Neurotransmitters are endogenous chemicals that enable neurotransmission. It is a type of chemical messenger which transmits signals across a chemical synapse, such as a neuromuscular junction, from one neuron to another "target" neuron, muscle cell, or gland cell. Neurotransmitters are released from synaptic vesicles in synapses into the synaptic cleft, where they are received by neurotransmitter receptors on the target cells. Many neurotransmitters are synthesized from simple and plentiful precursors such as amino acids, which are available from the diet and only require a small number of biosynthetic steps for conversion. Neurotransmitters play a major role in shaping everyday life and functions, their exact numbers are unknown, but more than 200 chemical messengers have been uniquely identified. Neurotransmitters are stored in synaptic vesicles, clustered close to the cell membrane at the axon terminal of the presynaptic neuron. Neurotransmitters are released into and diffuse across the synaptic cleft, where they bind to specific receptors on the membrane of the postsynaptic neuron.
Most neurotransmitters are about the size of a single amino acid. A released neurotransmitter is available in the synaptic cleft for a short time before it is metabolized by enzymes, pulled back into the presynaptic neuron through reuptake, or bound to a postsynaptic receptor. Short-term exposure of the receptor to a neurotransmitter is sufficient for causing a postsynaptic response by way of synaptic transmission. In response to a threshold action potential or graded electrical potential, a neurotransmitter is released at the presynaptic terminal. Low level "baseline" release occurs without electrical stimulation; the released neurotransmitter may move across the synapse to be detected by and bind with receptors in the postsynaptic neuron. Binding of neurotransmitters may influence the postsynaptic neuron in either an inhibitory or excitatory way; this neuron may be connected to many more neurons, if the total of excitatory influences are greater than those of inhibitory influences, the neuron will "fire".
It will create a new action potential at its axon hillock to release neurotransmitters and pass on the information to yet another neighboring neuron. Until the early 20th century, scientists assumed that the majority of synaptic communication in the brain was electrical. However, through the careful histological examinations by Ramón y Cajal, a 20 to 40 nm gap between neurons, known today as the synaptic cleft, was discovered; the presence of such a gap suggested communication via chemical messengers traversing the synaptic cleft, in 1921 German pharmacologist Otto Loewi confirmed that neurons can communicate by releasing chemicals. Through a series of experiments involving the vagus nerves of frogs, Loewi was able to manually slow the heart rate of frogs by controlling the amount of saline solution present around the vagus nerve. Upon completion of this experiment, Loewi asserted that sympathetic regulation of cardiac function can be mediated through changes in chemical concentrations. Furthermore, Otto Loewi is credited with discovering acetylcholine —the first known neurotransmitter.
Some neurons do, communicate via electrical synapses through the use of gap junctions, which allow specific ions to pass directly from one cell to another. There are four main criteria for identifying neurotransmitters: The chemical must be synthesized in the neuron or otherwise be present in it; when the neuron is active, the chemical must produce a response in some target. The same response must be obtained. A mechanism must exist for removing the chemical from its site of activation. However, given advances in pharmacology and chemical neuroanatomy, the term "neurotransmitter" can be applied to chemicals that: Carry messages between neurons via influence on the postsynaptic membrane. Have little or no effect on membrane voltage, but have a common carrying function such as changing the structure of the synapse. Communicate by sending reverse-direction messages that affect the release or reuptake of transmitters; the anatomical localization of neurotransmitters is determined using immunocytochemical techniques, which identify the location of either the transmitter substances themselves, or of the enzymes that are involved in their synthesis.
Immunocytochemical techniques have revealed that many transmitters the neuropeptides, are co-localized, that is, one neuron may release more than one transmitter from its synaptic terminal. Various techniques and experiments such as staining and collecting can be used to identify neurotransmitters throughout the central nervous system. There are many different ways. Dividing them into amino acids and monoamines is sufficient for some classification purposes. Major neurotransmitters: Amino acids: glutamate, aspartate, D-serine, γ-aminobutyric acid, glycine Gasotransmitters: nitric oxide, carbon monoxide, hydrogen sulfide Monoamines: dopamine, epinephrine, serotonin Trace amines: phenethylamine, N-methylphenethylamine, tyramine, 3-iodothyronamine, tryptamine, etc. Peptides: oxytocin, substance P, cocaine and amphetamine regulated transcript, opioid peptides Purines: adenosine triphosphate, adenosine Catecholamines: dopamine, epinephrine Others: acetylcholine, etc. In addition, over 50 neuroactive pepti
Wound healing is a complex process in which the skin, the tissues under it, repair themselves after injury. In this article, wound healing is depicted in a discrete timeline of physical attributes constituting the post-trauma repairing process. In undamaged skin, the epidermis and dermis form a protective barrier against the external environment; when the barrier is broken, a regulated sequence of biochemical events is set into motion to repair the damage. This process is divided into predictable phases: blood clotting, tissue growth, tissue remodeling. Blood clotting may be considered to be part of the inflammation stage instead of a separate stage; the wound healing process is not only complex but fragile, it is susceptible to interruption or failure leading to the formation of non-healing chronic wounds. Factors that contribute to non-healing chronic wounds are diabetes, venous or arterial disease and metabolic deficiencies of old age. Wound care encourages and speeds wound healing via cleaning and protection from reinjury or infection.
Depending on each patient's needs, it can range from the simplest first aid to entire nursing specialties such as wound and continence nursing and burn center care. Hemostasis: Within the first few minutes of injury, platelets in the blood begin to stick to the injured site; this activates the platelets. They change into an amorphous shape, more suitable for clotting, they release chemical signals to promote clotting; this results in the activation of fibrin, which forms a mesh and acts as "glue" to bind platelets to each other. This makes a clot that serves to plug the break in the blood vessel, slowing/preventing further bleeding. Inflammation: During this phase and dead cells are cleared out, along with bacteria and other pathogens or debris; this happens through the process of phagocytosis, where white blood cells "eat" debris by engulfing it. Platelet-derived growth factors are released into the wound that cause the migration and division of cells during the proliferative phase. Proliferation: In this phase, collagen deposition, granulation tissue formation, epithelialization, wound contraction occur.
In angiogenesis, vascular endothelial cells form new blood vessels. In fibroplasia and granulation tissue formation, fibroblasts grow and form a new, provisional extracellular matrix by excreting collagen and fibronectin. Concurrently, re-epithelialization of the epidermis occurs, in which epithelial cells proliferate and'crawl' atop the wound bed, providing cover for the new tissue. In wound contraction, myofibroblasts decrease the size of the wound by gripping the wound edges and contracting using a mechanism that resembles that in smooth muscle cells; when the cells' roles are close to complete, unneeded cells undergo apoptosis. Maturation: During maturation and remodeling, collagen is realigned along tension lines, cells that are no longer needed are removed by programmed cell death, or apoptosis. Timing is important to wound healing. Critically, the timing of wound reepithelialization can decide the outcome of the healing. If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months.
Wound healing is classically divided into hemostasis, inflammation and remodeling. Although a useful construct, this model employs considerable overlapping among individual phases. A complementary model has been described where the many elements of wound healing are more delineated; the importance of this new model becomes more apparent through its utility in the fields of regenerative medicine and tissue engineering. In this construct, the process of wound healing is divided into two major phases: the early phase and the cellular phase:The early phase, which begins following skin injury, involves cascading molecular and cellular events leading to hemostasis and formation of an early, makeshift extracellular matrix that provides structural staging for cellular attachment and subsequent cellular proliferation; the cellular phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, restore the epithelial layer. Subdivisions of the cellular phase are: Macrophages and inflammatory components, Epithelial-mesenchymal interaction: re-epithelialization and myofibroblasts: progressive alignment, collagen production, matrix contraction, Endothelial cells and angiogenesis, Dermal matrix: elements of fabrication and alteration/remodeling.
Just before the inflammatory phase is initiated, the clotting cascade occurs in order to achieve hemostasis, or stop blood loss by way of a fibrin clot. Thereafter, various soluble factors are released to attract cells that phagocytise debris and damaged tissue, in addition to releasing signaling molecules that initiate the proliferative phase of wound healing; when tissue is first wounded, blood comes in contact with collagen, triggering blood platelets to begin secreting inflammatory factors. Platelets express sticky glycoproteins on their cell membranes that allow them to aggregate, forming a mass. Fibrin and fibronectin cross-link together and form a plug that traps proteins and
The black mamba is a species of venomous snake, a member of the family Elapidae native to parts of Sub-Saharan Africa. First formally described by Albert Günther in 1864, it is the second-longest venomous snake after the king cobra. Specimens of 4.3 to 4.5 m have been reported. Its skin colour varies from grey to dark brown. Juvenile black mambas tend to be paler than adults and darken with age; the species is both arboreal. It is known to prey on birds and small mammals. Over suitable surfaces, it can move at speeds up to 16 km/h for short distances. Adult black mambas have few natural predators. In a threat display, the black mamba opens its inky-black mouth, spreads its narrow neck-flap and sometimes hisses, it is capable of striking at considerable range and may deliver a series of bites in rapid succession. Its venom is composed of neurotoxins that induce symptoms within ten minutes, is fatal unless antivenom is administered. Despite its reputation as a formidable and aggressive species, the black mamba only attacks humans if it is threatened or cornered.
It is rated as least concern on the International Union for Conservation of Nature's Red List of Threatened Species. The first formal description of the black mamba was made in 1864 by German-born British zoologist Albert Günther. A single specimen was one of many species of snake collected by John Kirk, a naturalist who accompanied David Livingstone on the 1858–1864 Second Zambesi expedition; this specimen is housed in the Natural History Museum, London. The generic name of the species is derived from the Ancient Greek words dendron, "tree", aspis "asp", the specific epithet polylepis is derived from the Ancient Greek poly meaning "many" and lepis meaning "scale"; the term "mamba" is derived from the Zulu word "imamba". In Tanzania, a local Ngindo name is ndemalunyayo because it clips grass. In 1873, German naturalist Wilhelm Peters described Dendraspis Antinorii from a specimen in the museum of Genoa, collected by Italian explorer Orazio Antinori in what is now northern Eritrea; this is no longer held to be distinct.
In 1896, Belgian-British zoologist George Albert Boulenger combined the species Dendroaspis polylepis as a whole with the eastern green mamba, a lumping diagnosis that remained in force until 1946 when South African herpetologist Vivian FitzSimons again split them into separate species. A 2016 genetic analysis showed the black and eastern green mambas are each others' closest relatives, are more distantly related to Jameson's mamba; the black mamba is a long, cylindrical snake. It has a "coffin-shaped" head with a medium-sized eye; the adult snake's length ranges from 2 to 3 m but specimens have grown to lengths of 4.3 to 4.5 m. It is the second-longest venomous snake species, exceeded in length only by the king cobra; the black mamba is a proteroglyphous snake, with fangs up to 6.5 mm in length, located at the front of the maxilla. The tail of the species is thin, the caudal vertebrae making up 17 -- 25 % of its body length. Black mambas weigh about 1.6 kg on average. Specimens vary in colour, including olive, yellowish-brown and gunmetal but are black.
The scales of some individuals may have a purplish glow. Individuals display dark mottling towards the posterior, which may appear in the form of diagonal crossbands. Black mambas have greyish-white underbellies and the inside of the mouth is dark bluish-grey to nearly black. Mamba eyes range between greyish-brown and shades of black. Juvenile snakes are lighter in colour than adults; the number and pattern of scales on a snake's body are a key element of identification to species level. The arrangement of scales of the black mamba's head and tail are as follows: The black mamba inhabits a wide range in Sub-Saharan Africa; the black mamba's distribution in parts of West Africa has been disputed. In 1954 the black mamba was recorded in the Dakar region of Senegal; this observation, a subsequent observation that identified a second specimen in the region in 1956, has not been confirmed and thus the snake's distribution in this area is inconclusive. The species prefers moderately dry environments such as light woodland and scrub, rocky outcrops and semi-arid savanna.
It inhabits moist savanna and lowland forests. It is not found at altitudes above 1,000 m, although its distribution does include locations at 1,800 m in Kenya and 1,650 m in Zambia, it is rated as a species of least concern on the International Union for Conservation of Nature's Red List of Endangered species, based on its huge range across sub-Saharan Africa and no documented decline. The black mamba is both arboreal. On the ground, it moves with its head and neck raised, uses termite mounds, abandoned burro
A contact lens, or contact, is a thin lens placed directly on the surface of the eye. Contact lenses are considered medical devices and can be worn to correct vision, or for cosmetic or therapeutic reasons. In 2004, it was estimated that 125 million people worldwide use contact lenses, including 28 to 38 million in the United States. In 2010, the worldwide market for contact lenses was estimated at $6.1 billion, while the US soft lens market was estimated at $2.1 billion. Multiple analysts estimated that the global market for contact lenses would reach $11.7 billion by 2015. As of 2010, the average age of contact lens wearers globally was 31 years old, two-thirds of wearers were female. People choose to wear contact lenses for many reasons. Aesthetics and cosmetics are the main motivating factors for people who want to avoid wearing glasses or to change the appearance of their eyes. Others wear contact lenses for optical reasons; when compared with spectacles, contact lenses provide better peripheral vision, do not collect moisture or perspiration.
This can make them preferable for other outdoor activities. Contact lens wearers can wear sunglasses, goggles, or other eyewear of their choice without having to fit them with prescription lenses or worry about compatibility with glasses. Additionally, there are conditions such as keratoconus and aniseikonia that are corrected better with contact lenses than with glasses. Leonardo da Vinci is credited with introducing the idea of contact lenses in his 1508 Codex of the eye, Manual D, wherein he described a method of directly altering corneal power by either submerging the head in a bowl of water or wearing a water-filled glass hemisphere over the eye. Neither idea was implementable in da Vinci's time, he did not suggest his idea be used for correcting vision, as he was more interested in learning about the mechanisms of accommodation of the eye. Descartes proposed another idea in 1636—a glass tube filled with liquid placed in direct contact with the cornea; the protruding end was to be composed of clear glass, shaped to correct vision.
In 1801, Thomas Young made a pair of basic contact lenses based on Descartes' model. He used wax to affix water-filled lenses to his eyes, he corrected for it with another pair of lenses. However, like da Vinci's, Young's device was not intended to correct refraction errors. Sir John Herschel, in a footnote of the 1845 edition of the Encyclopedia Metropolitana, posed two ideas for the visual correction: the first "a spherical capsule of glass filled with animal jelly", "a mould of the cornea" that could be impressed on "some sort of transparent medium". Though Herschel never tested these ideas, they were both advanced by several independent inventors such as Hungarian Dallos with István Komáromy, who perfected a method of making molds from living eyes; this enabled the manufacture of lenses that, for the first time, conformed to the actual shape of the eye. In 1888, German ophthalmologist Adolf Gaston Eugen Fick constructed and fitted the first successful contact lens. While working in Zürich, he described fabricating afocal scleral contact shells, which rested on the less sensitive rim of tissue around the cornea, experimentally fitting them.
These lenses were 18 -- 21 mm in diameter. Fick filled the empty space between glass with a dextrose solution, he published his work, "Contactbrille", in the journal Archiv für Augenheilkunde in March 1888. Fick's lens was large and unwieldy, could be worn only for a couple of hours at a time. August Müller in Kiel, corrected his own severe myopia with a more convenient blown-glass scleral contact lens of his own manufacture in 1888. In 1887, Louis J. Girard invented a similar scleral form of contact lens. Blown-glass scleral lenses remained the only form of contact lens until the 1930s when Perspex/Plexiglas was developed, allowing plastic scleral lenses to be manufactured for the first time. In 1936, optometrist William Feinbloom introduced plastic in lenses, making them lighter and more convenient; these lenses were a combination of plastic. In 1939, Hungarian optometrist Dr István Györffy produced first plastic lenses. In 1940, German optometrist Heinrich Wöhlk produced plastic lenses too, based on experiments performed during the 1930s.
In 1949, the first "corneal" lenses were developed. These were much smaller than the original scleral lenses, as they sat only on the cornea rather than across all of the visible ocular surface, could be worn up to sixteen hours a day. Polymethyl methacrylate corneal lenses became the first contact lenses to have mass appeal through the 1960s, as lens designs became more sophisticated with improving manufacturing technology. On Oct. 18, 1964, in a television studio in Washington, D. C, Lyndon Baines Johnson became the first President in the history of these United States to appear in public wearing contact lenses, under the supervision of Dr. Alan Isen, who developed the first commercially viable soft-contact lenses in the United states. Early corneal lenses of the 1950s and'60s were expensive and fragile, resulting in the development of a market for contact lens insurance. Replacement Lens Insurance, Inc. phased out its original flagship product in 1994 after contact lenses became more affordable and easier to replace.
One major disadvantage of PMMA lenses is that they allow no oxygen to get through to the conjunctiva and cornea, causing
Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, is a protective response involving immune cells, blood vessels, molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, initiate tissue repair; the five classical signs of inflammation are heat, redness and loss of function. Inflammation is a generic response, therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, specific for each pathogen. Too little inflammation could lead to progressive tissue destruction by the harmful stimulus and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, atherosclerosis, rheumatoid arthritis, cancer. Inflammation is therefore closely regulated by the body. Inflammation can be classified as either chronic.
Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, is characterized by simultaneous destruction and healing of the tissue from the inflammatory process. Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the body's inflammatory response—the two components are considered together when discussing an infection, the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the body's immunovascular response, whatever the cause may be.
But because of how the two are correlated, words ending in the suffix -itis are sometimes informally described as referring to infection. For example, the word urethritis means only "urethral inflammation", but clinical health care providers discuss urethritis as a urethral infection because urethral microbial invasion is the most common cause of urethritis, it is useful to differentiate inflammation and infection because there are typical situations in pathology and medical diagnosis where inflammation is not driven by microbial invasion – for example, trauma and autoimmune diseases including type III hypersensitivity. Conversely, there is pathology where microbial invasion does not cause the classic inflammatory response – for example, parasitosis or eosinophilia. Acute inflammation is a short-term process appearing within a few minutes or hours and begins to cease upon the removal of the injurious stimulus, it involves a coordinated and systemic mobilization response locally of various immune and neurological mediators of acute inflammation.
In a normal healthy response, it becomes activated, clears the pathogen and begins a repair process and ceases. It is characterized by five cardinal signs:An acronym that may be used to remember the key symptoms is "PRISH", for pain, immobility and heat; the traditional names for signs of inflammation come from Latin: Dolor Calor Rubor Tumor Functio laesa The first four were described by Celsus, while loss of function was added by Galen. However, the addition of this fifth sign has been ascribed to Thomas Sydenham and Virchow. Redness and heat are due to increased blood flow at body core temperature to the inflamed site. Loss of function has multiple causes. Acute inflammation of the lung does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings; the process of acute inflammation is initiated by resident immune cells present in the involved tissue resident macrophages, dendritic cells, Kupffer cells and mast cells. These cells possess surface receptors known as pattern recognition receptors, which recognize two subclasses of molecules: pathogen-associated molecular patterns and damage-associated molecular patterns.
PAMPs are compounds that are associated with various pathogens, but which are distinguishable from host molecules. DAMPs are compounds that are associated with host-related cell damage. At the onset of an infection, burn, or other injuries, these cells undergo activation and release inflammatory mediators responsible for the clinical signs of inflammation. Vasodilation and its resulting increased blood flow causes increased heat. Increased permeability of the blood vessels results in an exudation of plasma proteins and fluid into the tissue, which manifests itself as swelling; some of the released mediators such as bradykinin increase the sensitivity to pain. The mediator molecules alter the blood vessels to
A nerve is an enclosed, cable-like bundle of nerve fibres called axons, in the peripheral nervous system. A nerve provides a common pathway for the electrochemical nerve impulses called action potentials that are transmitted along each of the axons to peripheral organs or, in the case of sensory nerves, from the periphery back to the central nervous system; each axon within the nerve is an extension of an individual neuron, along with other supportive cells such as Schwann cells that coat the axons in myelin. Within a nerve, each axon is surrounded by a layer of connective tissue called the endoneurium; the axons are bundled together into groups called fascicles, each fascicle is wrapped in a layer of connective tissue called the perineurium. The entire nerve is wrapped in a layer of connective tissue called the epineurium. In the central nervous system, the analogous structures are known as tracts; each nerve is covered on the outside by a dense sheath of the epineurium. Beneath this is a layer of flat cells, the perineurium, which forms a complete sleeve around a bundle of axons.
Perineurial septae subdivide it into several bundles of fibres. Surrounding each such fibre is the endoneurium; this forms an unbroken tube from the surface of the spinal cord to the level where the axon synapses with its muscle fibres, or ends in sensory receptors. The endoneurium consists of an inner sleeve of material called the glycocalyx and an outer, meshwork of collagen fibres. Nerves are bundled and travel along with blood vessels, since the neurons of a nerve have high energy requirements. Within the endoneurium, the individual nerve fibres are surrounded by a low-protein liquid called endoneurial fluid; this acts in a similar way to the cerebrospinal fluid in the central nervous system and constitutes a blood-nerve barrier similar to the blood-brain barrier. Molecules are thereby prevented from crossing the blood into the endoneurial fluid. During the development of nerve edema from nerve irritation, the amount of endoneurial fluid may increase at the site of irritation; this increase in fluid can be visualized using magnetic resonance neurography, thus MR neurography can identify nerve irritation and/or injury.
Nerves are categorized into three groups based on the direction that signals are conducted: Afferent nerves conduct signals from sensory neurons to the central nervous system, for example from the mechanoreceptors in skin. Efferent nerves conduct signals from the central nervous system along motor neurons to their target muscles and glands. Mixed nerves contain both afferent and efferent axons, thus conduct both incoming sensory information and outgoing muscle commands in the same bundle. Nerves can be categorized into two groups based on where they connect to the central nervous system: Spinal nerves innervate much of the body, connect through the vertebral column to the spinal cord and thus to the central nervous system, they are given letter-number designations according to the vertebra through which they connect to the spinal column. Cranial nerves innervate parts of the head, connect directly to the brain, they are assigned Roman numerals from 1 to 12, although cranial nerve zero is sometimes included.
In addition, cranial nerves have descriptive names. Specific terms are used to describe their actions. A nerve that supplies information to the brain from an area of the body, or controls an action of the body is said to "innervate" that section of the body or organ. Other terms relate to whether the nerve affects the same side or opposite side of the body, to the part of the brain that supplies it. Nerve growth ends in adolescence, but can be re-stimulated with a molecular mechanism known as "Notch signaling". If the axons of a neuron are damaged, as long as the cell body of the neuron is not damaged, the axons would regenerate and remake the synaptic connections with neurons with the help of guidepost cells; this is referred to as neuroregeneration. The nerve begins the process by destroying the nerve distal to the site of injury allowing Schwann cells, basal lamina, the neurilemma near the injury to begin producing a regeneration tube. Nerve growth factors are produced causing many nerve sprouts to bud.
When one of the growth processes finds the regeneration tube, it begins to grow towards its original destination guided the entire time by the regeneration tube. Nerve regeneration is slow and can take up to several months to complete. While this process does repair some nerves, there will still be some functional deficit as the repairs are not perfect. A nerve conveys information in the form of electrochemical impulses carried by the individual neurons that make up the nerve; these impulses are fast, with some myelinated neurons conducting at speeds up to 120 m/s. The impulses travel from one neuron to another by crossing a synapse, the message is converted from electrical to chemical and back to electrical. Nerves can be categorized into two groups based on function: An afferent nerve fiber conducts sensory information from a sensory neuron to the central nervous system, where the information is processed. Bundles of fibres or axons, in the peripheral nervous system are called nerves, bundles of afferent fibers are known as sensory nerves.
An efferent nerve fiber conducts signals from a motor neuron in the central nervous system to muscles. Bundles of these fibres are known as efferent nerves; the nervous system is the part of an animal that coordinates its actions by transmitting signals to and from different parts of its body. In vertebrates it consists of two main par
Levator palpebrae superioris muscle
The levator palpebrae superioris is the muscle in the orbit that elevates the superior eyelid. The levator palpebrae superioris originates on the lesser wing of the sphenoid bone, just above the optic foramen, it decreases in thickness and becomes the levator aponeurosis. This portion inserts on the skin of the upper eyelid, as well as the superior tarsal plate, it is a skeletal muscle. The superior tarsal muscle, a smooth muscle, is attached to the levator palpebrae superioris, inserts on the superior tarsal plate as well; as with most of the muscles of the orbit, the levator palpebrae receives somatic motor input from the ipsilateral superior division of the oculomotor nerve. An adjoining smooth muscle, the superior tarsal muscle, confused to be a portion of the levator palpebrae superioris, is only attached, it is separately innervated by sympathetic fibers that originate in the cervical spinal cord; the levator palpebrae superioris muscle retracts the upper eyelid. Damage to this muscle or its innervation can cause ptosis, drooping of the eyelid.
Lesions in CN III can cause ptosis, because without stimulation from the oculomotor nerve the levator palpebrae cannot oppose the force of gravity, the eyelid droops. Ptosis can result from damage to the adjoining superior tarsal muscle or its sympathetic innervation; such damage to the sympathetic supply presents as a partial ptosis. It is important to distinguish between these two different causes of ptosis; this can be done clinically without issue, as each type of ptosis is accompanied by other distinct clinical findings. Blepharospasm Ptosis Superior tarsal muscle Anatomy figure: 29:01-01 at Human Anatomy Online, SUNY Downstate Medical Center lesson3 at The Anatomy Lesson by Wesley Norman