Autonomic Denervation
Sympathectomy
Parasympathectomy
Sympathetic Nervous System
Sympathectomy, Chemical
Muscular Atrophy
Pressoreceptors
Muscle, Skeletal
Vagotomy
Carotid Sinus
Kidney
Vagus Nerve
Cranial Nerve Diseases
Receptors, Cholinergic
Norepinephrine
Sciatic Nerve
3-Iodobenzylguanidine
Oxidopamine
Autonomic Nervous System Diseases
Parasympathetic Nervous System
Carotid Body
Reflex
Diaphragm
Rats, Inbred Strains
Dogs
Rats, Sprague-Dawley
Glossopharyngeal Nerve
Rats, Wistar
Hindlimb
Muscle Contraction
Electromyography
Chemoreceptor Cells
Motor Endplate
Muscle Proteins
Baroreflex
Edrophonium
Muscle Fibers, Skeletal
Muscle Fibers, Fast-Twitch
Tyramine
Shy-Drager Syndrome
Trigeminal Nerve
Diuresis
Hyperhidrosis
Sympatholytics
Cats
Ephedrine
Hypoglossal Nerve
Sodium Cyanide
Autonomic Fibers, Preganglionic
Autonomic Fibers, Postganglionic
Stellate Ganglion
Primary Dysautonomias
Hypertension
Nerve Degeneration
Pure Autonomic Failure
Atrophy
Myogenin
Ganglia, Sympathetic
Acetylcholine
Peripheral Nerves
Tongue
Nerve Fibers
Muscle Development
Neural Conduction
Botulinum Toxins
Acetylcholinesterase
Tibial Nerve
Sinoatrial Node
Nerve Endings
Catheter Ablation
Afferent Pathways
Nervous System Physiological Phenomena
Tetrodotoxin
Nictitating Membrane
Autonomic Nervous System
Muscle Fibers, Slow-Twitch
Ganglia, Parasympathetic
Muscular Disorders, Atrophic
Paralysis
Bungarotoxins
Masticatory Muscles
Ganglia, Autonomic
Guanethidine
Propranolol
Parkinson Disease
Neuromuscular Diseases
Hemodynamics
Ophthalmic Nerve
Disease Models, Animal
Sciatic Neuropathy
Atropine
Efferent Pathways
Diabetic Neuropathies
Mandibular Nerve
Iris
Receptors, Adrenergic
Facial Nerve
Reserpine
Respiration
Sympathomimetics
Striatonigral Degeneration
Action Potentials
Epinephrine
Schwann Cells
Phenylephrine
Calcitonin Gene-Related Peptide
Spinal Nerve Roots
Tyrosine 3-Monooxygenase
Hexamethonium Compounds
Dopamine
Chorda Tympani Nerve
Peroneal Nerve
Myosin Heavy Chains
Prenalterol
Corpus Striatum
Vascular Resistance
RNA, Messenger
Dihydroergotamine
Phentolamine
Sweat Glands
Sodium
Possible role of serotonin in Merkel-like basal cells of the taste buds of the frog, Rana nigromaculata. (1/1756)
Merkel-like basal cells in the taste buds of the frog were examined by fluorescence histochemistry, immunohistochemistry and electron microscopy. There were about 16-20 basal cells arranged in a radial fashion at the base of each taste bud. These cells were strongly immunopositive for serotonin antiserum. They were characterised by the presence of numerous dense-cored granules in the cytoplasm ranging from 80 to 120 nm in diameter, and of microvilli protruding from the cell surface. For 4 mo after sensory denervation by cutting the gustatory nerves, all cell types of the taste bud were well preserved and maintained their fine structure. Even at 4 mo after denervation, the basal cells exhibited a strong immunoreaction with serotonin antiserum. To investigate the function of serotonin in the basal cells in taste bud function, serotonin deficiency was induced by administration of p-chlorophenylalanine (PCPA), an inhibitor of tryptophan hydroxylase, and of p-chloroamphetamine (PCA), a depletor of serotonin. After administration of these agents to normal and denervated frogs for 2 wk, a marked decrease, or complete absence, of immunoreactivity for serotonin was observed in the basal cells. Ultrastructurally, degenerative changes were observed in both types of frog; numerous lysosome-like myelin bodies were found in all cell types of the taste buds. The number of dense-cored granules in the basal cells also was greatly decreased by treatment with these drugs. Serotonin in Merkel-like basal cells appears to have a trophic role in maintenance of the morphological integrity of frog taste bud cells. (+info)Expression of Mash1 in basal cells of rat circumvallate taste buds is dependent upon gustatory innervation. (2/1756)
Mash1, a mammalian homologue of the Drosophila achaete-scute proneural gene complex, plays an essential role in differentiation of subsets of peripheral neurons. In this study, using RT-PCR and in situ RT-PCR, we investigated if Mash1 gene expression occurs in rat taste buds. Further, we examined dynamics of Mash1 expression in the process of degeneration and regeneration in denervated rat taste buds. In rat tongue epithelium, Mash1 gene expression is confined to circumvallate, foliate, and fungiform papilla epithelia that include taste buds. In taste buds, Mash1-expressing cells are round cells in the basal compartment. In contrast, the mature taste bud cells do not express the Mash1 gene. Denervation and regeneration experiments show that the expression of Mash1 requires gustatory innervation. We conclude that Mash1 is expressed in cells of the taste bud lineage, and that the expression of Mash1 in rat taste buds is dependent upon gustatory innervation. (+info)Effect of central corticotropin-releasing factor on carbon tetrachloride-induced acute liver injury in rats. (3/1756)
Central neuropeptides play important roles in many instances of physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Stressors and sympathetic nerve activation are reported to exacerbate experimental liver injury. Some stressors are known to stimulate corticotropin-releasing factor (CRF) synthesis in the central nervous system and induce activation of sympathetic nerves in animal models. The effect of intracisternal CRF on carbon tetrachloride (CCl4)-induced acute liver injury was examined in rats. Intracisternal injection of CRF dose dependently enhanced elevation of the serum alanine aminotransferase (ALT) level induced by CCl4. Elevations of serum aspartate aminotransferase, alkaline phosphatase, and total bilirubin levels by CCl4 were also enhanced by intracisternal CRF injection. Intracisternal injection of CRF also aggravated CCl4-induced hepatic histological changes. Intracisternal CRF injection alone did not modify the serum ALT level. Intravenous administration of CRF did not influence CCl4-induced acute liver injury. The aggravating effect of central CRF on CCl4-induced acute liver injury was abolished by denervation of hepatic plexus with phenol and by denervation of noradrenergic fibers with 6-hydroxydopamine treatment but not by hepatic branch vagotomy or atropine treatment. These results suggest that CRF acts in the brain to exacerbate acute liver injury through the sympathetic-noradrenergic pathways. (+info)Nitric oxide mediates sympathetic vasoconstriction at supraspinal, spinal, and synaptic levels. (4/1756)
The purposes of this study were to investigate the level of the sympathetic nervous system in which nitric oxide (NO) mediates regional sympathetic vasoconstriction and to determine whether neural mechanisms are involved in vasoconstriction after NO inhibition. Ganglionic blockade (hexamethonium), alpha1-receptor blockade (prazosin), and spinal section at T1 were used to study sympathetic involvement. NO was blocked with Nomega-nitro-L-arginine methyl ester (L-NAME). Regional blood flow in the mesenteric and renal arteries and terminal aorta was monitored by electromagnetic flowmetry in conscious rats. L-NAME (3-5 mg/kg iv) increased arterial pressure and peripheral resistance. Ganglionic blockade (25 mg/kg iv) significantly reduced the increase in resistance in the mesentery and kidney in intact and spinal-sectioned rats. Ganglionic blockade significantly decreased hindquarter resistance in intact rats but not in spinal-sectioned rats. Prazosin (200 micrograms/kg iv) significantly reduced the increased hindquarter resistance. We concluded that NO suppresses sympathetic vasoconstriction in the mesentery and kidney at the spinal level, whereas hindquarter tone is mediated at supraspinal and synaptic levels. (+info)Erythromycin enhances early postoperative contractility of the denervated whole stomach as an esophageal substitute. (5/1756)
OBJECTIVE: To determine whether early postoperative administration of erythromycin accelerates the spontaneous motor recovery process after elevation of the denervated whole stomach up to the neck. SUMMARY BACKGROUND DATA: Spontaneous motor recovery after gastric denervation is a slow process that progressively takes place over years. METHODS: Erythromycin was administered as follows: continuous intravenous (i.v.) perfusion until postoperative day 10 in ten whole stomach (WS) patients at a dose of either 1 g (n = 5) or 2 g (n = 5) per day; oral intake at a dose of 1 g/day during 1.5 to 8 months after surgery in 11 WS patients, followed in 7 of them by discontinuation of the drug during 2 to 4 weeks. Gastric motility was assessed with intraluminal perfused catheters in these 21 patients, in 23 WS patients not receiving erythromycin, and in 11 healthy volunteers. A motility index was established by dividing the sum of the areas under the curves of >9 mmHg contractions by the time of recording. RESULTS: The motility index after IV or oral administration of erythromycin at and after surgery was significantly higher than that without erythromycin (i.v., 1 g: p = 0.0090; i.v., 2 g: p = 0.0090; oral, 1 g: p = 0.0017). It was similar to that in healthy volunteers (i.v., 1 g: p = 0.2818; oral, 1 g: p = 0.7179) and to that in WS patients with >3 years of follow-up who never received erythromycin (i.v., 1 g: p = 0.2206; oral, 1 g: p = 0.8326). The motility index after discontinuation of the drug was similar or superior to that recorded under medication in four patients who did not experience any modification of their alimentary comfort, whereas it dropped dramatically parallel to deterioration of the alimentary comfort in three patients. CONCLUSIONS: Early postoperative contractility of the denervated whole stomach pulled up to the neck under either i.v. or oral erythromycin is similar to that recovered spontaneously beyond 3 years of follow-up. In some patients, this booster effect persists after discontinuation of the drug. (+info)Heterogeneous cardiac sympathetic denervation and decreased myocardial nerve growth factor in streptozotocin-induced diabetic rats: implications for cardiac sympathetic dysinnervation complicating diabetes. (6/1756)
Heterogeneous myocardial sympathetic denervation complicating diabetes has been invoked as a factor contributing to sudden unexplained cardiac death. In subjects with diabetic autonomic neuropathy (DAN), distal left ventricular (LV) denervation contrasts with preservation of islands of proximal innervation, which exhibit impaired vascular responsiveness. The aims of this study were to determine whether this heterogeneous pattern of myocardial sympathetic denervation occurs in a rat model of diabetes and to explore a potential association with regional fluctuations in myocardial nerve growth factor (NGF) protein. Myocardial sympathetic denervation was characterized scintigraphically using the sympathetic neurotransmitter analog C-11 hydroxyephedrine ([11C]HED) and compared with regional changes in myocardial NGF protein abundance and norepinephrine content after 6 and 9 months in nondiabetic (ND) and streptozotocin-induced diabetic (STZ-D) rats. In ND rats, no difference in [11C]HED retention or norepinephrine content was detected in the proximal versus distal myocardium. After 6 months, compared with ND rats, myocardial [11C]HED retention had declined in the proximal segments of STZ-D rats by only 9% (NS) compared with a 33% decrease in the distal myocardium (P < 0.05). Myocardial norepinephrine content was similar in both ND and STZ-D rats. At 6 months, LV myocardial NGF protein content in STZ-D rats decreased by 52% in the proximal myocardial segments (P < 0.01 vs. ND rats) and by 82% distally (P < 0.01 vs. ND rats, P < 0.05 vs. proximal segments). By 9 months, [11C]HED retention had declined in both the proximal and distal myocardial segments of the STZ-D rats by 42% (P < 0.01 vs. ND rats), and LV norepinephrine content and NGF protein were decreased in parallel. Therefore, 6 months of STZ-induced diabetes results in heterogeneous cardiac sympathetic denervation in the rat, with maximal denervation occurring distally, and is associated with a proximal-to-distal gradient of LV NGF protein depletion. It is tempting to speculate that regional fluctuations of NGF protein in the diabetic myocardium contribute to heterogeneous cardiac sympathetic denervation complicating diabetes. (+info)Hypoxia inhibits baroreflex vagal bradycardia via a central action in anaesthetized rats. (7/1756)
It is known that arterial baroreflexes are suppressed in stressful conditions. The present study was designed to determine whether and how hypoxia affects arterial baroreflexes, especially the heart rate component, baroreflex vagal bradycardia. In chloralose-urethane-anaesthetized rats, baroreflex vagal bradycardia was evoked by electrical stimulation of the aortic depressor nerve, and the effect of 15 s inhalation of hypoxic gas (4% O2) was studied. Inhalation of hypoxic gas was found to inhibit baroreflex vagal bradycardia. The inhibition persisted after bilateral transection of the carotid sinus nerve. Cervical vagus nerves were cut bilaterally and their peripheral cut ends were stimulated to provoke vagal bradycardia of peripheral origin so as to determine whether hypoxia could inhibit vagal bradycardia by acting on a peripheral site. In contrast to baroreflex vagal bradycardia, the vagus-induced bradycardia was not affected by hypoxic gas inhalation. It is concluded that baroreflex vagal bradycardia is inhibited by hypoxia and the inhibition is largely mediated by its direct central action. (+info)A substituted dextran enhances muscle fiber survival and regeneration in ischemic and denervated rat EDL muscle. (8/1756)
Ischemia and denervation of EDL muscle of adult rat induce a large central zone of degeneration surrounded by a thin zone of peripheral surviving muscle fibers. Muscle regeneration is a complex phenomenon in which many agents interact, such as growth factors and heparan sulfate components of the extracellular matrix. We have shown that synthetic polymers, called RGTA (as regenerating agents), which imitate the heparan sulfates, are able to stimulate tissue repair when applied at the site of injury. In crushed muscles, RGTA were found to accelerate both regeneration and reinnervation. In vitro, RGTA act as protectors and potentiators of various heparin binding growth factors (HBGF). It was postulated that in vivo their tissue repair properties were due in part to an increase of bioavailability of endogenously released HBGF. In the present work, we show that ischemic and denervated EDL muscle treated by a unique injection of RGTA differs from the control after 1 wk in several aspects: 1) the epimysial postinflammatory reaction is inhibited and the area of fibrotic tissue among fibers is reduced; 2) the peripheral zone, as measured by the number of intact muscle fibers, was increased by more than twofold; and 3) In the central zone, RGTA enhances the regeneration of the muscle fibers as well as muscle revascularization. These results suggest that RGTA both protects muscle fibers from degeneration and preserves the differentiated state of the surviving fibers. For the first time it is demonstrated that a functionalized polymeric compound can prevent some of the damage resulting from muscle ischemia. RGTA may therefore open a new therapeutic approach for muscle fibrosis and other postischemic muscle pathologies. (+info)There are several types of muscular atrophy, including:
1. Disuse atrophy: This type of atrophy occurs when a muscle is not used for a long period, leading to its degeneration.
2. Neurogenic atrophy: This type of atrophy occurs due to damage to the nerves that control muscles.
3. Dystrophic atrophy: This type of atrophy occurs due to inherited genetic disorders that affect muscle fibers.
4. Atrophy due to aging: As people age, their muscles can degenerate and lose mass and strength.
5. Atrophy due to disease: Certain diseases such as cancer, HIV/AIDS, and muscular dystrophy can cause muscular atrophy.
6. Atrophy due to infection: Infections such as polio and tetanus can cause muscular atrophy.
7. Atrophy due to trauma: Traumatic injuries can cause muscular atrophy, especially if the injury is severe and leads to prolonged immobilization.
Muscular atrophy can lead to a range of symptoms depending on the type and severity of the condition. Some common symptoms include muscle weakness, loss of motor function, muscle wasting, and difficulty performing everyday activities. Treatment for muscular atrophy depends on the underlying cause and may include physical therapy, medication, and lifestyle changes such as exercise and dietary modifications. In severe cases, surgery may be necessary to restore muscle function.
Some common examples of cranial nerve diseases include:
1. Bell's palsy: A condition that affects the facial nerve, causing weakness or paralysis of one side of the face.
2. Multiple sclerosis: An autoimmune disease that damages the protective covering of nerve fibers, leading to communication problems between the brain and the rest of the body.
3. Trigeminal neuralgia: A condition that affects the trigeminal nerve, causing facial pain and numbness.
4. Meningitis: An inflammation of the meninges, the protective covering of the brain and spinal cord, which can damage the cranial nerves.
5. Acoustic neuroma: A type of non-cancerous tumor that grows on the nerve that connects the inner ear to the brain.
6. Cranial polyneuropathy: A condition where multiple cranial nerves are damaged, leading to a range of symptoms including muscle weakness, numbness, and pain.
7. Tumors: Both benign and malignant tumors can affect the cranial nerves, causing a variety of symptoms depending on their location and size.
8. Trauma: Head injuries or trauma can damage the cranial nerves, leading to a range of symptoms.
9. Infections: Bacterial or viral infections such as meningitis or encephalitis can damage the cranial nerves, leading to a range of symptoms.
10. Genetic disorders: Certain genetic disorders such as Charcot-Marie-Tooth disease can affect the cranial nerves, leading to a range of symptoms.
It's important to note that this is not an exhaustive list and there may be other causes of cranial nerve damage. If you are experiencing any symptoms that you think may be related to cranial nerve damage, it's important to seek medical attention as soon as possible for proper diagnosis and treatment.
There are many different types of ANS diseases, including:
1. Dysautonomia: a general term that refers to dysfunction of the autonomic nervous system.
2. Postural orthostatic tachycardia syndrome (POTS): a condition characterized by rapid heart rate and other symptoms that occur upon standing.
3. Neurocardiogenic syncope: a form of fainting caused by a sudden drop in blood pressure.
4. Multiple system atrophy (MSA): a progressive neurodegenerative disorder that affects the autonomic nervous system and other parts of the brain.
5. Parkinson's disease: a neurodegenerative disorder that can cause autonomic dysfunction, including constipation, urinary incontinence, and erectile dysfunction.
6. Dopamine deficiency: a condition characterized by low levels of the neurotransmitter dopamine, which can affect the ANS and other body systems.
7. Autonomic nervous system disorders associated with autoimmune diseases, such as Guillain-Barré syndrome and lupus.
8. Trauma: physical or emotional trauma can sometimes cause dysfunction of the autonomic nervous system.
9. Infections: certain infections, such as Lyme disease, can affect the autonomic nervous system.
10. Genetic mutations: some genetic mutations can affect the functioning of the autonomic nervous system.
Treatment for ANS diseases depends on the specific condition and its underlying cause. In some cases, medication may be prescribed to regulate heart rate, blood pressure, or other bodily functions. Lifestyle changes, such as regular exercise and stress management techniques, can also be helpful in managing symptoms. In severe cases, surgery may be necessary to correct anatomical abnormalities or repair damaged nerves.
The symptoms of Shy-Drager Syndrome can vary widely among individuals and may include:
* Cognitive decline
* Memory loss
* Difficulty with speech and language
* Loss of coordination and balance
* Dysphagia (difficulty swallowing)
* Weakness or paralysis of the limbs
* Bladder and bowel dysfunction
* Sleep disturbances
The exact cause of Shy-Drager Syndrome is not yet fully understood, but it is believed to be related to an autoimmune response, in which the body's immune system mistakenly attacks healthy cells in the brain. Genetic factors may also play a role in the development of the disorder.
There is no cure for Shy-Drager Syndrome, but various medications and therapies can help manage its symptoms. These may include:
* Cholinesterase inhibitors to improve cognitive function and slow the progression of dementia
* Anticholinergic drugs to reduce muscle rigidity and tremors
* Physical therapy to maintain mobility and strength
* Speech and language therapy to improve communication skills
* Occupational therapy to support daily living activities
The prognosis for Shy-Drager Syndrome is generally poor, with a median survival time of around 10-15 years after onset of symptoms. However, the rate of progression can vary widely among individuals, and some may experience a more gradual decline over several decades.
Overall, Shy-Drager Syndrome is a rare and complex disorder that requires careful management by a multidisciplinary team of healthcare professionals. While there is no cure for the condition, various therapies can help manage its symptoms and improve the quality of life for affected individuals.
There are two main types of hyperhidrosis: primary and secondary. Primary hyperhidrosis is idiopathic and has no identifiable cause, while secondary hyperhidrosis is caused by another medical condition or medication. Some common triggers for secondary hyperhidrosis include anxiety, stress, fever, infection, and certain medications such as antidepressants and beta blockers.
Symptoms of hyperhidrosis can vary in severity and can include:
* Excessive sweating on the palms, soles, face, or underarms
* Sweating that is not related to heat or physical activity
* Sweating that worsens at night or in cold temperatures
* Sweating that interferes with daily activities
* Skin irritation and infections due to excessive sweating
Hyperhidrosis can be diagnosed through a combination of medical history, physical examination, and laboratory tests. Treatment options for hyperhidrosis depend on the severity of symptoms and the underlying cause, but may include:
* Antiperspirants or deodorants that contain aluminum chloride or other active ingredients to reduce sweating
* Prescription medications such as beta blockers, anticholinergics, or botulinum toxin injections to reduce sweating
* Surgical procedures such as sympathectomy (nerve surgery) to destroy the nerves that regulate sweating
* Lifestyle modifications such as avoiding triggers and wearing loose, breathable clothing to manage symptoms.
It's important to note that hyperhidrosis can have a significant impact on quality of life, and seeking medical attention is recommended if symptoms are severe or persistent.
1. Difficulty regulating body temperature, leading to episodes of hyperthermia (elevated body temperature) or hypothermia (low body temperature).
2. Abnormal heart rate and rhythm, including bradycardia (slow heart rate) or tachycardia (fast heart rate).
3. Poor digestion and gastrointestinal problems such as constipation, diarrhea, nausea, and vomiting.
4. Difficulty swallowing, which can lead to respiratory problems.
5. Orthostatic intolerance, which can cause dizziness, lightheadedness, or fainting when standing up.
6. Seizures and other neurological symptoms such as tremors, muscle weakness, and loss of coordination.
7. Cognitive impairment, including developmental delays, intellectual disability, and learning disabilities.
8. Sleep disturbances, including insomnia and sleep apnea.
9. Emotional difficulties such as anxiety, depression, and mood swings.
10. Vision problems, including blurred vision, double vision, and light sensitivity.
Primary dysautonomias are caused by genetic mutations that affect the development or function of the autonomic nervous system. There are several subtypes of primary dysautonomias, each with distinct symptoms and characteristics. These conditions are rare and can be difficult to diagnose, as they often resemble other more common conditions such as anxiety disorders or attention deficit hyperactivity disorder (ADHD). Treatment for primary dysautonomias typically involves a combination of medication and lifestyle modifications, such as reducing stress, increasing fluid intake, and avoiding overexertion. In some cases, surgery may be necessary to correct anatomical abnormalities or to implant medical devices that help regulate the autonomic nervous system.
There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
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.
In other words, pure autonomic failure refers to a situation where an individual experiences a decline in their autonomic nervous system's ability to regulate involuntary functions, such as heart rate, blood pressure, digestion, and body temperature, without any identifiable underlying cause. This can result in a range of symptoms, including fatigue, dizziness, lightheadedness, and difficulty maintaining balance.
Pure autonomic failure is rare and often presents challenges for diagnosis and treatment. It may be associated with other medical conditions, such as autoimmune disorders or neurodegenerative diseases, but in some cases, the cause remains unknown. Treatment options are limited and may include medication, lifestyle modifications, and management of symptoms.
There are several types of atrophy that can occur in different parts of the body. For example:
1. Muscular atrophy: This occurs when muscles weaken and shrink due to disuse or injury.
2. Neuronal atrophy: This occurs when nerve cells degenerate, leading to a loss of cognitive function and memory.
3. Cardiac atrophy: This occurs when the heart muscle weakens and becomes less efficient, leading to decreased cardiac output.
4. Atrophic gastritis: This is a type of stomach inflammation that can lead to the wasting away of the stomach lining.
5. Atrophy of the testes: This occurs when the testes shrink due to a lack of use or disorder, leading to decreased fertility.
Atrophy can be diagnosed through various medical tests and imaging studies, such as MRI or CT scans. Treatment for atrophy depends on the underlying cause and may involve physical therapy, medication, or surgery. In some cases, atrophy can be prevented or reversed with proper treatment and care.
In summary, atrophy is a degenerative process that can occur in various parts of the body due to injury, disease, or disuse. It can lead to a loss of function and decreased quality of life, but with proper diagnosis and treatment, it may be possible to prevent or reverse some forms of atrophy.
Examples of atrophic muscular disorders include:
1. Muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength, leading to muscle wasting and weakness.
2. Myotonia congenita: An autosomal dominant disorder characterized by muscle stiffness and spasms, particularly in the neck, shoulder, and limb muscles.
3. Inclusion body myositis: An inflammatory muscle disease that leads to progressive muscle weakness and wasting, with deposits of abnormal protein called inclusion bodies in the muscle fibers.
4. Limb-girdle muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength in the arms and legs, leading to muscle wasting and weakness.
5. Facioscapulohumeral muscular dystrophy: An inherited disorder characterized by progressive weakness of the facial, shoulder, and upper arm muscles, with a loss of motor neurons in the spinal cord.
The symptoms of atrophic muscular disorders can vary depending on the specific disorder and its severity, but may include:
1. Muscle weakness and wasting
2. Muscle cramps and spasms
3. Difficulty walking or standing
4. Fatigue and decreased endurance
5. Loss of motor neurons in the spinal cord
6. Cognitive impairment
7. Developmental delays
8. Vision loss
9. Hearing loss
10. Skeletal deformities
Atrophic muscular disorders can be diagnosed through a combination of clinical evaluation, electromyography (EMG), and muscle biopsy. Treatment is focused on managing the symptoms and slowing the progression of the disease, and may include:
1. Physical therapy to maintain muscle strength and function
2. Medications to manage pain and spasms
3. Assistive devices such as braces and walkers
4. Respiratory support in advanced cases
5. Gene therapy is an area of ongoing research, but it is not yet widely available for the treatment of atrophic muscular disorders.
It is important to note that atrophic muscular disorders are a group of rare and complex conditions, and each type has its own unique set of symptoms and characteristics. If you suspect that you or someone you know may be experiencing symptoms of an atrophic muscular disorder, it is important to consult with a healthcare professional for proper evaluation and diagnosis.
1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.
Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.
Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease, affecting approximately 1% of the population over the age of 60. It is more common in men than women and has a higher incidence in Caucasians than in other ethnic groups.
The primary symptoms of Parkinson's disease are:
* Tremors or trembling, typically starting on one side of the body
* Rigidity or stiffness, causing difficulty with movement
* Bradykinesia or slowness of movement, including a decrease in spontaneous movements such as blinking or smiling
* Postural instability, leading to falls or difficulty with balance
As the disease progresses, symptoms can include:
* Difficulty with walking, gait changes, and freezing episodes
* Dry mouth, constipation, and other non-motor symptoms
* Cognitive changes, such as dementia, memory loss, and confusion
* Sleep disturbances, including REM sleep behavior disorder
* Depression, anxiety, and other psychiatric symptoms
The exact cause of Parkinson's disease is not known, but it is believed to involve a combination of genetic and environmental factors. The disease is associated with the degradation of dopamine-producing neurons in the substantia nigra, leading to a deficiency of dopamine in the brain. This deficiency disrupts the normal functioning of the basal ganglia, a group of structures involved in movement control, leading to the characteristic symptoms of the disease.
There is no cure for Parkinson's disease, but various treatments are available to manage its symptoms. These include:
* Medications such as dopaminergic agents (e.g., levodopa) and dopamine agonists to replace lost dopamine and improve motor function
* Deep brain stimulation, a surgical procedure that involves implanting an electrode in the brain to deliver electrical impulses to specific areas of the brain
* Physical therapy to improve mobility and balance
* Speech therapy to improve communication and swallowing difficulties
* Occupational therapy to improve daily functioning
It is important for individuals with Parkinson's disease to work closely with their healthcare team to develop a personalized treatment plan that addresses their specific needs and improves their quality of life. With appropriate treatment and support, many people with Parkinson's disease are able to manage their symptoms and maintain a good level of independence for several years after diagnosis.
1. Muscular dystrophy: A group of genetic disorders that cause progressive muscle weakness and degeneration.
2. 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.
3. Spinal muscular atrophy: A genetic disorder that affects the nerve cells responsible for controlling voluntary muscle movement.
4. Peripheral neuropathy: A condition that causes damage to the peripheral nerves, leading to weakness, numbness, and pain in the hands and feet.
5. Myasthenia gravis: An autoimmune disorder that affects the nerve-muscle connection, causing muscle weakness and fatigue.
6. Neuropathy: A term used to describe damage to the nerves, which can cause a range of symptoms including numbness, tingling, and pain in the hands and feet.
7. Charcot-Marie-Tooth disease: A group of inherited disorders that affect the peripheral nerves, leading to muscle weakness and wasting.
8. Guillain-Barré syndrome: An autoimmune disorder that causes inflammation and damage to the nerves, leading to muscle weakness and paralysis.
9. Botulism: A bacterial infection that can cause muscle weakness and paralysis by blocking the release of the neurotransmitter acetylcholine.
10. Myotonia congenita: A genetic disorder that affects the nerve-muscle connection, causing muscle stiffness and rigidity.
These are just a few examples of neuromuscular diseases, and there are many more conditions that can cause muscle weakness and fatigue. It's important to see a doctor if you experience persistent or severe symptoms to receive an accurate diagnosis and appropriate treatment.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are several types of diabetic neuropathies, including:
1. Peripheral neuropathy: This is the most common type of diabetic neuropathy and affects the nerves in the hands and feet. It can cause numbness, tingling, and pain in these areas.
2. Autonomic neuropathy: This type of neuropathy affects the nerves that control involuntary functions, such as digestion, bladder function, and blood pressure. It can cause a range of symptoms, including constipation, diarrhea, urinary incontinence, and sexual dysfunction.
3. Proximal neuropathy: This type of neuropathy affects the nerves in the legs and hips. It can cause weakness, pain, and stiffness in these areas.
4. Focal neuropathy: This type of neuropathy affects a single nerve, often causing sudden and severe pain.
The exact cause of diabetic neuropathies is not fully understood, but it is thought to be related to high blood sugar levels over time. Other risk factors include poor blood sugar control, obesity, smoking, and alcohol consumption. There is no cure for diabetic neuropathy, but there are several treatments available to manage the symptoms and prevent further nerve damage. These treatments may include medications, physical therapy, and lifestyle changes such as regular exercise and a healthy diet.
Striatonigral degeneration can be caused by various factors such as genetics, exposure to toxins, or certain medical conditions. It is also associated with other neurodegenerative disorders such as Parkinson's disease, Huntington's disease, and multiple system atrophy.
The diagnosis of striatonigral degeneration typically involves a combination of clinical evaluation, imaging studies, and laboratory tests to rule out other conditions that may cause similar symptoms. There is currently no cure for the condition, but various treatments can help manage its symptoms, including medications such as dopaminergic agonists and deep brain stimulation.
Overall, striatonigral degeneration is a rare and complex disorder that affects the brain's ability to regulate movement and cognitive function, leading to significant impairment in quality of life. Further research is needed to understand its underlying causes and develop more effective treatments for this debilitating condition.
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.
Denervation
Denervation supersensitivity
Targeted lung denervation
Renal sympathetic denervation
Ciliary ganglion
Ross' syndrome
Dysmenorrhea
Salomon Z. Langer
Inferior hypogastric plexus
Neural top-down control of physiology
Low back pain
Neck pain
Regional Acceleratory Phenomenon
John Thompson Shepherd
Reinnervation
Megavitamin-B6 syndrome
Familial amyloid polyneuropathy
Apraclonidine
Autosomal recessive axonal neuropathy with neuromyotonia
Linezolid
Posterior cricoarytenoid muscle
David A. Hood
Endoscopic thoracic sympathectomy
Loin pain hematuria syndrome
Trypanosoma cruzi
Teres minor muscle
Diabetic cardiomyopathy
Rabaptin
Quadrilateral space syndrome
Catecholaminergic polymorphic ventricular tachycardia
Impaired cardiac baroreflex sensitivity predicted renal denervation response
Renal Denervation Market Size & Analysis | Industry Report, 2020-2030
EROSION OF THE ALA NASI FOLLOWING TRIGEMINAL DENERVATION | Journal of Neurology, Neurosurgery & Psychiatry
The latest research shows that renal denervation may be an effective treatment for resistant hypertension - JusticeNewsFlash.com
Renal artery stenosis after renal sympathetic denervation<...
Disuse-associated loss of the protease LONP1 in muscle impairs mitochondrial function and causes reduced skeletal muscle mass...
Dynamic Reconstruction for Facial Nerve Paralysis: Overview, Anatomy of the Facial Nerve, Etiology in Prognosis and Treatment
Motility Clinic - Overview - Mayo Clinic
Renlane renal denervation system gets CE mark - Interventional News
Catheter-based renal artery denervation: facts and expectations. | Eur J Intern Med;2023 Aug 04. | MEDLINE
ESC 365 - Changes in nocturnal blood pressure post-renal denervation: comparison of treatment versus control groups in...
Renal denervation for hypertension. | Hospital Medicine Virtual Journal Club | Washington University in St. Louis
Renal denervation associated with SBP reduction in meta-analysis of sham-controlled trials - PACE-CME
Schwann cell processes guide regeneration of peripheral axons
Sympathetic Renal Denervation for the Treatment of Hypertension: A Review of Current Progress, Limitations, Techniques,...
ReCor Medical receives the CE mark for its second generation ultrasound-based Paradise Renal Denervation System -...
The effect of denervation on the heterogeneous material properties of the tibialis anterior tendon<...
Home - Dr James Howard
Renal denervation alters ambulatory blood pressure-derived salt sensitivity index in patients with uncontrolled hypertension -...
Catheter-based renal denervation reduces atrial nerve sprouting and complexity of atrial fibrillation in goats. - Radcliffe...
Benign Essential Blepharospasm Clinical Presentation: History, Physical, Causes
body composition and hepatic enzyme induction after food restriction in rats. Effect of liver denervation on compensatory...
Renal Denervation Attenuates Adverse Remodeling and Intramyocardial Inflammation in Acute Myocardial Infarction With Ischemia...
Renal denervation and the effect of peptide yy on renal blood flow in rats<...
Relevance of Targeting the Distal Renal Artery and Branches with Radiofrequency Renal Denervation Approaches-A Secondary...
NIOSHTIC-2 Search Results - Full View
High Blood Pressure
Acute Flaccid Paralysis and West Nile Virus Infection - Volume 9, Number 7-July 2003 - Emerging Infectious Diseases journal -...
Sympathetic denervation4
- Background: Although cardiac sympathetic denervation is associated with ventricular arrhythmias, limited data are available on the predictive value of sympathetic nerve imaging with 123-I MIBG on the occurrence of arrhythmias. (eur.nl)
- Conclusions: Cardiac sympathetic denervation predicts ventricular arrhythmias causing appropriate ICD therapy as well as the composite of appropriate ICD therapy or cardiac death. (eur.nl)
- The present experiments were undertaken to investigate the electrophysiological responses of the canine saphenous vein evoked by perivascular nerve stimulation, norepinephrine or selective alpha adrenergic agonists before and after chronic sympathetic denervation. (elsevier.com)
- Cardiac sympathetic denervation (CSD) is a surgical antiadrenergic procedure that can reduce sustained ventricular tachyarrhythmia (VT) and implanted cardioverter defibrillation (ICD) shocks. (ismics.org)
Renal artery3
- In SIMPLICITY HTN-3, patients had resistant hypertension (office SBP 180 mm Hg, with no diastolic cutoff), self-reported drug adherence to 5.1 medications prescribed at randomization, and received denervation of the main renal artery only performed by mostly inexperienced operators using a monoelectrode, sequential ablation system, Böhm said. (medscape.com)
- Catheter-based renal artery denervation: facts and expectations. (bvsalud.org)
- Catheter -based renal artery denervation (RAD) is entering a new era. (bvsalud.org)
Cardiac3
- A total of thirty-two patients underwent RATS cardiac denervation and thirty-three underwent VATS cardiac denervation. (ismics.org)
- The RATS approach to cardiac denervation has similar one year follow-up outcomes in reducing recurrent VT as the VATS approach, however, patients undergoing RATS denervation experienced better peri-operative outcomes. (ismics.org)
- Table 1: Pre-, peri-, and post-operative variables of patients undergoing RATS or VATS cardiac denervation. (ismics.org)
Radiofrequency denervation2
- To determine the clinical factors associated with the success and failure of radiofrequency denervation of the lumbar facet joints. (nih.gov)
- Clinical data were garnered from 3 academic medical centers on 192 patients with low back pain who underwent radiofrequency denervation after a positive response to diagnostic blocks. (nih.gov)
Underwent2
- some studies Recommendations can significantly reduce blood pressure.Others, such as a controlled trial in 2014 , Found that there was no significant difference in blood pressure reduction between people who underwent renal denervation and people who underwent mimic surgery. (justicenewsflash.com)
- Patients were stratified into two groups: those who underwent RATS denervation and those who underwent VATS denervation. (ismics.org)
Ablation1
- Medtronic has obtained approval in the Europe and Australia to market its next-generation components of Symplicity renal denervation system, designed to reduce ablation time and provide ease of deliverability during renal denervation procedures for patients with uncontrolled hypertension. (medicaldevice-network.com)
Chronic3
- After chronic denervation the maximum response of the tissue is increased by 30 to 50% to norepinephrine, acetylcimoline and histamine but not to potassium. (aspetjournals.org)
- Does anterior plus posterior interosseus neurectomy lead to better outcomes than isolated posterior interosseus denervation in the treatment of chronic wrist pain? (bioscientifica.com)
- Partial denervation for chronic wrist pain is a salvage procedure that leads to an overall success of 78.4% for pain relief, with no substantial complications. (bioscientifica.com)
Synaptic2
- Some of the AChR loss that follows denervation is correlated with failure of portions of the old synaptic site that lack SC coverage to be reinnervated. (jneurosci.org)
- In the adult animal, the terminal SCs (tSCs) extend processes away from the old synaptic site upon denervation ( Reynolds and Woolf, 1992 ), and these processes provide a substrate that leads regenerating axons to vacant synaptic sites and leads them to sprout beyond these sites ( Son and Thompson, 1995 ). (jneurosci.org)
Symplicity6
- Long-term follow up from the SYMPLICITY HTN-3 trial showed that renal denervation is safe, and no late-emerging complications were found," said Deepak L. Bhatt, MD, MPH, Executive Director of Interventional Cardiovascular Programs at Brigham and Women's Hospital Heart & Vascular Center and Professor of Medicine at Harvard Medical School. (crf.org)
- However, several devices are in trial, including Medtronic's Symplicity renal denervation system. (justicenewsflash.com)
- According to the company, the multi-electrode system is built upon the clinical success and strong safety profile of single-electrode Symplicity renal denervation system. (medicaldevice-network.com)
- The Symplicity renal denervation system is available for investigational use only in the US. (medicaldevice-network.com)
- Image: Symplicity Renal Denervation System. (medicaldevice-network.com)
- The Spyral HTN Off-Med trial was started to try to eliminate some of the factors that researchers believe confounded the data in the original pivotal trial, Symplicity HTN-3 ( Decision time for renal denervation firms as Symplicity trial yields little comfort , March 31, 2014 ). (evaluate.com)
Subacute1
- Fatty replacement was observed acutely in hypoglossal denervation but did not manifest until the subacute stage in V3 denervation. (elsevierpure.com)
Reinnervation1
- Reinnervation compared with denervation. (nih.gov)
Hypertension6
- In contrast, SPYRAL HTN-OFF MED enrolled patients with an office SBP of 150 to less than 180 mm Hg, an office DBP of at least 90 mm Hg, and a mean 24-hour ambulatory SBP of 140 to less than 170 mm Hg and excluded those with isolated systolic hypertension because they've been shown to be hyporesponsive to renal denervation. (medscape.com)
- Invited discussant Prof Bryan William (University College London, UK) agreed that the data provide proof of concept that renal denervation lowered blood pressure in "about 75% of patients studied" but said by excluding those with isolated systolic hypertension it missed "the most common and most difficult-to-treat hypertension phenotype. (medscape.com)
- BOSTON - September 18, 2022 - Long-term results from the first and largest randomized, sham-controlled clinical trial of renal denervation (RDN) for uncontrolled hypertension (HTN) show that the procedure could lower blood pressure (BP) in patients with resistant hypertension over three years. (crf.org)
- But new research There is some hope that renal denervation, which has long been considered an experimental treatment, may indeed be an effective solution for drug-resistant hypertension. (justicenewsflash.com)
- Since the 1990s, renal denervation has been considered a possible treatment for resistant hypertension, but it is still in the experimental stage due to the mixed results of clinical trials. (justicenewsflash.com)
- Cordis has announced receiving the CE mark for its Renlane renal denervation system for the treatment of patients with resistant hypertension and has completed the first successful cases in Europe. (interventionalnews.com)
Procedure1
- While denervation lowered blood pressure significantly further than a sham procedure, the effect was not huge, at just 5mmHg - too small to be able to say that these patients had their blood pressure controlled. (evaluate.com)
Spyral1
- Medtronic might have another crack at persuading European cardiologists - Spyral and many other denervation systems are long since CE marked - to pick their catheters back up. (evaluate.com)
Kidney2
- Kidney denervation is the process of transferring energy to overactive nerves to reduce energy A sympathy signal sent between the kidney and the brain. (justicenewsflash.com)
- The research was funded by Recor Medical Inc., a manufacturer of the heavenly kidney denervation system. (justicenewsflash.com)
Oxidative1
- Using HPLC measurement of the glutathione redox potential, we quantified oxidative stress in peripheral nerve and muscle at the onset of denervation. (nih.gov)
Patients7
- Finally, drug testing of serum and urine confirmed that 94.3% of patients in the renal-denervation group and 92.7% in the sham control group were not on antihypertensive medications. (medscape.com)
- Indeed, in 10 patients, blood pressure actually increased after denervation. (medscape.com)
- Based on the reduction in ambulatory SBP from an average of 154 to 148 mm Hg and in office-based SBP from 162 to 152 mm Hg, patients treated with denervation would still need to take medications to achieve currently recommended BP treatment targets, which are only likely to go lower with revision of guidelines around the world, he said. (medscape.com)
- Medtronic Renal Denervation vice-president and general manager Nina Goodheart said: "We have significantly enhanced our technology with sophisticated features designed to meet specific unmet needs and we believe these improvements, coupled with our strong safety and efficacy profile, will provide unprecedented benefit to both patients and physicians. (medicaldevice-network.com)
- The initial promise of denervation was that it could cut blood pressure in drug-resistant patients by something like 30mmHg - this was the kind of figure seen in some early trials with no sham control group. (evaluate.com)
- Discussing the results, Professor Bryan Williams of University College London, put it bluntly: "Renal denervation did not appear to control blood pressure in the patients treated to currently recommended targets. (evaluate.com)
- METHODS: Findings from 11 patients with V3 denervation and from seven patients with hypoglossal denervation resulting from a variety of abnormalities were reviewed retrospectively. (elsevierpure.com)
Pivotal trial1
- The study was not powered for statistical significance but "provides biologic proof of principle for the efficacy of renal denervation" and will inform the design of a larger pivotal trial, co-primary investigator Dr Michael Böhm (University Hospital of Saarland, Homburg/Saar, Germany) reported here at the European Society of Cardiology (ESC) Congress 2017 . (medscape.com)
Sensitivity1
- One week after preganglionie denervation (decentralization), there is a moderate increase in sensitivity to norepinephrine (2.5-fold) as well as supersensitivity to histamine (2-fold). (aspetjournals.org)
Clinical1
- So we can't become too excited about these data referable to clinical application, but what we can do is accept the fact that these data initiate the conversations again about renal denervation. (medscape.com)
Partial1
- Partial wrist denervation can be performed by isolated posterior interosseous nerve (PIN) or combined PIN plus (+) anterior interosseous nerve (AIN) neurectomy procedures. (bioscientifica.com)
Axon1
- New AChR clustering is also induced by axon terminals that follow SC processes extended during denervation. (jneurosci.org)
Patterns2
- Histologic samples can be assessed for patterns of innervation or denervation by the intrinsic nervous system of the gut. (mayoclinic.org)
- Recognition of MR imaging patterns of denervation may allow earlier diagnosis of a denervating lesion and may help to distinguish denervation from similar- appearing processes, such as infection or neoplasia. (elsevierpure.com)
Significantly1
- No conduction changes occurred as PR and QT intervals were not significantly different between pre- and post-op for both VATS and RATS denervation. (ismics.org)
Blood pressure1
- These findings indicate that durable blood pressure reductions with radio-frequency renal denervation in combination with maximal medical therapy can be safely achieved. (crf.org)
Functional2
- Facial nerve denervation and paralysis imposes significant psychological and functional impairment. (medscape.com)
- The motor denervation appearance and functional compromise of the affected musculature are described in terms of the chronicity of the denervation process. (elsevierpure.com)
Processes1
- During the period of denervation, SCs at the NMJ extend elaborate processes from the junction, as shown previously, but they also retract some processes from territory they previously occupied within the endplate. (jneurosci.org)
Response3
- One week after postganglionic denervation of the vas deferens there are marked changes in the response of the smooth muscle to stimulant drugs. (aspetjournals.org)
- There is also an increase in the duration of the response to all four stimulants after denervation. (aspetjournals.org)
- Denervation augments selectively the electrical response to alpha-2 adrenergic stimulation. (elsevier.com)
Results2
- RESULTS: The appearance of V3 and hypoglossal motor denervation varies with the chronicity of the process. (elsevierpure.com)
- Long-standing denervation results in extensive fatty replacement and a decrease in the size of the affected musculature. (elsevierpure.com)
Failure1
- The isolated PIN neurectomy technique showed a 15.1% pooled failure rate at a median follow-up of 22 months, while the combined AIN+PIN denervation had a pooled failure rate of 23.6% at a follow-up with a median of 29 months. (bioscientifica.com)
Show1
- Renal denervation, presumed dead in 2014, is starting to show signs of life. (evaluate.com)
Report2
- The report also includes profiles and for some of the leading companies in the Renal Denervation Market, with a focus on this segment of these companies' operations. (visiongain.com)
- We report preferential denervation of fast-twitch muscles beginning between 1 and 4 months of age, with relative sparing of slow-twitch muscle. (nih.gov)
Variable1
- CONCLUSION: V3 and hypoglossal denervation have a variable appearance depending on the chronicity of the process. (elsevierpure.com)
Market4
- Much opportunity remains in this growing Renal Denervation market. (visiongain.com)
- Along with revenue prediction for the overall world market, there are 3 segmentations of the Renal Denervation market, with forecasts for 4 Technologies, 3 Products, 3 End uses, each forecasted at a global and regional level. (visiongain.com)
- Revenue forecasts to 2030 for 5 regional and 18 key national markets - See forecasts for the Renal Denervation market in North America, Latin America, Europe, Asia-Pacific and MEA. (visiongain.com)
- Visiongain study is for everybody needing commercial analyses for the Renal Denervation market and leading companies. (visiongain.com)
Muscle1
- Branched chain aminoacid aminotransferase activity in the denervation atrophy of amphibian skeletal muscle. (who.int)