Hyperkalemia
Paralysis, Hyperkalemic Periodic
Paralyses, Familial Periodic
Paralysis
Myotonia Congenita
Heart Arrest, Induced
Pseudohypoaldosteronism
NAV1.4 Voltage-Gated Sodium Channel
Cardioplegic Solutions
Acidosis, Renal Tubular
Respiratory Paralysis
Myotonia
Vocal Cord Paralysis
Facial Paralysis
Sodium Channels
Potassium
Sleep Paralysis
Horses
Muscle Hypotonia
Hypokalemia
Poliomyelitis
Thyrotoxicosis
Paraplegia
Bell Palsy
Facial Nerve Diseases
Neuromuscular Blocking Agents
Quadriplegia
Recurrent Laryngeal Nerve
Paralysis, Obstetric
Poliovirus
Poliovirus Vaccine, Oral
Phrenic Nerve
Botulinum Toxins, Type A
Pancuronium
Hypokalemic Periodic Paralysis
Effects of temperature on slow and fast inactivation of rat skeletal muscle Na(+) channels. (1/16)
Patch-clamp studies of mammalian skeletal muscle Na(+) channels are commonly done at subphysiological temperatures, usually room temperature. However, at subphysiological temperatures, most Na(+) channels are inactivated at the cell resting potential. This study examined the effects of temperature on fast and slow inactivation of Na(+) channels to determine if temperature changed the fraction of Na(+) channels that were excitable at resting potential. The loose patch voltage clamp recorded Na(+) currents (I(Na)) in vitro at 19, 25, 31, and 37 degrees C from the sarcolemma of rat type IIb fast-twitch omohyoid skeletal muscle fibers. Temperature affected the fraction of Na(+) channels that were excitable at the resting potential. At 19 degrees C, only 30% of channels were excitable at the resting potential. In contrast, at 37 degrees C, 93% of Na(+) channels were excitable at the resting potential. Temperature did not alter the resting potential or the voltage dependencies of activation or fast inactivation. I(Na) available at the resting potential increased with temperature because the steady-state voltage dependence of slow inactivation shifted in a depolarizing direction with increasing temperature. The membrane potential at which half of the Na(+) channels were in the slow inactivated state was shifted by +16 mV at 37 degrees C compared with 19 degrees C. Consequently, the low availability of excitable Na(+) channels at subphysiological temperatures resulted from channels being in the slow, inactivated state at the resting potential. (+info)Phenotypic variation of a Thr704Met mutation in skeletal sodium channel gene in a family with paralysis periodica paramyotonica. (2/16)
OBJECTIVES: Patients with paralysis periodica paramyotonica exhibit a clinical syndrome with characteristics of both hyperkalaemic periodic paralysis and paramyotonia congenita. In several types of periodic paralysis associated with hyperkalaemia, mutations in the skeletal muscle sodium channel (SCN4A) gene have been previously reported. Phenotypic variations of mutations in SCN4A, however, have not been described yet. The present study aimed to evaluate genetic variations in a family with clinical and electrophysiological characteristics of paralysis periodica paramyotonia. METHODS: Seven members of a family affected with symptoms of paralysis periodica paramyotonia were studied by electrophysiological and genetic analyses. There were increased serum potassium concentrations in four members during paralytic attacks induced by hyperkalaemic periodic paralysis provocation tests. Short exercise tests before and after cold immersion were carried out in four patients to distinguish electrophysiological characteristics of hyperkalaemic periodic paralysis and paramyotonia. Sequencing analyses of SCN4A were performed on one patient and a normal control to identify polymorphisms. Restriction fragment length polymorphism (RFLP) analysis was then performed at the identified polymorphic sites. RESULTS: Electrophysiological studies showed both exercise sensitivity and temperature sensitivity. Compound motor action potential (CMAP) amplitudes were decreased (7.3%-28.6%) after short exercise tests. The CMAP amplitudes were even more severely decreased (21.7%-56.5%) in short exercise tests after cold exposure. Three polymorphic sites, Gln371Glu, Thr704Met, and Aspl376Asn were identified in SCN4A. RFLP analyses showed that all affected patients carried the Thr704Met mutation, whereas unaffected family members and a normal control did not. CONCLUSION: Phenotypic variation of the Thr704Met mutation, which was previously reported in patients with hyperkalaemic periodic paralysis, is described in a family affected with paralysis periodica paramyotonia. (+info)Severe infantile hyperkalaemic periodic paralysis and paramyotonia congenita: broadening the clinical spectrum associated with the T704M mutation in SCN4A. (3/16)
The authors describe an Italian kindred with nine individuals affected by hyperkalaemic periodic paralysis associated with paramyotonia congenita (hyperPP/PMC). Periodic paralysis was particularly severe, with several episodes a day lasting for hours. The onset of episodes was unusually early, beginning in the first year of life and persisting into adult life. The paralytic episodes were refractory to treatment. Patients described minimal paramyotonia, mainly of the eyelids and hands. All affected family members carried the threonine to methionine substitution at codon 704 (T704M) in exon 13 of the skeletal muscle voltage gated sodium channel gene (SCN4A). The association between T704M and the hyperPP/PMC phenotype has been only recently revealed. Nevertheless, such a severe phenotype has never been reported so far in families with either hyperPP or hyperPP/PMC. These data further broaden the clinical spectrum of T704M and support the evidence that this mutation is a common cause of hyperPP/PMC. (+info)Internal restriction sites: quality assurance aids in genotyping. (4/16)
Improvements to restriction fragment length polymorphism (RFLP)-based genotyping assays currently used for detection of mutations responsible for bovine ferrochelatase and myophosphorylase deficiencies, and equine hyperkalemic periodic paralysis (HYPP) are described. Reports of sporadic inhibition of restriction enzyme activity suggest a critical factor in RFLP-based genotyping assays should be assurance that restriction enzymes perform to specification with every sample. The RFLP genotyping assays that use either a mismatched recognition sequence in one or both of the oligonucleotides, or incorporate a second native site within the PCR amplicon, provide the mechanism by which efficiency of restriction enzymes can be assessed with every sample. The outcome is confirmation of the activity of the discriminating enzyme regardless of genotype. (+info)Cold-induced defects of sodium channel gating in atypical periodic paralysis plus myotonia. (5/16)
BACKGROUND: Missense mutations of the skeletal muscle voltage-gated sodium channel (NaV1.4) are an established cause of several clinically distinct forms of periodic paralysis and myotonia. The mechanistic basis for the phenotypic variability of these allelic disorders of muscle excitability remains unknown. An atypical phenotype with cold-induced hypokalemic paralysis and myotonia at warm temperatures was reported to segregate with the P1158S mutation. OBJECTIVE: This study extends the functional characterization of the P1158S mutation and tests the specific hypothesis that impairment of Na channel slow inactivation is a common feature of periodic paralysis. METHODS: Mutant NaV1.4 channels (P1158S) were transiently expressed in human embryonic kidney cells and characterized by voltage-clamp studies of Na currents. RESULTS: Wild-type and P1158S channels displayed comparable behavior at 37 degrees C, but upon cooling to 25 degrees C, mutant channels activated at more negative potentials and slow inactivation was destabilized. CONCLUSIONS: Consistent with other NaV1.4 mutations associated with a paralytic phenotype, the P1158S mutation disrupts slow inactivation. The unique temperature sensitivity of the channel defect may contribute to the unusual clinical phenotype. (+info)Targeted mutation of mouse skeletal muscle sodium channel produces myotonia and potassium-sensitive weakness. (6/16)
(+info)Voltage sensor charge loss accounts for most cases of hypokalemic periodic paralysis. (7/16)
(+info)Diagnostics and therapy of muscle channelopathies--Guidelines of the Ulm Muscle Centre. (8/16)
This article is dedicated to our teacher, Prof. Erich Kuhn, Heidelberg, on the occasion of his 88th birthday on 23rd November 2008. In contrast to muscular dystrophies, the muscle channelopathies, a group of diseases characterised by impaired muscle excitation or excitation-contraction coupling, can fairly well be treated with a whole series of pharmacological drugs. However, for a proper treatment proper diagnostics are essential. This article lists state-of-the-art diagnostics and therapies for the two types of myotonic dystrophies, for recessive and dominant myotonia congenita, for the sodium channel myotonias, for the primary dyskalemic periodic paralyses, for central core disease and for malignant hyperthermia susceptibility in detail. In addition, for each disorder a short summary of aetiology, symptomatology, and pathogenesis is provided. (+info)Hyperkalemia is a medical condition characterized by an elevated level of potassium (K+) in the blood serum, specifically when the concentration exceeds 5.0-5.5 mEq/L (milliequivalents per liter). Potassium is a crucial intracellular ion that plays a significant role in various physiological processes, including nerve impulse transmission, muscle contraction, and heart rhythm regulation.
Mild to moderate hyperkalemia might not cause noticeable symptoms but can still have harmful effects on the body, particularly on the cardiovascular system. Severe cases of hyperkalemia (potassium levels > 6.5 mEq/L) can lead to potentially life-threatening arrhythmias and heart failure.
Hyperkalemia may result from various factors, such as kidney dysfunction, hormonal imbalances, medication side effects, trauma, or excessive potassium intake. Prompt identification and management of hyperkalemia are essential to prevent severe complications and ensure proper treatment.
Hyperkalemic periodic paralysis (HypPK) is a rare genetic disorder characterized by episodes of muscle weakness or paralysis due to an abnormality in the ion channels that regulate the movement of potassium into and out of muscle fibers. This results in an excessive accumulation of potassium in the blood (hyperkalemia) during attacks, which can interfere with the ability of nerve cells to communicate with muscles and cause temporary muscle weakness or paralysis.
HypPK is caused by mutations in the SCN4A gene, which encodes a sodium channel protein found in skeletal muscle. These genetic changes disrupt the normal functioning of the ion channels, leading to an imbalance in the flow of ions across the muscle cell membrane and affecting muscle excitability.
Episodes of paralysis in HypPK typically begin in childhood or adolescence and can last from several hours to days. Triggers for attacks may include rest following exercise, cold or hot weather, stress, alcohol consumption, infection, or certain medications. Between episodes, individuals with HypPK usually have normal muscle strength and function.
Management of HypPK includes avoiding triggers, maintaining a low-potassium diet, and using medications to prevent or treat attacks. Medications such as thiazide diuretics, acetazolamide, or dichlorphenamide can help lower potassium levels in the blood and reduce the frequency and severity of episodes. In some cases, intravenous glucose and insulin may be used to drive potassium into cells during an attack, thereby reducing its concentration in the blood and alleviating symptoms.
Familial periodic paralysis is a group of rare genetic disorders characterized by episodes of muscle weakness or paralysis that recur over time. There are several types of familial periodic paralysis, including hypokalemic periodic paralysis, hyperkalemic periodic paralysis, and normokalemic periodic paralysis, each with its own specific genetic cause and pattern of symptoms.
In general, these disorders are caused by mutations in genes that regulate ion channels in muscle cells, leading to abnormalities in the flow of ions such as potassium in and out of the cells. This can result in changes in muscle excitability and contractility, causing episodes of weakness or paralysis.
The episodes of paralysis in familial periodic paralysis can vary in frequency, duration, and severity. They may be triggered by factors such as rest after exercise, cold or hot temperatures, emotional stress, alcohol consumption, or certain medications. During an episode, the affected muscles may become weak or completely paralyzed, often affecting the limbs but sometimes also involving the muscles of the face, throat, and trunk.
Familial periodic paralysis is typically inherited in an autosomal dominant pattern, meaning that a child has a 50% chance of inheriting the disorder if one parent is affected. However, some cases may arise from new mutations in the affected gene and occur in people with no family history of the disorder.
Treatment for familial periodic paralysis typically involves avoiding triggers and managing symptoms during episodes. In some cases, medications such as potassium-binding agents or diuretics may be used to help prevent or reduce the severity of episodes. Lifestyle modifications, such as a low-carbohydrate or high-sodium diet, may also be recommended in some cases.
Paralysis is a loss of muscle function in part or all of your body. It can be localized, affecting only one specific area, or generalized, impacting multiple areas or even the entire body. Paralysis often occurs when something goes wrong with the way messages pass between your brain and muscles. In most cases, paralysis is caused by damage to the nervous system, especially the spinal cord. Other causes include stroke, trauma, infections, and various neurological disorders.
It's important to note that paralysis doesn't always mean a total loss of movement or feeling. Sometimes, it may just cause weakness or numbness in the affected area. The severity and extent of paralysis depend on the underlying cause and the location of the damage in the nervous system.
Myotonia Congenita is a genetic muscle disorder characterized by delayed relaxation after voluntary muscle contraction, leading to stiffness or difficulty in relaxing the muscles following use. This muscle stiffness is called myotonia and can be aggravated by voluntary muscle action, such as handgrip or walking, and also occurs after periods of rest.
There are two main forms of Myotonia Congenita: Thomsen's disease (autosomal dominant inheritance) and Becker's disease (autosomal recessive inheritance). The disorder is caused by mutations in the CLCN1 gene, which encodes a chloride channel that helps regulate muscle excitability.
Myotonia Congenita primarily affects skeletal muscles, causing stiffness and cramping, but it does not typically affect muscle strength or size. Symptoms usually begin in childhood and may improve with repeated muscle use (warm-up phenomenon). Treatment options include medication to reduce muscle stiffness and physical therapy to maintain muscle flexibility and strength.
Induced heart arrest, also known as controlled cardiac arrest or planned cardiac arrest, is a deliberate medical intervention where cardiac activity is temporarily stopped through the use of medications or electrical disruption. This procedure is typically carried out during a surgical procedure, such as open-heart surgery, where the heart needs to be stilled to allow surgeons to work on it safely.
The most common method used to induce heart arrest is by administering a medication called potassium chloride, which stops the heart's electrical activity. Alternatively, an electrical shock may be delivered to the heart to achieve the same effect. Once the procedure is complete, the heart can be restarted using various resuscitation techniques, such as defibrillation or medication administration.
It's important to note that induced heart arrest is a carefully monitored and controlled medical procedure carried out by trained healthcare professionals in a hospital setting. It should not be confused with sudden cardiac arrest, which is an unexpected and often unpredictable event that occurs outside of a medical setting.
Pseudohypoaldosteronism is a group of disorders that are characterized by resistance to aldosterone, a hormone produced by the adrenal glands. Aldosterone plays a key role in regulating sodium and potassium balance in the body. In pseudohypoaldosteronism, the kidneys fail to respond to aldosterone, leading to an imbalance of electrolytes in the body.
There are two types of pseudohypoaldosteronism: type I and type II. Type I is further divided into two subtypes: severe neonatal or infantile forms, which are usually caused by genetic mutations that affect the function of the sodium-potassium pump in the kidney; and milder forms, which can be inherited or acquired and may be associated with other medical conditions.
Type II pseudohypoaldosteronism is a rare disorder that typically affects older children and adults. It is caused by genetic mutations that affect the function of the mineralocorticoid receptor in the kidney, which binds to aldosterone and triggers a response.
Symptoms of pseudohypoaldosteronism may include low sodium levels, high potassium levels, and metabolic acidosis (a buildup of acid in the body). Treatment typically involves supplementation with sodium and/or medications to help regulate electrolyte balance.
NAV1.4, also known as SCN4A, is a gene that encodes for the α subunit of the voltage-gated sodium channel in humans. This channel, specifically located in the skeletal muscle, is responsible for the rapid influx of sodium ions during the initiation and propagation of action potentials, which are critical for muscle contraction.
The NAV1.4 Voltage-Gated Sodium Channel plays a crucial role in the functioning of skeletal muscles. Mutations in this gene can lead to various neuromuscular disorders such as hyperkalemic periodic paralysis, paramyotonia congenita, and potassium-aggravated myotonia, which are characterized by muscle stiffness, cramps, and episodes of weakness or paralysis.
Cardioplegic solutions are specially formulated liquids used in medical procedures to induce cardiac arrest and protect the heart muscle during open-heart surgery. These solutions typically contain a combination of electrolytes, such as potassium and magnesium, which stop the heart from beating by interrupting its electrical activity. They may also include energy substrates, buffers, and other components to maintain the health and function of the heart cells during the period of arrest. The specific formulation of cardioplegic solutions can vary depending on the needs of the patient and the preferences of the medical team.
Renal tubular acidosis (RTA) is a medical condition that occurs when the kidneys are unable to properly excrete acid into the urine, leading to an accumulation of acid in the bloodstream. This results in a state of metabolic acidosis.
There are several types of RTA, but renal tubular acidosis type 1 (also known as distal RTA) is characterized by a defect in the ability of the distal tubules to acidify the urine, leading to an inability to lower the pH of the urine below 5.5, even in the face of metabolic acidosis. This results in a persistently alkaline urine, which can lead to calcium phosphate stones and bone demineralization.
Type 1 RTA is often caused by inherited genetic defects, but it can also be acquired due to various kidney diseases, drugs, or autoimmune disorders. Symptoms of type 1 RTA may include fatigue, weakness, muscle cramps, decreased appetite, and vomiting. Treatment typically involves alkali therapy to correct the acidosis and prevent complications.
Respiratory paralysis is a condition characterized by the inability to breathe effectively due to the failure or weakness of the muscles involved in respiration. This can include the diaphragm, intercostal muscles, and other accessory muscles.
In medical terms, it's often associated with conditions that affect the neuromuscular junction, such as botulism, myasthenia gravis, or spinal cord injuries. It can also occur as a complication of general anesthesia, sedative drugs, or certain types of poisoning.
Respiratory paralysis is a serious condition that requires immediate medical attention, as it can lead to lack of oxygen (hypoxia) and buildup of carbon dioxide (hypercapnia) in the body, which can be life-threatening if not treated promptly.
Myotonia is a condition characterized by the delayed relaxation of a muscle after voluntary contraction or electrical stimulation, resulting in stiffness or difficulty with relaxing the muscles. It's often associated with certain neuromuscular disorders such as myotonic dystrophy and myotonia congenita. The prolonged muscle contraction can cause stiffness, especially after periods of rest, and may improve with repeated contractions (warm-up phenomenon).
Vocal cord paralysis is a medical condition characterized by the inability of one or both vocal cords to move or function properly due to nerve damage or disruption. The vocal cords are two bands of muscle located in the larynx (voice box) that vibrate to produce sound during speech, singing, and breathing. When the nerves that control the vocal cord movements are damaged or not functioning correctly, the vocal cords may become paralyzed or weakened, leading to voice changes, breathing difficulties, and other symptoms.
The causes of vocal cord paralysis can vary, including neurological disorders, trauma, tumors, surgery, or infections. The diagnosis typically involves a physical examination, including a laryngoscopy, to assess the movement and function of the vocal cords. Treatment options may include voice therapy, surgical procedures, or other interventions to improve voice quality and breathing functions.
I understand you are asking for a medical definition of "Horse Diseases." However, it's important to note that there isn't a specific medical field dedicated to horse diseases as we typically categorize medical fields by human diseases and conditions. Veterinary medicine is the field responsible for studying, diagnosing, and treating diseases in animals, including horses.
Here's a general definition of 'Horse Diseases':
Horse diseases are health issues or medical conditions that affect equine species, particularly horses. These diseases can be caused by various factors such as bacterial, viral, fungal, or parasitic infections; genetic predispositions; environmental factors; and metabolic disorders. Examples of horse diseases include Strangles (Streptococcus equi), Equine Influenza, Equine Herpesvirus, West Nile Virus, Rabies, Potomac Horse Fever, Lyme Disease, and internal or external parasites like worms and ticks. Additionally, horses can suffer from musculoskeletal disorders such as arthritis, laminitis, and various injuries. Regular veterinary care, preventative measures, and proper management are crucial for maintaining horse health and preventing diseases.
Facial paralysis is a loss of facial movement due to damage or dysfunction of the facial nerve (cranial nerve VII). This nerve controls the muscles involved in facial expressions, such as smiling, frowning, and closing the eyes. Damage to one side of the facial nerve can cause weakness or paralysis on that side of the face.
Facial paralysis can result from various conditions, including:
1. Bell's palsy - an idiopathic (unknown cause) inflammation of the facial nerve
2. Trauma - skull fractures, facial injuries, or surgical trauma to the facial nerve
3. Infections - Lyme disease, herpes zoster (shingles), HIV/AIDS, or bacterial infections like meningitis
4. Tumors - benign or malignant growths that compress or invade the facial nerve
5. Stroke - damage to the brainstem where the facial nerve originates
6. Congenital conditions - some people are born with facial paralysis due to genetic factors or birth trauma
Symptoms of facial paralysis may include:
* Inability to move one or more parts of the face, such as the eyebrows, eyelids, mouth, or cheeks
* Drooping of the affected side of the face
* Difficulty closing the eye on the affected side
* Changes in saliva and tear production
* Altered sense of taste
* Pain around the ear or jaw
* Speech difficulties due to weakened facial muscles
Treatment for facial paralysis depends on the underlying cause. In some cases, such as Bell's palsy, spontaneous recovery may occur within a few weeks to months. However, physical therapy, medications, and surgical interventions might be necessary in other situations to improve function and minimize complications.
Sodium channels are specialized protein structures that are embedded in the membranes of excitable cells, such as nerve and muscle cells. They play a crucial role in the generation and transmission of electrical signals in these cells. Sodium channels are responsible for the rapid influx of sodium ions into the cell during the initial phase of an action potential, which is the electrical signal that travels along the membrane of a neuron or muscle fiber. This sudden influx of sodium ions causes the membrane potential to rapidly reverse, leading to the depolarization of the cell. After the action potential, the sodium channels close and become inactivated, preventing further entry of sodium ions and helping to restore the resting membrane potential.
Sodium channels are composed of a large alpha subunit and one or two smaller beta subunits. The alpha subunit forms the ion-conducting pore, while the beta subunits play a role in modulating the function and stability of the channel. Mutations in sodium channel genes have been associated with various inherited diseases, including certain forms of epilepsy, cardiac arrhythmias, and muscle disorders.
Potassium is a essential mineral and an important electrolyte that is widely distributed in the human body. The majority of potassium in the body (approximately 98%) is found within cells, with the remaining 2% present in blood serum and other bodily fluids. Potassium plays a crucial role in various physiological processes, including:
1. Regulation of fluid balance and maintenance of normal blood pressure through its effects on vascular tone and sodium excretion.
2. Facilitation of nerve impulse transmission and muscle contraction by participating in the generation and propagation of action potentials.
3. Protein synthesis, enzyme activation, and glycogen metabolism.
4. Regulation of acid-base balance through its role in buffering systems.
The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (milliequivalents per liter) or mmol/L (millimoles per liter). Potassium levels outside this range can have significant clinical consequences, with both hypokalemia (low potassium levels) and hyperkalemia (high potassium levels) potentially leading to serious complications such as cardiac arrhythmias, muscle weakness, and respiratory failure.
Potassium is primarily obtained through the diet, with rich sources including fruits (e.g., bananas, oranges, and apricots), vegetables (e.g., leafy greens, potatoes, and tomatoes), legumes, nuts, dairy products, and meat. In cases of deficiency or increased needs, potassium supplements may be recommended under the guidance of a healthcare professional.
Sleep paralysis is a temporary inability to move or speak while falling asleep or waking up, often accompanied by frightening hallucinations. These episodes typically last a few seconds to several minutes. During sleep paralysis, a person's body is immobile and cannot perform voluntary muscle movements even though they are fully conscious and awake. This condition can be quite alarming, but it is generally harmless and does not pose any serious threat to one's health. Sleep paralysis is often associated with certain sleep disorders, such as narcolepsy, or other medical conditions, as well as stress, lack of sleep, and changes in sleep patterns.
Tick paralysis is a condition caused by the saliva of certain species of tick that contains neurotoxins. When the tick feeds on the host's blood, the toxin is absorbed, leading to progressive ascending muscle weakness and eventually respiratory failure if not promptly treated. The symptoms typically begin in the lower extremities and progress upward, often within 2-7 days after attachment of the tick. Removal of the attached tick usually leads to improvement in symptoms and full recovery within a few days. It is more commonly seen in children and pets than adults.
I'm sorry for any confusion, but "horses" is not a medical term. It is the common name given to the species *Equus ferus caballus*, which are large domesticated mammals used for transportation, work, and recreation. If you have any questions about horses or a related topic that you would like a medical perspective on, please let me know and I'd be happy to help!
Muscle hypotonia, also known as decreased muscle tone, refers to a condition where the muscles appear to be flaccid or lacking in tension and stiffness. This results in reduced resistance to passive movements, making the limbs feel "floppy" or "like a rag doll." It can affect any muscle group in the body and can be caused by various medical conditions, including neurological disorders, genetic diseases, and injuries to the nervous system. Hypotonia should not be confused with muscle weakness, which refers to the inability to generate normal muscle strength.
Hypokalemia is a medical condition characterized by abnormally low potassium levels in the blood, specifically when the concentration falls below 3.5 milliequivalents per liter (mEq/L). Potassium is an essential electrolyte that helps regulate heart function, nerve signals, and muscle contractions.
Hypokalemia can result from various factors, including inadequate potassium intake, increased potassium loss through the urine or gastrointestinal tract, or shifts of potassium between body compartments. Common causes include diuretic use, vomiting, diarrhea, certain medications, kidney diseases, and hormonal imbalances.
Mild hypokalemia may not cause noticeable symptoms but can still affect the proper functioning of muscles and nerves. More severe cases can lead to muscle weakness, fatigue, cramps, paralysis, heart rhythm abnormalities, and in rare instances, respiratory failure or cardiac arrest. Treatment typically involves addressing the underlying cause and replenishing potassium levels through oral or intravenous (IV) supplementation, depending on the severity of the condition.
Poliomyelitis, also known as polio, is a highly infectious disease caused by a virus that invades the body through the mouth, usually from contaminated water or food. The virus multiplies in the intestine and can invade the nervous system, causing paralysis.
The medical definition of Poliomyelitis includes:
1. An acute viral infection caused by the poliovirus.
2. Characterized by inflammation of the gray matter of the spinal cord (poliomyelitis), leading to muscle weakness, and in some cases, paralysis.
3. The disease primarily affects children under 5 years of age.
4. Transmission occurs through the fecal-oral route or, less frequently, by respiratory droplets.
5. The virus enters the body via the mouth, multiplies in the intestines, and can invade the nervous system.
6. There are three types of poliovirus (types 1, 2, and 3), each capable of causing paralytic polio.
7. Infection with one type does not provide immunity to the other two types.
8. The disease has no cure, but vaccination can prevent it.
9. Two types of vaccines are available: inactivated poliovirus vaccine (IPV) and oral poliovirus vaccine (OPV).
10. Rare complications of OPV include vaccine-associated paralytic polio (VAPP) and circulating vaccine-derived polioviruses (cVDPVs).
Thyrotoxicosis is a medical condition that results from an excess of thyroid hormones in the body, leading to an overactive metabolic state. It can be caused by various factors such as Graves' disease, toxic adenoma, Plummer's disease, or excessive intake of thyroid hormone medication. Symptoms may include rapid heart rate, weight loss, heat intolerance, tremors, and increased sweating, among others. Thyrotoxicosis is not a diagnosis itself but a manifestation of various underlying thyroid disorders. Proper diagnosis and management are crucial to prevent complications and improve quality of life.
Dicistroviridae is a family of small, non-enveloped, positive-sense single-stranded RNA viruses that infect insects. These viruses are characterized by having two open reading frames (ORFs) in their genome, separated by an intergenic region (IGR). The first ORF encodes for the non-structural proteins involved in replication, while the second ORF encodes for the structural proteins needed for virion assembly.
The family Dicistroviridae includes several important insect pathogens, such as Cricket paralysis virus (CrPV), Rhopalisphum padi virus (RhPV), and Triatoma virus (TrV). These viruses can cause significant economic losses in agriculture by infecting and killing beneficial insects, such as honeybees and silkworms.
Dicistroviridae viruses are transmitted horizontally between hosts through various routes, including oral-fecal transmission, contact with contaminated surfaces, or via vectors such as parasitoids. They have a wide host range within the Insecta class, but they do not infect vertebrates or higher plants.
In terms of medical relevance, Dicistroviridae viruses are not known to infect humans or other mammals. However, understanding their replication and transmission strategies can provide valuable insights into the development of novel antiviral therapies and insect control methods.
Paraplegia is a medical condition characterized by partial or complete loss of motor function and sensation in the lower extremities, typically affecting both legs. This results from damage to the spinal cord, often due to trauma such as accidents, falls, or gunshot wounds, or from diseases like spina bifida, polio, or tumors. The specific area and extent of the injury on the spinal cord determine the severity and location of paralysis. Individuals with paraplegia may require assistive devices for mobility, such as wheelchairs, and may face various health challenges, including pressure sores, urinary tract infections, and chronic pain.
Bell palsy is a peripheral facial nerve palsy, which means that it is a weakness or paralysis of the facial nerves (cranial nerve VII) that causes sudden asymmetric weakness on one side of the face. The symptoms can vary from mild to severe and may include:
* Sudden weakness or paralysis on one side of the face
* Drooping of the mouth, causing difficulty with smiling, eating, drinking, or speaking
* Inability to close one eye
* Dryness of the eye and mouth
* Changes in taste sensation
* Discomfort around the jaw and behind the ear
* Headache
* Increased sensitivity to sound
The exact cause of Bell palsy is not known, but it is believed to be related to inflammation or swelling of the facial nerve. It may also be associated with viral infections such as herpes simplex virus or HIV. In most cases, Bell palsy resolves on its own within a few weeks to months, although some people may experience residual symptoms such as facial weakness or asymmetry. Treatment typically involves corticosteroids and antiviral medications, which can help reduce inflammation and speed up recovery.
Facial nerve diseases refer to a group of medical conditions that affect the function of the facial nerve, also known as the seventh cranial nerve. This nerve is responsible for controlling the muscles of facial expression, and it also carries sensory information from the taste buds in the front two-thirds of the tongue, and regulates saliva flow and tear production.
Facial nerve diseases can cause a variety of symptoms, depending on the specific location and extent of the nerve damage. Common symptoms include:
* Facial weakness or paralysis on one or both sides of the face
* Drooping of the eyelid and corner of the mouth
* Difficulty closing the eye or keeping it closed
* Changes in taste sensation or dryness of the mouth and eyes
* Abnormal sensitivity to sound (hyperacusis)
* Twitching or spasms of the facial muscles
Facial nerve diseases can be caused by a variety of factors, including:
* Infections such as Bell's palsy, Ramsay Hunt syndrome, and Lyme disease
* Trauma or injury to the face or skull
* Tumors that compress or invade the facial nerve
* Neurological conditions such as multiple sclerosis or Guillain-Barre syndrome
* Genetic disorders such as Moebius syndrome or hemifacial microsomia
Treatment for facial nerve diseases depends on the underlying cause and severity of the symptoms. In some cases, medication, physical therapy, or surgery may be necessary to restore function and relieve symptoms.
Neuromuscular blocking agents (NMBAs) are a class of drugs that act on the neuromuscular junction, the site where nerve impulses transmit signals to muscles to cause contraction. NMBAs prevent the transmission of these signals, leading to muscle paralysis. They are used in medical settings during surgical procedures and mechanical ventilation to facilitate intubation, control ventilation, and prevent patient movement. It is important to note that NMBAs do not have any effect on consciousness or pain perception; therefore, they are always used in conjunction with anesthetics and analgesics.
NMBAs can be classified into two main categories based on their mechanism of action:
1. Depolarizing Neuromuscular Blocking Agents: These drugs, such as succinylcholine, cause muscle fasciculations (brief, involuntary contractions) before inducing paralysis. They work by binding to the acetylcholine receptors at the neuromuscular junction and depolarizing the membrane, which results in muscle paralysis. However, the continuous depolarization also causes desensitization of the receptors, leading to a loss of effectiveness over time. Depolarizing NMBAs have a relatively short duration of action.
2. Non-depolarizing Neuromuscular Blocking Agents: These drugs, such as rocuronium, vecuronium, and pancuronium, do not cause muscle fasciculations. They work by binding to the acetylcholine receptors at the neuromuscular junction without depolarizing the membrane, which prevents the transmission of nerve impulses to muscles and leads to paralysis. Non-depolarizing NMBAs have a longer duration of action compared to depolarizing NMBAs.
Close monitoring of neuromuscular function is essential when using NMBAs to ensure adequate reversal of their effects before the patient regains consciousness. This can be achieved through the use of nerve stimulators, which assess the degree of blockade and help guide the administration of reversal agents when necessary.
Quadriplegia, also known as tetraplegia, is a medical condition characterized by paralysis affecting all four limbs and the trunk of the body. It results from damage to the cervical spinal cord, typically at levels C1-C8, which controls signals to the muscles in the arms, hands, trunk, legs, and pelvic organs. The extent of quadriplegia can vary widely, ranging from weakness to complete loss of movement and sensation below the level of injury. Other symptoms may include difficulty breathing, bowel and bladder dysfunction, and sexual dysfunction. The severity and prognosis depend on the location and extent of the spinal cord injury.
The Recurrent Laryngeal Nerve (RLN) is a branch of the vagus nerve (cranial nerve X), which is a mixed sensory, motor, and autonomic nerve. The RLN has important functions in providing motor innervation to the intrinsic muscles of the larynx, except for the cricothyroid muscle, which is supplied by the external branch of the superior laryngeal nerve.
The recurrent laryngeal nerve supplies all the muscles that are responsible for adduction (bringing together) of the vocal cords, including the vocalis muscle, lateral cricoarytenoid, thyroarytenoid, and interarytenoid muscles. These muscles play a crucial role in voice production, coughing, and swallowing.
The right recurrent laryngeal nerve has a longer course than the left one. It loops around the subclavian artery in the chest before ascending to the larynx, while the left RLN hooks around the arch of the aorta. This anatomical course makes them vulnerable to injury during various surgical procedures, such as thyroidectomy and neck dissection, leading to potential voice impairment or vocal cord paralysis.
Obstetric paralysis is a specific type of paralysis that can occur as a result of complications during childbirth. It is also known as "birth paralysis" or "puerperal paralysis."
The condition is typically caused by nerve damage or trauma to the brachial plexus, which is a network of nerves that runs from the spinal cord in the neck and provides movement and sensation to the shoulders, arms, and hands. Obstetric paralysis can occur when the brachial plexus is stretched or compressed during childbirth, particularly in difficult deliveries where forceps or vacuum extraction may be used.
There are several types of obstetric paralysis, including:
* Erb's palsy: This type of obstetric paralysis affects the upper brachial plexus and can cause weakness or paralysis in the arm, particularly the shoulder and elbow.
* Klumpke's palsy: This type of obstetric paralysis affects the lower brachial plexus and can cause weakness or paralysis in the hand and forearm.
* Total brachial plexus injury: This is a rare but severe form of obstetric paralysis that involves injury to all of the nerves in the brachial plexus, resulting in complete paralysis of the arm.
The severity of obstetric paralysis can vary widely, from mild weakness to complete paralysis. In some cases, the condition may resolve on its own within a few months, while in other cases, surgery or physical therapy may be necessary to help restore function.
Poliovirus is a human enterovirus, specifically a type of picornavirus, that is the causative agent of poliomyelitis (polio). It is a small, non-enveloped, single-stranded, positive-sense RNA virus. There are three serotypes of Poliovirus (types 1, 2 and 3) which can cause different degrees of severity in the disease. The virus primarily spreads through the fecal-oral route and infects the gastrointestinal tract, from where it can invade the nervous system and cause paralysis.
The Poliovirus has an icosahedral symmetry, with a diameter of about 30 nanometers. It contains a single stranded RNA genome which is encapsidated in a protein shell called capsid. The capsid is made up of 60 units of four different proteins (VP1, VP2, VP3 and VP4).
Poliovirus has been eradicated from most countries of the world through widespread vaccination with inactivated poliovirus vaccine (IPV) or oral poliovirus vaccine (OPV). However, it still remains endemic in a few countries and is considered a major public health concern.
Poliovirus Vaccine, Oral (OPV) is a vaccine used to prevent poliomyelitis (polio). It contains live attenuated (weakened) polioviruses, which stimulate an immune response in the body and provide protection against all three types of wild, infectious polioviruses. OPV is given by mouth, usually in drops, and it replicates in the gastrointestinal tract, where it induces a strong immune response. This response not only protects the individual who receives the vaccine but also helps to stop the spread of poliovirus in the community, providing indirect protection (herd immunity) to those who are not vaccinated. OPV is safe, effective, and easy to administer, making it an important tool for global polio eradication efforts. However, due to the risk of vaccine-associated paralytic polio (VAPP), inactivated poliovirus vaccine (IPV) is recommended for routine immunization in some countries.
The phrenic nerve is a motor nerve that originates from the cervical spine (C3-C5) and descends through the neck to reach the diaphragm, which is the primary muscle used for breathing. The main function of the phrenic nerve is to innervate the diaphragm and control its contraction and relaxation, thereby enabling respiration.
Damage or injury to the phrenic nerve can result in paralysis of the diaphragm, leading to difficulty breathing and potentially causing respiratory failure. Certain medical conditions, such as neuromuscular disorders, spinal cord injuries, and tumors, can affect the phrenic nerve and impair its function.
Botulinum toxins type A are neurotoxins produced by the bacterium Clostridium botulinum and related species. These toxins act by blocking the release of acetylcholine at the neuromuscular junction, leading to muscle paralysis. Botulinum toxin type A is used in medical treatments for various conditions characterized by muscle spasticity or excessive muscle activity, such as cervical dystonia, blepharospasm, strabismus, and chronic migraine. It is also used cosmetically to reduce the appearance of wrinkles by temporarily paralyzing the muscles that cause them. The commercial forms of botulinum toxin type A include Botox, Dysport, and Xeomin.
Pancuronium is defined as a non-depolarizing neuromuscular blocking agent, which is used in anesthesia practice to provide skeletal muscle relaxation during surgery. It works by competitively inhibiting the binding of acetylcholine to nicotinic receptors at the motor endplate, thereby preventing muscle contraction. Pancuronium has a intermediate duration of action and is often used for routine surgical procedures requiring muscle relaxation. It is administered intravenously and is typically reversed with an anticholinesterase agent such as neostigmine at the conclusion of surgery.
Laryngoplasty is a surgical procedure that involves reconstructing or reinforcing the larynx, specifically the vocal cords. The goal of this procedure can be to improve voice quality, restore breathing function, or manage airway obstructions caused by various conditions such as vocal cord paralysis, vocal fold bowing, or scarring.
There are different types of laryngoplasties, including:
1. Type I Thyroplasty (Medialization Laryngoplasty): This procedure involves placing an implant made of silicone, Gore-Tex, or other materials in the thyroid cartilage to medialize (move towards the midline) and support the paralyzed vocal cord. This helps improve voice quality and airway closure during speech and swallowing.
2. Arytenoid Adduction: In this procedure, the arytenoid cartilage is repositioned or fixed in place to help approximate (bring together) the vocal cords. It is often performed along with a Type I Thyroplasty for better voice and airway outcomes.
3. Laryngeal Framework Surgery: This is a more extensive procedure that involves reshaping the laryngeal framework, including the thyroid and cricoid cartilages, to improve voice, swallowing, or breathing function.
The choice of surgical technique depends on the underlying condition, its severity, and the patient's individual needs and goals.
Hypokalemic Periodic Paralysis (HPP) is a group of rare inherited disorders characterized by episodes of muscle weakness or paralysis, often associated with low potassium levels in the blood (hypokalemia). During an attack, muscles may become weak or fully paralyzed, typically affecting the legs and arms. The episodes can last from several hours to days. HPP is caused by genetic mutations that affect ion channels in muscle cells, leading to an imbalance of electrolytes and impaired muscle function. There are two main types: primary (or classic) HPP and secondary HPP. Primary HPP is further divided into thyrotoxic HPP and normokalemic HPP. Secondary HPP can be caused by various factors, such as medications or underlying medical conditions that cause hypokalemia.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Hyperkalemic periodic paralysis
Hyperkalemic periodic paralysis (equine)
Hyperkalemia
Ann T. Bowling
Impressive (horse)
List of OMIM disorder codes
Paramyotonia congenita
Appaloosa
Hypokalemic periodic paralysis
Nav1.4
Lameness (equine)
Periodic paralysis
Tiludronic acid
Myotonia
Louis Ptáček
Popular sire effect
Diclofenamide
Cav1.1
American Quarter Horse
Equine polysaccharide storage myopathy
List of MeSH codes (C05)
American Quarter Horse Association
Impressive
List of MeSH codes (C10)
List of MeSH codes (C18)
List of MeSH codes (C16)
List of diseases (H)
American Paint Horse
Muscular system of the horse
Myotonia congenita
Hyperkalemic periodic paralysis - Wikipedia
Hyperkalemic periodic paralysis: MedlinePlus Genetics
Hyperkalemic Periodic Paralysis - HYPP
Hyperkalemic Periodic Paralysis | Encyclopedia MDPI
Keveyis for the Treatment of Primary Hyperkalemic and Hypokalemic Periodic Paralysis - Clinical Trials Arena
Health Library | Rutgers Cancer Institute of New Jersey
Paralysis, Hyperkalemic Periodic; Hyperkalemic Periodic Paralysis; Myotonic Periodic Paralysis; Paralysis, Periodic,...
Hyperkalemic Periodic Paralysis
Periodic Paralyses: Background, Pathophysiology, Epidemiology
Periodic Paralyses Follow-up: Prognosis, Patient Education
New Brain Implant May Help People 'Locked In' With ALS: What to Know
Colic
JCI - A sodium channel knockin mutant (NaV1.4-R669H) mouse model of hypokalemic periodic paralysis
Acetazolamide Tablets - Heartland Vet Supply
Familial Periodic Paralysis - Pediatrics - MSD Manual Professional Edition
HORSE DIURETICS (Free Shipping) | Chewy
Acetazolamide 250 mg, 30 Tablets | VetDepot.com
Orphanet: Search a disease
Eastern Equine Encephalomyelitis Virus Infection in a Horse from California - Volume 8, Number 3-March 2002 - Emerging...
FeedXL Plans & Pricing
Pharmacokinetics of acetazolamide after intravenous and oral administration in horses in: American Journal of Veterinary...
Alok Sahay, MD | UC Health Provider Profile
Can Horses Eat Pumpkin? - The Horse
Familial Periodic Paralyses
Fugly Horse of the Day: By popular request: A few words on genetic Russian Roulette
Hybrid Vigor in Horses: Outcrossing Explained - AQHA
Familial Periodic Paralysis - Pediatrics - MSD Manual Professional Edition
March 2018 USDF Connection by USDF Publications - Issuu
Perioperative Management of Neuromuscular Disorders: Practice Essentials, Problem, Management
HYPP14
- Hyperkalemic periodic paralysis (HYPP, HyperKPP) is an inherited autosomal dominant disorder that affects sodium channels in muscle cells and the ability to regulate potassium levels in the blood. (wikipedia.org)
- DNA test for the Hyperkalemic Periodic Paralysis Disease (HYPP). (equigerminal.shop)
- Hyperkalemic Periodic paralysis (HYPP) is an inherited disease of the muscle, which is caused by an inherited genetic mutation. (equigerminal.shop)
- Acetazolamide Tablets are used for adjunctive therapy of hyperkalemic periodic paralysis (HYPP) in horses and adjunctive treatment of metabolic alkalosis or glaucoma in dogs and cats. (heartlandvetsupply.com)
- Acetazolamide Tablets are used to treat hyperkalemic periodic paralysis (HYPP) in horses. (heartlandvetsupply.com)
- Acetazolamide 250 mg, 30 Tablets is used to treat a genetic disease in horses called hyperkalemic periodic paralysis, or HYPP, which affects the neuromuscular system. (vetdepot.com)
- It helps manage HYPP symptoms like shaking, weakness, and paralysis. (vetdepot.com)
- HYPP (Hyperkalemic Periodic Paralysis) is a genetic defect that traces back to a popular Quarter Horse sire named Impressive. (blogspot.com)
- Among the genetic maladies the American Quarter Horse breed is currently addressing are GBED (glycogen branching enzyme deficiency), HERDA (hereditary equine regional dermal asthenia), HYPP (hyperkalemic periodic paralysis), MH (malignant hyperthermia) and PSSM (polysaccharide storage myopathy). (aqha.com)
- In addition to this, if your horse has a muscle disease like Hyperkalemic Periodic Paralysis - HYPP for short - you shouldn't give them bananas since the amount of potassium that they can consume is much more limited than that of a normal horse. (horses-arizona.com)
- Equine Hyperkalemic Periodic Paralysis Disease (HYPP) is a muscular disease caused by an inherited genetic mutation. (diamondktperformancehorses.com)
- Symptoms of HYPP may include muscle twitching, respiratory noises, and unpredictable paralysis attacks which can lead to sudden death. (diamondktperformancehorses.com)
- Hyperkalemic Periodic Paralysis Disease (HYPP) is a muscular disease that affects both horses and humans. (blueroans4u.com)
- The panel tests for Hyperkalemic Periodic Paralysis (HYPP), Polysaccharide Storage Myopathy type 1 (PSSM 1), Malignant Hyperthermia (MH), Hereditary Epidermal Regional Dermal Asthenia (HERDA), and Glycogen Branching Enzyme Deficiency (GBED). (springhillequine.com)
Hypokalemic19
- In contrast to HyperKPP, hypokalemic periodic paralysis (noted in humans) refers to loss-of-function mutations in channels that prevent muscle depolarisation and therefore are aggravated by low potassium ion concentrations. (wikipedia.org)
- Keveyis (dichlorphenamide) is the first medicine indicated for the treatment of primary hyperkalemic and hypokalemic periodic paralysis, which are a group of rare hereditary disorders that cause occasional episodes of muscle weakness or paralysis. (clinicaltrialsarena.com)
- Keveyis 50mg tablet was approved by US Food and Drug Administration (FDA) for the treatment for primary hyperkalemic and hypokalemic periodic paralysis and related variants in August 2015. (clinicaltrialsarena.com)
- Common types of primary PP include hyperkalemic and hypokalemic. (clinicaltrialsarena.com)
- The approval of Keveyis by the FDA was based on results from two clinical trials, namely Study 1 and Study 2, conducted to evaluate the efficacy of the drug in patients with hyperkalemic and hypokalemic periodic paralysis. (clinicaltrialsarena.com)
- Sub-study 1 was conducted on patients with hypokalemic periodic paralysis and the other on patients with hyperkalemic periodic paralysis. (clinicaltrialsarena.com)
- One sub-study was on patients with hypokalemic PP and the other was in those with hyperkalemic PP, including patients with paramyotonia congenita, a disorder that affects muscles used for movement. (clinicaltrialsarena.com)
- A clinically useful classification of primary periodic paralyses, shown in Table 1, includes hypokalemic, hyperkalemic, and paramyotonic forms. (medscape.com)
- Voltage sensor charge loss accounts for most cases of hypokalemic periodic paralysis. (medscape.com)
- Mutations in potassium channel Kir2.6 cause susceptibility to thyrotoxic hypokalemic periodic paralysis. (medscape.com)
- A mutation in the KCNE3 potassium channel gene is associated with susceptibility to thyrotoxic hypokalemic periodic paralysis. (medscape.com)
- Practical aspects in the management of hypokalemic periodic paralysis. (medscape.com)
- Acetazolamide efficacy in hypokalemic periodic paralysis and the predictive role of genotype. (medscape.com)
- Hypokalemic periodic paralysis (HypoPP) is an ion channelopathy of skeletal muscle characterized by attacks of muscle weakness associated with low serum K + . HypoPP results from a transient failure of muscle fiber excitability. (jci.org)
- Although the hypokalemic form is the most common form of familial periodic paralysis, it is nonetheless quite rare, with a prevalence of 1/100,000. (msdmanuals.com)
- The two most common types of periodic paralyses are:Hypokalemic periodic paralysis is characterized by a fall in potassium levels in the blood. (brainfacts.org)
- Neuromuscular disorders encompass a number of different disease processes, including myasthenia gravis (MG), Lambert-Eaton myasthenic syndrome (LEMS), Duchenne muscular dystrophy (DMD), Becker muscular dystrophy (BMD), and hypokalemic periodic paralysis. (medscape.com)
- Hypokalemic periodic paralysis is a rare autosomal dominant hereditary disorder that is characterized by transient episodes of skeletal muscle weakness/paralysis when the serum potassium level decreases. (medscape.com)
- The carbonic anhydrase inhibitor dichlorphenamide is indicated for long-term treatment of primary hyperkalemic periodic paralysis, primary hypokalemic periodic paralysis, and related variants. (medscape.com)
Familial periodic paralyses6
- Jurkat-Rott K, Lehmann-Horn F. Paroxysmal muscle weakness: the familial periodic paralyses. (medlineplus.gov)
- Familial periodic paralyses information page. (epnet.com)
- Available at: https://www.ninds.nih.gov/Disorders/All-Disorders/Familial-Periodic-Paralyses-Information-Page. (epnet.com)
- Familial periodic paralyses are a group of inherited neurological disorders caused by mutations in genes that regulate sodium and calcium channels in nerve cells. (brainfacts.org)
- The prognosis for the familial periodic paralyses varies. (brainfacts.org)
- The NINDS conducts and supports research on neuromuscular disorders such as the familial periodic paralyses. (brainfacts.org)
Mutations6
- citation needed] Mutations altering the usual structure and function of this sodium channel therefore disrupt regulation of muscle contraction, leading to episodes of severe muscle weakness or paralysis. (wikipedia.org)
- The pathological mechanism of SCN4A mutations in hyperkalemic periodic paralysis is complex, but explains the autosomal dominant and hyperkalemia-related aspects of the disease. (wikipedia.org)
- Mutations in the SCN4A gene can cause hyperkalemic periodic paralysis. (medlineplus.gov)
- Leaky sodium channels from voltage sensor mutations in periodic paralysis, but not paramyotonia. (medscape.com)
- Mutations of Na V 1.4 give rise to a heterogeneous group of muscle disorders, with gain-of-function defects causing myotonia or hyperkalemic periodic paralysis. (jci.org)
- The hyperkalemic form is due to mutations in the gene that encodes the alpha-subunit of the skeletal muscle sodium channel ( SCN4A ). (msdmanuals.com)
Characterized by episodes of flaccid2
- The heterogeneous group of muscle diseases known as periodic paralyses (PP) is characterized by episodes of flaccid muscle weakness occurring at irregular intervals. (medscape.com)
- Familial periodic paralysis is a rare autosomal dominant condition with considerable variation in penetrance characterized by episodes of flaccid paralysis with loss of deep tendon reflexes and failure of muscle to respond to electrical stimulation. (msdmanuals.com)
Flaccid paralysis1
- the altered potassium metabolism is a result of the PP. In primary and thyrotoxic PP, flaccid paralysis occurs with relatively small changes in the serum potassium level, whereas in secondary PP, serum potassium levels are markedly abnormal. (medscape.com)
Horses2
- Pharmacokinetic data generated by this study should facilitate estimation of appropriate dosages for acetazolamide use in horses with hyperkalemic periodic paralysis. (avma.org)
- As a result, the "Remarkable" line of horses became known as the hyperkalemic periodic paralysis line of horses. (horsyplanet.com)
Weakness8
- It is characterized by muscle hyperexcitability or weakness which, exacerbated by potassium, heat or cold, can lead to uncontrolled shaking followed by paralysis. (wikipedia.org)
- Hyperkalemic periodic paralysis causes episodes of extreme muscle weakness, with attacks often beginning in childhood. (wikipedia.org)
- Hyperkalemic periodic paralysis is a condition that causes episodes of extreme muscle weakness or paralysis, usually beginning in infancy or early childhood. (medlineplus.gov)
- These changes in ion transport reduce the ability of skeletal muscles to contract, leading to episodes of muscle weakness or paralysis. (medlineplus.gov)
- Periodic paralysis (PP) is a heterogeneous group of hereditary muscle disorders characterised by episodes of muscle weakness or paralysis occurring at irregular intervals. (clinicaltrialsarena.com)
- Normokalemic periodic paralysis is a closely related disorder marked by a lack of alterations in potassium levels during attacks of weakness. (lookfordiagnosis.com)
- With ALS, nerve cells gradually lose the ability to trigger specific muscles, causing weakness that develops into paralysis - which in some eventually leads to CLIS. (healthline.com)
- Some patients may develop chronic muscle weakness later in life.Hyperkalemic periodic paralysis is characterized by a rise in potassium levels in the blood. (brainfacts.org)
Thyrotoxic1
- Chaudhry MA, Wayangankar S. Thyrotoxic Periodic Paralysis: A Concise Review of the Literature. (medscape.com)
20201
- In November 2020, KonekoKitten was diagnosed with hyperkalemic periodic paralysis. (healthyceleb.com)
Potassium5
- Some people with hyperkalemic periodic paralysis have increased levels of potassium in their blood (hyperkalemia) during attacks. (wikipedia.org)
- Depolarization-activated gating pore current conducted by mutant sodium channels in potassium-sensitive normokalemicperiodic paralysis. (medscape.com)
- This type of periodic paralysis is characterized by hyperkalemia, or an increased level of potassium in the blood. (heartlandvetsupply.com)
- Eating carbohydrate-rich, low-potassium foods, and avoiding strenuous exercise and fasting, can help prevent hyperkalemic attacks. (brainfacts.org)
- Myotonia is a symptom seen certain inherited muscle dystrophies and pure channelopathies (Dystrophia myotonica type 1 and 2, Myotonia Congenita , Paramyotonia Congenita , Hyperkalæmisk periodic paralysis and Potassium-Aggravated myotonia). (go.jp)
Muscle2
- This makes the horse susceptible to sporadic episodes of muscle tremors or paralysis. (equigerminal.shop)
- Siddiqui FA, Sheikh A. Muscle paralysis in thyrotoxicosis. (medscape.com)
Affects1
- Hyperkalemic periodic paralysis affects an estimated 1 in 200,000 people. (medlineplus.gov)
Disorders1
- Periodic paralyses (PP) are a rare group of disorders. (epnet.com)
20231
- Hyperkalemic Periodic Paralysis" Encyclopedia , https://encyclopedia.pub/entry/4131 (accessed December 08, 2023). (encyclopedia.pub)
Attacks2
- Arzel-Hezode M, McGoey S, Sternberg D, Vicart S, Eymard B, Fontaine B. Glucocorticoids may trigger attacks in several types of periodic paralysis. (medscape.com)
- Treatment of the periodic paralyses focuses on preventing further attacks and relieving acute symptoms. (brainfacts.org)
Gene2
- To address the question of specificity for the allele encoding the Na V 1.4-R669H variant as a cause of HypoPP and to produce a model system in which to characterize functional defects of the mutant channel and susceptibility to paralysis, we generated knockin mice carrying the ortholog of the gene encoding the Na V 1.4-R669H variant (referred to herein as R669H mice). (jci.org)
- Each form of familial periodic paralysis involves a different gene and electrolyte channel. (msdmanuals.com)
Therapeutic1
- Jurkat-Rott K, Lehmann-Horn F. Genotype-phenotype correlation and therapeutic rationale in hyperkalemic periodic paralysis. (medlineplus.gov)
Glucose1
- Initial therapy included intravenous corticosteroids, fluid therapy (including glucose to treat possible hyperkalemic periodic paralysis), and diazepam for intermittent seizures. (cdc.gov)
Hereditary1
- Most of the conditions are hereditary and are more episodic than periodic. (medscape.com)
Treatment2
- Treatment for periodic paralysis. (epnet.com)
- Review of the Diagnosis and Treatment of Periodic Paralysis. (medscape.com)
Trigger1
- This can be caused by the same things that trigger the paralysis, dependent on the type of myotonia. (wikipedia.org)
Respiratory1
- Levels higher than 7 mEq/L can lead to significant hemodynamic and neurologic consequences, whereas levels exceeding 8.5 mEq/L can cause respiratory paralysis or cardiac arrest and can quickly be fatal. (medscape.com)
Muscles1
- and paralysis of the muscles surrounding the heart and/or lungs, causing death due to heart attack or suffocation. (blogspot.com)
People1
- According to one researcher, it was thought people with complete paralysis might no longer be capable of communicating, even mentally. (healthline.com)