Optic Nerve Injuries
Optic Nerve
Retinal Ganglion Cells
Optic Disk
Optic Nerve Diseases
Axotomy
Sciatic Nerve
Cranial Nerve Injuries
Evoked Potentials, Visual
Glaucoma
Retina
Optic Neuritis
Wounds, Nonpenetrating
Optic Chiasm
Wounds and Injuries
Facial Nerve Injuries
Peripheral Nerves
Optic Atrophy
Nerve Fibers
Spinal Nerves
Optic Nerve Neoplasms
Sciatic Neuropathy
Cell Count
Disease Models, Animal
Neuralgia
Trigeminal Nerve Injuries
Lingual Nerve Injuries
Neuroprotective Agents
Brain-Derived Neurotrophic Factor
Cell Survival
Trauma, Nervous System
Brain Injuries
Optic Nerve Glioma
Optic Neuropathy, Ischemic
Immunohistochemistry
Spinal Cord Injuries
Hyperalgesia
Rats, Sprague-Dawley
Peripheral Nervous System Diseases
Facial Nerve
Ulnar Nerve
Reperfusion Injury
Tibial Nerve
Nerve Compression Syndromes
Nerve Block
Median Nerve
Ganglia, Spinal
Papilledema
Femoral Nerve
Accessory Nerve Injuries
Recurrent Laryngeal Nerve Injuries
Myelin Sheath
Sural Nerve
Optic Lobe, Nonmammalian
Nerve Degeneration
Eye Injuries
Optic Atrophies, Hereditary
Wallerian Degeneration
Spinal Cord
Axonal Transport
Spinal Nerve Roots
Nerve Growth Factors
Injury Severity Score
Injury-induced gelatinase and thrombin-like activities in regenerating and nonregenerating nervous systems. (1/264)
It is now widely accepted that injured nerves, like any other injured tissue, need assistance from their extracellular milieu in order to heal. We compared the postinjury activities of thrombin and gelatinases, two types of proteolytic activities known to be critically involved in tissue healing, in nonregenerative (rat optic nerve) and regenerative (fish optic nerve and rat sciatic nerve) neural tissue. Unlike gelatinases, whose induction pattern was comparable in all three nerves, thrombin-like activity differed clearly between regenerating and nonregenerating nervous systems. Postinjury levels of this latter activity seem to dictate whether it will display beneficial or detrimental effects on the capacity of the tissue for repair. The results of this study further highlight the fact that tissue repair and nerve regeneration are closely linked and that substances that are not unique to the nervous system, but participate in wound healing in general, are also crucial for regeneration or its failure in the nervous system. (+info)Experimental induction of retinal ganglion cell death in adult mice. (2/264)
PURPOSE: Retinal ganglion cells die by apoptosis during development and after trauma such as axonal damage and exposure to excitotoxins. Apoptosis is associated with changes in the expression of genes that regulate this process. The genes that regulate apoptosis in retinal ganglion cells have not been characterized primarily because previous studies have been limited to animal models in which gene function is not easily manipulated. To overcome this limitation, the rate and mechanism of retinal ganglion cell death in mice was characterized using optic nerve crush and intravitreal injections of the glutamate analog N-methyl-D-aspartate (NMDA). METHODS: To expose retinal ganglion cells (RGCs) to excitotoxins, adult CB6F1 mice were injected intravitreally in one eye with NMDA. In an alternative protocol to physically damage the axons in the optic nerve, the nerve was crushed using self-closing fine forceps. Each animal had one or the other procedure carried out on one eye. Loss of RGCs was monitored as a percentage of cells lost relative to the fellow untreated eye. Thy1 expression was examined using in situ hybridization. DNA fragmentation in dying cells was monitored using terminal transferase-dUTP nick-end labeling (TUNEL). RESULTS: RGCs comprise 67.5% +/- 6.5% (mean +/- SD) of cells in the ganglion cell layer (GCL) of control mice based on nuclear morphology and the presence of mRNA for the ganglion cell marker Thy1. One week after optic nerve crush, these cells started to die, progressing to a maximum loss of 57.8% +/- 8.1% of the cells in the GCL by 3 weeks. Cell loss after NMDA injection was dose dependent, with injections of 10 nanomoles having virtually no effect to a maximum loss of 72.5% +/- 12.1% of the cells in the GCL within 6 days after injection of 160 nanomoles NMDA. Cell death exhibited features of apoptosis after both optic nerve crush and NMDA injection, including the formation of pyknotic nuclei and TUNEL staining. CONCLUSIONS: Quantitative RGC death can be induced in mice using two distinct signaling pathways, making it possible to test the roles of genes in this process using transgenic animals. (+info)Differential T cell response in central and peripheral nerve injury: connection with immune privilege. (3/264)
The central nervous system (CNS), unlike the peripheral nervous system (PNS), is an immune-privileged site in which local immune responses are restricted. Whereas immune privilege in the intact CNS has been studied intensively, little is known about its effects after trauma. In this study, we examined the influence of CNS immune privilege on T cell response to central nerve injury. Immunocytochemistry revealed a significantly greater accumulation of endogenous T cells in the injured rat sciatic nerve than in the injured rat optic nerve (representing PNS and CNS white matter trauma, respectively). Use of the in situ terminal deoxytransferase-catalyzed DNA nick end labeling (TUNEL) procedure revealed extensive death of accumulating T cells in injured CNS nerves as well as in CNS nerves of rats with acute experimental autoimmune encephalomyelitis, but not in injured PNS nerves. Although Fas ligand (FasL) protein was expressed in white matter tissue of both systems, it was more pronounced in the CNS. Expression of major histocompatibility complex (MHC) class II antigens was found to be constitutive in the PNS, but in the CNS was induced only after injury. Our findings suggest that the T cell response to central nerve injury is restricted by the reduced expression of MHC class II antigens, the pronounced FasL expression, and the elimination of infiltrating lymphocytes through cell death. (+info)Bilateral optic nerve injury. (4/264)
Bilateral optic nerve injury is a rare condition and is reported in 5-6 percent of all optic nerve injuries. However, there is no published series on bilateral optic nerve injury. Analysis of 31 cases of bilateral optic nerve involvement seen amongst 275 patients with optic nerve injury (11.5 percent) is discussed. Road traffic accident which is the most common cause of optic nerve injury, was recorded in 61 percent. Shotgun injury and blast in jury was the cause in 22.5 percent of cases. All the patients except 4 received steroids. Anterior cranial fossa fracture and opacity of paranasal sinuses were recorded in a third of the patients. Visual evoked potentials were recorded in 27 patients. Improvement in vision was noticed in 23 patients (74 percent). However, among the 62 eyes, 39 eyes showed improvement (62.8 percent). Possible reasons for better outcome in bilateral optic nerve injury are discussed. (+info)Bax antisense oligonucleotides reduce axotomy-induced retinal ganglion cell death in vivo by reduction of Bax protein expression. (5/264)
Following transection of the optic nerve (ON), retinal ganglion cells (RGCs) upregulate Bax protein expression and undergo apoptosis. The present study aimed at reducing Bax expression in order to test whether Bax plays a causative role in the induction of secondary RGC apoptosis. Following injection into the vitreous, fluoresceinated oligonucleotides transfected RGCs in vivo at the injection site in the temporal superior retina. Following ON lesion, and repeated injections of a partially phosphorothioated Bax antisense oligonucleotide, but not following injection of control oligonucleotides, expression of Bax protein was locally inhibited, and the number of surviving RGCs was increased in Bax antisense treated rats 8 days after axotomy. Our results indicate that Bax induction is a prerequisite for the execution of RGC apoptosis following ON axotomy. While the Bax antisense strategy offers an exciting perspective to inhibit secondary neuronal degeneration in vivo, both limited transfection efficacy, and the temporal restriction of this effect currently limit the use of this approach with respect to clinical applications for the treatment of neurodegeneration. (+info)R-esp1, a rat homologue of drosophila groucho, is differentially expressed after optic nerve crush and mediates NGF-induced survival of PC12 cells. (6/264)
The differential display reverse transcription polymerase chain reaction method was used to detect alterations in gene expression in the superior colliculus after optic nerve crush in adult rats. One of the most prominent changes observed was the selective induction of R-esp1, a homologue of the Drosophila enhancer of split locus (Groucho). Therefore, we studied the influence of R-esp1 on nerve growth factor (NGF)-induced cell survival of PC12 cells. Overexpression of R-esp1 promotes cell survival even in the absence of NGF and, conversely, it is reduced by antisense-mediated inhibition of R-esp1 expression. In conclusion, we propose a novel model in which R-esp1 protein mediates the NGF-signaling pathway. (+info)Optic nerve crush: axonal responses in wild-type and bcl-2 transgenic mice. (7/264)
Retinal ganglion cells of transgenic mice overexpressing the anti-apoptotic protein Bcl-2 in neurons show a dramatic increase of survival rate after axotomy. We used this experimental system to test the regenerative potentials of central neurons after reduction of nonpermissive environmental factors. Survival of retinal ganglion cells 1 month after intracranial crush of the optic nerve was found to be 100% in adult bcl-2 mice and 44% in matched wild-type (wt) mice. In the optic nerve, and particularly at the crush site, fibers regrowing spontaneously or simply sprouting were absent in both wt and bcl-2 mice. We attempted to stimulate regeneration implanting in the crushed nerves hybridoma cells secreting antibodies that neutralize central myelin proteins, shown to inhibit regeneration (IN-1 antibodies) (Caroni and Schwab, 1988). Again, we found that regeneration of fibers beyond the site of crush was virtually absent in the optic nerves of both wt and bcl-2 mice. However, in bcl-2 animals treated with IN-1 antibodies, fibers showed sprouting in the proximity of the hybridoma implant. These results suggest that neurons overexpressing bcl-2 are capable of surviving axotomy and sprout when faced with an environment in which inhibition of regeneration has been reduced. Nevertheless, extensive regeneration does not occur, possibly because other factors act by preventing it. (+info)Visual outcome in optic nerve injury patients without initial light perception. (8/264)
PURPOSE: To assess the prognosis for recovery of vision in patients with blindness due to head injury, and to analyse the predictive value of visual evoked potential (VEP). METHODS: One hundred consecutive patients with unilateral/bilateral blindness as a result of minor head injury were studied with regard to their visual status, CT scan, MRI scan and serial VEPs. Steroids were given to those presenting within one month of injury, 5 patients among them received methyl prednisolone. Transethmoidal decompression was done in 6 patients. RESULTS: Visual improvement was recorded in 23 patients. Initial VEP failed to reveal any wave in 29 patients and was abnormal in 71. All the 14 patients in whom VEPs were repeatedly normal, irrespective of initial VEP status, showed varying degrees of visual improvement and none of the 15 patients with persistently negative VEPs showed visual improvement. CONCLUSION: Recovery of VEP from no response to abnormal wave or abnormal wave to normal VEP were indicators of relatively good visual prognosis. Overall, 23 patients showed visual improvement, but did not return to normal. Mode of injury, CT findings and timing of surgery did not influence the outcome. (+info)Optic nerve injuries refer to damages or trauma inflicted on the optic nerve, which is a crucial component of the visual system. The optic nerve transmits visual information from the retina to the brain, enabling us to see. Injuries to the optic nerve can result in various visual impairments, including partial or complete vision loss, decreased visual acuity, changes in color perception, and reduced field of view.
These injuries may occur due to several reasons, such as:
1. Direct trauma to the eye or head
2. Increased pressure inside the eye (glaucoma)
3. Optic neuritis, an inflammation of the optic nerve
4. Ischemia, or insufficient blood supply to the optic nerve
5. Compression from tumors or other space-occupying lesions
6. Intrinsic degenerative conditions affecting the optic nerve
7. Toxic exposure to certain chemicals or medications
Optic nerve injuries are diagnosed through a comprehensive eye examination, including visual acuity testing, slit-lamp examination, dilated fundus exam, and additional diagnostic tests like optical coherence tomography (OCT) and visual field testing. Treatment options vary depending on the cause and severity of the injury but may include medications, surgery, or vision rehabilitation.
The optic nerve, also known as the second cranial nerve, is the nerve that transmits visual information from the retina to the brain. It is composed of approximately one million nerve fibers that carry signals related to vision, such as light intensity and color, from the eye's photoreceptor cells (rods and cones) to the visual cortex in the brain. The optic nerve is responsible for carrying this visual information so that it can be processed and interpreted by the brain, allowing us to see and perceive our surroundings. Damage to the optic nerve can result in vision loss or impairment.
A nerve crush injury is a type of peripheral nerve injury that occurs when there is excessive pressure or compression applied to a nerve, causing it to become damaged or dysfunctional. This can happen due to various reasons such as trauma from accidents, surgical errors, or prolonged pressure on the nerve from tight casts, clothing, or positions.
The compression disrupts the normal functioning of the nerve, leading to symptoms such as numbness, tingling, weakness, or pain in the affected area. In severe cases, a nerve crush injury can cause permanent damage to the nerve, leading to long-term disability or loss of function. Treatment for nerve crush injuries typically involves relieving the pressure on the nerve, providing supportive care, and in some cases, surgical intervention may be necessary to repair the damaged nerve.
Retinal Ganglion Cells (RGCs) are a type of neuron located in the innermost layer of the retina, the light-sensitive tissue at the back of the eye. These cells receive visual information from photoreceptors (rods and cones) via intermediate cells called bipolar cells. RGCs then send this visual information through their long axons to form the optic nerve, which transmits the signals to the brain for processing and interpretation as vision.
There are several types of RGCs, each with distinct morphological and functional characteristics. Some RGCs are specialized in detecting specific features of the visual scene, such as motion, contrast, color, or brightness. The diversity of RGCs allows for a rich and complex representation of the visual world in the brain.
Damage to RGCs can lead to various visual impairments, including loss of vision, reduced visual acuity, and altered visual fields. Conditions associated with RGC damage or degeneration include glaucoma, optic neuritis, ischemic optic neuropathy, and some inherited retinal diseases.
Peripheral nerve injuries refer to damage or trauma to the peripheral nerves, which are the nerves outside the brain and spinal cord. These nerves transmit information between the central nervous system (CNS) and the rest of the body, including sensory, motor, and autonomic functions. Peripheral nerve injuries can result in various symptoms, depending on the type and severity of the injury, such as numbness, tingling, weakness, or paralysis in the affected area.
Peripheral nerve injuries are classified into three main categories based on the degree of damage:
1. Neuropraxia: This is the mildest form of nerve injury, where the nerve remains intact but its function is disrupted due to a local conduction block. The nerve fiber is damaged, but the supporting structures remain intact. Recovery usually occurs within 6-12 weeks without any residual deficits.
2. Axonotmesis: In this type of injury, there is damage to both the axons and the supporting structures (endoneurium, perineurium). The nerve fibers are disrupted, but the connective tissue sheaths remain intact. Recovery can take several months or even up to a year, and it may be incomplete, with some residual deficits possible.
3. Neurotmesis: This is the most severe form of nerve injury, where there is complete disruption of the nerve fibers and supporting structures (endoneurium, perineurium, epineurium). Recovery is unlikely without surgical intervention, which may involve nerve grafting or repair.
Peripheral nerve injuries can be caused by various factors, including trauma, compression, stretching, lacerations, or chemical exposure. Treatment options depend on the type and severity of the injury and may include conservative management, such as physical therapy and pain management, or surgical intervention for more severe cases.
Nerve regeneration is the process of regrowth and restoration of functional nerve connections following damage or injury to the nervous system. This complex process involves various cellular and molecular events, such as the activation of support cells called glia, the sprouting of surviving nerve fibers (axons), and the reformation of neural circuits. The goal of nerve regeneration is to enable the restoration of normal sensory, motor, and autonomic functions impaired due to nerve damage or injury.
The optic disk, also known as the optic nerve head, is the point where the optic nerve fibers exit the eye and transmit visual information to the brain. It appears as a pale, circular area in the back of the eye, near the center of the retina. The optic disk has no photoreceptor cells (rods and cones), so it is insensitive to light. It is an important structure to observe during eye examinations because changes in its appearance can indicate various ocular diseases or conditions, such as glaucoma, optic neuritis, or papilledema.
An axon is a long, slender extension of a neuron (a type of nerve cell) that conducts electrical impulses (nerve impulses) away from the cell body to target cells, such as other neurons or muscle cells. Axons can vary in length from a few micrometers to over a meter long and are typically surrounded by a myelin sheath, which helps to insulate and protect the axon and allows for faster transmission of nerve impulses.
Axons play a critical role in the functioning of the nervous system, as they provide the means by which neurons communicate with one another and with other cells in the body. Damage to axons can result in serious neurological problems, such as those seen in spinal cord injuries or neurodegenerative diseases like multiple sclerosis.
Optic nerve diseases refer to a group of conditions that affect the optic nerve, which transmits visual information from the eye to the brain. These diseases can cause various symptoms such as vision loss, decreased visual acuity, changes in color vision, and visual field defects. Examples of optic nerve diseases include optic neuritis (inflammation of the optic nerve), glaucoma (damage to the optic nerve due to high eye pressure), optic nerve damage from trauma or injury, ischemic optic neuropathy (lack of blood flow to the optic nerve), and optic nerve tumors. Treatment for optic nerve diseases varies depending on the specific condition and may include medications, surgery, or lifestyle changes.
Axotomy is a medical term that refers to the surgical cutting or severing of an axon, which is the long, slender projection of a neuron (nerve cell) that conducts electrical impulses away from the cell body and toward other cells. Axons are a critical component of the nervous system, allowing for communication between different parts of the body.
Axotomy is often used in research settings to study the effects of axonal injury on neuronal function and regeneration. This procedure can provide valuable insights into the mechanisms underlying neurodegenerative disorders and potential therapies for nerve injuries. However, it is important to note that axotomy can also have significant consequences for the affected neuron, including changes in gene expression, metabolism, and overall survival.
The sciatic nerve is the largest and longest nerve in the human body, running from the lower back through the buttocks and down the legs to the feet. It is formed by the union of the ventral rami (branches) of the L4 to S3 spinal nerves. The sciatic nerve provides motor and sensory innervation to various muscles and skin areas in the lower limbs, including the hamstrings, calf muscles, and the sole of the foot. Sciatic nerve disorders or injuries can result in symptoms such as pain, numbness, tingling, or weakness in the lower back, hips, legs, and feet, known as sciatica.
Cranial nerve injuries refer to damages or trauma to one or more of the twelve cranial nerves (CN I through CN XII). These nerves originate from the brainstem and are responsible for transmitting sensory information (such as vision, hearing, smell, taste, and balance) and controlling various motor functions (like eye movement, facial expressions, swallowing, and speaking).
Cranial nerve injuries can result from various causes, including head trauma, tumors, infections, or neurological conditions. The severity of the injury may range from mild dysfunction to complete loss of function, depending on the extent of damage to the nerve. Treatment options vary based on the type and location of the injury but often involve a combination of medical management, physical therapy, surgical intervention, or rehabilitation.
Evoked potentials, visual, also known as visually evoked potentials (VEPs), are electrical responses recorded from the brain following the presentation of a visual stimulus. These responses are typically measured using electroencephalography (EEG) and can provide information about the functioning of the visual pathways in the brain.
There are several types of VEPs, including pattern-reversal VEPs and flash VEPs. Pattern-reversal VEPs are elicited by presenting alternating checkerboard patterns, while flash VEPs are elicited by flashing a light. The responses are typically analyzed in terms of their latency (the time it takes for the response to occur) and amplitude (the size of the response).
VEPs are often used in clinical settings to help diagnose and monitor conditions that affect the visual system, such as multiple sclerosis, optic neuritis, and brainstem tumors. They can also be used in research to study the neural mechanisms underlying visual perception.
Cranial sutures are the fibrous joints that connect and hold together the bones of the skull (cranium) in humans and other animals. These sutures provide flexibility for the skull during childbirth and growth, allowing the skull to expand as the brain grows in size, especially during infancy and early childhood.
There are several cranial sutures in the human skull, including:
1. The sagittal suture, which runs along the midline of the skull, connecting the two parietal bones.
2. The coronal suture, which connects the frontal bone to the two parietal bones.
3. The lambdoid suture, which connects the occipital bone to the two parietal bones.
4. The squamosal suture, which connects the temporal bone to the parietal bone.
5. The frontosphenoidal and sphenoethmoidal sutures, which connect the frontal bone, sphenoid bone, and ethmoid bone in the anterior cranial fossa.
These sutures are typically made up of a specialized type of connective tissue called Sharpey's fibers, which interdigitate with each other to form a strong yet flexible joint. Over time, as the skull bones fully fuse together, these sutures become less prominent and eventually ossify (turn into bone). In some cases, abnormalities in cranial suture development or fusion can lead to medical conditions such as craniosynostosis.
Glaucoma is a group of eye conditions that damage the optic nerve, often caused by an abnormally high pressure in the eye (intraocular pressure). This damage can lead to permanent vision loss or even blindness if left untreated. The most common type is open-angle glaucoma, which has no warning signs and progresses slowly. Angle-closure glaucoma, on the other hand, can cause sudden eye pain, redness, nausea, and vomiting, as well as rapid vision loss. Other less common types of glaucoma also exist. While there is no cure for glaucoma, early detection and treatment can help slow or prevent further vision loss.
The retina is the innermost, light-sensitive layer of tissue in the eye of many vertebrates and some cephalopods. It receives light that has been focused by the cornea and lens, converts it into neural signals, and sends these to the brain via the optic nerve. The retina contains several types of photoreceptor cells including rods (which handle vision in low light) and cones (which are active in bright light and are capable of color vision).
In medical terms, any pathological changes or diseases affecting the retinal structure and function can lead to visual impairment or blindness. Examples include age-related macular degeneration, diabetic retinopathy, retinal detachment, and retinitis pigmentosa among others.
Optic neuritis is a medical condition characterized by inflammation and damage to the optic nerve, which transmits visual information from the eye to the brain. This condition can result in various symptoms such as vision loss, pain with eye movement, color vision disturbances, and pupillary abnormalities. Optic neuritis may occur in isolation or be associated with other underlying medical conditions, including multiple sclerosis, neuromyelitis optica, and autoimmune disorders. The diagnosis typically involves a comprehensive eye examination, including visual acuity testing, dilated funduscopic examination, and possibly imaging studies like MRI to evaluate the optic nerve and brain. Treatment options may include corticosteroids or other immunomodulatory therapies to reduce inflammation and prevent further damage to the optic nerve.
Hypoglossal nerve injuries refer to damages or impairments to the twelfth cranial nerve, also known as the hypoglossal nerve. This nerve is primarily responsible for controlling the movements of the tongue.
An injury to this nerve can result in various symptoms, depending on the severity and location of the damage. These may include:
1. Deviation of the tongue to one side when protruded (usually away from the side of the lesion)
2. Weakness or paralysis of the tongue muscles
3. Difficulty with speaking, swallowing, and articulation
4. Changes in taste and sensation on the back of the tongue (in some cases)
Hypoglossal nerve injuries can occur due to various reasons, such as trauma, surgical complications, tumors, or neurological disorders like stroke or multiple sclerosis. Treatment for hypoglossal nerve injuries typically focuses on managing symptoms and may involve speech and language therapy, exercises to strengthen the tongue muscles, and, in some cases, surgical intervention.
Nonpenetrating wounds are a type of trauma or injury to the body that do not involve a break in the skin or underlying tissues. These wounds can result from blunt force trauma, such as being struck by an object or falling onto a hard surface. They can also result from crushing injuries, where significant force is applied to a body part, causing damage to internal structures without breaking the skin.
Nonpenetrating wounds can cause a range of injuries, including bruising, swelling, and damage to internal organs, muscles, bones, and other tissues. The severity of the injury depends on the force of the trauma, the location of the impact, and the individual's overall health and age.
While nonpenetrating wounds may not involve a break in the skin, they can still be serious and require medical attention. If you have experienced blunt force trauma or suspect a nonpenetrating wound, it is important to seek medical care to assess the extent of the injury and receive appropriate treatment.
The optic chiasm is a structure in the brain where the optic nerves from each eye meet and cross. This allows for the integration of visual information from both eyes into the brain's visual cortex, creating a single, combined image of the visual world. The optic chiasm plays an important role in the processing of visual information and helps to facilitate depth perception and other complex visual tasks. Damage to the optic chiasm can result in various visual field deficits, such as bitemporal hemianopsia, where there is a loss of vision in the outer halves (temporal fields) of both eyes' visual fields.
A wound is a type of injury that occurs when the skin or other tissues are cut, pierced, torn, or otherwise broken. Wounds can be caused by a variety of factors, including accidents, violence, surgery, or certain medical conditions. There are several different types of wounds, including:
* Incisions: These are cuts that are made deliberately, often during surgery. They are usually straight and clean.
* Lacerations: These are tears in the skin or other tissues. They can be irregular and jagged.
* Abrasions: These occur when the top layer of skin is scraped off. They may look like a bruise or a scab.
* Punctures: These are wounds that are caused by sharp objects, such as needles or knives. They are usually small and deep.
* Avulsions: These occur when tissue is forcibly torn away from the body. They can be very serious and require immediate medical attention.
Injuries refer to any harm or damage to the body, including wounds. Injuries can range from minor scrapes and bruises to more severe injuries such as fractures, dislocations, and head trauma. It is important to seek medical attention for any injury that is causing significant pain, swelling, or bleeding, or if there is a suspected bone fracture or head injury.
In general, wounds and injuries should be cleaned and covered with a sterile bandage to prevent infection. Depending on the severity of the wound or injury, additional medical treatment may be necessary. This may include stitches for deep cuts, immobilization for broken bones, or surgery for more serious injuries. It is important to follow your healthcare provider's instructions carefully to ensure proper healing and to prevent complications.
Facial nerve injuries refer to damages or trauma inflicted on the facial nerve, also known as the seventh cranial nerve (CN VII). This nerve is responsible for controlling the muscles involved in facial expressions, eyelid movement, and taste sensation in the front two-thirds of the tongue.
There are two main types of facial nerve injuries:
1. Peripheral facial nerve injury: This type of injury occurs when damage affects the facial nerve outside the skull base, usually due to trauma from cuts, blunt force, or surgical procedures in the parotid gland or neck region. The injury may result in weakness or paralysis on one side of the face, known as Bell's palsy, and may also impact taste sensation and salivary function.
2. Central facial nerve injury: This type of injury occurs when damage affects the facial nerve within the skull base, often due to stroke, brain tumors, or traumatic brain injuries. Central facial nerve injuries typically result in weakness or paralysis only on the lower half of the face, as the upper motor neurons responsible for controlling the upper face receive innervation from both sides of the brain.
Treatment for facial nerve injuries depends on the severity and location of the damage. For mild to moderate injuries, physical therapy, protective eyewear, and medications like corticosteroids and antivirals may be prescribed. Severe cases might require surgical intervention, such as nerve grafts or muscle transfers, to restore function. In some instances, facial nerve injuries may heal on their own over time, particularly when the injury is mild and there is no ongoing compression or tension on the nerve.
Peripheral nerves are nerve fibers that transmit signals between the central nervous system (CNS, consisting of the brain and spinal cord) and the rest of the body. These nerves convey motor, sensory, and autonomic information, enabling us to move, feel, and respond to changes in our environment. They form a complex network that extends from the CNS to muscles, glands, skin, and internal organs, allowing for coordinated responses and functions throughout the body. Damage or injury to peripheral nerves can result in various neurological symptoms, such as numbness, weakness, or pain, depending on the type and severity of the damage.
Intraocular pressure (IOP) is the fluid pressure within the eye, specifically within the anterior chamber, which is the space between the cornea and the iris. It is measured in millimeters of mercury (mmHg). The aqueous humor, a clear fluid that fills the anterior chamber, is constantly produced and drained, maintaining a balance that determines the IOP. Normal IOP ranges from 10-21 mmHg, with average values around 15-16 mmHg. Elevated IOP is a key risk factor for glaucoma, a group of eye conditions that can lead to optic nerve damage and vision loss if not treated promptly and effectively. Regular monitoring of IOP is essential in diagnosing and managing glaucoma and other ocular health issues.
Optic atrophy is a medical term that refers to the degeneration and shrinkage (atrophy) of the optic nerve, which transmits visual information from the eye to the brain. This condition can result in various vision abnormalities, including loss of visual acuity, color vision deficiencies, and peripheral vision loss.
Optic atrophy can occur due to a variety of causes, such as:
* Traumatic injuries to the eye or optic nerve
* Glaucoma
* Optic neuritis (inflammation of the optic nerve)
* Ischemic optic neuropathy (reduced blood flow to the optic nerve)
* Compression or swelling of the optic nerve
* Hereditary or congenital conditions affecting the optic nerve
* Toxins and certain medications that can damage the optic nerve.
The diagnosis of optic atrophy typically involves a comprehensive eye examination, including visual acuity testing, refraction assessment, slit-lamp examination, and dilated funduscopic examination to evaluate the health of the optic nerve. In some cases, additional diagnostic tests such as visual field testing, optical coherence tomography (OCT), or magnetic resonance imaging (MRI) may be necessary to confirm the diagnosis and determine the underlying cause.
There is no specific treatment for optic atrophy, but addressing the underlying cause can help prevent further damage to the optic nerve. In some cases, vision rehabilitation may be recommended to help patients adapt to their visual impairment.
Nerve fibers are specialized structures that constitute the long, slender processes (axons) of neurons (nerve cells). They are responsible for conducting electrical impulses, known as action potentials, away from the cell body and transmitting them to other neurons or effector organs such as muscles and glands. Nerve fibers are often surrounded by supportive cells called glial cells and are grouped together to form nerve bundles or nerves. These fibers can be myelinated (covered with a fatty insulating sheath called myelin) or unmyelinated, which influences the speed of impulse transmission.
Spinal nerves are the bundles of nerve fibers that transmit signals between the spinal cord and the rest of the body. There are 31 pairs of spinal nerves in the human body, which can be divided into five regions: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each spinal nerve carries both sensory information (such as touch, temperature, and pain) from the periphery to the spinal cord, and motor information (such as muscle control) from the spinal cord to the muscles and other structures in the body. Spinal nerves also contain autonomic fibers that regulate involuntary functions such as heart rate, digestion, and blood pressure.
Optic nerve neoplasms refer to abnormal growths or tumors that develop within or near the optic nerve. These tumors can be benign (non-cancerous) or malignant (cancerous).
Benign optic nerve neoplasms include optic nerve meningiomas and schwannomas, which originate from the sheaths surrounding the optic nerve. They usually grow slowly and may not cause significant vision loss, but they can lead to compression of the optic nerve, resulting in visual field defects or optic disc swelling (papilledema).
Malignant optic nerve neoplasms are rare but more aggressive. The most common type is optic nerve glioma, which arises from the glial cells within the optic nerve. These tumors can quickly damage the optic nerve and cause severe vision loss.
It's important to note that any optic nerve neoplasm requires prompt medical evaluation and treatment, as they can potentially lead to significant visual impairment or even blindness if left untreated.
Microsurgery is a surgical technique that requires the use of an operating microscope and fine instruments to perform precise surgical manipulations. It is commonly used in various fields such as ophthalmology, neurosurgery, orthopedic surgery, and plastic and reconstructive surgery. The magnification provided by the microscope allows surgeons to work on small structures like nerves, blood vessels, and tiny bones. Some of the most common procedures that fall under microsurgery include nerve repair, replantation of amputated parts, and various types of reconstructions such as free tissue transfer for cancer reconstruction or coverage of large wounds.
Sciatic neuropathy is a condition that results from damage or injury to the sciatic nerve, which is the largest nerve in the human body. The sciatic nerve originates from the lower spine (lumbar and sacral regions) and travels down through the buttocks, hips, and legs to the feet.
Sciatic neuropathy can cause various symptoms, including pain, numbness, tingling, weakness, or difficulty moving the affected leg or foot. The pain associated with sciatic neuropathy is often described as sharp, shooting, or burning and may worsen with movement, coughing, or sneezing.
The causes of sciatic neuropathy include compression or irritation of the nerve due to conditions such as herniated discs, spinal stenosis, bone spurs, tumors, or piriformis syndrome. Trauma or injury to the lower back, hip, or buttocks can also cause sciatic neuropathy.
Diagnosing sciatic neuropathy typically involves a physical examination and medical history, as well as imaging tests such as X-rays, MRI, or CT scans to visualize the spine and surrounding structures. Treatment options may include pain management, physical therapy, steroid injections, or surgery, depending on the severity and underlying cause of the condition.
"Cell count" is a medical term that refers to the process of determining the number of cells present in a given volume or sample of fluid or tissue. This can be done through various laboratory methods, such as counting individual cells under a microscope using a specialized grid called a hemocytometer, or using automated cell counters that use light scattering and electrical impedance techniques to count and classify different types of cells.
Cell counts are used in a variety of medical contexts, including hematology (the study of blood and blood-forming tissues), microbiology (the study of microscopic organisms), and pathology (the study of diseases and their causes). For example, a complete blood count (CBC) is a routine laboratory test that includes a white blood cell (WBC) count, red blood cell (RBC) count, hemoglobin level, hematocrit value, and platelet count. Abnormal cell counts can indicate the presence of various medical conditions, such as infections, anemia, or leukemia.
Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.
The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.
Examples of animal disease models include:
1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.
Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.
Neuralgia is a type of pain that occurs along the pathway of a nerve, often caused by damage or irritation to the nerve. It is typically described as a sharp, stabbing, burning, or electric-shock like pain that can be severe and debilitating. Neuralgia can affect any nerve in the body, but it most commonly occurs in the facial area (trigeminal neuralgia) or in the nerves related to the spine (postherpetic neuralgia). The pain associated with neuralgia can be intermittent or constant and may be worsened by certain triggers such as touch, temperature changes, or movement. Treatment for neuralgia typically involves medications to manage pain, as well as other therapies such as nerve blocks, surgery, or lifestyle modifications.
Trigeminal nerve injuries refer to damages or traumas affecting the trigeminal nerve, also known as the fifth cranial nerve. This nerve is responsible for sensations in the face and motor functions such as biting and chewing. Trigeminal nerve injuries can result in various symptoms depending on the severity and location of the injury, including:
1. Loss or reduction of sensation in the face, lips, gums, teeth, or tongue.
2. Pain, often described as burning, aching, or stabbing, in the affected areas.
3. Numbness or tingling sensations.
4. Difficulty with biting, chewing, or performing other motor functions.
5. Impaired taste sensation.
6. Headaches or migraines.
7. Eye dryness or excessive tearing.
Trigeminal nerve injuries can occur due to various reasons, such as trauma during facial surgeries, accidents, tumors, infections, or neurological conditions like multiple sclerosis. Treatment options depend on the cause and severity of the injury and may include medication, physical therapy, surgical intervention, or pain management strategies.
A lingual nerve injury refers to damage or trauma to the lingual nerve, which is a branch of the mandibular nerve (itself a branch of the trigeminal nerve). The lingual nerve provides sensation to the anterior two-thirds of the tongue and the floor of the mouth. It also contributes to taste perception on the front two-thirds of the tongue through its connection with the chorda tympani nerve.
Lingual nerve injuries can result from various causes, such as surgical procedures (e.g., dental extractions, implant placements, or third molar surgeries), pressure from tumors or cysts, or direct trauma to the mouth and tongue area. The injury may lead to symptoms like numbness, altered taste sensation, pain, or difficulty speaking and swallowing. Treatment for lingual nerve injuries typically involves a combination of symptom management and possible surgical intervention, depending on the severity and cause of the injury.
Neuroprotective agents are substances that protect neurons or nerve cells from damage, degeneration, or death caused by various factors such as trauma, inflammation, oxidative stress, or excitotoxicity. These agents work through different mechanisms, including reducing the production of free radicals, inhibiting the release of glutamate (a neurotransmitter that can cause cell damage in high concentrations), promoting the growth and survival of neurons, and preventing apoptosis (programmed cell death). Neuroprotective agents have been studied for their potential to treat various neurological disorders, including stroke, traumatic brain injury, Parkinson's disease, Alzheimer's disease, and multiple sclerosis. However, more research is needed to fully understand their mechanisms of action and to develop effective therapies.
Brain-Derived Neurotrophic Factor (BDNF) is a type of protein called a neurotrophin, which is involved in the growth and maintenance of neurons (nerve cells) in the brain. BDNFA is encoded by the BDNF gene and is widely expressed throughout the central nervous system. It plays an essential role in supporting the survival of existing neurons, encouraging the growth and differentiation of new neurons and synapses, and contributing to neuroplasticity - the ability of the brain to change and adapt as a result of experience. Low levels of BDNF have been associated with several neurological disorders, including depression, Alzheimer's disease, and Huntington's disease.
Cell survival refers to the ability of a cell to continue living and functioning normally, despite being exposed to potentially harmful conditions or treatments. This can include exposure to toxins, radiation, chemotherapeutic drugs, or other stressors that can damage cells or interfere with their normal processes.
In scientific research, measures of cell survival are often used to evaluate the effectiveness of various therapies or treatments. For example, researchers may expose cells to a particular drug or treatment and then measure the percentage of cells that survive to assess its potential therapeutic value. Similarly, in toxicology studies, measures of cell survival can help to determine the safety of various chemicals or substances.
It's important to note that cell survival is not the same as cell proliferation, which refers to the ability of cells to divide and multiply. While some treatments may promote cell survival, they may also inhibit cell proliferation, making them useful for treating diseases such as cancer. Conversely, other treatments may be designed to specifically target and kill cancer cells, even if it means sacrificing some healthy cells in the process.
Nervous system trauma, also known as neurotrauma, refers to damage or injury to the nervous system, including the brain and spinal cord. This type of trauma can result from various causes, such as vehicular accidents, sports injuries, falls, violence, or penetrating traumas. Nervous system trauma can lead to temporary or permanent impairments in sensory, motor, or cognitive functions, depending on the severity and location of the injury.
Traumatic brain injury (TBI) is a common form of nervous system trauma that occurs when an external force causes brain dysfunction. TBIs can be classified as mild, moderate, or severe, based on factors such as loss of consciousness, memory loss, and neurological deficits. Mild TBIs, also known as concussions, may not cause long-term damage but still require medical attention to ensure proper healing and prevent further complications.
Spinal cord injuries (SCI) are another form of nervous system trauma that can have severe consequences. SCI occurs when the spinal cord is damaged due to a sudden, traumatic blow or cut, causing loss of motor function, sensation, or autonomic function below the level of injury. The severity and location of the injury determine the extent of impairment, which can range from partial to complete paralysis.
Immediate medical intervention is crucial in cases of nervous system trauma to minimize secondary damage, prevent complications, and optimize recovery outcomes. Treatment options may include surgery, medication, rehabilitation, or a combination of these approaches.
A brain injury is defined as damage to the brain that occurs following an external force or trauma, such as a blow to the head, a fall, or a motor vehicle accident. Brain injuries can also result from internal conditions, such as lack of oxygen or a stroke. There are two main types of brain injuries: traumatic and acquired.
Traumatic brain injury (TBI) is caused by an external force that results in the brain moving within the skull or the skull being fractured. Mild TBIs may result in temporary symptoms such as headaches, confusion, and memory loss, while severe TBIs can cause long-term complications, including physical, cognitive, and emotional impairments.
Acquired brain injury (ABI) is any injury to the brain that occurs after birth and is not hereditary, congenital, or degenerative. ABIs are often caused by medical conditions such as strokes, tumors, anoxia (lack of oxygen), or infections.
Both TBIs and ABIs can range from mild to severe and may result in a variety of physical, cognitive, and emotional symptoms that can impact a person's ability to perform daily activities and function independently. Treatment for brain injuries typically involves a multidisciplinary approach, including medical management, rehabilitation, and supportive care.
Laryngeal nerve injuries refer to damages or injuries to the recurrent laryngeal nerve (RLN) and/or the superior laryngeal nerve (SLN), which are the primary nerves that supply the larynx, or voice box. These nerves play crucial roles in controlling the vocal cord movements and protecting the airway during swallowing.
The recurrent laryngeal nerve provides motor function to all intrinsic muscles of the larynx, except for the cricothyroid muscle, which is innervated by the superior laryngeal nerve. The RLN also carries sensory fibers from a small area of the mucous membrane below the vocal folds.
Injuries to these nerves can result in voice changes, breathing difficulties, and swallowing problems. Depending on the severity and location of the injury, patients may experience hoarseness, weak voice, breathy voice, coughing while swallowing, or even complete airway obstruction in severe cases. Laryngeal nerve injuries can occur due to various reasons, such as surgical complications (e.g., thyroid, esophageal, and cardiovascular surgeries), neck trauma, tumors, infections, or iatrogenic causes.
An Optic Nerve Glioma is a type of brain tumor that arises from the glial cells (supportive tissue) within the optic nerve. It is most commonly seen in children, particularly those with neurofibromatosis type 1 (NF1). These tumors are typically slow-growing and may not cause any symptoms, especially if they are small. However, as they grow larger, they can put pressure on the optic nerve, leading to vision loss or other visual disturbances. In some cases, these tumors can also affect nearby structures in the brain, causing additional neurological symptoms. Treatment options may include observation, chemotherapy, radiation therapy, or surgery, depending on the size and location of the tumor, as well as the patient's age and overall health.
Ischemic optic neuropathy (ION) is a medical condition that refers to the damage or death of the optic nerve due to insufficient blood supply. The optic nerve is responsible for transmitting visual information from the eye to the brain.
In ION, the blood vessels that supply the optic nerve become blocked or narrowed, leading to decreased blood flow and oxygen delivery to the nerve fibers. This results in inflammation, swelling, and ultimately, damage to the optic nerve. The damage can cause sudden, painless vision loss, often noticed upon waking up in the morning.
There are two types of ION: anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). AION affects the front part of the optic nerve, while PION affects the back part of the nerve. AION is further classified into arteritic and non-arteritic types, depending on whether it is caused by giant cell arteritis or not.
Risk factors for ION include age (most commonly occurring in people over 50), hypertension, diabetes, smoking, sleep apnea, and other cardiovascular diseases. Treatment options depend on the type and cause of ION and may include controlling underlying medical conditions, administering corticosteroids, or undergoing surgical procedures to improve blood flow.
Immunohistochemistry (IHC) is a technique used in pathology and laboratory medicine to identify specific proteins or antigens in tissue sections. It combines the principles of immunology and histology to detect the presence and location of these target molecules within cells and tissues. This technique utilizes antibodies that are specific to the protein or antigen of interest, which are then tagged with a detection system such as a chromogen or fluorophore. The stained tissue sections can be examined under a microscope, allowing for the visualization and analysis of the distribution and expression patterns of the target molecule in the context of the tissue architecture. Immunohistochemistry is widely used in diagnostic pathology to help identify various diseases, including cancer, infectious diseases, and immune-mediated disorders.
Spinal cord injuries (SCI) refer to damage to the spinal cord that results in a loss of function, such as mobility or feeling. This injury can be caused by direct trauma to the spine or by indirect damage resulting from disease or degeneration of surrounding bones, tissues, or blood vessels. The location and severity of the injury on the spinal cord will determine which parts of the body are affected and to what extent.
The effects of SCI can range from mild sensory changes to severe paralysis, including loss of motor function, autonomic dysfunction, and possible changes in sensation, strength, and reflexes below the level of injury. These injuries are typically classified as complete or incomplete, depending on whether there is any remaining function below the level of injury.
Immediate medical attention is crucial for spinal cord injuries to prevent further damage and improve the chances of recovery. Treatment usually involves immobilization of the spine, medications to reduce swelling and pressure, surgery to stabilize the spine, and rehabilitation to help regain lost function. Despite advances in treatment, SCI can have a significant impact on a person's quality of life and ability to perform daily activities.
Hyperalgesia is a medical term that describes an increased sensitivity to pain. It occurs when the nervous system, specifically the nociceptors (pain receptors), become excessively sensitive to stimuli. This means that a person experiences pain from a stimulus that normally wouldn't cause pain or experiences pain that is more intense than usual. Hyperalgesia can be a result of various conditions such as nerve damage, inflammation, or certain medications. It's an important symptom to monitor in patients with chronic pain conditions, as it may indicate the development of tolerance or addiction to pain medication.
Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.
Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.
These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.
Athletic injuries are damages or injuries to the body that occur while participating in sports, physical activities, or exercise. These injuries can be caused by a variety of factors, including:
1. Trauma: Direct blows, falls, collisions, or crushing injuries can cause fractures, dislocations, contusions, lacerations, or concussions.
2. Overuse: Repetitive motions or stress on a particular body part can lead to injuries such as tendonitis, stress fractures, or muscle strains.
3. Poor technique: Using incorrect form or technique during exercise or sports can put additional stress on muscles, joints, and ligaments, leading to injury.
4. Inadequate warm-up or cool-down: Failing to properly prepare the body for physical activity or neglecting to cool down afterwards can increase the risk of injury.
5. Lack of fitness or flexibility: Insufficient strength, endurance, or flexibility can make individuals more susceptible to injuries during sports and exercise.
6. Environmental factors: Extreme weather conditions, poor field or court surfaces, or inadequate equipment can contribute to the risk of athletic injuries.
Common athletic injuries include ankle sprains, knee injuries, shoulder dislocations, tennis elbow, shin splints, and concussions. Proper training, warm-up and cool-down routines, use of appropriate protective gear, and attention to technique can help prevent many athletic injuries.
Peripheral Nervous System (PNS) diseases, also known as Peripheral Neuropathies, refer to conditions that affect the functioning of the peripheral nervous system, which includes all the nerves outside the brain and spinal cord. These nerves transmit signals between the central nervous system (CNS) and the rest of the body, controlling sensations, movements, and automatic functions such as heart rate and digestion.
PNS diseases can be caused by various factors, including genetics, infections, toxins, metabolic disorders, trauma, or autoimmune conditions. The symptoms of PNS diseases depend on the type and extent of nerve damage but often include:
1. Numbness, tingling, or pain in the hands and feet
2. Muscle weakness or cramps
3. Loss of reflexes
4. Decreased sensation to touch, temperature, or vibration
5. Coordination problems and difficulty with balance
6. Sexual dysfunction
7. Digestive issues, such as constipation or diarrhea
8. Dizziness or fainting due to changes in blood pressure
Examples of PNS diseases include Guillain-Barre syndrome, Charcot-Marie-Tooth disease, diabetic neuropathy, and peripheral nerve injuries. Treatment for these conditions varies depending on the underlying cause but may involve medications, physical therapy, lifestyle changes, or surgery.
The facial nerve, also known as the seventh cranial nerve (CN VII), is a mixed nerve that carries both sensory and motor fibers. Its functions include controlling the muscles involved in facial expressions, taste sensation from the anterior two-thirds of the tongue, and secretomotor function to the lacrimal and salivary glands.
The facial nerve originates from the brainstem and exits the skull through the internal acoustic meatus. It then passes through the facial canal in the temporal bone before branching out to innervate various structures of the face. The main branches of the facial nerve include:
1. Temporal branch: Innervates the frontalis, corrugator supercilii, and orbicularis oculi muscles responsible for eyebrow movements and eyelid closure.
2. Zygomatic branch: Supplies the muscles that elevate the upper lip and wrinkle the nose.
3. Buccal branch: Innervates the muscles of the cheek and lips, allowing for facial expressions such as smiling and puckering.
4. Mandibular branch: Controls the muscles responsible for lower lip movement and depressing the angle of the mouth.
5. Cervical branch: Innervates the platysma muscle in the neck, which helps to depress the lower jaw and wrinkle the skin of the neck.
Damage to the facial nerve can result in various symptoms, such as facial weakness or paralysis, loss of taste sensation, and dry eyes or mouth due to impaired secretion.
The Ulnar nerve is one of the major nerves in the forearm and hand, which provides motor function to the majority of the intrinsic muscles of the hand (except for those innervated by the median nerve) and sensory innervation to the little finger and half of the ring finger. It originates from the brachial plexus, passes through the cubital tunnel at the elbow, and continues down the forearm, where it runs close to the ulna bone. The ulnar nerve then passes through the Guyon's canal in the wrist before branching out to innervate the hand muscles and provide sensation to the skin on the little finger and half of the ring finger.
Reperfusion injury is a complex pathophysiological process that occurs when blood flow is restored to previously ischemic tissues, leading to further tissue damage. This phenomenon can occur in various clinical settings such as myocardial infarction (heart attack), stroke, or peripheral artery disease after an intervention aimed at restoring perfusion.
The restoration of blood flow leads to the generation of reactive oxygen species (ROS) and inflammatory mediators, which can cause oxidative stress, cellular damage, and activation of the immune system. This results in a cascade of events that may lead to microvascular dysfunction, capillary leakage, and tissue edema, further exacerbating the injury.
Reperfusion injury is an important consideration in the management of ischemic events, as interventions aimed at restoring blood flow must be carefully balanced with potential harm from reperfusion injury. Strategies to mitigate reperfusion injury include ischemic preconditioning (exposing the tissue to short periods of ischemia before a prolonged ischemic event), ischemic postconditioning (applying brief periods of ischemia and reperfusion after restoring blood flow), remote ischemic preconditioning (ischemia applied to a distant organ or tissue to protect the target organ), and pharmacological interventions that scavenge ROS, reduce inflammation, or improve microvascular function.
The Tibial nerve is a major branch of the sciatic nerve that originates in the lower back and runs through the buttock and leg. It provides motor (nerve impulses that control muscle movement) and sensory (nerve impulses that convey information about touch, temperature, and pain) innervation to several muscles and skin regions in the lower limb.
More specifically, the Tibial nerve supplies the following structures:
1. Motor Innervation: The Tibial nerve provides motor innervation to the muscles in the back of the leg (posterior compartment), including the calf muscles (gastrocnemius and soleus) and the small muscles in the foot (intrinsic muscles). These muscles are responsible for plantarflexion (pointing the foot downward) and inversion (turning the foot inward) of the foot.
2. Sensory Innervation: The Tibial nerve provides sensory innervation to the skin on the sole of the foot, as well as the heel and some parts of the lower leg.
The Tibial nerve travels down the leg, passing behind the knee and through the calf, where it eventually joins with the common fibular (peroneal) nerve to form the tibial-fibular trunk. This trunk then divides into several smaller nerves that innervate the foot's intrinsic muscles and skin.
Damage or injury to the Tibial nerve can result in various symptoms, such as weakness or paralysis of the calf and foot muscles, numbness or tingling sensations in the sole of the foot, and difficulty walking or standing on tiptoes.
Nerve compression syndromes refer to a group of conditions characterized by the pressure or irritation of a peripheral nerve, causing various symptoms such as pain, numbness, tingling, and weakness in the affected area. This compression can occur due to several reasons, including injury, repetitive motion, bone spurs, tumors, or swelling. Common examples of nerve compression syndromes include carpal tunnel syndrome, cubital tunnel syndrome, radial nerve compression, and ulnar nerve entrapment at the wrist or elbow. Treatment options may include physical therapy, splinting, medications, injections, or surgery, depending on the severity and underlying cause of the condition.
A nerve block is a medical procedure in which an anesthetic or neurolytic agent is injected near a specific nerve or bundle of nerves to block the transmission of pain signals from that area to the brain. This technique can be used for both diagnostic and therapeutic purposes, such as identifying the source of pain, providing temporary or prolonged relief, or facilitating surgical procedures in the affected region.
The injection typically contains a local anesthetic like lidocaine or bupivacaine, which numbs the nerve, preventing it from transmitting pain signals. In some cases, steroids may also be added to reduce inflammation and provide longer-lasting relief. Depending on the type of nerve block and its intended use, the injection might be administered close to the spine (neuraxial blocks), at peripheral nerves (peripheral nerve blocks), or around the sympathetic nervous system (sympathetic nerve blocks).
While nerve blocks are generally safe, they can have side effects such as infection, bleeding, nerve damage, or in rare cases, systemic toxicity from the anesthetic agent. It is essential to consult with a qualified medical professional before undergoing this procedure to ensure proper evaluation, technique, and post-procedure care.
The median nerve is one of the major nerves in the human body, providing sensation and motor function to parts of the arm and hand. It originates from the brachial plexus, a network of nerves that arise from the spinal cord in the neck. The median nerve travels down the arm, passing through the cubital tunnel at the elbow, and continues into the forearm and hand.
In the hand, the median nerve supplies sensation to the palm side of the thumb, index finger, middle finger, and half of the ring finger. It also provides motor function to some of the muscles that control finger movements, allowing for flexion of the fingers and opposition of the thumb.
Damage to the median nerve can result in a condition called carpal tunnel syndrome, which is characterized by numbness, tingling, and weakness in the hand and fingers.
Spinal ganglia, also known as dorsal root ganglia, are clusters of nerve cell bodies located in the peripheral nervous system. They are situated along the length of the spinal cord and are responsible for transmitting sensory information from the body to the brain. Each spinal ganglion contains numerous neurons, or nerve cells, with long processes called axons that extend into the periphery and innervate various tissues and organs. The cell bodies within the spinal ganglia receive sensory input from these axons and transmit this information to the central nervous system via the dorsal roots of the spinal nerves. This allows the brain to interpret and respond to a wide range of sensory stimuli, including touch, temperature, pain, and proprioception (the sense of the position and movement of one's body).
Papilledema is a medical term that refers to swelling of the optic nerve head, also known as the disc, which is the point where the optic nerve enters the back of the eye (the retina). This swelling can be caused by increased pressure within the skull, such as from brain tumors, meningitis, or idiopathic intracranial hypertension. Papilledema is usually detected through a routine eye examination and may be accompanied by symptoms such as headaches, visual disturbances, and nausea. If left untreated, papilledema can lead to permanent vision loss.
The femoral nerve is a major nerve in the thigh region of the human body. It originates from the lumbar plexus, specifically from the ventral rami (anterior divisions) of the second, third, and fourth lumbar nerves (L2-L4). The femoral nerve provides motor and sensory innervation to various muscles and areas in the lower limb.
Motor Innervation:
The femoral nerve is responsible for providing motor innervation to several muscles in the anterior compartment of the thigh, including:
1. Iliacus muscle
2. Psoas major muscle
3. Quadriceps femoris muscle (consisting of four heads: rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius)
These muscles are involved in hip flexion, knee extension, and stabilization of the hip joint.
Sensory Innervation:
The sensory distribution of the femoral nerve includes:
1. Anterior and medial aspects of the thigh
2. Skin over the anterior aspect of the knee and lower leg (via the saphenous nerve, a branch of the femoral nerve)
The saphenous nerve provides sensation to the skin on the inner side of the leg and foot, as well as the medial malleolus (the bony bump on the inside of the ankle).
In summary, the femoral nerve is a crucial component of the lumbar plexus that controls motor functions in the anterior thigh muscles and provides sensory innervation to the anterior and medial aspects of the thigh and lower leg.
Accessory nerve injuries refer to damage or trauma to the eleventh cranial nerve, also known as the accessory nerve. This nerve has both a cranial and spinal root, and it primarily controls the movement of some muscles in the neck and shoulder.
Injuries to the accessory nerve can result in weakness or paralysis of the affected muscles, leading to difficulty turning the head or lifting the arm. The severity of the symptoms depends on the extent and location of the injury. Accessory nerve injuries can occur due to various reasons, such as trauma during surgery (particularly neck or shoulder surgeries), penetrating injuries, tumors, or neurological disorders.
Treatment for accessory nerve injuries typically involves a combination of physical therapy, pain management, and, in some cases, surgical intervention to repair the damaged nerve. The prognosis for recovery varies depending on the severity and cause of the injury.
Recurrent laryngeal nerve injuries refer to damages or trauma inflicted on the recurrent laryngeal nerve, which is a branch of the vagus nerve that supplies motor function to the intrinsic muscles of the larynx, except for the cricothyroid muscle. This nerve plays a crucial role in controlling vocal fold movement and swallowing.
Injuries to this nerve can result in voice changes, hoarseness, or even complete loss of voice, depending on the severity and location of the injury. Additionally, it may also lead to breathing difficulties, coughing, and choking while swallowing due to impaired laryngeal function.
Recurrent laryngeal nerve injuries can occur due to various reasons, such as surgical complications (particularly during thyroid or neck surgeries), tumors, infections, inflammation, or direct trauma to the neck region. In some cases, these injuries may be temporary and resolve on their own or through appropriate treatment; however, severe or prolonged injuries might require medical intervention, including possible surgical repair.
The myelin sheath is a multilayered, fatty substance that surrounds and insulates many nerve fibers in the nervous system. It is essential for the rapid transmission of electrical signals, or nerve impulses, along these nerve fibers, allowing for efficient communication between different parts of the body. The myelin sheath is produced by specialized cells called oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS). Damage to the myelin sheath, as seen in conditions like multiple sclerosis, can significantly impair nerve function and result in various neurological symptoms.
The sural nerve is a purely sensory peripheral nerve in the lower leg and foot. It provides sensation to the outer ( lateral) aspect of the little toe and the adjacent side of the fourth toe, as well as a small portion of the skin on the back of the leg between the ankle and knee joints.
The sural nerve is formed by the union of branches from the tibial and common fibular nerves (branches of the sciatic nerve) in the lower leg. It runs down the calf, behind the lateral malleolus (the bony prominence on the outside of the ankle), and into the foot.
The sural nerve is often used as a donor nerve during nerve grafting procedures due to its consistent anatomy and relatively low risk for morbidity at the donor site.
The optic lobe in non-mammals refers to a specific region of the brain that is responsible for processing visual information. It is a part of the protocerebrum in the insect brain and is analogous to the mammalian visual cortex. The optic lobes receive input directly from the eyes via the optic nerves and are involved in the interpretation and integration of visual stimuli, enabling non-mammals to perceive and respond to their environment. In some invertebrates, like insects, the optic lobe is further divided into subregions, including the lamina, medulla, and lobula, each with distinct functions in visual processing.
Nerve degeneration, also known as neurodegeneration, is the progressive loss of structure and function of neurons, which can lead to cognitive decline, motor impairment, and various other symptoms. This process occurs due to a variety of factors, including genetics, environmental influences, and aging. It is a key feature in several neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. The degeneration can affect any part of the nervous system, leading to different symptoms depending on the location and extent of the damage.
Eye injuries refer to any damage or trauma caused to the eye or its surrounding structures. These injuries can vary in severity and may include:
1. Corneal abrasions: A scratch or scrape on the clear surface of the eye (cornea).
2. Chemical burns: Occurs when chemicals come into contact with the eye, causing damage to the cornea and other structures.
3. Eyelid lacerations: Cuts or tears to the eyelid.
4. Subconjunctival hemorrhage: Bleeding under the conjunctiva, the clear membrane that covers the white part of the eye.
5. Hyphema: Accumulation of blood in the anterior chamber of the eye, which is the space between the cornea and iris.
6. Orbital fractures: Breaks in the bones surrounding the eye.
7. Retinal detachment: Separation of the retina from its underlying tissue, which can lead to vision loss if not treated promptly.
8. Traumatic uveitis: Inflammation of the uvea, the middle layer of the eye, caused by trauma.
9. Optic nerve damage: Damage to the optic nerve, which transmits visual information from the eye to the brain.
Eye injuries can result from a variety of causes, including accidents, sports-related injuries, violence, and chemical exposure. It is important to seek medical attention promptly for any suspected eye injury to prevent further damage and potential vision loss.
Hereditary optic atrophies (HOAs) are a group of genetic disorders that cause degeneration of the optic nerve, leading to vision loss. The optic nerve is responsible for transmitting visual information from the eye to the brain. In HOAs, this nerve degenerates over time, resulting in decreased visual acuity, color vision deficits, and sometimes visual field defects.
There are several types of HOAs, including dominant optic atrophy (DOA), Leber hereditary optic neuropathy (LHON), autosomal recessive optic atrophy (AROA), and Wolfram syndrome. Each type has a different inheritance pattern and is caused by mutations in different genes.
DOA is the most common form of HOA and is characterized by progressive vision loss that typically begins in childhood or early adulthood. It is inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the disease-causing mutation from an affected parent.
LHON is a mitochondrial disorder that primarily affects males and is characterized by sudden, severe vision loss that typically occurs in young adulthood. It is caused by mutations in the mitochondrial DNA and is inherited maternally.
AROA is a rare form of HOA that is inherited in an autosomal recessive manner, meaning that both copies of the gene must be mutated to cause the disease. It typically presents in infancy or early childhood with progressive vision loss.
Wolfram syndrome is a rare genetic disorder that affects multiple organs, including the eyes, ears, and endocrine system. It is characterized by diabetes insipidus, diabetes mellitus, optic atrophy, and hearing loss. It is inherited in an autosomal recessive manner.
There is currently no cure for HOAs, but treatments such as low-vision aids and rehabilitation may help to manage the symptoms. Research is ongoing to develop new therapies for these disorders.
Wallerian degeneration is a process that occurs following damage to the axons of neurons (nerve cells). After an axon is severed or traumatically injured, it undergoes a series of changes including fragmentation and removal of the distal segment of the axon, which is the part that is separated from the cell body. This process is named after Augustus Waller, who first described it in 1850.
The degenerative changes in the distal axon are characterized by the breakdown of the axonal cytoskeleton, the loss of myelin sheath (the fatty insulating material that surrounds and protects the axon), and the infiltration of macrophages to clear away the debris. These events lead to the degeneration of the distal axon segment, which is necessary for successful regeneration of the injured nerve.
Wallerian degeneration is a crucial process in the nervous system's response to injury, as it enables the regrowth of axons and the reestablishment of connections between neurons. However, if the regenerative capacity of the neuron is insufficient or the environment is not conducive to growth, functional recovery may be impaired, leading to long-term neurological deficits.
The spinal cord is a major part of the nervous system, extending from the brainstem and continuing down to the lower back. It is a slender, tubular bundle of nerve fibers (axons) and support cells (glial cells) that carries signals between the brain and the rest of the body. The spinal cord primarily serves as a conduit for motor information, which travels from the brain to the muscles, and sensory information, which travels from the body to the brain. It also contains neurons that can independently process and respond to information within the spinal cord without direct input from the brain.
The spinal cord is protected by the bony vertebral column (spine) and is divided into 31 segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each segment corresponds to a specific region of the body and gives rise to pairs of spinal nerves that exit through the intervertebral foramina at each level.
The spinal cord is responsible for several vital functions, including:
1. Reflexes: Simple reflex actions, such as the withdrawal reflex when touching a hot surface, are mediated by the spinal cord without involving the brain.
2. Muscle control: The spinal cord carries motor signals from the brain to the muscles, enabling voluntary movement and muscle tone regulation.
3. Sensory perception: The spinal cord transmits sensory information, such as touch, temperature, pain, and vibration, from the body to the brain for processing and awareness.
4. Autonomic functions: The sympathetic and parasympathetic divisions of the autonomic nervous system originate in the thoracolumbar and sacral regions of the spinal cord, respectively, controlling involuntary physiological responses like heart rate, blood pressure, digestion, and respiration.
Damage to the spinal cord can result in various degrees of paralysis or loss of sensation below the level of injury, depending on the severity and location of the damage.
Axonal transport is the controlled movement of materials and organelles within axons, which are the nerve fibers of neurons (nerve cells). This intracellular transport system is essential for maintaining the structural and functional integrity of axons, particularly in neurons with long axonal processes. There are two types of axonal transport: anterograde transport, which moves materials from the cell body toward the synaptic terminals, and retrograde transport, which transports materials from the synaptic terminals back to the cell body. Anterograde transport is typically slower than retrograde transport and can be divided into fast and slow components based on velocity. Fast anterograde transport moves vesicles containing neurotransmitters and their receptors, as well as mitochondria and other organelles, at speeds of up to 400 mm/day. Slow anterograde transport moves cytoskeletal elements, proteins, and RNA at speeds of 1-10 mm/day. Retrograde transport is primarily responsible for recycling membrane components, removing damaged organelles, and transmitting signals from the axon terminal to the cell body. Dysfunctions in axonal transport have been implicated in various neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS).
Optic flow is not a medical term per se, but rather a term used in the field of visual perception and neuroscience. It refers to the pattern of motion of objects in the visual field that occurs as an observer moves through the environment. This pattern of motion is important for the perception of self-motion and the estimation of egocentric distance (the distance of objects in the environment relative to the observer). Optic flow has been studied in relation to various clinical populations, such as individuals with vestibular disorders or visual impairments, who may have difficulty processing optic flow information.
Spinal nerve roots are the initial parts of spinal nerves that emerge from the spinal cord through the intervertebral foramen, which are small openings between each vertebra in the spine. These nerve roots carry motor, sensory, and autonomic fibers to and from specific regions of the body. There are 31 pairs of spinal nerve roots in total, with 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal pair. Each root has a dorsal (posterior) and ventral (anterior) ramus that branch off to form the peripheral nervous system. Irritation or compression of these nerve roots can result in pain, numbness, weakness, or loss of reflexes in the affected area.
Nerve Growth Factors (NGFs) are a family of proteins that play an essential role in the growth, maintenance, and survival of certain neurons (nerve cells). They were first discovered by Rita Levi-Montalcini and Stanley Cohen in 1956. NGF is particularly crucial for the development and function of the peripheral nervous system, which connects the central nervous system to various organs and tissues throughout the body.
NGF supports the differentiation and survival of sympathetic and sensory neurons during embryonic development. In adults, NGF continues to regulate the maintenance and repair of these neurons, contributing to neuroplasticity – the brain's ability to adapt and change over time. Additionally, NGF has been implicated in pain transmission and modulation, as well as inflammatory responses.
Abnormal levels or dysfunctional NGF signaling have been associated with various medical conditions, including neurodegenerative diseases (e.g., Alzheimer's and Parkinson's), chronic pain disorders, and certain cancers (e.g., small cell lung cancer). Therefore, understanding the role of NGF in physiological and pathological processes may provide valuable insights into developing novel therapeutic strategies for these conditions.
The Injury Severity Score (ISS) is a medical scoring system used to assess the severity of trauma in patients with multiple injuries. It's based on the Abbreviated Injury Scale (AIS), which classifies each injury by body region on a scale from 1 (minor) to 6 (maximum severity).
The ISS is calculated by summing the squares of the highest AIS score in each of the three most severely injured body regions. The possible ISS ranges from 0 to 75, with higher scores indicating more severe injuries. An ISS over 15 is generally considered a significant injury, and an ISS over 25 is associated with a high risk of mortality. It's important to note that the ISS has limitations, as it doesn't consider the number or type of injuries within each body region, only the most severe one.
The eye is the organ of sight, primarily responsible for detecting and focusing on visual stimuli. It is a complex structure composed of various parts that work together to enable vision. Here are some of the main components of the eye:
1. Cornea: The clear front part of the eye that refracts light entering the eye and protects the eye from harmful particles and microorganisms.
2. Iris: The colored part of the eye that controls the amount of light reaching the retina by adjusting the size of the pupil.
3. Pupil: The opening in the center of the iris that allows light to enter the eye.
4. Lens: A biconvex structure located behind the iris that further refracts light and focuses it onto the retina.
5. Retina: A layer of light-sensitive cells (rods and cones) at the back of the eye that convert light into electrical signals, which are then transmitted to the brain via the optic nerve.
6. Optic Nerve: The nerve that carries visual information from the retina to the brain.
7. Vitreous: A clear, gel-like substance that fills the space between the lens and the retina, providing structural support to the eye.
8. Conjunctiva: A thin, transparent membrane that covers the front of the eye and the inner surface of the eyelids.
9. Extraocular Muscles: Six muscles that control the movement of the eye, allowing for proper alignment and focus.
The eye is a remarkable organ that allows us to perceive and interact with our surroundings. Various medical specialties, such as ophthalmology and optometry, are dedicated to the diagnosis, treatment, and management of various eye conditions and diseases.
Lomerizine
Intraocular hemorrhage
Max Talmey
Blacklight paint
Anesthesia for eye surgery
Blast-related ocular trauma
SARM1
Wilbrand's knee
Coluracetam
Military career of L. Ron Hubbard
1996 Dura Lube 200
Posterior ischemic optic neuropathy
Nasal surgery
Role of microglia in disease
Paint mixing
Pseudobiography of L. Ron Hubbard
Suter MMX2
Protective autoimmunity
Red eye (medicine)
Optic nerve
Center for the Partially Sighted
Scotoma
Emergency ultrasound
Wallerian degeneration
List of MeSH codes (C10)
Bob Switzer
Optic neuropathy
2011-12 Notre Dame Fighting Irish men's basketball team
Orbital emphysema
Digestion chambers
2014 ICD-9-CM Diagnosis Code 950.9 : Injury to unspecified optic nerve and pathways
Optic Nerve Disorders: MedlinePlus
Optic nerve as a source of activated retinal microglia post-injury<...
Retinal genomic fabric remodeling after optic nerve injury<...
Optic Nerve Injuries | Profiles RNS
Chelation Therapy - Medical Clinical Policy Bulletins | Aetna
Optic Nerve Decompression for Traumatic Optic Neuropathy: Practice Essentials, History of the Procedure, Problem
Optic Nerve Injuries; Optic Nerve Trauma; Optic Neuropathy, Traumatic; Second Cranial Nerve Trauma
Prognostic Effect of Optic Nerve Sheath Diameter Measurement in Traumatic Brain Injury Patients Admitted to Emergency Department
Optic Nerve Decompression Surgery - Medical Clinical Policy Bulletins | Aetna
Exogenous Modulation of Retinoic Acid Signaling Affects Adult RGC Survival in the Frog Visual System after Optic Nerve Injury -...
Human embryonic stem cell-derived mesenchymal cells preserve kidney function and extend lifespan in NZB/W F1 mouse model of...
Lomerizine - Wikipedia
M1 News Research Articles
NEI Office of Regenerative Medicine: Vision Innovation Seminars | National Eye Institute
Low-Tension Glaucoma Medication: Alpha2-adrenergic agonists, Carbonic anhydrase inhibitors, Beta-adrenergic blockers,...
Table of Contents - June 15, 2000, 20 (12) | Journal of Neuroscience
Prevention and Treatment of Common Eye Injuries in Sports | AAFP
Retrobulbar Block: Overview, Periprocedural Care, Technique
SciELO - Brazil - Comparative study of the distribution and expression of Neuroglobin and Hypoxia-inducible factor-1α in the...
Glaucoma - Symptoms and causes - Mayo Clinic
KoreaMed
Bioline International Official Site (site up-dated regularly)
Frontiers | Why Most Traumatic Brain Injuries are Not Caused by Linear Acceleration but Skull Fractures are
2023 ICD-10-CM Diagnosis Code H54: Blindness and low vision
Involvement of Nrf2 in Ocular Diseases
Cells | Free Full-Text | Low-Intensity Blue Light Exposure Reduces Melanopsin Expression in Intrinsically Photosensitive...
Astrocytes | Harvard Catalyst Profiles | Harvard Catalyst
Glaucoma16
- Glaucoma usually happens when the fluid pressure inside the eyes slowly rises and damages the optic nerve. (medlineplus.gov)
- This drug is currently used clinically for the treatment of migraines, while also being used experimentally for the treatment of glaucoma and optic nerve injury. (wikipedia.org)
- Glaucoma is a group of eye conditions that damage the optic nerve. (mayoclinic.org)
- Glaucoma develops when the optic nerve becomes damaged. (mayoclinic.org)
- Glaucoma is a collection of eye diseases that affect the optic nerve, which is essential for good vision. (trustedhealthproducts.com)
- The injury to the optic nerve causes glaucoma. (trustedhealthproducts.com)
- Your optic nerve is injured with normal-tension glaucoma even though your eye pressure is within the usual range. (trustedhealthproducts.com)
- Researchers recently reported a technique that increases the regenerative capacity of retinal axons in a mouse model of optic nerve injury, a model commonly used to study glaucoma and other optic neuropathies. (nih.gov)
- Newswise - A form of gene therapy protects optic nerve cells and preserves vision in mouse models of glaucoma, according to research supported by NIH's National Eye Institute. (newswise.com)
- Glaucoma results from irreversible neurodegeneration of the optic nerve, the bundle of axons from retinal ganglion cells that transmits signals from the eye to the brain to produce vision. (newswise.com)
- Our study is the first to show that activating the CaMKII pathway helps protect retinal ganglion cells from a variety of injuries and in multiple glaucoma models," said the study's lead investigator, Bo Chen, Ph.D., associate professor of ophthalmology and neuroscience at the Icahn School of Medicine at Mount Sinai in New York City. (newswise.com)
- Optic nerve crush has been used as a model neuronal injury, including glaucoma, traumatic optic neuropathies, neurodegeneration and CNS injury. (pharmoptima.com)
- Applications include traumatic optic neuropathy, glaucoma and neurodegenerative disease. (pharmoptima.com)
- Glaucomatous injury is a pathohistological feature of glaucoma in the optic nerve. (pharmoptima.com)
- The optic nerve crush model can test agents treating glaucoma, traumatic optic neuropathies, neurodegeneration, and CNS injury and inflammation. (pharmoptima.com)
- In fact, studies have shown that red light may protect vision and even support a reversal of age-related ocular (eye) disorders such as macular degeneration and glaucoma, as well as eye injuries. (platinumtherapylights.com)
Neuropathies3
- A review of optic neuropathies. (uchicago.edu)
- Hereditary optic neuropathies result from genetic defects that cause vision loss and occasionally cardiac or neurologic abnormalities. (msdmanuals.com)
- It is believed to be the most common of the hereditary optic neuropathies, with prevalence in the range of 1:10,000 to 1:50,000. (msdmanuals.com)
Retinal ganglion cell2
- Park KK , Luo X, Mooney SJ , Yungher BJ , Belin S , Wang C , Holmes MM , He Z . Retinal ganglion cell survival and axon regeneration after optic nerve injury in naked mole-rats. (neurotree.org)
- Using an antibody marker of CaMKII activity, Chen's team discovered that CaMKII pathway signaling was compromised whenever retinal ganglion cells were exposed to toxins or trauma from a crush injury to the optic nerve, suggesting a correlation between CaMKII activity and retinal ganglion cell survival. (newswise.com)
Retina7
- Comparison of optic nerve to retina following an ONC showed a much greater concentration of GFPhi cells and GFPlo microglia in the optic nerve. (umn.edu)
- Optic nerve injury also induced Ki67+ cells in the optic nerve but not in the retina. (umn.edu)
- Comparison of the retinal myeloid cell response after full versus partial ONT revealed fewer GFPhi cells and GFPlo microglia in the retina following a full ONT despite it being a more severe injury, suggesting that full transection of the optic nerve can block the migration of responding myeloid cells to the retina. (umn.edu)
- Our results suggest that the optic nerve can be a reservoir for activated microglia and other retinal myeloid cells in the retina following optic nerve injury. (umn.edu)
- We profiled the retina transcriptome of Lister Hooded rats at 2 weeks after optic nerve crush (ONC) and analyzed the data from the genomic fabric paradigm (GFP) to bring additional insights into the molecular mechanisms of the retinal remodeling after induction of RGC degeneration. (elsevierpure.com)
- Goldberg and colleagues have demonstrated through a series of interventions in mice with optic nerve injury that they can successfully regenerate retinal ganglion cells axons, which form the optic nerve that transmits visual information from the retina to the brain. (nih.gov)
- Crush injury to the optic nerve severs the retinal ganglion cell (RGC) axons leading to the gradual death of RGC neurons in the retina. (pharmoptima.com)
Ischemic optic neur4
- Haemodilution and head-down tilting induce functional injury in the rat optic nerve: A model for peri-operative ischemic optic neuropathy. (uchicago.edu)
- Non-arteritic anterior ischemic optic neuropathy (NAION) is a common cause of sudden loss of vision, especially in the elderly. (aetna.com)
- To resolve the controversy over the effectiveness of optic nerve decompression for NAION, the National Eye Institute sponsored the Ischemic Optic Neuropathy Decompression Trial, a multicenter, randomized controlled clinical trial of optic nerve decompression surgery for patients with NAION. (aetna.com)
- A structured evidence review (Dickersin and Manheimer, 2002) concluded that "[r]esults from the Ischemic Optic Neuropathy Decompression Trial indicate that optic nerve decompression surgery for nonarteritic ischemic optic neuropathy is not effective. (aetna.com)
Neuropathy15
- Traumatic optic neuropathy is a devastating potential complication of closed head injury. (medscape.com)
- The hallmark of an optic neuropathy, traumatic or otherwise, is a loss of visual function, which can manifest by subnormal visual acuity, visual field loss, or color vision dysfunction. (medscape.com)
- The presence of an afferent pupillary defect strongly suggests a prechiasmal location for the injury and is necessary to support the diagnosis of traumatic optic neuropathy. (medscape.com)
- Vision loss associated with traumatic optic neuropathy can be partial or complete and temporary or permanent. (medscape.com)
- In polytraumatized patients with poor awareness, CT scanning with clinical exploration is the most important method for the assessment of traumatic optic neuropathy in the acute emergency setting. (medscape.com)
- Patients suspected of sustaining traumatic optic neuropathy should undergo visual field testing. (medscape.com)
- Although no visual field defects are pathognomonic of traumatic optic neuropathy, quantification of visual field defects is useful to assess convalescent visual improvements. (medscape.com)
- Historically, the 3 treatment paradigms advocated for traumatic optic neuropathy are observation, medical corticosteroid therapy, or optic canal decompression. (medscape.com)
- [ 8 ] In the early 1900s, transcranial unroofing of the optic canal was the surgical procedure of choice for traumatic optic neuropathy treatment. (medscape.com)
- During this period, systemic corticosteroid treatment was also extended to treatment of traumatic optic neuropathy. (medscape.com)
- Recent advances in endoscopic instrumentation and intranasal sinus surgical techniques have refined extracranial surgical approaches for traumatic optic neuropathy. (medscape.com)
- The traumatic optic neuropathy occurs in 0.5 to 5% of closed head trauma cases. (koreamed.org)
- Vision loss in patients with Leber hereditary optic neuropathy typically begins between 15 and 35 years (range, 1 to 80 years). (msdmanuals.com)
- Some patients with Leber hereditary optic neuropathy have cardiac conduction defects. (msdmanuals.com)
- Optic nerve crush serves as a useful model for traumatic optic neuropathy and mimics glaucomatous injury, similarly inducing RGC cell death and degeneration. (pharmoptima.com)
Intraocular2
- Retrobulbar block is type of regional anesthetic nerve block used in intraocular surgery. (medscape.com)
- If that system is blocked or isn't functioning well, the pressure inside the eye (intraocular pressure) builds, which in turn damages the optic nerve. (mayoclinic.org)
Cause optic nerve2
- Drainage blockages or an underlying medical issue could cause optic nerve injury. (trustedhealthproducts.com)
- The condition involves a build up of fluid in the brain, which can cause optic nerve damage and other injuries, and often can only be relieved through a lumbar puncture. (aboutlawsuits.com)
Regeneration13
- Researchers identified a small molecule capable of stimulating nerve regeneration and restoring vision following injury to the optic nerve. (neurosciencenews.com)
- Optic nerve diseases and regeneration: How far are we from the promised land? (neurotree.org)
- Subtype-specific survival and regeneration of retinal ganglion cells in response to injury. (neurotree.org)
- Retinal ganglion cell expression of cytokine enhances occupancy of NG2 cell-derived astrocytes at the nerve injury site: Implication for axon regeneration. (neurotree.org)
- Proteomics and systems biology in optic nerve regeneration. (neurotree.org)
- Optic nerve regeneration in mammals: Regenerated or spared axons? (neurotree.org)
- Wnt signaling promotes axonal regeneration following optic nerve injury in the mouse. (neurotree.org)
- Here we show through systematic epigenetic studies that the histone acetyltransferase p300/CBP-associated factor (PCAF) promotes acetylation of histone 3 Lys 9 at the promoters of established key regeneration-associated genes following a peripheral but not a central axonal injury. (nature.com)
- Finally, PCAF is necessary for conditioning-dependent axonal regeneration and also singularly promotes regeneration after spinal cord injury. (nature.com)
- Interestingly, the lack of regeneration of injured ascending sensory fibres in the spinal cord can be partially enhanced by an injury to the peripheral branch (conditioning lesion) of DRG neurones 7 . (nature.com)
- Finally, we established that PCAF is required for regeneration following a conditioning lesion and PCAF overexpression promotes axonal regeneration similar to that of a conditioning lesion after CNS injury in spinal ascending sensory fibres. (nature.com)
- The model provides an opportunity to study neuronal outcomes following injury, including survival, apoptosis, regeneration and associated biomarkers. (pharmoptima.com)
- qRT-PCR of Atf3, Sprr1a, Ddit3 (Chop), and Gfap from retinal RNA four days after optic nerve crush (ONC) compared to uninjured contralateral control (CTL): upregulation of regeneration-associated genes Atf3 and Sprr1a, pro-apoptotic transcription factor Ddit3 (Chop), and reactive astrocyte marker Gfap demonstrates a robust response to injury following ONC. (pharmoptima.com)
Clinical1
- Diagnosis of dominant optic atrophy and Leber hereditary optic atrophy is mainly clinical. (msdmanuals.com)
Axonal9
- Use of immunocytochemical labeling techniques has recently demonstrated that axonal injury (AI) and the ensuing reactive axonal change is, probably, more widespread and occurs over a longer posttraumatic time in the injured brain than had previously been appreciated. (nih.gov)
- The comparability of AI in animal models to human diffuse AI (DAI) is discussed and the conclusion drawn that, although animal models allow the analysis of morphologic changes, the spatial distribution within the brain and the time course of reactive axonal change differs to some extent both between species and with the mode of brain injury. (nih.gov)
- Recent work has provided a consensus that reactive axonal change is linked to pertubation of the axolemma resulting in disruption of ionic homeostatic mechanisms within injured nerve fibers. (nih.gov)
- Recent studies of responses by the axonal cytoskeleton after nondisruptive AI have demonstrated loss of axonal microtubules over a period up to 24 h after injury. (nih.gov)
- Axonal regenerative failure is a major cause of neurological impairment following central nervous system (CNS) but not peripheral nervous system (PNS) injury. (nature.com)
- The regenerative response initiated following axonal injury in the peripheral nervous system (PNS) versus the central nervous system (CNS) leads to differential growth capacities and repair. (nature.com)
- However, the final link between axonal injury-induced retrograde signalling and the regulation of essential regenerative gene expression remains elusive. (nature.com)
- We examined both DNA methylation and various key histone modifications with regards to gene regulation following axonal injury. (nature.com)
- We found that p300/CBP-associated factor (PCAF)-dependent acetylation of histone 3 lysine 9 (H3K9ac), paralleled by a reduction in methylation of H3K9 (H3K9me2), occurred at the promoters of select genes only after PNS axonal injury. (nature.com)
Neurodegeneration1
- Mitochondria dysregulation contributes to secondary neurodegeneration progression post-contusion injury in human 3D in vitro triculture brain tissue model. (harvard.edu)
Axons3
- Using mice expressing green fluorescent protein (GFP) from a transgenic CD11c promoter we found that a controlled optic nerve crush (ONC) injury attracted GFPhi retinal myeloid cells to the dying retinal ganglion cells and their axons. (umn.edu)
- Axons are particularly at risk in human diffuse head injury. (nih.gov)
- In addition, there is developing in the literature considerable variance in the terminology applied to injured axons or nerve fibers. (nih.gov)
Diseases1
- ICD-9-CM codes are used in medical billing and coding to describe diseases, injuries, symptoms and conditions. (icd9data.com)
Disorders4
- Tests for optic nerve disorders may include eye exams, ophthalmoscopy (an examination of the back of your eye), and imaging tests . (medlineplus.gov)
- With some optic nerve disorders, you may get your vision back. (medlineplus.gov)
- For the recent 10 years, we summarized the experience of the rhinology unit of our department regarding orbital injury and complications of ESS for sinonasal inflammatory disorders. (scirp.org)
- For the 10 years from 2003 to 2012, we summarized the experience of the rhinology unit of our department regarding orbital injury and complications of ESS for sinonasal inflammatory disorders. (scirp.org)
Glaucomatous Injury1
- Astrocytes in the Optic Nerve Are Heterogeneous in Their Reactivity to Glaucomatous Injury. (harvard.edu)
Atrophy5
- Optic nerve atrophy is damage to the optic nerve. (medlineplus.gov)
- By the time optic atrophy is detected, substantial optic nerve injury has already occurred. (msdmanuals.com)
- Dominant optic atrophy is inherited in an autosomal dominant fashion. (msdmanuals.com)
- Most patients with dominant optic atrophy have no associated neurologic abnormalities, although nystagmus and hearing loss have been reported. (msdmanuals.com)
- Eventually, optic atrophy supervenes. (msdmanuals.com)
Pathways3
- Following targeted motor and sensory reinnervation, a procedure that reroutes residual limb nerves to intact muscles and skin in amputees, the brain remaps both motor and sensory pathways. (neurosciencenews.com)
- Western blot of retinal tissue three days following optic nerve crush compared to uninjured control: upregulation of injury marker, pcJun, demonstrates activation of signaling pathways important for neuronal outcome following ONC. (pharmoptima.com)
- Immunostained whole mount retinas following optic nerve crush (ONC): upregulation of injury marker, pcJun, demonstrates activation of injury signaling pathways resulting in retinal ganglion cell (RGC) death following ONC. (pharmoptima.com)
Drusen1
- Visual loss secondary to optic nerve drusen. (aetna.com)
Traumatic brain3
- Therefore, rotational kinematics should be a better indicator of traumatic brain injury risk than linear acceleration. (frontiersin.org)
- Therefore, distortional strain was used as an indicator of the risk of traumatic brain injury in the current study. (frontiersin.org)
- In the presence of normal neurologic and ophthalmologic examinations, the most common conditions associated with photophobia are migraine, blepharospasm, and traumatic brain injury. (researchgate.net)
Decompression7
- Hemostasis is essential during optic canal decompression. (medscape.com)
- In the 1920s, Sewell performed a transethmoidal optic canal decompression by removing the lamina papyracea and medial wall of the optic canal. (medscape.com)
- Currently, endoscopic optic nerve decompression (OND) via an intranasal and transethmoidal or transsphenoidal approach has gained popular support. (medscape.com)
- Optic nerve decompression surgery (also known as optic nerve sheath decompression surgery) involves cutting slits or a window in the optic nerve sheath to allow cerebrospinal fluid to escape, thereby reducing the pressure around the optic nerve. (aetna.com)
- Initial results of uncontrolled studies suggested that optic nerve sheath decompression was a promising treatment of progressive visual loss in patients with NAION. (aetna.com)
- The investigators concluded that optic nerve decompression surgery is not an effective treatment for NAION, and in fact, may increase the risk of progressive visual loss in NAION patients. (aetna.com)
- A Cochrane review (Dickersin et al, 2012) concluded that results from the single trial indicate no evidence of a beneficial effect of optic nerve decompression surgery for NAION. (aetna.com)
Damage6
- Damage to an optic nerve can cause vision loss . (medlineplus.gov)
- Damage to the optic nerve is often related to high pressure in your eye. (mayoclinic.org)
- For reasons that doctors don't fully understand, this nerve damage is usually related to increased pressure in the eye. (mayoclinic.org)
- Optic nerve damage is usually permanent and in some cases progressive. (msdmanuals.com)
- Administering the gene therapy to mice just prior to the toxic insult (which initiates rapid damage to the cells), and just after optic nerve crush (which causes slower damage), increased CaMKII activity and robustly protected retinal ganglion cells. (newswise.com)
- Bottle rockets accounted for 58 (83%) injuries, including eight of 10 injuries resulting in permanent damage to the optic nerve and all those resulting in enucleation. (cdc.gov)
Inflammation1
- Optic neuritis is an inflammation of the optic nerve. (medlineplus.gov)
Fiber layer2
- Ophthalmoscopic examination may show telangiectatic microangiopathy, swelling of the nerve fiber layer around the optic disk, and an absence of leakage on fluorescein angiography. (msdmanuals.com)
- Retinal nerve fiber layer thickness measurement may elucidate the risk of structural and functional sequelae. (researchgate.net)
Degeneration3
- Lomerizine also shows neuroprotective effects against secondary degeneration resulting from injury in retinal ganglion cells. (wikipedia.org)
- It is thought to be optic abiotrophy, premature degeneration of the optic nerve leading to progressive vision loss. (msdmanuals.com)
- Axon degeneration occurs in the nerve tissue, giving rise to anesthesia, paresthesia and paralysis. (bvsalud.org)
Microglia1
- They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury. (harvard.edu)
Cranial nerve7
- Structures located within the cone (after passing through the annulus of Zinn) include the motor innervations to the rectus muscles (cranial nerves III and VI) and the afferent sensory fibers from the globe, which are carried by the short and long posterior ciliary nerves before joining the nasociliary nerve (a branch of cranial nerve V1). (medscape.com)
- Cranial nerve VI (abducens) innervates the lateral rectus muscle. (medscape.com)
- Cranial nerve IV (trochlear) innervates the superior oblique muscle. (medscape.com)
- Cranial nerve III (oculomotor) innervates all other extraocular muscles. (medscape.com)
- While cranial nerves III and VI pass within the cone, cranial nerve IV travels outside of the muscle cone to innervate the superior oblique muscle. (medscape.com)
- The fibers then join the nasociliary nerve, which is a branch of the superior division of the trigeminal nerve (cranial nerve V1). (medscape.com)
- Additional complications include cranial nerve palsies, hydrocephalus, and apoplexy (from hemorrhage/infarction into the tumor). (medscape.com)
Endoscopic1
- Orbital injury and complications are commonly encountered in endoscopic sinus surgery (ESS) despite advances in techniques and instrumentation. (scirp.org)
Ocular injury2
- By the 18th century, the relationship between frontal trauma and vision loss with an absence of ocular injury was well appreciated. (medscape.com)
- 1 Among young persons five to 14 years of age, baseball is most frequently associated with ocular injury, while among persons 15 to 64 years of age, basketball is the leading cause of eye injuries. (aafp.org)
Peripheral nerve1
- A possible therapeutic effect of acetyl-L carnitine (ALCAR) on peripheral nerve injuries and the expression of Jun, the protein products of immediate-early genes(IEGs), in the spinal cord were investigated after. (koreamed.org)
Secondary1
- In reality, pure radial impacts are very rare and would mainly cause skull fractures and injuries secondary to those. (frontiersin.org)
Sensory1
- Retrobulbar block also provides sensory anesthesia of the cornea, uvea, and conjunctiva by blocking the ciliary nerves. (medscape.com)
Mice1
- In this study we use transgenic mice in conjunction with ONC, partial and full optic nerve transection (ONT), and parabiosis to determine the origin of injury induced retinal myeloid cells. (umn.edu)
Medial1
- Diamox, Lasix, corticosteroids), and disc swelling with visual field loss progresses, direct fenestration of the optic nerve sheaths via medial or lateral orbitotomy has been shown to be an effective and relatively simple procedure for relief of papilledema. (aetna.com)
Fibers2
- The optic nerve is a bundle of more than 1 million nerve fibers that carry visual messages. (medlineplus.gov)
- Afferent fibers from the globe travel via the long and short posterior ciliary nerves. (medscape.com)
Deteriorates2
- As this nerve gradually deteriorates, blind spots develop in your vision. (mayoclinic.org)
- Blind patches form in your visual field when this nerve deteriorates. (trustedhealthproducts.com)
Examination3
- In 1879, Berlin described the first pathologic examination of the optic nerve after head trauma. (medscape.com)
- A preparticipation eye examination is helpful in identifying persons who may be at increased risk for eye injury. (aafp.org)
- Sports-related eye injuries should be evaluated on site with an adequate examination of the eye and adnexa. (aafp.org)
Pathophysiology1
- The 20th century saw significant progress in defining the classification, pathophysiology, and management of traumatic optic nerve injuries. (medscape.com)
Lamina papyracea3
- Eight patients showed herniation of orbital fat alone through the injury of the lamina papyracea. (scirp.org)
- All injuries and complications were brought about by injury of the lamina papyracea. (scirp.org)
- Eight patients showed herniation of orbital fat alone through the injury of the lamina papyracea, where the presence of fat in the surgical field was confirmed by gentle ballottement of the eye ( Figure 1 ). (scirp.org)
Surgical1
- With each athlete, physicians should obtain an ocular history, paying special attention to prior conditions such as a high degree of myopia, surgical aphakia, retinal detachment, eye surgery, and injury or infection. (aafp.org)
Model2
- Evidence for proteolysis of neurofilaments has been obtained recently in the optic nerve stretch injury model and is correlated with disruption of the axolemma. (nih.gov)
- The Optic Nerve Crush model provides an effective tool for analyzing the pathogenic mechanisms associated with neuronal injury signaling in vivo . (pharmoptima.com)
Complications3
- Orbital injury and complications were observed in 13 patients (13 sides), which corresponded to 0.7% of the operated sides and 1.2% of the patients. (scirp.org)
- Especially, exposure of the periorbit and herniation of orbital fat after lamina injury with powered instrumentation dramatically increases the potential for more severe complications. (scirp.org)
- This can occur after eye injury, or even complications brought on by chronic stress, and it can destroy eye tissue. (platinumtherapylights.com)
Head3
- Injuries to the optic nerve induced by a trauma to the face or head. (uchicago.edu)
- By blocking these channels and preventing Ca2+ release, lomerizine increases circulation in the optic nerve head. (wikipedia.org)
- The primary verification tool in the design process is the Head Injury Criterion (HIC) applied in a free motion head-form experimental set-up, where a rigid dummy head is launched toward specific locations ( National Highway Traffic Safety Administration, 1995 ). (frontiersin.org)
Visual3
- The optic nerve sends visual information from your eye to your brain and is vital for good vision. (mayoclinic.org)
- Both afferent and efferent visual systems are sensitive to brain injury. (researchgate.net)
- Eye injuries caused by fireworks are often severe and can cause permanently reduced visual acuity or blindness. (cdc.gov)
Oxidative2
- Oxidative stress can denature lipids and proteins [ 10 , 12 - 14 ], as well as induce DNA and RNA fragmentation [ 15 - 17 ], leading to cell dysfunction, injury, and death. (hindawi.com)
- It puts in place a sequence of events that ultimately protect the cell from oxidative injury. (hindawi.com)
Vision1
- Treating optic nerve injuries with red light therapy has been shown to promote healing and restore vision . (sunhomesaunas.com)
Spinal cord i1
- Awakening dormant neurons long after spinal cord injury. (neurotree.org)