoroughly scraped with a curette. The patient should be warned that the swelling will remain for some time since the cavity becomes filled with blood. Sometimes, especially if the curettage has not been sufficient, granulation tissue sprouts from the wound. Very hard chalazia are occasionally met with, particularly near the canthi, which may be adenomata of the glands and require excision. However, in all cases with recurrences or those occurring in elderly individuals, the lesion should be biopsied to rule out a meibomian cell carcinoma. Chalazia are often multiple, occurring in crops, and are more common among adults than in children. Essential blepharospasm has an insidious onset between the ages of 45 and 65 years, with brief involuntary closing of the eye affecting one or both eyes and leading to an inability to open the lids. Treatment may be medical by an injection of botulinum toxin in a total dosage of 43 units distributed to the upper eyelids, above the eyebrows, the glabellar and the lateral canthal area in divided doses of 2. If this method fails, only then should the lower lid be injected with three separate injections of 2. The mandibular branch of the facial nerve is identified and the function of its branches assessed by electrical stimulation. Sensory or reflex blepharospasm is commonly caused by bright light, corneal or eyelid irritation. Patients may complain of photophobia, a vague discomfort and a foreign body sensation. Trichiasis may prevent corneal ulcers from healing despite therapy, thereby threatening vision. A few of the lashes may be affected or the condition may be due to entropion involving the whole margin of the lid. The symptoms are those of a foreign body continually present in the eye with irritation, pain, conjunctival congestion, reflex blepharospasm and lacrimation. Recurrent erosions, superficial opacities, vascularization of the cornea and frequent, recurrent corneal ulcers are eventually produced. Electrolysis: Destruction of the hair follicle by diathermy or electrolysis is preferable. Cryosurgery may be used to treat segmental trichiasis, but can lead to necrosis and depigmentation of the lid. Diathermy: In diathermy, a fine needle is inserted into the hair follicle and a current of 30 mA applied for 10 seconds. In electrolysis, the flat positive pole is applied to the temple, while the negative, a fine steel needle, is introduced into the hair follicle and a current of 2 mA is used. The negative pole is determined by placing the terminals in saline-bubbles of hydrogen are given off by it. It should be remembered that electrolysis is both painful and tedious, but pain may be avoided by injecting local anaesthetic into the margin of the lid. If the current is of the proper strength, the bubbles produced at the puncture site cause the formation of slight foam, and the lash with its bulbous root can be easily lifted out. Cryoepilation Surgery If many cilia are displaced, operative procedures, as for entropion, must be undertaken. Entropion Positioning of the sharp posterior lid margin against the cornea is essential for the integrity of the tear film and the health of the ocular surface. Clinical features: the symptoms are those of disturbances of the stability of the tear film and the induced trichiasis. Involutional Entropion There is a general instability of the lid structures with age. A weakness or dehiscence of the posterior retractors of the lid occurs, together with a laxity of the medial and lateral canthal ligaments. This is accompanied by a loss of posterior support, as atrophy of the orbital fat leads to enophthalmos. The pre-tarsal orbicularis is attached to the tarsus, but the pre-septal orbicularis has more tenuous attachments and a tendency to override the pre-tarsal orbicularis. The lower border of the tarsal plate is therefore rotated forward and the margin of the lid onto the globe. Surgery for involutional entropion addresses the pathogenesis-reattachment of the retractors to the tarsal plate, shortening of the horizontal width of the tarsal plate and forming a cicatrix between the pre-tarsal and pre-septal parts of the orbicularis. The aim of the surgery is to restore the vertical and horizontal tautness of the lid. In involutional entropion affecting bed-ridden patients or those for whom surgery is a medical risk, a simple suturing of the lower lid with double-arm 5-0 vicryl chromic catgut may prove efficacious. The needle is passed through the lid from the conjunctiva to the skin adjacent to , but not through, the inferior border of the tarsus. Slight downward traction is applied to the skin when the needle is passed through the muscle and skin. Tissue reaction to the gut suture helps to create a cicatricial barrier that maintains the eyelid in the everted position. In patients with significant horizontal laxity of the lower lids and entropion it is necessary to remove some of the excessive lid tissue next to the lateral canthus. One 4-0 silk suture is brought through the skin of the medial edge 2 mm from the wound margin. The suture is carried through two-thirds of the thickness of the tarsus and does not penetrate the conjunctiva. The needle is then carried through the equivalent tissue of the lateral margin before piercing the lateral canthal tendon.

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IgG and complement have been demonstrated in the glomeruli of lupus erythematosus patients blood pressure 7949 order generic exforge line. Systemic lupus erythematosus affects young women nine times more commonly than men heart attack humor buy generic exforge on line. It may be due to an innate tendency to produce auto-antibodies because the defective T-lymphocytes fail to exercise their restraining influence on B-lymphocyte function blood pressure medication vivid dreams generic exforge 80mg line. Obstruction of the Arterial Circulation Obstruction of a retinal artery is usually due to an embolus; superadded spasm often completes the occlusion pulse pressure glaucoma purchase exforge 80mg free shipping. It may occur without obvious general vascular disease or blood pressure chart bpm buy exforge amex, when widespread blood pressure medication night sweats exforge 80mg sale, there may be associated arteriosclerosis, hypertension or Buerger disease. The eye becomes suddenly blind, although when the causative factor is minute emboli, premonitory obscurations of vision may occur. The larger arteries are reduced to threads, the smaller are invisible but the veins are little altered except on the disc where they are contracted. Within a few hours the retina loses its transparency, becoming opaque and milky-white, especially in the neighbourhood of the disc and macula. At the fovea centralis, where the retina is extremely thin, the red reflex from the choroid is visible and appears as a round cherry-red spot, presenting a strong contrast to the cloudy white background. When obstruction to the blood flow is not complete, the flow may be partially restored in the course of a few days, in which case gentle pressure upon the globe may break up the column of venous blood into red beads separated by clear interspaces. If the veins are easily emptied of blood or arterial pulsation is produced by slight pressure on the eyeball, it is evidence of incomplete blockage. The white appearance of the retina takes several weeks to clear up but eventually the membrane regains its transparency and appears normal; it is, however, completely atrophic apart from the outer layers which receive their nourishment from the choroid. The vessels are contracted or reduced to white threads although some of them refill at a later stage due to the establishment of a feeble collateral circulation through an anastomoses with the ciliary system round the disc. In some cases a certain degree of central vision persists in spite of apparent complete occlusion of the central artery. This is due to the presence of cilioretinal arteries which, when present, always supply the macular region and naturally escape occlusion; or to a macular branch of the central artery given off proximal to the block. In the early stages the corresponding scotoma is usually somewhat indefinite, but later settles down to form a permanent sector-shaped defect. Treatment seldom helps, but attempts should be made to relieve spasm or drive an embolus into a less important branch if the patient is seen early. Massaging the globe is probably the most effective method but paracentesis has been employed for this purpose; to be effective such measures must be adopted without delay. Obstruction of the Venous Circulation Venous Stasis Retinopathy Venous stasis retinopathy is a well-defined clinical entity that consists of unilateral disc oedema with variable retinal vascular changes in young healthy adults. The retinal vascular abnormality may be minimal or present as markedly engorged, dilated, tortuous veins and haemorrhages at the posterior pole extending into the retinal periphery. Neuro-ophthalmological examination is negative and fluorescein angiography shows venous stasis with delayed venous drainage. Systemic corticosteroids are occasionally used but the disease can safely be followed without neurodiagnostic studies in a healthy young adult where there are no abnormal systemic or neuro-ophthalmological findings. The fundus picture simulates that of central venous thrombosis and probably results from phlebitis affecting the central vein within the optic nerve head. The essential difference between venous stasis retinopathy and central venous thrombosis is that in the former there is a stasis of the venous circulation in the absence of ischaemia of the retina. In these cases the obstruction is usually in the central vein just behind the lamina cribrosa where the vein shares a common sheath with the artery so that the two are affected by the same sclerotic process. At other times in arteriosclerotic patients, the block may be peripheral, usually at a bifurcation or where a sclerosed artery crosses a vein, an event which is particularly prone to occur in the superior temporal vein. Thrombosis may also be due to local causes, such as a chronic glaucoma, orbital cellulitis or facial erysipelas. In all cases the condition is to be regarded as a danger signal and constitutional investigation and treatment should be assiduously undertaken. Sight is much impaired, though not as rapidly as in obstruction of the central retinal artery. In these cases the visual defect is partial but not exactly sectorial as in the case of occlusion of a branch of the artery. No treatment is effective in cases of venous occlusion once the blockage has become complete. If there is widespread capillary occlusion, panphotocoagulation of the retina (or cryoapplications if the media are hazy) may forestall neovascular glaucoma and rubeosis iridis. Widespread capillary occlusion is associated with cotton-wool spots, delayed arteriovenous transit time, large vessel leakage and retinal oedema. In branch occlusion, destruction of areas of poor perfusion (as seen by closure of retinal capillaries in an angiogram) may relieve persistent oedema and inhibit neovascularization. Photocoagulation should not be done until most of the intraretinal blood is absorbed. Although rare, retinal venous occlusive disease is known to occur in serpiginous choroidopathy, as the subretinal inflammatory process extends superiorly to produce a focal retinitis and vascular obstruction (not necessarily at an arteriole venous-venous crossing). There is always microscopic evidence of haemorrhage between the retina and choroid and in the deep layers of the retina, and the ophthalmoscopic appearance is usually characterized by a number of small aneurysms and a varying amount of exudation, sometimes with masses of cholesterol crystals embedded in it. Development of new vessels is also a feature in age-related macular degeneration (neovascular form) and retinopathy of prematurity. Photocoagulation remains the standard treatment of choice, but has frequent adverse effects. Adjunctive modes of inhibiting vascular endothelial growth factor allow greater success in controlling the neovascularization. The characteristic feature is the presence of round or oval white spots (Roth spots). There is little general reaction in the retina although some oedema and papilloedema may occur, but the disease is frequently fatal and vision may be seriously impaired before death. This is a very serious problem and often results in loss of all vision or even the eye. Endophthalmitis usually occurs after intraocular surgery or following a penetrating injury. It is treated with antibiotics given intravenously, as eye drops, as periocular injections, or intravitreal injections. If the endophthalmitis is severe and does not respond to this conservative management, vitrectomy is carried out. Vitrectomy is done to remove infectious material inside the eye, decrease the bacterial load and allow antibiotics to be in direct contact with the infected tissues. The visual prognosis in any case of endophthalmitis is guarded; severe visual loss can occur if the endophthalmitis is not treated early. Retinal detachment occurs in 75% of patients, usually within 3 months of the onset of symptoms secondary to holes within the necrotic retina and in association with vitreous traction. Intravenous acyclovir has been shown to induce some regression of the retinal lesions (see also Chapter 13, Ocular Therapeutics). These may be divided into purulent inflammations caused by pyogenic organisms and inflammations caused by specific infections. Cytomegalovirus Infection Human cytomegalovirus infection is characterized by distended tissue cells in which nuclei contain large acidophilic inclusion bodies. The eye may be affected by an isolated macular lesion or by a severe haemorrhagic or granular form of retinitis. The acute forms, due to the lodgement of organisms in the retina in the course of a pyaemia, lead to metastatic endophthalmitis or panophthalmitis. Subacute Infective Retinitis (Septic Retinitis of Roth) this occurs in less virulent infections of a metastatic nature, typically in bacterial endocarditis and sometimes in puerperal septicaemia. The posterior part of the fundus is generally affected, where numerous recurrent haemorrhages of Syphilis Most syphilitic retinal affections are secondary to choroidal inflammations but certain ill-defined changes may occur primarily in the retina. In the more definite forms, there are larger atrophic and pigmented areas at the periphery (anterior retinitis), a condition often seen with interstitial keratitis. In acquired syphilis endarteritis may be prominent with whitish exudates along the course of the vessels. A diffuse retinitis may occur, particularly in the secondary stage of the disease wherein the retina, especially in the central area, becomes grey and cloudy. As the condition subsides the typical picture which develops consists of an atrophic optic disc, attenuated vessels, and a generally depigmented retina with the pigment aggregated in corpuscles, particularly at the periphery, in a distribution resembling pigmentary retinal dystrophy. The subjective symptoms are defective central vision, night blindness, irregular and concentric contraction of the field with or without central, paracentral, or ring scotomata and metamorphopsia. Toxocariasis When tissues other than the skin are invaded by nematode larvae the condition is referred to as visceral larva migrans. Toxocara canis and Toxocara catis are round-worms and are common causes of ocular disease. Children eat infected material so that the eggs of the worm hatch in the duodenum and larvae then penetrate the intestinal wall, enter the venous circulation and migrate across the pulmonary capillary bed to reach the respiratory tree. If the infection is heavy, the children suffer from fever, anorexia, eosinophilia and hepatomegaly. The larvae produce an intraocular granuloma consisting of eosinophils and IgE, which is situated centrally or peripherally in the retina as a white lesion. During the acute stage antibody titres rise in the blood stream and a skin test with antigens may produce a reaction. Vitritis may respond to topical steroids which may be supported by thiabendazole and systemic steroids. Tractional detachments of the retina are common and in such cases vitrectomy and/or scleral buckling may have a part to play. Ascaris lumbricoides may also produce ocular inflammation as a result of larval migration. Sarcoidosis the characteristic histological lesion in sarcoidosis is an epithelioid cell granuloma, similar to a tubercle without caseation. The mediastinal lymph nodes are a common site of such lesions but the lungs, liver, spleen, skin and eyes together with the parotid glands are also affected. The tuberculin test is usually negative but the Kveim reaction, which is a test for skin sensitivity to sarcoid material, may be useful. X-rays of the chest may show bilateral lymph node involvement in the hilar region of the lungs and this may lead eventually to pulmonary fibrosis. Occasionally the bones of the hand are affected so that the phalanges show cystic areas. The optic nerve head may be oedematous and also affected by nodular granulomata leading to atrophy. There may be patches of chorioretinitis and periphlebitis in association with posterior uveitis. Of patients with ocular sarcoid, 25% show evidence of posterior segment involvement during their illness. When the retina is involved there is often an associated affection of the central nervous system. Periphlebitis Retinae this is a relatively common disease which manifests itself clinically by inflammation of the veins and progressive Toxoplasmosis (See Chapter 32, Ocular Manifestations of Systemic Disorders). This leads to a proliferation of new vessels on the retinal surface or as fronds, and repeated haemorrhages into the vitreous. Practically all the visible rays, ultraviolet and many infrared rays pass unimpeded to the retina and these are absorbed by the pigmentary epithelium. The lesion is, in fact, a burn of the retina, generally seen in the paramacular area. The symptoms are persistence of the after-image, progressing later into a positive scotoma, and metamorphopsia. Ophthalmoscopically, there may be no signs at first, or a pale spot is seen at the fovea with a brownish-red ring round it. Later there are usually deposits of pigment and small, grey punctate spots around the fovea, or even the formation of a retinal hole. Prognosis must be guarded; although improvement often occurs, some defect usually remains and the scotoma may persist permanently. Light-induced maculopathy due to the strong focused light of the operating microscope has been recorded in patients who have undergone cataract surgery with posterior chamber lens implantation. The exudative form of the disease usually leads to more serious vision loss and is responsible for 90% of the blindness due to this disease. Macular degeneration is more common in people over 65 years of age, Whites and females. Pathogenesis the atrophic form possibly results in thinning of macular tissues, amorphous deposits and pigmentation in the macula. Exudative macular degeneration occurs when new vessels form a choroidal neovascular membrane. Photograph of the peripheral retina showing an area of healed perivasculitis, with retinal sheathing, a fibrovascular vitreoretinal frond and scars of previous photocoagulation.

These autonomic activities include increase in pulse and blood pressure blood pressure jokes order exforge with mastercard, metabolism blood pressure medication weight loss purchase 80mg exforge with visa, and blood flow in the brain arteria iliaca externa generic 80 mg exforge. In this phase heart attack fast food buy 80mg exforge, the eye movements are slow blood pressure chart hospital generic 80mg exforge with amex, and muscles maintain tone with normal deep tendon reflexes blood pressure ranges low normal high purchase exforge no prescription. Autonomic activities are minimal, although secretion of growth hormone and prolactin increases during this phase. This stage usually lasts only a few minutes in the first cycle and is transitional to stage 4. Stages 3 and 4 are often referred to as slow-wave sleep, delta sleep, or deep sleep. In contrast, long-term arousal may result from increased secretion of the catecholamines from this nucleus. The balanced opposing effects of serotonergic and noradrenergic neurons regulate the sleep states. Narcolepsy is a condition in which patients enter into brief, often unpredictable, and irresistible episodes of sleep during waking hours (when conducting activities that require constant attention). Sleep attacks during a single day may range between 1 to as many as 20, and each attack may last from a few minutes to as much as a few hours. It has been estimated that up to 50% of these individuals suffer from memory loss. Some narcoleptics may experience automatic behaviors that may include rapid blinking, repetitive motor activities, and irrelevant speech. This condition starts in the second decade of life between adolescence and age 25 years and may follow traumatic emotional situations. Excessive daytime sleepiness, preceded by a feeling of overwhelming fatigue, may be an initial sign of narcolepsy. Presence of excessive daytime somnolence, cataplexy, sleep (hypnagogic and hypnopomic) hallucinations, and sleep paralysis represents the narcolepsy tetrad that is essential for the diagnosis of narcolepsy. Most narcoleptics present with cataplexy, which may be brought on by excitement, anger, or fear. Cataplexy usually occurs months to years following the initial onset of sleep attacks. Visual and/or auditory hallucinations may be detected in individuals with prolonged cataplectic attacks. It is characterized by sudden loss of muscle tone, which may lead to sudden collapse of the patient to the ground. Hypnagogic hallucination refers to the hallucinations that occur prior to falling asleep, whereas hypnopompic hallucination occurs upon awakening. Sleep paralysis is similar to cataplexy but refers to the paralysis that may be experienced by the patient slightly before the onset of sleep or shortly after awakening. The individual is aware of the paralysis and often describes the struggle to get up. This paralysis is temporary and may be terminated spontaneously or after mild sensory stimulation. In this diagnostic method, the patient is allowed an adequate amount of sleep approximately 10 days prior to the study. Narcoleptics usually require less than 4 min to fall asleep, a considerably smaller amount of time compared to normal individuals. Although the inheritance pattern is believed to be autosomal dominant, environmental factors should also be considered in the assessment of this condition. First-degree relatives of narcoleptics may exhibit excessive daytime somnolence and have much greater incidence of narcolepsy. Prolonged administration of this medication may cause insomnia, irritability psychosis, and possible tolerance. Centrally acting -1 adrenergic agonists such as modafinil and selegiline, a monoamine oxidase type B inhibitor, although less effective than methylphenidate, may be used as second-line agents. Different cardiovascular neuron groups in the ventral reticular formation of the rostral medulla in rabbits: Single neurone studies. Effects of lesion of pontomedullary reticular formation on visually triggered vertical and oblique head orienting movements in alert cats. Neurotoxic lesions of the dorsolateral pontomesencephalic tegmentum-cholinergic cell area in the cat. M2 muscarinic receptor subtype in the feline medial pontine reticular formation modulates the amount of rapid eye movement sleep. Evidence for the existence of monaminecontaining neurons in the central nervous system. Experimentally induced changes in the intraneuronal amine levels of bulbospinal neuron systems. The topography and cellular organization of the reticular formation of the thoracic part of the spinal cord in the cat. The projection of the nucleus reticularis tegmenti pontis and adjacent regions of the pontine nuclei to the central cerebellar nuclei in the cat. Narcolepsy in children: A practical guide to its diagnosis, treatment and follow-up. It decussates in the caudal mesencephalon and enters the cerebellum to join afferent fibers of the spinocerebellar tract. The corpus cerebelli comprises two lateral hemispheres, which are connected by the midline vermis. These hemispheres are separated posteriorly by the posterior cerebellar notch that contains the falx cerebelli. This deep notch continues inferiorly with the cerebellar vallecula, a median fossa between the two hemispheres. Each cerebellar hemisphere consists of a peripheral cortical gray matter, which is thrown into lamina or cerebellar folia, and a central white medullary substance, containing the cerebellar nuclei. In contrast, the spinal gray matter and white matter pursue a reverse arrangement. The fourth ventricle extends into the white matter as a transverse gap, the fastigium, marking the junction of the superior and inferior medullary velum (white matter bands that extend rostrally and caudally in the roof of the fourth ventricle). The fastigium in the roof of the fourth ventricle contains the fastigial, nuclei whereas the floor of the fourth ventricle contains the vestibular area that overlies the vestibular nuclei. Parieto-occipital fissure the cerebellum is derived from the rhombic lip of the alar plate and constitutes an important part of the rhombencephalon. It is located in the posterior cranial fossa, covered by the tentorium cerebelli, and separated by the fourth ventricle from the dorsal surfaces of the pons and medulla. The tentorium cerebelli is lodged between the cerebellum and the occipital lobes of the brain. It is connected to circuits that establish a link between the motor ans sensory cortices of the brain. It receives sensory input from the vestibular, reticular, and trigeminal nuclei as well as the spinal neurons and cerebral input via the pontine nuclei. It influences motor activity through projection to the motor cortices via specific thalamic nuclei. The cerebellum, also termed the motor autopilot, coordinates (synchronizes) fine voluntary motor activity, adjustment during motion, and eye movements; regulates phonation; maintains equilibrium; and processes exteroceptive impulses. It is also a critical structure in reflex modification, motor learning, and cognitive and emotional control. Lesions of the cerebellum or its connections produce muscular incoordination in the muscles of the eye (nystagmus), speech (dysarthria), and extremities and trunk (ataxia). Despite the remarkable motor deficits associated with cerebellar lesions, a great deal of functional recovery over time is attainable. Gross examination of the cerebellum reveals a corpus cerebelli with inputs from the spinal cord and pontine and trigeminal nuclei, and a flocculonodular lobe that maintains primary connections to the vestibular nuclei. The corpus cerebelli is subdivided into regions that receive spinal and pontine inputs and is connected to the midbrain, pons, and medulla via the superior, middle, and inferior cerebellar peduncles, respectively. The inferior cerebellar peduncle is medial to the middle cerebellar peduncle and consists of a dorsolateral part, the restiform body that contains afferents derived from the spinal cord and medulla (olivocerebellar, spinocerebellar, cuneocerebellar, and trigeminocerebellar tracts), and a medial part, which consists of mainly of efferent fibers (fastigiovestibular, Purkinje, and cerebellovestibular fibers) with some vestibular afferent (secondary and primary vestibulocerebellar fibers) fibers. The middle cerebellar peduncle is the largest that passes laterally from the basilar pons and contains the fibers of the pontocerebellar tract. The cerebellum lies inferior to the occipital lobe and is separated by the tentorium cerebelli. Developmentally, the posterolateral fissure is the first fissure to appear, marking the caudal boundary of the flocculonodular lobe. The primary fissure serves as a landmark that separates the rostrally located anterior lobe from the more caudally positioned posterior lobe. The cerebellum is further divided into superior and inferior surfaces by the horizontal fissure, which also divides the ansiform lobule (cerebellar cortical areas that correspond to the folium and tuber vermis) into superior and inferior semilunar lobules. The superior vermis and the corresponding parts of the cortical hemispheric areas are shown. The central lobule is separated from the lingula by a postlingual fissure, whereas the central lobule is demarcated from the anterior quadrangular lobule via the postcentral fissure. The flocculi remain attached to the midline nodule and form the flocculonodular lobe. The prepyramidal fissure bounds the tuber vermis caudally, and the postpyramidal fissure separates the uvula from the pyramid. Larsell classified the vermis in a simplified pattern in which each hemispheric lobule can be related to one of the vermian parts. Voogd divided the cerebellar cortex into longitudinal zone that maintains discrete connections to the cerebellar nuclei. On the basis of this mapping, the efferent fibers from the cerebellar cortex to the cerebellar nuclei appear to arise in cortical zones that belong to the same compartment as the nuclear region to which they project. The vermis and its cortical expansions are sites of somatotopic representation of the body. Case in point, the head and face are represented in the simple lobule and the leg in the Middle cerebellar peduncle Horizontal fissure central lobule, whereas the arm occupies a distinct area in the culmen. Blood supply and Venous drainage Blood flow to the cerebellum is sustained by the superior cerebellar, anterior, and posterior inferior cerebellar arteries. The superior cerebellar artery supplies the superior portion of the cerebellum, middle and inferior cerebellar peduncles, superior medullary velum, and choroid plexus of the fourth ventricle. This vessel originates from the basilar artery (an artery formed at the pontobulbar sulcus by union of the two vertebral arteries). Note the branches of the anterior and posterior inferior cerebellar arteries on this surface. Note that the morphologic divisions may correspond to a great extent to the functional classification. The posterior inferior cerebellar artery supplies the cerebellar hemispheres and the inferior vermis, uvula, nodule, cerebellar tonsils, choroid plexus of the fourth ventricle, and dentate nuclei. This syndrome manifests lateral gaze and facial palsies, vertigo with nystagmus (fast phase) toward the same side, deafness, ataxia, and contralateral hemianesthesia. The superior cerebellar veins drain into the great cerebral vein of Galen, the inferior cerebellar veins open into the straight sinus, and the lateral veins drain into the transverse, superior, and inferior petrosal sinuses. Most of the cerebellar hemispheres (posterior lobe) and part of the posterior vermis are the latest to appear phylogenetically, forming the neocerebellum. Functionally, the classification of the cerebellum comprises the vestibulocerebellum, spinocerebellum, and pontocerebellum. The vestibulocerebellum is comprised of the flocculonodular lobe and caudal part of the uvula. It has reciprocal connections with the vestibular nuclei, maintaining equilibrium and mediating vestibulo-ocular reflex. The interrelationship between the vestibular nuclei, oculomotor system, and cerebellum plays an important role in the coordination of voluntary eye movements. The spinocerebellum includes most of the anterior lobe, pyramis, and corresponding cortical parts (biventral lobules). It receives input from the spinal cord and mesencephalic trigeminal nucleus and deals with propulsive movements. The flocculonodular lobe deals with activities that govern posture and movement through its connections to the brainstem and spinal cord. The posterior lobe, with the exception of the simple lobule, the gracile and biventral, lobule and the corresponding vermal parts (declive and pyramis), comprises the pontocerebellum. It coordinates fine movements through its connections to the cerebral cortex and possibly planning for anticipated movement. The archicerebellum, which corresponds to the flocculonodular lobe, represents the oldest and most primitive part of the cerebellum. The paleocerebellum, the second-oldest cerebellar component, consists cereBellar cortex the cerebellar cortex consists of granular, Purkinje, and molecular layers. The granular layer (innermost layer) consists of small, densely packed granule cells, Golgi neurons, and mossy fiber rosettes. Note the single Purkinje layer between the outer molecular and inner granular layer. They have a number of dendrites that form clawlike terminal expansions that establish synapses with the terminals of the mossy fibers and Golgi neuronal axons in the cerebellar glomeruli. It must be realized that receptors mediating cholinergic (nicotinic and muscuranic) receptors also exist in the granule cells. During their course, axons of the granule cells establish extensive contacts with the successive Purkinje cells like telephone poles. Transmission between Purkinje and parallel fibers may be blocked by adenosine that binds to A1-adenosine receptors of the parallel fibers. The excitatory input mediated by the parallel fibers and incoming mossy fibers results in repetitive firing of the Purkinje neurons with the conventional type of action potentials. Their dendrites and axonal branches extend in a radially symmetrical pattern, in exact contrast to the pattern of branching of other inhibitory neurons and Purkinje cells.