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Conjunctivitis gonorrhoica adultorum
Gonorrhea can cause pose a risk to the newborn infant quite easily, especially when it’s contracted during childbirth and not caught until the eye is significantly pustular and weeping, but when gonorrheal infection manages to take hold in the adult eye, it’s often far more damaging, much more quickly than in the infant. The eye can begin producing an excess of clear tears in the morning, by noon have the lachrymation become turbid and milky, and by evening have a steady stream of pus coming from the eye.
As you can see in this illustration, sometimes the entire cornea is broken down into pus by the gonococci, leaving the iris exposed, and precluding possibility of maintaining sight in the infected eye. The unaffected eye is covered by a watch-glass here, and surrounded by an adhesive bandage, to keep any gonococci from spreading over from the infected eye. Though they can easily establish themselves and do massive damage when entrenched in the body (such as in the eyes, or the mucous membranes of the genitalia), gonorrheal bacteria are very delicate and cannot infect across the skin, unless there’a break or tear present.
Atlas of External Diseases of the Eye. Richard Greeff, 1914.
The Optic Nerve - Histology and Anatomy
Special sensory (special somatic efferent)—special sense of vision
The organization of the mammalian retina is perhaps counterintuitive. Light traverses through numerous cell layers before reaching the light sensing layer of rods and cones. The light signal received by the photosensing apparatus is turned in to electrical impulses and transmitted via a number of levels. Axons from retinal ganglion cells form the nerve itself.
The optic nerve as an anatomic structure begins at the optic disk. A smaller, disc-shaped depression, called the optic cup, lies slightly temporal to the center of the optic disk. Sheets of persistent glial tissue (developmental remnants) which produce a slightly grey filmy (gossamer) appearance may sometimes be seen over a portion or the entire surface of the disk. Moreover, a developmental remnant of the hyaloid artery—Bergmeister’s papilla—located nasal and inferior, may also be seen (micrograph below). (During fetal eye development, the hyaloid artery supplies the lens, running from the optic disk to the anterior part of the developing eye. It regresses by the time the eyelid opens.)
Nerve bundles (of unmyelinated ganglion cell axons) penetrate the collagen of the sclera through a sieve perforations, termed the lamina cribrosa. As the non-myelinated nerves pass this point the optic nerve becomes myelinated; axons are enveloped by a sheath of doubled plasmalemma, to form the myelin produced by oligodendrocytes. Myelination doubles the cross-sectional thickness of the nerve.
The arterial supply to the optic nerve anterior to the lamina cribosa is derived from the short ciliary arteries. Immediately behind the lamina cribosa vessels derived from the Circle of Zinn (#2 in the diagram below), which is itself supplied by the short ciliary arteries, enter the optic nerve. The orbital portion of the optic nerve derives its blood supply from the pial circulation (#3 below) and perhaps also to some extent from the ophthalmic artery (#1 below) and its branches, including the central retinal artery. That portion of the optic nerve lying in the optic canal derives its arterial blood supply from the ophthalmic artery, whilst the intra-cranial part of the optic nerve is supplied centripetally through the pial vessels. Venous drainage from the ocular and orbital portions of the optic nerve is chiefly into the central retinal vein.
The nerve passes posteromedially in the orbit and exits through the optic canal, entering the middle cranial fossa.The optic nerve diameter increases from about 1.6 mm within the eye to 3.5 mm in the orbit to 4.5 mm within the cranial space. The optic nerve component lengths are 1 mm in the globe, 24 mm in the orbit, 9 mm in the optic canal, and 16 mm in the cranial space before joining the optic chiasm.
Just anterosuperior to the pituitary gland, fibers from the nasal half of each retina (about 53% of the fibers) decussate in the optic chiasm and join uncrossed fibers from the temporal half of the retina to form the optic tract. In this way, information from the right half of the visual field is transmitted by the left optic tract and vice versa. Most fibers of the optic tracts terminate in the lateral geniculate nuclei of the thalamus.
From the lateral geniculate body, fibers of the optic radiation pass to the visual cortex in the occipital lobe of the brain. In more specific terms, fibers carrying information from the contralateral superior visual field traverse Meyer’s loop to terminate in the lingual gyrus below the calcarine fissure in the occipital lobe, and fibers carrying information from the contralateral inferior visual field terminate more superiorly, to the cuneus.
Fibers from the optic nerve that do not terminate in the lateral geniculate bodies project to the pretectal and suprachiasmatic nuclei. These fibers comprise the so called accessory optic system and are among the only sensory cranial nerve fibers (along with those of the olfactory nerve) that connect directly to the cortex without passing through the thalamus. The pretectal area of the midbrain is responsible for the pupillary light reflex—it projects axons to the Edinger-Westphal nuclei (the accessory parasympathetic nucleus of the oculomotor nerve). The suprachiasmatic nucleus is situated in the anterior part of the hypothalamus, just dorsal to the optic chiasm. This nucleus controls circadian rhythms.
Optic nerve disease
Developmental, vascular, glaucoma, demyelinating, toxic, tumor, drusen, trauma
- Aplasia or hypoplasia may be sporadic or familial. This may lead to a variety of visual field defects.
- Coloboma - incomplete closure of the fetal cleft - appears inferiorly. See below.
- Morning glory syndrome - rare dysplastic coloboma of the optic disk. Presumably named after the flower.
- Optic nerve pit - not related to coloboma. Rare (1 per 11,000) . Bilateral in 15% of cases. Usually positioned inferotemporal quadrant of papilla. Leads to visual field defects of various types. Cause not certain.
- Aneurysms and subarachnoid hemorrhages that impinge on the optic nerve may arise from the internal carotid or anterior branches of circle of Willis. Slow growing aneurysms may present like tumors—compression induced visual field defects and optic nerve atrophy. Aneurysms that bleed present in a similar way as subarachnoid hemorrhages from other causes (i.e. excruciating headache). Subarachnoid bleeds (see image A below) may cause bilateral optic disk swelling and optic nerve hemorrhage (see cross section below). Clinical pearl - always check to make sure that you can visually locate the limiting edge of a subconjunctival hemorrhage.
- Inflammation, ischemia or infarction (or some combination thereof) of the blood vessels supplying the optic nerve. Central retinal artery/vein thrombi or emboli, giant cell arteritis (see arterial cross section below), temporal arteritis, polyarteritis nodosa, thromboangiitis obliterans, optic disk vasculitis, syphilitic meningitis, and atherosclerotic vaso-occlusive disease (esp. of the posterior ciliary artery) are all causes of optic nerve damage. In addition, sarcoidosis, toxoplasmosis and SLE can cause vasculitis of the vessels of the retina.
Demyelination of the optic nerve
- Also known as optic neuritis—the name is misleading as it is not always the result of an inflammatory condition. Optic neuritis can be caused by some of the diseases mentioned above (i.e. syphilis, mumps, sarcoidosis, lupus, ischemic vascular diseases). But, by far, the most common cause is multiple sclerosis. Usually optic neuritis due to MS presents as an acute loss of vision which improves or stabilizes after about 10 days. Additional ocular signs include eye pain, tenderness of the globe, dyschromatopsia, decreased brightness sense, decreased color perception, a relative afferent pupillary defect and assorted other visual field defects.
- The hallmark of glaucomatous optic neuropathy is thinning and excavation of the neuroretinal rim. The neuroretinal rim is a region just within the scleral ring which contains a dense packing of nerve fibers. It can be visualized as the region where small and medium blood vessels bend and enter the optic cup. The first image below shows a normal retina and the second shows glaucomatous optic neuropathy (arrows point to splinter hemorrhages, taken from Bourne 2006).
Tumors - compressive optic neuropathy
- Slowly progressive, unilateral loss of vision. The optic nerve is most vulnerable to injury by a compressive force where it is adjacent to bone or in a confined space (eg, orbital apex, optic canal).
- Optic nerve sheath meningioma - rare, benign tumors
- Optic nerve glioma - most common primary tumor of the optic nerve. Seen in neurofibromatosis type I.
- Blunt trauma to the face can lead to sudden, severe, unilateral loss of vision. Certain portions of the optic nerve do not have Schwann cells to regenerate a damaged myelin sheath and nerve. This leads to optic atrophy which does not have any specific features at the time of examination; the disc may be edematous, hemorrhagic or pale.
— Coco Chanel
Histology of the Pancreas
The Olfactory Nerve - Anatomy and Histology
(This information is compiled from Wikipedia, Moore’s Clinically Oriented Anatomy, The NCBI Bookshelf and other sources. Please ask if you have any specific questions.)
Originating in the olfactory mucosa in the roof of the nasal cavity and along the nasal septum and medial wall of the superior concha, this special sensory (special visceral afferent) nerve terminates in the olfactory bulb, at the rostral end of the olfactory tract that attaches directly to the base of the forebrain (prosencephalon).
The above rendition (by Vesalius) shows olfactory bulbs (colored red) resting along the orbital surfaces of the frontal lobes of the cerebral hemispheres.
The olfactory epithelia house the cell bodies of neurosensory cells (also known as primary olfactory neurons or olfactory cells). The olfactory epithelium occupies about 2.5 cm2 of area at the apex of each nostril. This patch of yellowish brown mucosa is located in a small cavity off the main nasal passage. For this reason, “sniffing” provides more rapid stimulation than normal breathing. Within the lamina propria, below the olfactory epithelium, lie Bowman’s glands. These structures secrete mucus and IgA.
The central processes of the bipolar olfactory neurosensory cells form about 20 bundles of olfactory nerve fibers that together form the olfactory nerve. The arrowhead below points to the cell body of a bipolar cell.
Olfactory epithelium is a primitive type of sensory epithelium, lending support to the concept that olfaction is phylogenetically the oldest of the senses. The cell is both a receptor and a bipolar first-order neuron. A single dendrite projects from the apical pole of the cell to the surface of the epithelium. This dendrite ends in an apical dendritic knob (olfactory knob). Each knob gives rise to 5 to 20 long delicate nonmotile cilia, which extend into the mucus covering the sensory epithelium.
The olfactory neuron, unlike most other neurons, has a life span of only 30 to 40 days. New neurons differentiate from stem cells in the deepest or basal region of the olfactory epithelium. The basal pole of the neuron gives rise to a single unmyelinated axon. The axons form bundles, sheathed in Schwann cells, that traverse rostrally through the cribriform plate of the ethmoid bone, pierce the dura/arachnoid, and synapse in the olfactory bulb in the anterior cranial fossa.
The olfactory nerve fibers synapse with mitral cells (“mitral” comes from mitre meaning “bishop’s tall hat,” late 14c., from O.Fr.) in the olfactory bulb. The axons of these mitral cells form the olfactory tract. Each olfactory tract splits in to lateral and medial olfactory striae (distinct fiber bands).
The detection threshold for odorants is quite low: 10−13 to 10−4 molecules in air. Studies suggest that the volume concentration of receptor molecules in the mucus is in the range of 10−5 M. Each olfactory neuron has about 106 receptor molecules on its cilia. Odors penetrate the mucus overlying the sensory epithelium and gain access to the receptors by virtue of their partition and diffusion coefficients in the olfactory mucus. An odorant traverses the mucus in the range of a few dozen milliseconds, and forms a complex with the receptor in about the same time span. The odorant molecule combines with integral membrane proteins that form the receptor. The proteins and odorant-gated channels that mediate sensory transduction are located in the membranes of the olfactory cilia and the apical dendritic olfactory knob. Voltage-gated channels, located in the initial axonal segment and the axolemma, are associated with impulse initiation and propagation. The second messenger system is probably a G protein-adenylate cyclase cascade.
The olfactory nerve/tract has the shortest course of any cranial nerve. (Which has the longest?) Also peculiar to the olfactory nerve is that it is one of only two cranial nerves (the other being fibers from the optic nerve) which does not synapse in the brainstem but rather connects directly to the cortex. The lateral stria terminates in the piriform cortex—a highly evolutionarily conserved region from mammals to amphibians—while the medial olfactory stria projects through the anterior commissure to contralateral olfactory structures. There are also direct projections to the amygdaloid nucleus and to the anterior perforated substance. In addition, there are secondary and tertiary connections to the limbic system.
Clinical Significance -
Hyperosmia, or lowered threshold for odors, occurs with Addison’s disease and mucoviscidosis. Clinical perception of hyperosmia is ordinarily just about impossible either by history taking or by bedside testing.
Hypoosmia is usually caused by local processes that involve both the nasal and olfactory mucosa. Examples include rhinitis due to the common cold or allergy, smoking, certain industrial fumes, and intranasal polyps or carcinoma. Pernicious anemia, diabetes, and vitamin A deficiency cause diminished olfactory acuity. Pernicious anemia can also cause anosmia. Hypoosmia can occur after total laryngectomy. The reasons are not known.
Anosmia may be bilateral or unilateral. The patient can recognize bilateral anosmia, but unilateral anosmia is usually not perceived.
- Traumatic - head trauma is probably the most frequent cause, with an incidence of 7.5% in one large series. Blows to the occiput are five times more likely to produce anosmia than blows to the forehead because of the contrecoup effect. The injury can be so trivial as to go almost unnoticed.
- Neoplastic - tumors of the floor of the anterior fossa, such as meningiomas of the sphenoid ridge or olfactory groove, can produce anosmia, which is usually unilateral.
- Infectious - meningitis or abscess associated with osteomyelitis of the frontal or ethmoid bones can produce anosmia.
- Congenital absence of smell is present in albinos. (Interesting!)
- Vascular - Subarachnoid hemorrhage can cause anosmia.
- Psychiatric - hysteria is another cause for anosmia. Hysteria can be identified by comparing perception for coffee or vanilla with ammonia perception. Coffee and vanilla principally stimulate the olfactory cell receptors. Ammonia is a trigeminal nerve stimulator. In anosmia of organic cause the ammonia can be detected but the coffee or vanilla odor cannot.
Smell and Mate Preference - nanoreview by me
In 1976 Yamazaki et al published a seminal study showing that mice prefer to mate with partners that have dissimilar major histocompatibility (MHC) haplotypes. The evolutionary implications are fascinating. As Santos et al puts it,
It has been suggested, therefore, that animals use body odor as a guide to identify possible mates as MHC-similar or MHC-dissimilar from their own genotype. Preference for a MHC-dissimilar partner enhances MHC heterozygosity of an individual’s offspring. The possible adaptive advantages are clear: it is a mechanism of avoiding inbreeding and MHC-heterozygous offspring may have enhanced immunocompetence.
Numerous studies since 1976 have aimed to see if the same trend exists in Homo sapiens as it does in Mus musculus. Indeed, there is mounting evidence that mate choice in humans is influenced by “pheromones.” There is also genetic evidence showing that MHC and olfactory neuron receptor genes are linked, but the significance of this evidence is still not clear.
In the above Santos study, men and women were instructed to smell the sweat and urine of members of the opposite sex and rate whether or not they found the odors pleasing. Only one trend emerged: women find the sweat of a man who is MHC-dissimilar to have “pleasant” smelling sweat. Besides invoking the downright revolting image of smelling another person’s urine, this study suggests that there are perhaps evolutionary mechanisms in place that determine who we mate with—mechanisms which are out of our control. Fascinating.
Anatomy 101: Muscles - Upper Neck and Face
As humans, a huge amount of our communication is non-verbal, and subconscious queues given by facial movements can say as much as any exclamation.
Almost all muscle on the head and neck is considered skeletal (voluntary) muscle, and the muscles that control the finest expressions originate from the facial bones, and insert on the skin. Aside from the chewing muscles, there are few that both insert and originate on bone.
Like skeletal muscles in the rest of the body, the muscles of the face sometimes have an antagonistic partner - that is, a muscle that performs the opposite action. Since muscles cannot perform a pushing action, the antagonist is needed to pull its partner back into place. One of the more obvious examples of this is the biceps brachii and the triceps brachii - if you had one without the other, the arm would only be able to move in one direction! Unlike the rest of the body, however, the muscles of the head and neck do not control limbs or need to push body parts, and don’t always need one or more antagonists.
Some of the significant facial muscles include:
- Frontalis and corrugator: Control the forehead and eyebrows, respectively. When they’re used repeatedly, furrows in the brow develop. The corrugator muscle is generally where people getting Botox of the eyebrow have injections.
- Obicularis oculi and obicularis oris: Circular muscles that work to “purse” the eyelids and lips, respectively.
- Temporalis; masseter; and medial and lateral pterygoid: Muscles that are primary in chewing. The temporalis comes from the temple and elevates and retracts the jaw. The masseter and medial pterygoid also work to elevate and retract the jaw, and the lateral pterygoid depresses, opens, and protrudes the mandible, as well as moving it laterally.
- Buccinator: Draws the lips wide and tight, and keeps food in contact with the teeth.
- Levator labii: Raises the upper lip.
- Depressor labii: Lowers the lower lips.
- Risoris: Draws the lips into a smile (by the way, the whole “13 muscles required to smile/56 required to frown” is nonsense).
— Voltaire to Casanova from J. Rives Childs (1988) “Casanova: A New Perspective” Paragon House.
— Giacomo Casanova to François-Marie Voltaire from J. Rives Childs (1988) “Casanova: A New Perspective” Paragon House.