Is there pain receptors in the eye ball?


The eyeball itself does not contain pain receptors; however, many of the nerves and fibers surrounding the eyeball do.

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The optic nerve, also known as cranial nerve II, transmits visual information from the retina to the brain. Derived from the embryonic retinal ganglion cell, a diverticulum located in the diencephalon, the optic nerve does not regenerate after transection. The optic nerve is the second of twelve paired cranial nerves but is considered to be part of the central nervous system, as it is derived from an outpouching of the diencephalon during embryonic development. As a consequence, the fibers are covered with myelin produced by oligodendrocytes, rather than Schwann cells, which are found in the peripheral nervous system, and are encased within the meninges. Peripheral neuropathies like Guillain-Barré syndrome do not affect the optic nerve. The optic nerve is ensheathed in all three meningeal layers (dura, arachnoid, and pia mater) rather than the epineurium, perineurium, and endoneurium found in peripheral nerves. Fiber tracks of the mammalian central nervous system (as opposed to the peripheral nervous system) are incapable of regeneration, and, hence, optic nerve damage produces irreversible blindness. The fibres from the retina run along the optic nerve to nine primary visual nuclei in the brain, from which a major relay inputs into the primary visual cortex. The optic nerve is composed of retinal ganglion cell axons and support cells. It leaves the orbit (eye socket) via the optic canal, running postero-medially towards the optic chiasm, where there is a partial decussation (crossing) of fibres from the temporal visual fields (the nasal hemi-retina) of both eyes. The proportion of decussating fibers varies between species, and is correlated with the degree of binocular vision enjoyed by a species. Most of the axons of the optic nerve terminate in the lateral geniculate nucleus from where information is relayed to the visual cortex, while other axons terminate in the pretectal nucleus and are involved in reflexive eye movements. Other axons terminate in the suprachiasmatic nucleus and are involved in regulating the sleep-wake cycle. Its 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. There, partial decussation occurs, and about 53% of the fibers cross to form the optic tracts. Most of these fibres terminate in the lateral geniculate body.][ 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. The eye's blind spot is a result of the absence of photoreceptors in the area of the retina where the optic nerve leaves the eye. Each human optic nerve contains between 770,000 and 1.7 million nerve fibers, which are axons of the retinal ganglion cells of one retina. In the fovea, which has high acuity, these ganglion cells connect to as few as 5 photoreceptor cells; in other areas of retina, they connect to many thousand photoreceptors. SSA, special somatic afferent, vision Damage to the optic nerve typically causes permanent and potentially severe loss of vision, as well as an abnormal pupillary reflex, which is diagnostically important. The type of visual field loss will depend on which portions of the optic nerve were damaged. In general: Injury to the optic nerve can be the result of congenital or inheritable problems like Leber's Hereditary Optic Neuropathy, glaucoma, trauma, toxicity, inflammation, ischemia, infection (very rarely), or compression from tumors or aneurysms. By far, the three most common injuries to the optic nerve are from glaucoma, optic neuritis (especially in those younger than 50 years of age), and anterior ischemic optic neuropathy (usually in those older than 50). Glaucoma is a group of diseases involving loss of retinal ganglion cells causing optic neuropathy in a pattern of peripheral vision loss, initially sparing central vision. Optic neuritis is inflammation of the optic nerve. It is associated with a number of diseases, the most notable one being multiple sclerosis. Anterior Ischemic Optic Neuropathy is a particular type of infarct that affects patients with an anatomical predisposition and cardiovascular risk factors. Optic nerve hypoplasia is the underdevelopment of the optic nerve causing little to no vision in the affected eye. Ophthalmologists and optometrists can detect and diagnose some optic nerve diseases but, those sub-specialists that are neuro-ophthalmologists, are often best suited to diagnose and treat diseases of the optic nerve. The International Foundation for Optic Nerve Diseases (IFOND) sponsors research and information on a variety of optic nerve disorders and may provide general direction. MRI scan of human eye showing optic nerve. The ophthalmic artery and its branches. (optic nerve is yellow) Dura mater and its processes exposed by removing part of the right half of the skull, and the brain. Tentorium cerebelli from above. Superficial dissection of brain-stem. Lateral view. Dissection of brain-stem. Lateral view. Mesal aspect of a brain sectioned in the median sagittal plane. Scheme showing central connections of the optic nerves and optic tracts. Optic nerve Optic nerve The fornix and corpus callosum from below. Nerves of the orbit. Seen from above. Nerves of the orbit, and the ciliary ganglion. Side view. The arteries of the choroid and iris. The greater part of the sclera has been removed. The veins of the choroid. The terminal portion of the optic nerve and its entrance into the eyeball, in horizontal section. Human brain dura mater (reflections) Optic nerve Optic nerve Optic nerve Optic nerve Optic nerve Structures of the eye labeled This image shows another labeled view of the structures of the eye Extrinsic eye muscle. Nerves of orbita. Deep dissection. Extrinsic eye muscle. Nerves of orbita. Deep dissection. Extrinsic eye muscle. Nerves of orbita. Deep dissection. Extrinsic eye muscle. Nerves of orbita. Deep dissection. Extrinsic eye muscle. Nerves of orbita. Deep dissection. Extrinsic eye muscle. Nerves of orbita. Deep dissection. Extrinsic eye muscle. Nerves of orbita. Deep dissection. Cerebrum. Deep dissection. Inferior dissection. Tympanic cavity. Facial canal. Internal carotid artery. M: PNS anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp noco/auto/cong/tumr, sysi/epon, injr proc, drug (N1B) M: EYE anat (g/a/p)/phys/devp/prot noco/cong/tumr, epon proc, drug (S1A/1E/1F/1L)
The parasympathetic nervous system (PSNS, or occasionally PNS) is one of three main divisions of the autonomic nervous system (ANS), the other two being the sympathetic and enteric systems. The ANS is responsible for regulation of internal organs and glands, which occurs unconsciously. To be specific, the parasympathetic system is responsible for stimulation of "rest-and-digest" or "feed and breed"][ activities that occur when the body is at rest, especially after eating, including sexual arousal, salivation, lacrimation (tears), urination, digestion and defecation. Its action is described as being complementary to that of one of the other main branches of the ANS, the sympathetic nervous system, which is responsible for stimulating activities associated with the fight-or-flight response. Sympathetic and parasympathetic divisions typically function in opposition to each other. This natural opposition is better understood as complementary in nature rather than antagonistic. For an analogy, one may think of the sympathetic division as the police responders and the parasympathetic division as the court system. The sympathetic division typically functions in actions requiring quick responses. The parasympathetic division functions with actions that do not require immediate reaction. A useful mnemonic to summarize the functions of the parasympathetic nervous system is SLUDD (salivation, lacrimation, urination, digestion and defecation). The parasympathetic nervous system may also be known as Parasympathetic division. The parasympathetic nerves (PSNS) are autonomic (aka "visceral") branches of the peripheral nervous system (PNS). Parasympathetic nerve fibers arise from the central nervous system with the S2, S3, and S4 spinal nerves and from the third, seventh, ninth, and tenth cranial nerves. Because of its location, the parasympathetic system is commonly referred to as having "craniosacral outflow", which stands in contrast to the sympathetic nervous system, which is said to have "thoracolumbar outflow". The parasympathetic nerves that arise from the S2, S3, and S4 spinal nerves are commonly referred to as the pelvic splanchnic nerves or the "nervi erigentes". As is true in the sympathetic nervous system, efferent parasympathetic nerve signals are carried from the central nervous system to their targets by a system of two neurons. The first neuron in this pathway is referred to as the preganglionic or presynaptic neuron. Its cell body sits in the central nervous system and its axon usually extends to a ganglion somewhere else in the body where it synapses with the dendrites of the second neuron in the chain. This second neuron is referred to as the postganglionic or postsynaptic neuron. The axons of presynaptic parasympathetic neurons are usually long: They extend from the CNS into a ganglion that is either very close to or embedded in their target organ. As a result, the postsynaptic parasympathetic nerve fibers are very short. In the cranium, preganglionic PSN (CN III, CN VII, and CN IX) usually arise from specific nuclei in the Central Nervous System (CNS) and synapse at one of four parasympathetic ganglia: ciliary, pterygopalatine, otic, or submandibular. From these four ganglia the PSN complete their journey to target tissues via CN V (trigeminal) branches (ophthalmic nerve CN V1, maxillary nerve CN V2, mandibular nerve CN V3). The vagus nerve (CN X) does not participate in these cranial ganglia as most of its PSN fibers are destined for a broad array of ganglia on or near thoracic viscera (esophagus, trachea, heart, lungs) and abdominal viscera (stomach, pancreas, liver, kidneys). It travels all the way down to the midgut/hindgut junction, which occurs just before the splenic flexure of the transverse colon. The efferent preganglionic nerve cell bodiespelvic splanchnic reside in the lateral gray horn of the spinal cord at the T12-L1 vertebral levels (the spinal cord terminates at the L1-L2 vertebrae with the conus medullaris), and their axons exit the vertebral column as S2-S4 spinal nerves through the sacral foramina. Their axons continue away from the CNS to synapse at an autonomic ganglion. The PSN ganglion where these preganglionic neurons synapse will be close to the organ of innervation. This differs from the sympathetic nervous system, where synapses between pre- and post-ganglionic efferent nerves in general occur at ganglia that are farther away from the target organ. The afferent fibers of the autonomic nervous system, which transmit sensory information from the internal organs of the body back to the central nervous system, are not divided into parasympathetic and sympathetic fibers as the efferent fibers are. Instead, autonomic sensory information is conducted by general visceral afferent fibers. General visceral afferent sensations are mostly unconscious visceral motor reflex sensations from hollow organs and glands that are transmitted to the CNS. While the unconscious reflex arcs normally are undetectable, in certain instances they may send pain sensations to the CNS masked as referred pain. If the peritoneal cavity becomes inflamed or if the bowel is suddenly distended, the body will interpret the afferent pain stimulus as somatic in origin. This pain is usually non-localized. The pain is also usually referred to dermatomes that are at the same spinal nerve level as the visceral afferent synapse. The oculomotor nerve is responsible for several parasympathetic functions related to the eye. The oculomotor PNS fibers originate in the Edinger-Westphal nucleus in the CNS and travel through the superior orbital fissure to synapse in the ciliary ganglion located just behind the orbit (eye). From the ciliary ganglion the postganglionic PSN fibers leave via short ciliary nerve fibers, a continuation of the nasociliary nerve (a branch of ophthalmic division of the trigeminal nerve, CN V1). The short ciliary nerves innervate the orbit to control the ciliary muscle (responsible for accommodation) and the sphincter pupillae muscle, which is responsible for miosis or constriction of the pupil (in response to light or accommodation). The parasympathetic aspect of the facial nerve (CN VII) controls secretion of the sublingual and submandibular salivary glands, the lacrimal gland, and the glands associated with the nasal cavity. The preganglionic fibers originate within the CNS in the superior salivatory nucleus and leave as the intermediate nerve (which some consider a separate cranial nerve altogether) to connect with the facial nerve just distal (further out) to it surfacing the CNS. Just after the facial nerve geniculate ganglion (general sensory ganglion) in the temporal bone, the facial nerve gives off two separate parasympathetic nerves. The first is the greater petrosal nerve and the second is the chorda tympani. The greater petrosal nerve travels through the middle ear and eventually combines with the deep petrosal nerve (sympathetic fibers) to form the nerve of the pterygoid canal. The PSN fibers of the nerve of the pterygoid canal synapse at the pterygopalatine ganglion, which is closely associated with the maxillary division of the trigeminal nerve (CN V2). The postganglionic PSN fibers leave the pterygopalatine ganglion in several directions. One division leaves on the zygomatic division of CN V2 and travels on a communicating branch to unite with the lacrimal nerve (branch of the ophthalmic nerve of CN V1) before synapsing at the lacrimal gland. These PSN to the lacrimal gland control tear production. A separate group of PSN leaving from the pterygopalatine ganglion are the descending palatine nerves (CN V2 branch), which include the greater and lesser palatine nerves. The greater palatine PSN synapse on the hard palate and regulate mucus glands located there. The lesser palatine nerve synapses at the soft palate and controls sparse taste receptors and mucus glands. Yet another set of divisions from the pterygopalatine ganglion are the posterior, superior, and inferior lateral nasal nerves; and the nasopalatine nerves (all branches of CN V2, maxillary division of the trigeminal nerve) that bring PSN to glands of the nasal mucosa. The second PSN branch that leaves the facial nerve is the chorda tympani. This nerve carries secretomotor fibers to the submandibular and sublingual glands. The chorda tympani travels through the middle ear and attaches to the lingual nerve (mandibular division of trigeminal, CN V3). After joining the lingual nerve, the preganglionic fibers synapse at the submandibular ganglion and send postganglionic fibers to the sublingual and submandibular salivary glands. The glossopharyngeal nerve, CN IX, has parasympathetic fibers that innervate the parotid salivary gland. The preganglionic fibers depart CN IX as the tympanic nerve and continue to the middle ear where they make up a tympanic plexus on the cochlear promontory of the mesotympanum. The tympanic plexus of nerves rejoin and form the lesser petrosal nerve and exit through the foramen ovale to synapse at the otic ganglion. From the otic ganglion postganglionic parasympathetic fibers travel with the auriculotemporal nerve (mandibular branch of trigeminal, CN V3) to the parotid salivary gland. The vagus nerve, named from the Latin word vagus means literally "Wandering", since the nerve controls such a broad range of target tissues, has PSN that originate in the dorsal nucleus of the vagus nerve and the nucleus ambiguus in the CNS. The vagus nerve is an unusual cranial PSN in that it doesn't join the trigeminal nerve in order to get to its target tissues. Another peculiarity is that the vagus has an autonomic ganglion associated with it at approximately the level of C1 vertebra. The vagus gives no PSN to the cranium. The vagus nerve is hard to track definitively due to its ubiquitous nature in the thorax and abdomen so the major contributions will be discussed. Several PSN nerves come off the vagus nerve as it enters the thorax. One nerve is the recurrent laryngeal nerve, which becomes the inferior laryngeal nerve. From the left vagus nerve the recurrent laryngeal nerve hooks around the aorta to travel back up to the larynx and proximal esophagus while, from the right vagus nerve, the recurrent laryngeal nerve hooks around the right subclavian artery to travel back up to the same location as its counterpart. These different paths are a direct result of embryological development of the circulatory system. Each recurrent laryngeal nerve supplies the trachea and the esophagus with parasympathetic secretomotor innervation for glands associated with them (and other fibers that are not PSN). Another nerve that comes off the vagal nerves approximately at the level of entering the thorax are the cardiac nerves. These cardiac nerves go on to form cardiac and pulmonary plexuses around the heart and lungs. As the main vagus nerves continue into the thorax they become intimately linked with the esophagus and sympathetic nerves from the sympathetic trunks to form the esophageal plexus. This is very efficient as the major function of the vagus nerve from there on will be control of the gut smooth muscles and glands. As the esophageal plexus enter the abdomen through the esophageal hiatus anterior and posterior vagal trunks form. The vagal trunks then join with preaortic sympathetic ganglion around the aorta to disperse with the blood vessels and sympathetic nerves throughout the abdomen. The extent of the PSN in the abdomen include the pancreas, kidneys, liver, gall bladder, stomach and gut tube. The vagal contribution of PSN continues down the gut tube until the end of the midgut. The midgut ends 2/3 of the way across the transverse colon near the splenic flexure. The pelvic splanchnic nerves, S2-4, work in tandem to innervate the pelvic viscera. Unlike in the cranium, where one PSN was in charge of one particular tissue or region, for the most part the pelvic splanchnics each contribute fibers to pelvic viscera by first traveling to one or more plexuses before being dispersed to the target tissue. These plexuses are composed of mixed autonomic nerve fibers (PSN and SN) and include the vesical, prostatic, rectal, uterovaginal, and inferior hypogastric plexus. The preganglionic neurons in the neurons do not synapse in named ganglion as in the cranium but rather in the walls of the tissues or organs that they innervate. The fiber paths are variable and each individual's autonomic nervous system in the pelvis is unique. The visceral tissues in the pelvis that the PSN control include: urinary bladder, ureters, urinary sphincter, anal sphincter, uterus, prostate, glands, vagina and penis. Unconsciously, the PSN will cause peristaltic movements of the ureters helping to move urine from the kidneys into the bladder and move feces down the intestinal tract and upon necessity, the PSN will assist excreting urine from the bladder or defecation. Stimulation of the PSN will cause the detrusor muscle (urinary bladder wall) to contract and simultaneously relax the internal sphincter urethrae muscle to relax allowing void of urine. Also, PSN stimulation to the internal anal sphincter will relax this muscle and allow defecation. There are other skeletal muscles involved with these processes but the PSN play a huge role in continence. Another role that the PSN play in the pelvis is in sexual activity. In males, the cavernous nerves from the prostatic plexus stimulate smooth muscle in the fibrous trabeculae of the coiled helicene arteries to relax and allow blood to fill the corpora cavernosum and the corpus spongiosum of the penis, making it rigid to prepare for sexual activity. Upon emission of ejaculate, the sympathetics participate and cause peristalsis of the ductus deferens and closure of the internal urethral sphincter to prevent semen from entering the bladder. At the same time, parasympathetics cause peristalsis of the urethral muscle, and the pudendal nerve causes contraction of the bulbospongiosus (skeletal muscle is not via PSN), to forcibly emit the semen. During remission the penis becomes flaccid again. In the female, there is erectile tissue analogous to the male yet less substantial that plays a large role in sexual stimulation. The PSN cause release of secretions in the female that decrease friction. Also in the female, the parasympathetics innervate the fallopian tubes, which helps peristaltic contractions and movement of the oocyte to the uterus for implantation. The secretions from the female genital tract aids in semen migration. The PSN (and SN to a lesser extent) play a huge role in reproduction. The parasympathetic nervous system promotes digestion and the synthesis of glycogen, and allows for normal function and behavior. The parasympathetic nervous system uses chiefly acetylcholine (ACh) as its neurotransmitter, although peptides (such as cholecystokinin) may act on the PSNS as a neurotransmitter. The ACh acts on two types of receptors, the muscarinic and nicotinic cholinergic receptors. Most transmissions occur in two stages: When stimulated, the preganglionic nerve releases ACh at the ganglion, which acts on nicotinic receptors of postganglionic neurons. The postganglionic nerve then releases ACh to stimulate the muscarinic receptors of the target organ. The five main types of muscarinic receptors: In vertebrates, nicotinic receptors are broadly classified into two subtypes based on their primary sites of expression: muscle-type nicotinic receptors and neuronal-type nicotinic receptors.][ M: CNS anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr proc, drug (N1A/2AB/C/3/4/7A/B/C/D) M: PNS anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp noco/auto/cong/tumr, sysi/epon, injr proc, drug (N1B) M: PNS anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp noco/auto/cong/tumr, sysi/epon, injr proc, drug (N1B)
The nasociliary nerve is a branch of the ophthalmic nerve. It is intermediate in size between the two other main branches of the ophthalmic nerve, the frontal nerve and the lacrimal nerve, and is more deeply placed. The nasociliary nerve enters the orbit between the two heads of the lateral rectus muscles and between the superior and inferior rami of the oculomotor nerve (CN III). It passes across the optic nerve (CN II) and runs obliquely beneath the superior rectus muscle and superior oblique muscle to the medial wall of the orbital cavity. It passes through the anterior ethmoidal opening as the anterior ethmoidal nerve and enters the cranial cavity just above the cribriform plate of the ethmoid bone. It supplies branches to the mucous membrane of the nasal cavity and finally emerges between the inferior border of the nasal bone and the side nasal cartilages as the external nasal branch. Since both the short and long ciliary nerves carry the afferent limb of the corneal blink reflex, one can test the integrity of the nasociliary nerve (and, ultimately, the trigeminal nerve) by examining this reflex in the patient. Normally both eyes should blink when either cornea (not the conjunctiva, which is supplied by the adjacent cutaneous nerves) is irritated. If neither eye blinks, then either the ipsilateral nasociliary nerve is damaged, or the facial nerve (CN VII, which carries the efferent limb of this reflex) is bilaterally damaged. If only the contralateral eye blinks, then the ipsilateral facial nerve is damaged. If only the ipsilateral eye blinks, then the contralateral facial nerve is damaged. The nasociliary nerve gives off the following branches: PLICA is a mnemonic often used to remember these branches. Base of the skull. Upper surface. Plan of oculomotor nerve. Nerves of the orbit. Seen from above. Distribution of the maxillary and mandibular nerves, and the submaxillary ganglion. The sphenopalatine ganglion and its branches. Dissection showing origins of right ocular muscles, and nerves entering by the superior orbital fissure. Pathways in the Ciliary Ganglion. Extrinsic eye muscle. Nerves of orbita. Deep dissection. Extrinsic eye muscle. Nerves of orbita. Deep dissection. This article incorporates text from a public domain edition of Gray's Anatomy. frontal: supratrochlear  supraorbital (lateral branch, medial branch) nasociliary: long ciliary  infratrochlear  posterior ethmoidal  anterior ethmoidal (external nasal, internal nasal)  sensory root of ciliary ganglion (ciliary ganglion) M: PNS anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp noco/auto/cong/tumr, sysi/epon, injr proc, drug (N1B)
The vagus nerve ( ), also called pneumogastric nerve and cranial nerve X is the tenth of twelve (excluding CN0) paired cranial nerves. Upon leaving the medulla between the medullary pyramid and the inferior cerebellar peduncle, it extends through the jugular foramen, then passes into the carotid sheath between the internal carotid artery and the internal jugular vein down below the head, to the neck, chest and abdomen, where it contributes to the innervation of the viscera. Besides output to the various organs in the body, the vagus nerve conveys sensory information about the state of the body's organs to the central nervous system. 80-90% of the nerve fibers in the vagus nerve are afferent (sensory) nerves communicating the state of the viscera to the brain. The medieval Latin word vagus means literally "wandering" (the words vagrant, vagabond, and vague come from the same root). Sometimes the branches are spoken of in the plural and are thus called vagi (, US dict: ). The vagus is also called the pneumogastric nerve since it innervates both the lungs and the stomach. The motor division of the vagus nerve is derived from the basal plate of the embryonic medulla oblongata, while the sensory division originates from the cranial neural crest. The vagus nerve includes axons which emerge from or converge onto four nuclei of the medulla: The vagus runs posterior to the common carotid artery and internal jugular vein inside the carotid sheath. Right and left vagus nerves descend from the cranial vault through the jugular foramina, penetrating the carotid sheath between the internal and external carotid arteries, then passing posterolateral to the common carotid artery. The cell bodies of visceral afferent fibers of the vagus nerve are located bilaterally in the inferior ganglion of the vagus nerve (nodose ganglia). The right vagus nerve gives rise to the right recurrent laryngeal nerve, which hooks around the right subclavian artery and ascends into the neck between the trachea and esophagus. The right vagus then crosses anteriorly to the right subclavian artery and runs posterior to the superior vena cava and descends posterior to the right main bronchus and contributes to cardiac, pulmonary, and esophageal plexuses. It forms the posterior vagal trunk at the lower part of the esophagus and enters the diaphragm through the esophageal hiatus. The left vagus nerve enters the thorax between left common carotid artery and left subclavian artery and descends on the aortic arch. It gives rise to the left recurrent laryngeal nerve, which hooks around the aortic arch to the left of the ligamentum arteriosum and ascends between the trachea and esophagus. The left vagus further gives off thoracic cardiac branches, breaks up into pulmonary plexus, continues into the esophageal plexus, and enters the abdomen as the anterior vagal trunk in the esophageal hiatus of the diaphragm. The vagus nerve supplies motor parasympathetic fibers to all the organs except the suprarenal (adrenal) glands, from the neck down to the second segment of the transverse colon. The vagus also controls a few skeletal muscles, notable ones being: This means that the vagus nerve is responsible for such varied tasks as heart rate, gastrointestinal peristalsis, sweating, and quite a few muscle movements in the mouth, including speech (via the recurrent laryngeal nerve) and keeping the larynx open for breathing (via action of the posterior cricoarytenoid muscle, the only abductor of the vocal folds). It also has some afferent fibers that innervate the inner (canal) portion of the outer ear, via the Auricular branch (also known as Alderman's nerve) and part of the meninges. This explains why a person may cough when tickled on the ear (such as when trying to remove ear wax with a cotton swab). Parasympathetic innervation of the heart is controlled by the vagus nerve. To be specific, the vagus nerve acts to lower the heart rate. The right vagus innervates the sinoatrial node. Parasympathetic hyperstimulation predisposes those affected to bradyarrhythmias. The left vagus when hyperstimulated predisposes the heart to atrioventricular (AV) blocks. At this location, neuroscientist Otto Loewi first demonstrated that nerves secrete substances called neurotransmitters, which have effects on receptors in target tissues. In his experiment, Loewi electrically stimulated the vagus nerve of a frog heart, which slowed the heart. Then he took the fluid from the heart and transferred it to a second frog heart without a vagus nerve. The second heart slowed down without an electrical stimulation. Loewi described the substance released by the vagus nerve as vagusstoff, which was later found to be acetylcholine. Drugs that inhibit the muscarinic cholinergic receptor (anticholinergics) such as atropine and scopolamine are called vagolytic because they inhibit the action of the vagus nerve on the heart, gastrointestinal tract, and other organs. Anticholinergic drugs increase heart rate and are used to treat bradycardia (slow heart rate). Atropine is no longer indicated for the treatment of pulseless electrical activity (PEA) or asystole per the 2010 ACLS guidelines, as it has not been shown to improve outcomes in these clinical scenarios. Vagus nerve stimulation (VNS) therapy using a pacemaker-like device implanted in the chest is a treatment used since 1997 to control seizures in epilepsy patients and has recently been approved for treating drug-resistant cases of clinical depression. A non-invasive VNS device that stimulates an afferent branch of the vagus nerve is also being developed and will soon undergo trials.][ Clinical trials are currently underway in Antwerp, Belgium using VNS for the treatment of tonal tinnitus after a breakthrough study published in early 2011 by researchers at the University of Texas - Dallas showed successful tinnitus suppression in rats when tones were paired with brief pulses of stimulation of the vagus nerve. VNS may also be achieved by one of the vagal maneuvers: holding the breath for a few seconds, dipping the face in cold water, coughing, or tensing the stomach muscles as if to bear down to have a bowel movement. Patients with supraventricular tachycardia, atrial fibrillation, and other illnesses may be trained to perform vagal maneuvers (or find one or more on their own). Vagus nerve blocking (VBLOC) therapy is similar to VNS but used only during the day. In a six-month open-label trial involving three medical centers in Australia, Mexico, and Norway, vagus nerve blocking has helped 31 obese participants lose an average of nearly 15 percent of their excess weight. A year-long 300-participant double-blind, phase II trial has begun. Vagotomy (cutting of the vagus nerve) is a now-obsolete therapy that was performed for peptic ulcer disease. Vagotomy is currently being researched as a less invasive alternative weight-loss procedure to gastric bypass surgery. The procedure curbs the feeling of hunger and is sometimes performed in conjunction with putting bands on patients' stomachs, resulting in average weight loss of 43% at six months with diet and exercise. One serious side-effect of a vagotomy is a 12vitamin B deficiency later in life - i.e., 10 years - that is similar to pernicious anemia. The vagus normally stimulates the stomach's parietal cells to secrete acid and intrinsic factor. Intrinsic factor is needed to absorb vitamin B12 from food. The vagotomy reduces this secretion and ultimately leads to the deficiency, which, if left untreated, causes nerve damage, tiredness, dementia, paranoia, and ultimately death. Activation of the vagus nerve typically leads to a reduction in heart rate, blood pressure, or both. This occurs commonly in the setting of gastrointestinal illness such as viral gastroenteritis or acute cholecystitis, or in response to other stimuli, including carotid sinus massage, Valsalva maneuver, or pain from any cause, in particular, having blood drawn. When the circulatory changes are great enough, vasovagal syncope results. Relative dehydration tends to amplify these responses. Symptoms of Irritable Bowel Syndrome are thought to cause activation of the vagus nerve with many people reporting fainting, vision disturbances and dizziness, but there has been little research into this area as it is not deemed necessary and/or life threatening. Excessive activation of the vagal nerve during emotional stress, which is a parasympathetic overcompensation of a strong sympathetic nervous system response associated with stress, can also cause vasovagal syncope because of a sudden drop in blood pressure and heart rate. Vasovagal syncope affects young children and women more than other groups. It can also lead to temporary loss of bladder control under moments of extreme fear. Research has shown that women having had complete spinal cord injury can experience orgasms through the vagus nerve, which can go from the uterus, cervix, and, it is presumed, the vagina to the brain. Liver - Insulin signaling activates the adenosine triphosphate (ATP)-sensitive potassium (KATP) channels in the Arcuate nucleus, decreases AgRP release, and through the vagus nerve, leads to decreased glucose production by the liver by decreasing gluconeogenic enzymes: Phosphoenolpyruvate carboxykinase, Glucose 6-phosphatase The patient complains of hoarse voice, difficulty in swallowing (dysphagia), and choking when drinking fluid. There is also loss of gag reflex. Uvula deviates away from the side of lesion, and there is failure of palate elevation. Interior view of the human brain, with the cranial nerves labeled. Vagus nerve Section of the neck at about the level of the sixth cervical vertebra Transverse section of thorax, showing relations of pulmonary artery The arch of the aorta, and its branches Dura mater and its processes exposed by removing part of the right half of the skull, and the brain The tracheobronchial lymph glands Section of the medulla oblongata at about the middle of the olive Hind- and mid-brains; postero-lateral view Upper part of medulla spinalis and hind- and mid-brains; posterior aspect, exposed in situ The right sympathetic chain and its connections with the thoracic, abdominal, and pelvic plexuses The celiac ganglia with the sympathetic plexuses of the abdominal viscera radiating from the ganglia The position and relation of the esophagus in the cervical region and in the posterior mediastinum, seen from behind The thyroid gland and its relations The thymus of a full-term fetus, exposed in situ Vagus nerve Vagus nerve Vagus nerve Vagus nerve Vagus nerve Muscles, arteries and nerves of neck. Newborn dissection. Muscles, arteries and nerves of neck. Newborn dissection. Muscles, nerves and arteries of neck.Deep dissection. Anterior view. M: PNS anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp noco/auto/cong/tumr, sysi/epon, injr proc, drug (N1B)
Muscarinic receptors, or mAChRs, are acetylcholine receptors that form G protein-receptor complexes in the cell membranes of certain neurons and other cells. They play several roles, including acting as the main end-receptor stimulated by acetylcholine released from postganglionic fibers in the parasympathetic nervous system. Muscarinic receptors were named as such because they are more sensitive to muscarine than to nicotine. Their counterparts are nicotinic acetylcholine receptors (nAChRs), receptor ion channels that are also important in the autonomic nervous system. Many drugs and other substances (for example pilocarpine and scopolamine) manipulate these two distinct receptors by acting as selective agonists or antagonists. Acetylcholine (ACh) is a neurotransmitter found extensively in the brain and the autonomic ganglia. Muscarinic receptors are used in the following roles: ACh is always used as the transmitter within the autonomic ganglion. Nicotinic receptors on the postganglionic neuron are responsible for the initial fast depolarization (Fast EPSP) of that neuron. As a consequence of this, nicotinic receptors are often cited as the receptor on the postganglionic neurons at the ganglion. However, the subsequent hyperpolarization (IPSP) and slow depolarization (Slow EPSP) that represent the recovery of the postganglionic neuron from stimulation are actually mediated by muscarinic receptors, types M2 and M1 respectively (discussed below). Peripheral autonomic fibers (sympathetic and parasympathetic fibers) are categorized anatomically as either preganglionic or postganglionic fibers, then further generalized as either adrenergic fibers with their corresponding adrenergic receptors, or cholinergic fibers with their cholinergic receptors. Both preganglionic sympathetic fibers and preganglionic parasympathetic fibers are cholinergic. All postganglionic sympathetic fibers are adrenergic; their neurotransmitter is norepinephrine, except for the postganglionic sympathetic fibers to the sweat glands, piloerectile muscles of the body hairs and the skeletal muscle arterioles. The adrenal medulla is considered a sympathetic ganglion and like other sympathetic ganglia, is supplied by cholinergic preganglionic sympathetic fibers; acetylcholine is its neurotransmitter. The other postganglionic fibers of the peripheral autonomic system belong to the parasympathetic division; all are cholinergic fibers, and use acetylcholine (ACh) as their neurotransmitter. Another role for these receptors is at the junction of the innervated tissue and the postganglionic neuron in the parasympathetic division of the autonomic nervous system. Here acetylcholine is again used as a neurotransmitter, and muscarinic receptors form the principal receptors on the innervated tissue. Very few parts of the sympathetic system use cholinergic receptors. In sweat glands the receptors are of the muscarinic type. The sympathetic nervous system also has some preganglionic nerves terminating at the chromaffin cells in the adrenal medulla, which secrete epinephrine and norepinephrine into the bloodstream. Some believe that chromaffin cells are modified postganglionic CNS fibers. In the adrenal medulla, acetylcholine is used as a neurotransmitter, and the receptor is of the nicotinic type. The somatic nervous system uses a nicotinic receptor to acetylcholine at the neuromuscular junction. Muscarinic acetylcholine are also present and distributed throughout the central nervous system, in post-synaptic and pre-synaptic positions. There is also some evidence for postsynaptic receptors on sympathetic neurons allowing the parasympathetic nervous system to inhibit sympathetic effects. It's now known they also appear on the pre-synaptic membrane of somatic neurons in the neuro-muscular junction, where they are involved in the regulation of acetylcholine release. Muscarinic acetylcholine receptors belong to a class of metabotropic receptors that use G proteins as their signalling mechanism. In such receptors, the signaling molecule (the ligand) binds to a receptor that has seven transmembrane regions; in this case, the ligand is ACh. This receptor is bound to intracellular proteins, known as G proteins, which begin the information cascade within the cell. By contrast, nicotinic receptors use a ligand-gated ion channel mechanism for signaling. In this case, binding of the ligands with the receptor causes an ion channel to open, permitting either one or more specific type(s) of ion (e.g., K+, Na+, Ca+2) to diffuse into or out of the cell. By the use of selective radioactively labeled agonist and antagonist substances, five subtypes of muscarinic receptors have been determined, named M1-M5 (using an upper case M and subscript number). For example, the drug pirenzepine is a muscarinic antagonist (decreases the effect of ACh), which is much more potent at M1 receptors than it is at other subtypes. The acceptance of the various subtypes has proceeded in numerical order: therefore, sources that recognize only the M1/M2 distinction exist. More recent studies tend to recognize M3 and the most recent M4. Meanwhile, geneticists and molecular biologists have characterised five genes that appear to encode muscarinic receptors, named m1-m5 (lowercase m; no subscript number). The first four code for pharmacologic types M1-M4. The fifth, M5, corresponds to a subtype of receptor that had until recently not been detected pharmacologically. The receptors m1 and m2 were determined based upon partial sequencing of M1 and M2 receptor proteins. The others were found by searching for homology, using bioinformatic techniques. G proteins contain an alpha-subunit that is critical to the functioning of receptors. These subunits can take a number of forms. There are four broad classes of form of G-protein: Gs, Gi, Gq, and G12/13. Muscarinic receptors vary in the G protein to which they are bound, with some correlation according to receptor type. G proteins are also classified according to their susceptibility to cholera toxin (CTX) and pertussis toxin (PTX, whooping cough). Gs and some subtypes of Gi (Gαt and Gαg) are susceptible to CTX. Only Gi is susceptible to PTX, with the exception of one subtype of Gi (Gαz) which is immune. Also, only when bound with an agonist, those G proteins normally sensitive to PTX also become susceptible to CTX. The various G-protein subunits act differently upon secondary messengers, upregulating Phospholipases, downregulating cAMP, and so on. Because of the strong correlations to muscarinic receptor type, CTX and PTX are useful experimental tools in investigating these receptors. This receptor is found mediating slow EPSP at the ganglion in the postganglionic nerve, is common in exocrine glands and in the CNS. It is predominantly found bound to G proteins of class qG, which use upregulation of phospholipase C and, therefore, inositol trisphosphate and intracellular calcium as a signaling pathway. A receptor so bound would not be susceptible to CTX or PTX. However, Gi (causing a downstream decrease in cAMP) and Gs (causing an increase in cAMP) have also been shown to be involved in interactions in certain tissues, and so would be susceptible to PTX and CTX, respectively. The M2 muscarinic receptors are located in the heart, where they act to slow the heart rate down to normal sinus rhythm after stimulatory actions of the parasympathetic nervous system, by slowing the speed of depolarization. They also reduce contractile forces of the atrial cardiac muscle, and reduce conduction velocity of the atrioventricular node (AV node). It also serves to slightly decrease the contractile forces of the ventricular muscle. M2 muscarinic receptors act via a iG type receptor, which causes a decrease in cAMP in the cell, inhibition of voltage-gated Ca2+ channels, and increasing efflux of K+, in general, leading to inhibitory-type effects. The M3 muscarinic receptors are located at many places in the body. They are located in the smooth muscles of the blood vessels, as well as in the lungs. Because the M3 receptor is Gq-coupled and mediates an increase in intracellular calcium, it typically causes contraction of smooth muscle, such as that observed during bronchoconstriction. However, with respect to vasculature, activation of M3 on vascular endothelial cells causes increased synthesis of nitric oxide, which diffuses to adjacent vascular smooth muscle cells and causes their relaxation, thereby explaining the paradoxical effect of parasympathomimetics on vascular tone and bronchiolar tone. Indeed, direct stimulation of vascular smooth muscle, M3 mediates vasconstriction in pathologies wherein the vascular endothelium is disrupted. The M3 receptors are also located in many glands, which help to stimulate secretion in, for example, the salivary glands, as well as other glands of the body. Like the M1 muscarinic receptor, M3 receptors are G proteins of class qG that upregulate phospholipase C and, therefore, inositol trisphosphate and intracellular calcium as a signaling pathway. M4 receptors are found in the CNS. Receptors work via iG receptors to decrease cAMP in the cell and, thus, produce generally inhibitory effects. Possible bronchospasm may result if stimulated by muscarinic agonists Location of M5 receptors is not well known. Like the M1 and M3 muscarinic receptor, M5 receptors are coupled with G proteins of class qG that upregulate phospholipase C and, therefore, inositol trisphosphate and intracellular calcium as a signaling pathway. Ligands targeting the mAChR that are currently approved for clinical use include non-selective antagonists for the treatment of Parkinson's disease, atropine (to dilate the pupil), Scopolamine (used to prevent motion sickness), and ipratropium (used in the treatment of COPD).
The trigeminal nerve (the fifth cranial nerve, also called the fifth nerve, or simply CNV or CN5) is a nerve responsible for sensation in the face and certain motor functions such as biting and chewing. It is the largest of the cranial nerves. Its name ("trigeminal" = tri- or three, and -geminus or twin, or thrice twinned) derives from the fact that each trigeminal nerve, one on each side of the pons, has three major branches: the ophthalmic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3). The ophthalmic and maxillary nerves are purely sensory. The mandibular nerve has both cutaneous and motor functions. Sensory information from the face and body is processed by parallel pathways in the central nervous system. The motor division of the trigeminal nerve is derived from the basal plate of the embryonic pons, while the sensory division originates from the cranial neural crest. The sensory function of the trigeminal nerve is to provide the tactile, proprioceptive, and nociceptive afference of the face and mouth. The motor function activates the muscles of mastication, the tensor tympani, tensor veli palatini, mylohyoid, and anterior belly of the digastric. The three major branches of the trigeminal nerve, the ophthalmic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3) converge on the trigeminal ganglion (also called the semilunar ganglion or gasserian ganglion), located within Meckel's cave, and contains the cell bodies of incoming sensory nerve fibers. The trigeminal ganglion is analogous to the dorsal root ganglia of the spinal cord, which contain the cell bodies of incoming sensory fibers from the rest of the body. From the trigeminal ganglion, a single large sensory root enters the brainstem at the level of the pons. Immediately adjacent to the sensory root, a smaller motor root emerges from the pons at the same level. Motor fibers pass through the trigeminal ganglion on their way to peripheral muscles, but their cell bodies are located in the nucleus of the fifth nerve, deep within the pons. The areas of cutaneous distribution (dermatomes) of the three branches of the trigeminal nerve have sharp borders with relatively little overlap (unlike dermatomes in the rest of the body, which show considerable overlap). Injection of local anesthetics such as lidocaine results in the complete loss of sensation from well-defined areas of the face and mouth. For example, the teeth on one side of the jaw can be numbed by injecting the mandibular nerve. Occasionally, injury or disease processes, though, may affect two or all three branches of the trigeminal nerve, and in these cases the involved branches may be termed: Notably, nerves on the left side of the jaw outnumber slightly the number of nerves on the right side of the jaw. The ophthalmic, maxillary and mandibular branches leave the skull through three separate foramina: the superior orbital fissure, the foramen rotundum and the foramen ovale. The mnemonic standing room only can be used to remember that V1 passes through the superior orbital fissure, V2 through the foramen rotundum, and V3 through the foramen ovale. The many branches within the three trigeminal divisions are best represented in this chart. Motor branches of the trigeminal nerve are distributed in the mandibular nerve. These fibers originate in the motor nucleus of the fifth nerve, which is located near the main trigeminal nucleus in the pons. Motor nerves are functionally quite different from sensory nerves, and their association in the peripheral branches of the mandibular nerve is more a matter of convenience than of necessity. In classical anatomy, the trigeminal nerve is said to have general somatic afferent (sensory) components, as well as special visceral efferent (motor) components. The motor branches of the trigeminal nerve control the movement of eight muscles, including the four muscles of mastication. With the exception of tensor tympani, all of these muscles are involved in biting, chewing and swallowing. All have 'bilateral' cortical representation. A unilateral central lesion (e.g., a stroke), no matter how large, is unlikely to produce any observable deficit. Injury to the peripheral nerve can cause paralysis of muscles on one side of the jaw. The jaw deviates to the paralyzed side when it opens. This direction of the mandible is due to the action of normal pterygoids on the opposite side. The two basic types of sensation are touch/position and pain/temperature. They are distinguished, roughly speaking, by the fact that touch/position input comes to attention immediately, whereas pain/temperature input reaches the level of consciousness only after a perceptible delay. When stepping on a pin, awareness of stepping on something is immediate, but the pain associated with it is delayed. In general, touch/position information is carried by myelinated (fast-conducting) nerve fibers, whereas pain/temperature information is carried by unmyelinated (slow-conducting) nerve fibers. The primary sensory receptors for touch/position (Meissner’s corpuscles, Merkel's receptors, Pacinian corpuscles, Ruffini’s corpuscles, hair receptors, muscle spindle organs, and Golgi tendon organs) are structurally more complex than the primitive receptors for pain/temperature, which are bare nerve endings. The term "sensation", as used in this article, refers to the conscious perception of touch/position and pain/temperature information. It does not refer to the so-called "special senses" (smell, sight, taste, hearing and balance), which are processed by different cranial nerves and sent to the cerebral cortex through different pathways. The perception of magnetic fields, electrical fields, low-frequency vibrations and infrared radiation by certain nonhuman vertebrates is processed by the equivalent of the fifth cranial nerve in these animals. The term "touch", as used in this article, refers to the perception of detailed, localized tactile information, such as "two-point discrimination" (the difference between touching one point and two closely spaced points) or the difference between grades of sandpaper (coarse, medium and fine). People who lack touch/position perception can still "feel" the surface of their bodies, and can therefore perceive "touch" in a crude, yes-or-no way, but they lack the rich perceptual detail others normally experience. The term "position", as used in this article, refers to conscious proprioception. Proprioceptors (muscle spindle organs and Golgi tendon organs) provide information about joint position and muscle movement. Much of this information is processed at an unconscious level (mainly by the cerebellum and the vestibular nuclei). However, some of this information is available at a conscious level. The two types of sensation in humans, touch/position and pain/temperature, are processed by different pathways in the central nervous system. The distinction is hard-wired, and it is maintained all the way to the cerebral cortex. Within the cerebral cortex, sensations are further hard-wired to (associated with) other cortical areas. Sensory pathways from the periphery to the cortex are summarized below. Pathways are separate for touch/position sensation and pain/temperature sensation. All sensory information is sent to specific nuclei in the thalamus. Thalamic nuclei, in turn, send information to specific areas in the cerebral cortex. Each pathway consists of three bundles of nerve fibers, connected in series: The 'secondary' neurons in each pathway decussate (cross to the other side of the spinal cord or brainstem), because the spinal cord initially forms segmentally. Later on, decussated fibres reach and connect these segments with the higher centres. The main reason for decussation is the optic chiasma occurs (nasal fibres of the optic nerve cross so each cerebral hemisphere receives the contralateral vision) to keep interneuronal connections short (responsible for processing of information), and all sensory and motor pathways converge and diverge respectively to the contralateral hemisphere Sensory pathways are often depicted as chains of 'individual' neurons connected in series; this is an oversimplification. Sensory information is processed and modified at each level in the chain by interneurons and by input from other areas of the nervous system. For example, cells in the main trigeminal nucleus ("Main V" in the diagram) receive input (not shown) from the reticular formation and from the cerebral cortex. This information contributes to the final output of the cells in Main V to the thalamus. Touch/position information from the body is carried to the thalamus by the medial lemniscus; this information from the face is carried to the thalamus by the trigeminal lemniscus. Pain/temperature information from the body is carried to the thalamus by the spinothalamic tract; this information from the face is carried to the thalamus by the trigeminothalamic ' (or quintothalamic) tract. Pathways for touch/position sensation from the face and body merge in the brainstem. A single touch/position sensory map of the entire body is projected onto the thalamus. Likewise, pathways for pain/temperature sensation from the face and body merge in the brainstem. A single pain/temperature sensory map of the entire body is projected onto the thalamus. From the thalamus, touch/position and pain/temperature information is projected onto various areas of the cerebral cortex. Exactly where, when, and how this information becomes conscious is entirely beyond our understanding at present. The explanation of consciousness is one of the great unsolved mysteries in science. The details of the pathways connecting the lower body to the cerebral cortex are beyond the scope of this article. The details of the pathways connecting the face and mouth to the cerebral cortex are discussed below. It is not widely appreciated that all sensory information from the face (all touch/position information and all pain/temperature information) is sent to the trigeminal nucleus. In classical anatomy, most sensory information from the face is carried by the fifth nerve, but sensation from certain parts of the mouth, certain parts of the ear and certain parts of the meninges is carried by "general somatic afferent" fibers in cranial nerves VII (the facial nerve), IX (the glossopharyngeal nerve) and X (the vagus nerve). Without exception, however, all sensory fibers from these nerves terminate in the trigeminal nucleus. On entering the brainstem, sensory fibers from V, VII, IX, and X are sorted out and sent to the trigeminal nucleus, which thus contains a complete sensory map of the face and mouth. The spinal counterparts of the trigeminal nucleus (cells in the dorsal horn and dorsal column nuclei of the spinal cord) contain a complete sensory map of the rest of the body. The trigeminal nucleus extends throughout the entire brainstem, from the midbrain to the medulla, and continues into the cervical cord, where it merges with the dorsal horn cells of the spinal cord. The nucleus is divided anatomically into three parts, visible in microscopic sections of the brainstem. From caudal to rostral (i.e., going up from the medulla to the midbrain) they are the spinal trigeminal nucleus, the main trigeminal nucleus, and the mesencephalic trigeminal nucleus. The three parts of the trigeminal nucleus receive different types of sensory information. The spinal trigeminal nucleus receives pain/temperature fibers. The main trigeminal nucleus receives touch/position fibers. The mesencephalic nucleus receives proprioceptor and mechanoreceptor fibers from the jaws and teeth. The spinal trigeminal nucleus represents pain/temperature sensation from the face. Pain/temperature fibers from peripheral nociceptors are carried in cranial nerves V, VII, IX, and X. On entering the brainstem, sensory fibers are grouped together and sent to the spinal trigeminal nucleus. This bundle of incoming fibers can be identified in cross sections of the pons and medulla as the spinal tract of the trigeminal nucleus, which parallels the spinal trigeminal nucleus itself. The spinal tract of V is analogous to, and continuous with, Lissauer's tract in the spinal cord. The spinal trigeminal nucleus contains a pain/temperature sensory map of the face and mouth. From the spinal trigeminal nucleus, secondary fibers cross the midline and ascend in the trigeminothalamic (quintothalamic) tract to the contralateral thalamus. Pain/temperature fibers are sent to multiple thalamic nuclei. As discussed below, the central processing of pain/temperature information is markedly different from the central processing of touch/position information. Exactly how pain/temperature fibers from the face are distributed to the spinal trigeminal nucleus has been a subject of considerable controversy. The present understanding is that all pain/temperature information from all areas of the human body is represented (in the spinal cord and brainstem) in an ascending, caudal-to-rostral fashion. Information from the lower extremities is represented in the lumbar cord. Information from the upper extremities is represented in the thoracic cord. Information from the neck and the back of the head is represented in the cervical cord. Information from the face and mouth is represented in the spinal trigeminal nucleus. Within the spinal trigeminal nucleus, information is represented in an onion skin fashion. The lowest levels of the nucleus (in the upper cervical cord and lower medulla) represent peripheral areas of the face (the scalp, ears and chin). Higher levels (in the upper medulla) represent more central areas (nose, cheeks, lips). The highest levels (in the pons) represent the mouth, teeth, and pharyngeal cavity. The onion skin distribution is entirely different from the dermatome distribution of the peripheral branches of the fifth nerve. Lesions that destroy lower areas of the spinal trigeminal nucleus (but which spare higher areas) preserve pain/temperature sensation in the nose (V1), upper lip (V2) and mouth (V3) while removing pain/temperature sensation from the forehead (V1), cheeks (V2) and chin (V3). Analgesia in this distribution is "nonphysiologic" in the traditional sense, because it crosses over several dermatomes. Nevertheless, analgesia in exactly this distribution is found in humans after surgical sectioning of the spinal tract of the trigeminal nucleus. The spinal trigeminal nucleus sends pain/temperature information to the thalamus. It also sends information to the mesencephalon and the reticular formation of the brainstem. The latter pathways are analogous to the spinomesencephalic and spinoreticular tracts of spinal cord, which send pain/temperature information from the rest of the body to the same areas. The mesencephalon modulates painful input before it reaches the level of consciousness. The reticular formation is responsible for the automatic (unconscious) orientation of the body to painful stimuli. The main trigeminal nucleus represents touch/position sensation from the face. It is located in the pons, close to the entry site of the fifth nerve. Fibers carrying touch/position information from the face and mouth (via cranial nerves V, VII, IX, and X) are sent to the main trigeminal nucleus when they enter the brainstem. The main trigeminal nucleus contains a touch/position sensory map of the face and mouth, just as the spinal trigeminal nucleus contains a complete pain/temperature map. The main nucleus is analogous to the dorsal column nuclei (the gracile and cuneate nuclei) of the spinal cord, which contain a touch/position map of the rest of the body. From the main trigeminal nucleus, secondary fibers cross the midline and ascend in the trigeminal lemniscus to the contralateral thalamus. The trigeminal lemniscus runs parallel to the medial lemniscus, which carries touch/position information from the rest of the body to the thalamus. Some sensory information from the teeth and jaws is sent from the main trigeminal nucleus to the ipsilateral thalamus, via the small dorsal trigeminal tract. Thus touch/position information from the teeth and jaws of one side of the face is represented bilaterally in the thalamus (and hence in the cortex). The reason for this special processing is discussed below. The mesencephalic trigeminal nucleus is not really a "nucleus"; rather, it is a sensory ganglion (like the trigeminal ganglion) that happens to be embedded in the brainstem.][ The mesencephalic "nucleus" is the sole exception to the general rule that sensory information passes through peripheral sensory ganglia before entering the central nervous system. Only certain types of sensory fibers have cell bodies in the mesencephalic nucleus: proprioceptor fibers from the jaw and mechanoreceptor fibers from the teeth. Some of these incoming fibers go to the motor nucleus of V, thus entirely bypassing the pathways for conscious perception. The jaw jerk reflex is an example. Tapping the jaw elicits a reflex closure of the jaw, in exactly the same way that tapping the knee elicits a reflex kick of the lower leg. Other incoming fibers from the teeth and jaws go to the main nucleus of V. As noted above, this information is projected bilaterally to the thalamus. It is available for conscious perception. Activities such as biting, chewing and swallowing require symmetrical, simultaneous coordination of both sides of the body. They are essentially automatic activities, requiring little conscious attention. They involve a sensory component (feedback about touch/position), processed at a largely unconscious level. The unusual anatomy of "mesencephalic V" has been found in all vertebrates, with the exception of lampreys and hagfishes. Lampreys and hagfishes are the only vertebrates without jaws. Information about biting, chewing and swallowing evidently is singled out for special processing in the vertebrate brainstem, specifically in the mesencephalic nucleus. Lampreys and hagfishes have cells in their brainstems that can be identified as the evolutionary precursors of the mesencephalic nucleus. These "internal ganglion" cells were discovered in the latter part of the 19th century by then young medical student Sigmund Freud. Sensation has beed defined herein as the conscious perception of touch/proprioception and pain/temperature information. With the sole exception of smell, all sensory input (touch/position, pain/temperature, sight, taste, hearing, and balance) is sent to the thalamus before being sent to the cortex. The thalamus is anatomically subdivided into a number of separate nuclei. The thalamic nuclei involved in sensation, and their cortical projections, are discussed below. Touch/position information from the body is sent to the ventral posterolateral nucleus (VPL) of the thalamus. Touch/position information from the face is sent to the ventral posteromedial nucleus (VPM) of the thalamus. From the VPL and VPM, information is projected to the primary sensory cortex (SI) in the postcentral gyrus of the parietal lobe. The representation of sensory information in SI is organized somatotopically. Adjacent areas in the body are represented by adjacent areas in the cortex. When body parts are drawn in proportion to the density of their innervation, however, the result is a strangely distorted "little man", the sensory homunculus. Many textbooks reproduce the classic Penfield-Rasmussen diagram, which is now outdated. For example, the toes and genitals are shown in the classic diagram on the mesial surface of the cortex, when in fact they are represented on the convexity. What is more important, the classic diagram implies a single primary sensory map of the body, when in fact there are multiple primary maps. At least four separate, anatomically distinct sensory homunculi have been identified in SI. They represent different blends of input from surface receptors, deep receptors, rapidly adapting receptors, and slowly adapting peripheral receptors. For example, smooth objects will activate certain cells, whereas edged objects will activate other cells. Information from all four maps in the SI is sent to the secondary sensory cortex (SII) in the parietal lobe. SII contains two more sensory homunculi. In general, information from one side of the body is represented on the opposite side in SI, but on both sides in SII. Functional MRI imaging of a defined stimulus (e.g., stroking the skin with a toothbrush) "lights up" a single focus in SI and two foci in SII. Pain/temperature information is sent to the VPL (body) and VPM (face) of the thalamus (the same nuclei that receive touch/position information). From the thalamus, pain/temperature and touch/position information is projected onto SI. In marked contrast to touch/position information, however, pain/temperature information is also sent to other thalamic nuclei, and is projected onto additional areas of the cerebral cortex. Some pain/temperature fibers are sent to the medial dorsal thalamic nucleus (MD), which projects to the anterior cingulate cortex. Other fibers are sent to the ventromedial (VM) nucleus of the thalamus, which projects to the insular cortex. Finally, some fibers are sent to the intralaminar (IL) nuclei of the thalamus via the reticular formation. The IL project diffusely to all parts of the cerebral cortex. The insula and cingulate cortex are areas of the brain that represent our perception of touch/position and pain/temperature in the context of other simultaneous perceptions (sight, smell, taste, hearing and balance), and in the context of our memories and present emotional state. It is noteworthy that peripheral pain/temperature information is channeled directly into the brain at these deep levels, without prior processing. This contrasts markedly with the way that touch/position information is handled. Diffuse thalamic projections from the IL and other thalamic nuclei are responsible for one’s overall level of consciousness. The thalamus and reticular formation "activate" the entire brain. It is noteworthy that peripheral pain/temperature information feeds directly into this system as well. GSA, general somatic afferent, skin of the face via ophthalmic (V1), maxillary (V2), and mandibular (V3) divisions SVE, special visceral efferent, muscles of mastication via mandibular (V3) division The complex processing of pain/temperature information in the thalamus and cerebral cortex (as opposed to the relatively simple, straightforward processing of touch/position information) reflects a phylogenetically older, more primitive sensory system. The rich, detailed information we receive from peripheral touch/position receptors is superimposed on a background of awareness, memory and emotions that is set, in part, by peripheral pain/temperature receptors. The thresholds for touch/position perception are relatively easy to measure, and are similar in all humans. The thresholds for pain/temperature perception are difficult to define and even more difficult to measure. "Touch" is an objective sensation. "Pain" is a highly individualized, personal sensation that varies markedly among different people. It is conditioned by their memories and by their emotions. The fundamental anatomical differences between the pathways for touch/position perception and pain/temperature sensation help to explain why pain, especially chronic pain, is so difficult to manage. Wallenberg syndrome (also called the lateral medullary syndrome) is a classic clinical demonstration of the anatomy of the fifth nerve. It provides a useful summary of essential points about the processing of sensory information by the trigeminal nerve. A stroke usually affects only one side of the body. If a stroke causes loss of sensation, the deficit will be lateralized to the right side or the left side of the body. The only exceptions to this rule are certain spinal cord lesions and the medullary syndromes, of which Wallenberg syndrome is the most famous example. In Wallenberg syndrome, a stroke causes loss of pain/temperature sensation from one side of the face and the other side of the body. The explanation involves the anatomy of the brainstem. In the medulla, the ascending spinothalamic tract (which carries pain/temperature information from the opposite side of the body) is adjacent to the ascending spinal tract of the fifth nerve (which carries pain/temperature information from the same side of the face). A stroke that cuts off the blood supply to this area (e.g., a clot in the posterior inferior cerebellar artery) destroys both tracts simultaneously. The result is loss of pain/temperature sensation (but not touch/position sensation) in a unique "checkerboard" pattern (ipsilateral face, contralateral body) that is entirely diagnostic. Cerebrum. Deep dissection. Inferior dissection. M: PNS anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp noco/auto/cong/tumr, sysi/epon, injr proc, drug (N1B) frontal: supratrochlear  supraorbital (lateral branch, medial branch) nasociliary: long ciliary  infratrochlear  posterior ethmoidal  anterior ethmoidal (external nasal, internal nasal)  sensory root of ciliary ganglion (ciliary ganglion) M: PNS anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp noco/auto/cong/tumr, sysi/epon, injr proc, drug (N1B)
Cranial nerves are nerves that emerge directly from the brain, in contrast to spinal nerves, which emerge from segments of the spinal cord. In humans, there are traditionally twelve pairs of cranial nerves. Only the first and the second pair emerge from the cerebrum; the remaining ten pairs emerge from the brainstem. The cranial nerves are part of the peripheral nervous system (PNS) with the exception of cranial nerve II or 'optic nerve', along with the retina, which is not a true peripheral nerve but a tract of the diencephalon. Cranial nerve nuclei are found in the central nervous system (CNS). The remaining eleven axons extend beyond the brain and are therefore considered part of the PNS. Human cranial nerves are nerves similar to those found in many other vertebrates. Cranial nerves XI and XII evolved in other species to amniotes (non-amphibian tetrapods), thus totaling twelve pairs. In some primitive cartilaginous fishes, such as the spiny dogfish or mud shark (Squalus acanthias), there is a terminal nerve numbered zero, since it exits the brain before the traditionally designated first cranial nerve.
There are many mnemonic devices in circulation to help remember the names and order of the cranial nerves. Because the mind recalls rhymes well, the best mnemonics often use rhyming schemes. An example mnemonic sentence for the initial letters "OOOTTAFAGVSH" is "On old Olympus's towering tops, a Finn and German viewed some hops," and for the initial letters "OOOTTAFVGVAH" is "Oh, oh, oh, to touch and feel very good velvet...ah, heaven." The differences between these depend on "acoustic" versus "vestibulocochlea" and "spinal-accessory" versus "accessory". A useful mnemonic for remembering which nerves are motor (M), sensory (S), or both (B) is, "Some Say Marry Money But My Brother Says Big Brains Matter More". There are many more mnemonics from many sources, for example OLd OPie OCcasionally TRies TRIGonometry And Feels VEry GLOomy, VAGUe, And HYPOactive. Animations of cranial nerve input to extraocular muscles can be found here (University of Liverpool Veterinary School). M: CNS anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr proc, drug (N1A/2AB/C/3/4/7A/B/C/D) M: PNS anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp noco/auto/cong/tumr, sysi/epon, injr proc, drug (N1B) M: PNS anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp noco/auto/cong/tumr, sysi/epon, injr proc, drug (N1B)
Sensory receptors Sensory system Perception Pain Cranial nerves Nociceptor Sense Trigeminal nerve Mind Nervous system Nociception Health Medical Pharma Health Medical Pharma

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