Axotomy
Facial Nerve Injuries
Facial Nerve
Sciatic Nerve
Ganglia, Spinal
Retrograde Degeneration
Wallerian Degeneration
GAP-43 Protein
Optic Nerve
Red Nucleus
Optic Nerve Injuries
Retinal Ganglion Cells
Axonal Transport
Autonomic Fibers, Postganglionic
Peripheral Nerves
Ganglia, Sympathetic
Self Mutilation
Neurofilament Proteins
Hypoglossal Nerve
Nerve Degeneration
Rats, Sprague-Dawley
Neurons
Spinal Nerves
Nissl Bodies
Schwann Cells
Glossopharyngeal Nerve
Nerve Growth Factors
Spinal Cord
Sciatic Neuropathy
Lampreys
Neurites
Femoral Neuropathy
Neural Conduction
Sensory Receptor Cells
Intermediate Filaments
Cell Survival
Activating Transcription Factor 3
Trauma, Nervous System
Aplysia
Medial Forebrain Bundle
Neurotrophin 3
Tubulin
Galanin
The optically determined size of exo/endo cycling vesicle pool correlates with the quantal content at the neuromuscular junction of Drosophila larvae. (1/532)
According to the current theory of synaptic transmission, the amplitude of evoked synaptic potentials correlates with the number of synaptic vesicles released at the presynaptic terminals. Synaptic vesicles in presynaptic boutons constitute two distinct pools, namely, exo/endo cycling and reserve pools (). We defined the vesicles that were endocytosed and exocytosed during high K+ stimulation as the exo/endo cycling vesicle pool. To determine the role of exo/endo cycling vesicle pool in synaptic transmission, we estimated the quantal content electrophysiologically, whereas the pool size was determined optically using fluorescent dye FM1-43. We then manipulated the size of the pool with following treatments. First, to change the state of boutons of nerve terminals, motoneuronal axons were severed. With this treatment, the size of exo/endo cycling vesicle pool decreased together with the quantal content. Second, we promoted the FM1-43 uptake using cyclosporin A, which inhibits calcineurin activities and enhances endocytosis. Cyclosporin A increased the total uptake of FM1-43, but neither the size of exo/endo cycling vesicle pool nor the quantal content changed. Third, we increased the size of exo/endo cycling vesicle pool by forskolin, which enhances synaptic transmission. The forskolin treatment increased both the size of exo/endo cycling vesicle pool and the quantal content. Thus, we found that the quantal content was closely correlated with the size of exo/endo cycling vesicle pool but not necessarily with the total uptake of FM1-43 fluorescence by boutons. The results suggest that vesicles in the exo/endo cycling pool primarily participate in evoked exocytosis of vesicles. (+info)Central peptidergic neurons are hyperactive during collateral sprouting and inhibition of activity suppresses sprouting. (2/532)
Little is known regarding the effect of chronic changes in neuronal activity on the extent of collateral sprouting by identified CNS neurons. We have investigated the relationship between activity and sprouting in oxytocin (OT) and vasopressin (VP) neurons of the hypothalamic magnocellular neurosecretory system (MNS). Uninjured MNS neurons undergo a robust collateral-sprouting response that restores the axon population of the neural lobe (NL) after a lesion of the contralateral MNS (). Simultaneously, lesioned rats develop chronic urinary hyperosmolality indicative of heightened neurosecretory activity. We therefore tested the hypothesis that sprouting MNS neurons are hyperactive by measuring changes in cell and nuclear diameters, OT and VP mRNA pools, and axonal cytochrome oxidase activity (COX). Each of these measures was significantly elevated during the period of most rapid axonal growth between 1 and 4 weeks after the lesion, confirming that both OT and VP neurons are hyperactive while undergoing collateral sprouting. In a second study the hypothesis that chronic inhibition of neuronal activity would interfere with the sprouting response was tested. Chronic hyponatremia (CH) was induced 3 d before the hypothalamic lesion and sustained for 4 weeks to suppress neurosecretory activity. CH abolished the lesion-induced increases in OT and VP mRNA pools and virtually eliminated measurable COX activity in MNS terminals. Counts of the total number of axon profiles in the NL revealed that CH also prevented axonal sprouting from occurring. These results are consistent with the hypothesis that increased neuronal activity is required for denervation-induced collateral sprouting to occur in the MNS. (+info)Differential expression of the mRNA for the vanilloid receptor subtype 1 in cells of the adult rat dorsal root and nodose ganglia and its downregulation by axotomy. (3/532)
Sensitivity to the pungent vanilloid, capsaicin, defines a subpopulation of primary sensory neurons that are mainly polymodal nociceptors. The recently cloned vanilloid receptor subtype 1 (VR1) is activated by capsaicin and noxious heat. Using combined in situ hybridization and histochemical methods, we have characterized in sensory ganglia the expression of VR1 mRNA. We show that this receptor is almost exclusively expressed by neurofilament-negative small- and medium-sized dorsal root ganglion cells. Within this population, VR1 mRNA is detected at widely varying levels in both the NGF receptor (trkA)-positive, peptide-producing cells that elicit neurogenic inflammation and the functionally less characterized glial cell line-derived neurotrophic factor-responsive cells that bind lectin Griffonia simplicifolia isolectin B4 (IB4). Cells without detectable levels of VR1 mRNA are found in both classes. A subpopulation of the IB4-binding cells that produce somatostatin has relatively low levels of VR1 mRNA. A previously uncharacterized population of very small cells that express the receptor tyrosine kinase (RET) and that do not label for trkA or IB4-binding has the highest relative levels of VR1 mRNA. The majority of small visceral sensory neurons of the nodose ganglion also express VR1 mRNA, in conjunction with the BDNF receptor trkB but not trkA. Axotomy results in the downregulation of VR1 mRNA in dorsal root ganglion cells. Our data emphasize the heterogeneity of VR1 mRNA expression by subclasses of small sensory neurons, and this may result in their differential sensitivity to chemical and noxious heat stimuli. Our results also indicate that peripherally derived trophic factors may regulate levels of VR1 mRNA. (+info)Cannabinoid suppression of noxious heat-evoked activity in wide dynamic range neurons in the lumbar dorsal horn of the rat. (4/532)
The effects of cannabinoid agonists on noxious heat-evoked firing of 62 spinal wide dynamic range (WDR) neurons were examined in urethan-anesthetized rats (1 cell/animal). Noxious thermal stimulation was applied with a Peltier device to the receptive fields in the ipsilateral hindpaw of isolated WDR neurons. To assess the site of action, cannabinoids were administered systemically in intact and spinally transected rats and intraventricularly. Both the aminoalkylindole cannabinoid WIN55,212-2 (125 microg/kg iv) and the bicyclic cannabinoid CP55,940 (125 microg/kg iv) suppressed noxious heat-evoked activity. Responses evoked by mild pressure in nonnociceptive neurons were not altered by CP55,940 (125 microg/kg iv), consistent with previous observations with another cannabinoid agonist, WIN55,212-2. The cannabinoid induced-suppression of noxious heat-evoked activity was blocked by pretreatment with SR141716A (1 mg/kg iv), a competitive antagonist for central cannabinoid CB1 receptors. By contrast, intravenous administration of either vehicle or the receptor-inactive enantiomer WIN55,212-3 (125 microg/kg) failed to alter noxious heat-evoked activity. The suppression of noxious heat-evoked activity induced by WIN55,212-2 in the lumbar dorsal horn of intact animals was markedly attenuated in spinal rats. Moreover, intraventricular administration of WIN55,212-2 suppressed noxious heat-evoked activity in spinal WDR neurons. By contrast, both vehicle and enantiomer were inactive. These findings suggest that cannabinoids selectively modulate the activity of nociceptive neurons in the spinal dorsal horn by actions at CB1 receptors. This modulation represents a suppression of pain neurotransmission because the inhibitory effects are selective for pain-sensitive neurons and are observed with different modalities of noxious stimulation. The data also provide converging lines of evidence for a role for descending antinociceptive mechanisms in cannabinoid modulation of spinal nociceptive processing. (+info)CNTF, not other trophic factors, promotes axonal regeneration of axotomized retinal ganglion cells in adult hamsters. (5/532)
PURPOSE: To investigate the in vivo effects of trophic factors on the axonal regeneration of axotomized retinal ganglion cells in adult hamsters. METHODS: The left optic nerve was transected intracranially or intraorbitally, and a peripheral nerve graft was apposed or sutured to the axotomized optic nerve to enhance regeneration. Trophic factors were applied intravitreally every 5 days. Animals were allowed to survive for 3 or 4 weeks. Regenerating retinal ganglion cells (RGCs) were labeled by applying the dye Fluoro-Gold to the distal end of the peripheral nerve graft 3 days before the animals were killed. RESULTS: Intravitreal application of ciliary neurotrophic factor substantially enhanced the regeneration of damaged axons into a sciatic nerve graft in both experimental conditions (intracranial and intraorbital optic nerve transections) but did not increase the survival of distally axotomized RGCs. Basic fibroblast growth factor and neurotrophins such as nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 failed to enhance axonal regeneration of distally axotomized RGCs. CONCLUSIONS: Neurons of the adult central nervous system can regenerate in response to trophic supply after injury, and ciliary neurotrophic factor is at least one of the trophic factors that can promote axonal regeneration of axotomized RGCs. (+info)Neurotrophin modulation of the monosynaptic reflex after peripheral nerve transection. (6/532)
The effects of neurotrophin-3 (NT-3) and NT-4/5 on the function of axotomized group Ia afferents and motoneurons comprising the monosynaptic reflex pathway were investigated. The axotomized medial gastrocnemius (MG) nerve was provided with NT-3 or NT-4/5 for 8-35 d via an osmotic minipump attached to its central end at the time of axotomy. After this treatment, monosynaptic EPSPs were recorded intracellularly from MG or lateral gastrocnemius soleus (LGS) motoneurons in response to stimulation of the heteronymous nerve under pentobarbital anesthesia. Controls were preparations with axotomized nerves treated directly with vehicle; other axotomized controls were administered subcutaneous NT-3. Direct NT-3 administration (60 microgram/d) not only prevented the decline in EPSP amplitude from axotomized afferents (stimulate MG, record LGS) observed in axotomy controls but, after 5 weeks, led to EPSPs larger than those from intact afferents. These central changes were paralleled by recovery of group I afferent conduction velocity. Removal of NT-3 4-5 weeks after beginning treatment resulted in a decline of conduction velocity and EPSP amplitude within 1 week to values characteristic of axotomy. The increased synaptic efficacy after NT-3 treatment was associated with enhanced connectivity of single afferents to motoneurons. NT-4/5 induced modest recovery in group I afferent conduction velocity but not of the EPSPs they elicited. NT-3 or NT-4/5 had no effect on the properties of treated motoneurons or their monosynaptic EPSPs. We conclude that NT-3, and to a limited extent NT-4/5, promotes recovery of axotomized group Ia afferents but not axotomized motoneurons or the synapses on them. (+info)Ultrastructural analysis of ectopic synaptic boutons arising from peripherally regenerated primary afferent fibers. (7/532)
The central axons of peripherally regenerated Abeta primary sensory neurons were impaled in the dorsal columns of alpha-chloralose-anesthetized cats 9-12 mo after axotomy. The adequate peripheral stimulus was determined, and the afferent fibers intracellularly stimulated while simultaneously recording the resulting cord dorsum potentials (CDPs). Fibers that successfully had reinnervated the skin responded to light tactile stimulation, and evoked CDPs that suggested dorsally located boutons were stained intracellularly with horseradish peroxidase (HRP). Two HRP-stained regenerated Abeta afferent fibers were recovered that supported large numbers of axon collaterals and swellings in laminae I, IIo, and IIi. Sections containing the ectopic collateral fibers and terminals in the superficial dorsal horn were embedded in plastic. Analyses of serial ultrathin sections revealed that ectopic projections from both regenerated fibers supported numerous synaptic boutons filled with clear round vesicles, a few large dense core vesicles (LDCVs) and several mitochondria (>3). All profiles examined in serial sections (19) formed one to three asymmetric axo-dendritic contacts. Unmyelinated portions of ectopic fibers giving rise to en passant and terminal boutons often contained numerous clear round vesicles. Several boutons (47%) received asymmetric contacts from axon terminals containing pleomorphic vesicles. These results strongly suggest that regenerated Abeta fibers activated by light tactile stimuli support functional connections in the superficial dorsal horn that have distinct ultrastructural features. In addition, the appearance of LDCVs suggests that primary sensory neurons are capable of changing their neurochemical phenotype. (+info)Nature of the retrograde signal from injured nerves that induces interleukin-6 mRNA in neurons. (8/532)
In previous studies, interleukin-6 was shown to be synthesized in approximately one-third of lumbar dorsal root ganglion neurons during the first week after nerve transection. In present studies, interleukin-6 mRNA was found to be induced also in axotomized facial motor neurons and sympathetic neurons. The nature of the signal that induces interleukin-6 mRNA in neurons after nerve injury was analyzed. Blocking of retrograde axonal transport by injection of colchicine into an otherwise normal nerve did not induce interleukin-6 mRNA in primary sensory neurons, but injection of colchicine into the nerve stump prevented induction of interleukin-6 mRNA by nerve transection. Therefore, it was concluded that interleukin-6 is induced by an injury factor arising from the nerve stump rather than by interruption of normal retrograde trophic support from target tissues or distal nerve segments. Next, injection into the nerve of a mast cell degranulating agent was shown to stimulate interleukin-6 mRNA in sensory neurons and systemic administration of mast cell stabilizing agents to mitigate the induction of interleukin-6 mRNA in sensory neurons after nerve injury. These data implicate mast cells as one possible source of the factors that lead to induction of interleukin-6 mRNA after nerve injury. In search of a possible function of inducible interelukin-6, neuronal death after nerve transection was assessed in mice with null deletion of the interleukin-6 gene. Retrograde death of neurons in the fifth lumbar dorsal root ganglion was 45% greater in knockout than in wild-type mice. Thus, endogenous interleukin-6 contributes to the survival of axotomized neurons. (+info)There are several types of facial nerve injuries, including:
1. Bell's palsy: This is a condition that affects the facial nerve and causes weakness or paralysis of the muscles on one side of the face. It is often temporary and resolves on its own within a few weeks.
2. Facial paralysis: This is a condition in which the facial nerve is damaged, leading to weakness or paralysis of the muscles of facial expression. It can be caused by trauma, tumors, or viral infections.
3. Ramsay Hunt syndrome: This is a rare condition that occurs when the facial nerve is affected by a virus, leading to symptoms such as facial paralysis and pain in the ear.
4. Traumatic facial nerve injury: This can occur as a result of trauma to the head or face, such as a car accident or a fall.
5. Tumor-related facial nerve injury: In some cases, tumors can grow on the facial nerve and cause damage.
6. Ischemic facial nerve injury: This occurs when there is a reduction in blood flow to the facial nerve, leading to damage to the nerve fibers.
7. Neurofibromatosis type 2: This is a rare genetic disorder that can cause tumors to grow on the facial nerve, leading to damage and weakness of the facial muscles.
Treatment for facial nerve injuries depends on the underlying cause and severity of the injury. In some cases, physical therapy may be recommended to help regain strength and control of the facial muscles. Surgery may also be necessary in some cases to repair damaged nerve fibers or remove tumors.
1. Neurodegenerative diseases: In conditions such as Alzheimer's disease and Parkinson's disease, there is evidence of retrograde degeneration of neurons, whereby affected neurons lose their mature characteristics and adopt more primitive features.
2. Retinal degeneration: In certain eye disorders, such as retinitis pigmentosa, there is retrograde degeneration of the retina, leading to loss of vision.
3. Cardiac disease: In some cases of heart failure, there is evidence of retrograde degeneration of the heart muscle, whereby the heart becomes less efficient and cannot pump blood effectively.
4. Cancer: Retrograde degeneration can occur in cancer, whereby tumor cells undergo a process of de-differentiation, losing their mature characteristics and adopting more primitive features.
In each of these cases, retrograde degeneration is often associated with a loss of function and can lead to severe clinical consequences. Understanding the mechanisms of retrograde degeneration is important for developing effective treatments and improving outcomes for patients with these conditions.
The process of Wallerian degeneration begins with the loss of myelin sheaths that surround the axons and are essential for their proper functioning. As a result of this degeneration, the axoplasm (the cytoplasmic contents of an axon) is exposed to the extracellular space, leading to a series of degradative changes within the axon. These changes include:
1. Breakdown of organelles and their membranes
2. Release of cellular contents into the extracellular space
3. Activation of proteolytic enzymes that degrade axonal structures
4. Influx of ionic fluids and water into the axon, leading to swelling and eventually rupture of the axon.
The onset and progression of Wallerian degeneration depend on various factors, including the severity of the initial injury, the age of the individual, and the presence of any underlying medical conditions. The degenerative process can be slowed down or even halted by various interventions, such as local application of neurotrophic factors or axonal regeneration promoters.
Wallerian degeneration is a common phenomenon in many neurodegenerative diseases and injuries, including traumatic brain injury, multiple sclerosis, and peripheral nerve damage. Understanding the mechanisms of Wallerian degeneration can provide valuable insights into the pathogenesis of these conditions and may lead to the development of novel therapeutic strategies for their management.
Types of Optic Nerve Injuries:
1. Traumatic optic neuropathy: This type of injury is caused by direct damage to the optic nerve as a result of trauma, such as a car accident or sports injury.
2. Ischemic optic neuropathy: This type of injury is caused by a lack of blood flow to the optic nerve, which can lead to cell death and vision loss.
3. Inflammatory optic neuropathy: This type of injury is caused by inflammation of the optic nerve, which can be caused by conditions such as multiple sclerosis or sarcoidosis.
4. Tumor-induced optic neuropathy: This type of injury is caused by a tumor that compresses or damages the optic nerve.
5. Congenital optic nerve disorders: These are present at birth and can cause vision loss or blindness. Examples include optic nerve hypoplasia and coloboma.
Symptoms of Optic Nerve Injuries:
* Blurred vision or double vision
* Loss of peripheral vision
* Difficulty seeing in dim lighting
* Pain or discomfort in the eye or head
* Redness or swelling of the eye
Diagnosis and Treatment of Optic Nerve Injuries:
Diagnosis is typically made through a combination of physical examination, imaging tests such as MRI or CT scans, and visual field testing. Treatment depends on the underlying cause of the injury, but may include medication, surgery, or vision rehabilitation. In some cases, vision loss may be permanent, but early diagnosis and treatment can help to minimize the extent of the damage.
Prognosis for Optic Nerve Injuries:
The prognosis for optic nerve injuries varies depending on the underlying cause and severity of the injury. In some cases, vision may be partially or fully restored with treatment. However, in other cases, vision loss may be permanent. It is important to seek medical attention immediately if any symptoms of an optic nerve injury are present, as early diagnosis and treatment can improve outcomes.
Self-mutilation is not the same as suicide, although it can be a risk factor for suicidal behavior. People who engage in self-mutilation may do so as a way to try to regulate their emotions, express feelings that they cannot put into words, or cope with traumatic events. It is important to note that self-mutilation is not a healthy or effective way to manage emotions or cope with stress, and it can lead to physical and emotional scars, infections, and worsening mental health.
Self-mutilation can be difficult to recognize, as it often occurs in secret and can be hidden by clothing or makeup. However, some common signs that someone may be engaging in self-mutilation include:
* Unexplained cuts, scars, or bruises
* Frequent injuries or wounds that do not heal properly
* Difficulty concentrating or memory problems
* Mood swings or emotional instability
* Withdrawal from social activities or relationships
* Substance abuse or addiction
If you suspect that someone you know is engaging in self-mutilation, it is important to approach the situation with sensitivity and compassion. Encourage them to seek professional help from a mental health provider, such as a therapist or counselor. A mental health professional can work with the individual to identify the underlying causes of their behavior and develop healthy coping strategies.
Treatment for self-mutilation typically involves a combination of psychotherapy and medication. Therapy can help individuals understand the underlying causes of their behavior, develop healthy coping strategies, and learn how to manage negative emotions in a more productive way. Medications such as antidepressants or mood stabilizers may be prescribed to help regulate mood and reduce impulsivity.
In summary, self-mutilation is a behavior where an individual intentionally causes harm to their own body, often as a coping mechanism for emotional pain or distress. It can take many forms, including cutting, burning, or hitting oneself. Treatment typically involves a combination of psychotherapy and medication, and it is important to approach the situation with sensitivity and compassion. If you suspect that someone you know is engaging in self-mutilation, encourage them to seek professional help from a mental health provider.
There are many different types of nerve degeneration that can occur in various parts of the body, including:
1. Alzheimer's disease: A progressive neurological disorder that affects memory and cognitive function, leading to degeneration of brain cells.
2. Parkinson's disease: A neurodegenerative disorder that affects movement and balance, caused by the loss of dopamine-producing neurons in the brain.
3. Amyotrophic lateral sclerosis (ALS): A progressive neurological disease that affects nerve cells in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death.
4. Multiple sclerosis: An autoimmune disease that affects the central nervous system, causing inflammation and damage to nerve fibers.
5. Diabetic neuropathy: A complication of diabetes that can cause damage to nerves in the hands and feet, leading to pain, numbness, and weakness.
6. Guillain-Barré syndrome: An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and paralysis.
7. Chronic inflammatory demyelinating polyneuropathy (CIDP): An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and numbness.
The causes of nerve degeneration are not always known or fully understood, but some possible causes include:
1. Genetics: Some types of nerve degeneration may be inherited from one's parents.
2. Aging: As we age, our nerve cells can become damaged or degenerate, leading to a decline in cognitive and physical function.
3. Injury or trauma: Physical injury or trauma to the nervous system can cause nerve damage and degeneration.
4. Infections: Certain infections, such as viral or bacterial infections, can cause nerve damage and degeneration.
5. Autoimmune disorders: Conditions such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) are caused by the immune system attacking and damaging nerve cells.
6. Toxins: Exposure to certain toxins, such as heavy metals or pesticides, can damage and degenerate nerve cells.
7. Poor nutrition: A diet that is deficient in essential nutrients, such as vitamin B12 or other B vitamins, can lead to nerve damage and degeneration.
8. Alcoholism: Long-term alcohol abuse can cause nerve damage and degeneration due to the toxic effects of alcohol on nerve cells.
9. Drug use: Certain drugs, such as chemotherapy drugs and antiviral medications, can damage and degenerate nerve cells.
10. Aging: As we age, our nerve cells can deteriorate and become less functional, leading to a range of cognitive and motor symptoms.
It's important to note that in some cases, nerve damage and degeneration may be irreversible, but there are often strategies that can help manage symptoms and improve quality of life. If you suspect you have nerve damage or degeneration, it's important to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.
Types of Peripheral Nerve Injuries:
1. Traumatic Nerve Injury: This type of injury occurs due to direct trauma to the nerve, such as a blow or a crush injury.
2. Compression Neuropathy: This type of injury occurs when a nerve is compressed or pinched, leading to damage or disruption of the nerve signal.
3. Stretch Injury: This type of injury occurs when a nerve is stretched or overstretched, leading to damage or disruption of the nerve signal.
4. Entrapment Neuropathy: This type of injury occurs when a nerve is compressed or trapped between two structures, leading to damage or disruption of the nerve signal.
Symptoms of Peripheral Nerve Injuries:
1. Weakness or paralysis of specific muscle groups
2. Numbness or tingling in the affected area
3. Pain or burning sensation in the affected area
4. Difficulty with balance and coordination
5. Abnormal reflexes
6. Incontinence or other bladder or bowel problems
Causes of Peripheral Nerve Injuries:
1. Trauma, such as a car accident or fall
2. Sports injuries
3. Repetitive strain injuries, such as those caused by repetitive motions in the workplace or during sports activities
4. Compression or entrapment of nerves, such as carpal tunnel syndrome or tarsal tunnel syndrome
5. Infections, such as Lyme disease or diphtheria
6. Tumors or cysts that compress or damage nerves
7. Vitamin deficiencies, such as vitamin B12 deficiency
8. Autoimmune disorders, such as rheumatoid arthritis or lupus
9. Toxins, such as heavy metals or certain chemicals
Treatment of Peripheral Nerve Injuries:
1. Physical therapy to improve strength and range of motion
2. Medications to manage pain and inflammation
3. Surgery to release compressed nerves or repair damaged nerves
4. Electrical stimulation therapy to promote nerve regeneration
5. Platelet-rich plasma (PRP) therapy to stimulate healing
6. Stem cell therapy to promote nerve regeneration
7. Injection of botulinum toxin to relieve pain and reduce muscle spasticity
8. Orthotics or assistive devices to improve mobility and function
It is important to seek medical attention if you experience any symptoms of a peripheral nerve injury, as early diagnosis and treatment can help prevent long-term damage and improve outcomes.
The hypoglossal nerve is a cranial nerve that controls the movement of the tongue and is responsible for its protrusion, withdrawal, and lateral movement. Hypoglossal nerve injuries can occur due to various reasons such as trauma, surgery, or tumors. These injuries can result in symptoms such as tongue weakness or paralysis, difficulty speaking or swallowing, and loss of taste sensation on the tip of the tongue.
The severity of hypoglossal nerve injuries can vary from mild to severe, and the treatment options depend on the cause and extent of the injury. Mild cases may resolve on their own with time, while more severe cases may require surgical intervention or other treatments such as physical therapy or medications. In this article, we will discuss the causes, symptoms, diagnosis, and treatment options for hypoglossal nerve injuries in detail.
Causes of Hypoglossal Nerve Injuries:
Hypoglossal nerve injuries can occur due to various reasons such as:
Trauma: Traumatic injuries to the face or neck can cause damage to the hypoglossal nerve, resulting in tongue weakness or paralysis.
Surgery: Surgical procedures in the head and neck region can sometimes result in injury to the hypoglossal nerve.
Tumors: Tumors in the head and neck region can compress or injure the hypoglossal nerve, leading to tongue weakness or paralysis.
Infections: Infections such as meningitis or abscesses in the head and neck region can damage the hypoglossal nerve.
Neurodegenerative diseases: Certain neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) can affect the hypoglossal nerve, leading to tongue weakness or paralysis.
Symptoms of Hypoglossal Nerve Injuries:
The symptoms of hypoglossal nerve injuries can vary depending on the severity and location of the injury. Common symptoms include:
Tongue weakness or paralysis: Weakness or paralysis of the tongue can make it difficult to speak, eat, or swallow.
Drooling: Inability to control salivation due to tongue weakness or paralysis can lead to drooling.
Difficulty articulating words: Slurred speech or difficulty articulating words due to tongue weakness or paralysis.
Facial weakness or paralysis: Weakness or paralysis of the facial muscles can cause drooping or weakness in the face.
Difficulty swallowing: Difficulty swallowing due to tongue weakness or paralysis can lead to dysphagia.
Causes of Hypoglossal Nerve Injuries:
Hypoglossal nerve injuries can occur due to various reasons, including:
Trauma: Traumatic injuries to the face or neck can cause damage to the hypoglossal nerve, resulting in tongue weakness or paralysis.
Surgery: Surgical procedures in the head and neck region can sometimes cause nerve damage, leading to hypoglossal nerve injuries.
Neurological conditions: Certain neurological conditions such as stroke, multiple sclerosis, or tumors can cause hypoglossal nerve injuries.
Viral infections: Viral infections such as HIV or Lyme disease can cause inflammation of the nerves, including the hypoglossal nerve.
Treatment options for Hypoglossal Nerve Injuries:
Treatment options for hypoglossal nerve injuries depend on the underlying cause and severity of the injury. Some possible treatment options include:
Physical therapy: Physical therapy exercises can help improve tongue strength and mobility.
Medications: Medications such as antiviral drugs or steroids may be prescribed to manage symptoms.
Surgery: In some cases, surgery may be necessary to relieve compression or repair damaged nerve tissue.
Speech therapy: Speech therapy can help improve communication skills and address swallowing difficulties.
It's important to seek medical attention if you experience any symptoms of hypoglossal nerve injuries, as prompt treatment can help prevent long-term complications and improve outcomes.
Femoral neuropathy is a type of peripheral neuropathy that affects the femoral nerve, which runs from the lower back down to the thigh and leg. This condition can cause a range of symptoms, including pain, numbness, and weakness in the affected limb.
Causes of Femoral Neuropathy
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There are several potential causes of femoral neuropathy, including:
1. Trauma or injury to the nerve
2. Compression or entrapment of the nerve due to a herniated disc or other soft tissue abnormality
3. Inflammation or infection of the nerve
4. Vitamin deficiencies, such as vitamin B12 deficiency
5. Chronic conditions such as diabetes or rheumatoid arthritis
Symptoms of Femoral Neuropathy
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The symptoms of femoral neuropathy can vary depending on the severity and location of the nerve damage. Common symptoms include:
1. Pain, numbness, or tingling in the thigh or leg
2. Weakness or muscle wasting in the affected limb
3. Difficulty moving the affected limb or maintaining balance
4. Sensitivity to touch or temperature changes
5. Loss of reflexes in the affected limb
Diagnosis and Treatment of Femoral Neuropathy
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Femoral neuropathy can be difficult to diagnose, as it may be mistaken for other conditions such as a muscle strain or sciatica. To diagnose femoral neuropathy, a healthcare provider will typically perform a physical examination and order imaging tests such as an MRI or EMG to confirm the presence of nerve damage.
Treatment for femoral neuropathy depends on the underlying cause of the condition. Conservative treatments may include:
1. Pain management with medication or injections
2. Physical therapy to improve strength and balance
3. Lifestyle changes such as weight loss or avoiding activities that exacerbate the condition
4. Electrical stimulation or other alternative therapies
In some cases, surgery may be necessary to relieve compression on the nerve or repair any structural issues. It is important to seek medical attention if symptoms persist or worsen over time, as early treatment can improve outcomes and reduce the risk of long-term complications.
Living with Femoral Neuropathy
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Living with femoral neuropathy can be challenging, but there are several strategies that can help manage symptoms and improve quality of life. These may include:
1. Pain management: Maintaining a consistent pain management plan can help reduce discomfort and improve mobility.
2. Assistive devices: Using canes, walkers, or other assistive devices can help improve balance and stability.
3. Physical therapy: Regular physical therapy sessions can help maintain strength and flexibility in the affected limb.
4. Lifestyle changes: Making lifestyle changes such as losing weight, avoiding activities that exacerbate the condition, and taking regular breaks to rest the affected limb can help manage symptoms.
5. Alternative therapies: Electrical stimulation or other alternative therapies may be helpful in managing symptoms.
6. Support groups: Joining a support group can provide emotional support and connect individuals with others who are experiencing similar challenges.
It is important to remember that each person's experience with femoral neuropathy is unique, and what works for one person may not work for another. It is essential to work closely with a healthcare provider to develop a personalized treatment plan that addresses individual needs and goals. With the right treatment and support, it is possible to manage symptoms of femoral neuropathy and improve quality of life.
Trauma to the nervous system can have a profound impact on an individual's quality of life, and can lead to a range of symptoms including:
* Headaches
* Dizziness and vertigo
* Memory loss and difficulty concentrating
* Mood changes such as anxiety, depression, or irritability
* Sleep disturbances
* Changes in sensation, such as numbness or tingling
* Weakness or paralysis of certain muscle groups
Trauma to the nervous system can also have long-lasting effects, and may lead to chronic conditions such as post-traumatic stress disorder (PTSD), chronic pain, and fibromyalgia.
Treatment for trauma to the nervous system will depend on the specific nature of the injury and the severity of the symptoms. Some common treatments include:
* Medication to manage symptoms such as pain, anxiety, or depression
* Physical therapy to help regain strength and mobility
* Occupational therapy to help with daily activities and improve function
* Cognitive-behavioral therapy (CBT) to address any emotional or psychological issues
* Alternative therapies such as acupuncture, massage, or meditation to help manage symptoms and promote relaxation.
It's important to seek medical attention if you experience any symptoms of trauma to the nervous system, as prompt treatment can help reduce the risk of long-term complications and improve outcomes.
Axotomy
Yishi Jin
Chromatolysis
DBN1
Haptotaxis
Nerve injury
Glial cell line-derived neurotrophic factor
Michal Schwartz
AGTPBP1 (gene)
Protective autoimmunity
John Graham Nicholls
Diffuse axonal injury
ANTXR1
Arimoclomol
Stephen Brendan McMahon
Darcy Kelley
Gap-43 protein
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Enolase 2
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Programmed cell death
PJA2
Aurora kinase B
Wallerian degeneration
POU4F2
Neurotrophic factors
Gliosis
Optical transfection
Neurotrophin mimetics
Georg Kreutzberg
Pain control through selective chemo-axotomy of centrally projecting TRPV1+ sensory neurons - PubMed
Impairment of microglial responses to facial nerve axotomy in cathepsin S-deficient mice<...
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Dynamic Reconstruction for Facial Nerve Paralysis: Overview, Anatomy of the Facial Nerve, Etiology in Prognosis and Treatment
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Integrin-Driven Axon Regeneration in the Spinal Cord Activates a Distinctive CNS Regeneration Program - PubMed
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NLM History of Medicine Division Finding Aids
Neuronal2
- Finally, we compared axotomy-induced neuronal death in the two groups and found that the percentage of motoneurons that survived in CS-/- mice was significantly smaller than that in wildtype mice. (elsevierpure.com)
- Methamphetamine-induced deficits of brain monoaminergic neuronal markers: distal axotomy or neuronal plasticity. (nih.gov)
Neurons3
- Axotomy of roundworm neurons was performed by femtosecond laser surgery, after which the axons functionally regenerated. (nanowerk.com)
- For in vitro studies, mouse P0 primary cortical neurons were plated on an axon chamber and axotomy was performed on 7DIV when axons were sufficiently grown into the other side of the axon chamber. (nih.gov)
- During her PhD (advised by Dr. Martin Schwab) she investigated the reorganization of corticospinal neurons after axotomy and their role in the recovery of forelimb motor function in rats. (nih.gov)
Optic nerve4
- 2006. Examination of cellular and molecular events associated with optic nerve axotomy. (nih.gov)
- Regenerative failure in the mammalian optic nerve is generally attributed to axotomy-induced retinal ganglion cell (RGC) death, an insufficient intrinsic regenerative capacity, and an extrinsic inhibitory environment. (neurosciencenews.com)
- This thesis focuses on the effects of CDNF and MANF treatment in vivo on optic nerve axotomy. (medipol.edu.tr)
- In order to study these mechanisms, optic nerve axotomy was performed. (medipol.edu.tr)
Peripheral2
- Neuropeptide Y and galanin binding sites in rat and monkey lumbar dorsal root ganglia and spinal cord and effect of peripheral axotomy. (duke.edu)
- In rats with a spinal dorsal column crush injury, a preconditioning peripheral sciatic nerve axotomy, or NgR1(310)ecto-Fc decoy protein treatment or ChondroitinaseABC (ChABC) treatment independently support similar degrees of regeneration by ascending primary afferent fibers into the vicinity of the injury site. (listlabs.com)
Dorsal1
- Prominent expression of bFGF in dorsal root ganglia after axotomy. (duke.edu)
Vivo1
- To understand the underlying mechanisms, we established in vivo laser axotomy assay in C. elegans . (nih.gov)
Axons1
- Seems to prevent the degeneration of motor axons after axotomy. (nih.gov)
Responses2
- To better understand the role of CS in microglia, we investigated microglial responses after a facial nerve axotomy in CS-deficient (CS-/-) and wild-type mice. (elsevierpure.com)
- Hai, PH , Doh-Ura, K & Nakanishi, H 2007, ' Impairment of microglial responses to facial nerve axotomy in cathepsin S-deficient mice ', Journal of Neuroscience Research , vol. 85, no. 10, pp. 2196-2206. (elsevierpure.com)
Transplantation1
- Ventral root axotomy regeneration after mesenchymal stem cell transplantation. (bvsalud.org)
Role1
- The present study strongly suggests that CS plays a role in the migration and activation of microglia to protect facial motoneurons against axotomy-induced injury. (elsevierpure.com)
Motor1
- Microglia in both groups accumulated in the facial motor nucleus following axotomy. (elsevierpure.com)
Optic nerve axotomy2
- Neurotrophins, such as NGF and BDNF, have been tested in animal models of glaucoma and while some studies have shown them to reduce RGC death, [ 46 ] exogenous BDNF may not provide long-lasting neuroprotection to RGC in optic nerve axotomy or glaucoma models. (medscape.com)
- 2006. Examination of cellular and molecular events associated with optic nerve axotomy. (nih.gov)
Axon3
- Traumatic injury to the peripheral and central nervous systems very often causes axotomy, where an axon loses connections with its target resulting in loss of function. (nih.gov)
- For in vitro studies, mouse P0 primary cortical neurons were plated on an axon chamber and axotomy was performed on 7DIV when axons were sufficiently grown into the other side of the axon chamber. (nih.gov)
- Axon growth after axotomy was also promoted by synaptamide addition to either side of the chamber. (nih.gov)
Regeneration1
- In contrast, spontaneous regeneration rarely occurs after axotomy in the spinal cord and brain. (nih.gov)
Protein1
- Reduction of either protein increases axonal regrowth following axotomy. (bvsalud.org)
Brain1
- Methamphetamine-induced deficits of brain monoaminergic neuronal markers: distal axotomy or neuronal plasticity. (nih.gov)