Recurrent Laryngeal Nerve
Respiratory Physiological Phenomena
Peripheral Nervous System Diseases
Brachial Plexus Neuritis
Trauma, Nervous System
Sympathetic Nervous System
Posterior Thalamic Nuclei
Nerve Growth Factor
Nerve Growth Factors
Vocal Cord Paralysis
Spinal Cord Injuries
Spinal Nerve Roots
Nerve Compression Syndromes
Nerve terminal damage by beta-bungarotoxin: its clinical significance. (1/947)We report here original data on the biological basis of prolonged neuromuscular paralysis caused by the toxic phospholipase A2 beta-bungarotoxin. Electron microscopy and immunocytochemical labeling with anti-synaptophysin and anti-neurofilament have been used to show that the early onset of paralysis is associated with the depletion of synaptic vesicles from the motor nerve terminals of skeletal muscle and that this is followed by the destruction of the motor nerve terminal and the degeneration of the cytoskeleton of the intramuscular axons. The postjunctional architecture of the junctions were unaffected and the binding of fluorescein-isothiocyanate-conjugated alpha-bungarotoxin to acetylcholine receptor was not apparently affected by exposure to beta-bungarotoxin. The re-innervation of the muscle fiber was associated by extensive pre- and post-terminal sprouting at 3 to 5 days but was stable by 7 days. Extensive collateral innervation of adjacent muscle fibers was a significant feature of the re-innervated neuromuscular junctions. These findings suggest that the prolonged and severe paralysis seen in victims of envenoming bites by kraits (elapid snakes of the genus Bungarus) and other related snakes of the family Elapidae is caused by the depletion of synaptic vesicles from motor nerve terminals and the degeneration of the motor nerve terminal and intramuscular axons. (+info)
Diaphragm electromyogram measured with unilateral magnetic stimulation. (2/947)The purpose of this study was to establish the phrenic nerve conduction time (PNCT) for magnetic stimulation and further assess the relatively new technique of anterior unilateral magnetic stimulation (UMS) of the phrenic nerves in evaluating the diaphragm electromyogram (EMG). An oesophageal electrode was used to record the diaphragm compound muscle action potential (CMAP) elicited by supramaximal percutaneous electrical phrenic nerve stimulation (ES) and UMS from eight normal subjects. The oesophageal electrode used for recording the CMAP was positioned at the level of the hiatus and 3 cm below. The diaphragm CMAP was also recorded from chest wall surface electrodes in five subjects. All of the phrenic nerves could be maximally stimulated with UMS. A clear plateau of the amplitude of the CMAP was achieved for the right and left phrenic nerves. The mean amplitudes of the CMAP recorded from the oesophageal electrode were, for the right side, 0.74+/-0.29 mV (mean+SD) for ES and 0.76+/-0.30 mV for UMS with maximal power output, and for the left side 0.88+/-0.33 mV for ES and 0.80+/-0.24 mV for UMS. PNCT measured by the oesophageal electrode with ES and UMS with maximal output were, for the right side, 7.0+/-0.8 ms and 6.9+/-0.8 ms, respectively, and for the left side 7.8+/-1.2 ms and 7.7+/-1.3 ms, respectively. However, the CMAP recorded from chest wall surface electrodes with UMS was unsuitable for the measurement of PNCT. The results suggest that unilateral magnetic stimulation of the phrenic nerves combined with an oesophageal electrode can be used to assess diaphragmatic electrical activity and measure the phrenic nerve conduction time. (+info)
Concurrent inhibition and excitation of phrenic motoneurons during inspiration: phase-specific control of excitability. (3/947)The movements that define behavior are controlled by motoneuron output, which depends on the excitability of motoneurons and the synaptic inputs they receive. Modulation of motoneuron excitability takes place over many time scales. To determine whether motoneuron excitability is specifically modulated during the active versus the quiescent phase of rhythmic behavior, we compared the input-output properties of phrenic motoneurons (PMNs) during inspiratory and expiratory phases of respiration. In neonatal rat brainstem-spinal cord preparations that generate rhythmic respiratory motor outflow, we blocked excitatory inspiratory synaptic drive to PMNs and then examined their phase-dependent responses to superthreshold current pulses. Pulses during inspiration elicited fewer action potentials compared with identical pulses during expiration. This reduced excitability arose from an inspiratory-phase inhibitory input that hyperpolarized PMNs in the absence of excitatory inspiratory inputs. Local application of bicuculline blocked this inhibition as well as the difference between inspiratory and expiratory firing. Correspondingly, bicuculline locally applied to the midcervical spinal cord enhanced fourth cervical nerve (C4) inspiratory burst amplitude. Strychnine had no effect on C4 output. Nicotinic receptor antagonists neither potentiated C4 output nor blocked its potentiation by bicuculline, further indicating that the inhibition is not from recurrent inhibitory pathways. We conclude that it is bulbospinal in origin. These data demonstrate that rapid changes in motoneuron excitability occur during behavior and suggest that integration of overlapping, opposing synaptic inputs to motoneurons is important in controlling motor outflow. Modulation of phasic inhibition may represent a means for regulating the transfer function of PMNs to suit behavioral demands. (+info)
An overview of phrenic nerve and diaphragm muscle development in the perinatal rat. (4/947)In this overview, we outline what is known regarding the key developmental stages of phrenic nerve and diaphragm formation in perinatal rats. These developmental events include the following. Cervical axons emerge from the spinal cord during embryonic (E) day 11. At approximately E12.5, phrenic and brachial axons from the cervical segments merge at the brachial plexi. Subsequently, the two populations diverge as phrenic axons continue to grow ventrally toward the diaphragmatic primordium and brachial axons turn laterally to grow into the limb bud. A few pioneer axons extend ahead of the majority of the phrenic axonal population and migrate along a well-defined track toward the primordial diaphragm, which they reach by E13.5. The primordial diaphragmatic muscle arises from the pleuroperitoneal fold, a triangular protrusion of the body wall composed of the fusion of the primordial pleuroperitoneal and pleuropericardial tissues. The phrenic nerve initiates branching within the diaphragm at approximately E14, when myoblasts in the region of contact with the phrenic nerve begin to fuse and form distinct primary myotubes. As the nerve migrates through the various sectors of the diaphragm, myoblasts along the nerve's path begin to fuse and form additional myotubes. The phrenic nerve intramuscular branching and concomitant diaphragmatic myotube formation continue to progress up until E17, at which time the mature pattern of innervation and muscle architecture are approximated. E17 is also the time of the commencement of inspiratory drive transmission to phrenic motoneurons (PMNs) and the arrival of phrenic afferents to the motoneuron pool. During the period spanning from E17 to birth (gestation period of approximately 21 days), there is dramatic change in PMN morphology as the dendritic branching is rearranged into the rostrocaudal bundling characteristic of mature PMNs. This period is also a time of significant changes in PMN passive membrane properties, action-potential characteristics, and firing properties. (+info)
Comparison between huperzine A, tacrine, and E2020 on cholinergic transmission at mouse neuromuscular junction in vitro. (5/947)AIM: To compare the effects of huperzine A (Hup A), tacrine, and E2020 on cholinergic transmission at mouse neuromuscular junction in vitro. METHODS: The isolated mouse phrenic nerve-hemidiaphragm preparations were used with the conventional intracellular recording technique. The miniature end-plate potentials (MEPP), the mean quantal content of end-plate potentials (EPP), and the resting membrane potentials of muscle fiber were recorded. RESULTS: Hup A, tacrine, and E2020 at the concentration of 1.0 mumol.L-1 increased the amplitude, time-to-peak, and half-decay time of MEPP in the potencies of E2020 > Hup A > tacrine. Hup A did not significantly change the frequency of MEPP, the appearance of giant MEPP or slow MEPP, the resting membrane potentials, and the mean quantal content of EPP. CONCLUSION: Hup A is a selective and potent cholinesterase inhibitor, by which activity it facilitates the cholinergic transmission at mouse neuromuscular junction, and devoid of pre- and post-synaptic actions. (+info)
Patterns of phrenic motor output evoked by chemical stimulation of neurons located in the pre-Botzinger complex in vivo. (6/947)The pre-Botzinger complex (pre-BotC) has been proposed to be essential for respiratory rhythm generation from work in vitro. Much less, however, is known about its role in the generation and modulation of respiratory rhythm in vivo. Therefore we examined whether chemical stimulation of the in vivo pre-BotC manifests respiratory modulation consistent with a respiratory rhythm generator. In chloralose- or chloralose/urethan-anesthetized, vagotomized cats, we recorded phrenic nerve discharge and arterial blood pressure in response to chemical stimulation of neurons located in the pre-BotC with DL-homocysteic acid (DLH; 10 mM; 21 nl). In 115 of the 122 sites examined in the pre-BotC, unilateral microinjection of DLH produced an increase in phrenic nerve discharge that was characterized by one of the following changes in cycle timing and pattern: 1) a rapid series of high-amplitude, rapid rate of rise, short-duration bursts, 2) tonic excitation (with or without respiratory oscillations), 3) an integration of the first two types of responses (i.e., tonic excitation with high-amplitude, short-duration bursts superimposed), or 4) augmented bursts in the phrenic neurogram (i.e., eupneic breath ending with a high-amplitude, short-duration burst). In 107 of these sites, the phrenic neurogram response was accompanied by an increase or decrease (>/=10 mmHg) in arterial blood pressure. Thus increases in respiratory burst frequency and production of tonic discharge of inspiratory output, both of which have been seen in vitro, as well as modulation of burst pattern can be produced by local perturbations of excitatory amino acid neurotransmission in the pre-BotC in vivo. These findings are consistent with the proposed role of this region as the locus for respiratory rhythm generation. (+info)
Electrophysiological properties of rat phrenic motoneurons during perinatal development. (7/947)Past studies determined that there is a critical period at approximately embryonic day (E)17 during which phrenic motoneurons (PMNs) undergo a number of pivotal developmental events, including the inception of functional recruitment via synaptic drive from medullary respiratory centers, contact with spinal afferent terminals, the completion of diaphragm innervation, and a major transformation of PMN morphology. The objective of this study was to test the hypothesis that there would be a marked maturation of motoneuron electrophysiological properties occurring in conjunction with these developmental processes. PMN properties were measured via whole cell patch recordings with a cervical slice-phrenic nerve preparation isolated from perinatal rats. From E16 to postnatal day 1, there was a considerable transformation in a number of motoneuron properties, including 1) 10-mV increase in the hyperpolarization of the resting membrane potential, 2) threefold reduction in the input resistance, 3) 12-mV increase in amplitude and 50% decrease duration of action potential, 4) major changes in the shapes of potassium- and calcium-mediated afterpotentials, 5) decline in the prominence of calcium-dependent rebound depolarizations, and 6) increases in rheobase current and steady-state firing rates. Electrical coupling among PMNs was detected in 15-25% of recordings at all ages studied. Collectively, these data and those from parallel studies of PMN-diaphragm ontogeny describe how a multitude of regulatory mechanisms operate in concert during the embryonic development of a single mammalian neuromuscular system. (+info)
The rostral ventrolateral medulla mediates the sympathoactivation produced by chemical stimulation of the rat nasal mucosa. (8/947)1. We sought to outline the brainstem circuit responsible for the increase in sympathetic tone caused by chemical stimulation of the nasal passages with ammonia vapour. Experiments were performed in alpha-chloralose-anaesthetized, paralysed and artificially ventilated rats. 2. Stimulation of the nasal mucosa increased splanchnic sympathetic nerve discharge (SND), elevated arterial blood pressure (ABP), raised heart rate slightly and inhibited phrenic nerve discharge. 3. Bilateral injections of the broad-spectrum excitatory amino acid receptor antagonist kynurenate (Kyn) into the rostral part of the ventrolateral medulla (RVLM; rostral C1 area) greatly reduced the effects of nasal mucosa stimulation on SND (-80 %). These injections had no effect on resting ABP, resting SND or the sympathetic baroreflex. 4. Bilateral injections of Kyn into the ventrolateral medulla at the level of the obex (caudal C1 area) or into the nucleus tractus solitarii (NTS) greatly attenuated the baroreflex and significantly increased the baseline levels of both SND and ABP. However they did not reduce the effect of nasal mucosa stimulation on SND. 5. Single-unit recordings were made from 39 putative sympathoexcitatory neurons within the rostral C1 area. Most neurons (24 of 39) were activated by nasal mucosa stimulation (+65.8 % rise in discharge rate). Responding neurons had a wide range of conduction velocities and included slow-conducting neurons identified previously as C1 cells. The remaining putative sympathoexcitatory neurons were either unaffected (n = 8 neurons) or inhibited (n = 7) during nasal stimulation. We also recorded from ten respiratory-related neurons, all of which were silenced by nasal stimulation. 6. In conclusion, the sympathoexcitatory response to nasal stimulation is largely due to activation of bulbospinal presympathetic neurons within the RVLM. We suggest that these neurons receive convergent and directionally opposite polysynaptic inputs from arterial baroreceptors and trigeminal afferents. These inputs are integrated within the rostral C1 area as opposed to the NTS or the caudal C1 area. (+info)
Respiratory paralysis can manifest in different ways depending on the underlying cause and severity of the condition. Some common symptoms include:
1. Difficulty breathing: Patients may experience shortness of breath, wheezing, or a feeling of suffocation.
2. Weakened cough reflex: The muscles used for coughing may be weakened or paralyzed, making it difficult to clear secretions from the lungs.
3. Fatigue: Breathing can be tiring and may leave the patient feeling exhausted.
4. Sleep disturbances: Respiratory paralysis can disrupt sleep patterns and cause insomnia or other sleep disorders.
5. Chest pain: Pain in the chest or ribcage can be a symptom of respiratory paralysis, particularly if it is caused by muscle weakness or atrophy.
Diagnosis of respiratory paralysis typically involves a physical examination, medical history, and diagnostic tests such as electroencephalogram (EEG), electromyography (EMG), or nerve conduction studies (NCS). Treatment options vary depending on the underlying cause but may include:
1. Medications: Drugs such as bronchodilators, corticosteroids, and anticholinergics can be used to manage symptoms and improve lung function.
2. Respiratory therapy: Techniques such as chest physical therapy, respiratory exercises, and non-invasive ventilation can help improve lung function and reduce fatigue.
3. Surgery: In some cases, surgery may be necessary to correct anatomical abnormalities or repair damaged nerves.
4. Assistive devices: Patients with severe respiratory paralysis may require the use of assistive devices such as oxygen therapy, ventilators, or wheelchairs to help improve their quality of life.
5. Rehabilitation: Physical therapy, occupational therapy, and speech therapy can all be helpful in improving function and reducing disability.
6. Lifestyle modifications: Patients with respiratory paralysis may need to make lifestyle changes such as avoiding smoke, dust, and other irritants, getting regular exercise, and managing stress to help improve their condition.
The term "decerebrate" comes from the Latin word "cerebrum," which means brain. In this context, the term refers to a state where the brain is significantly damaged or absent, leading to a loss of consciousness and other cognitive functions.
Some common symptoms of the decerebrate state include:
* Loss of consciousness
* Flaccid paralysis (loss of muscle tone)
* Dilated pupils
* Lack of responsiveness to stimuli
* Poor or absent reflexes
* Inability to speak or communicate
The decerebrate state can be caused by a variety of factors, including:
* Severe head injury
* Stroke or cerebral vasculature disorders
* Brain tumors or cysts
* Infections such as meningitis or encephalitis
* Traumatic brain injury
Treatment for the decerebrate state is typically focused on addressing the underlying cause of the condition. This may involve medications to control seizures, antibiotics for infections, or surgery to relieve pressure on the brain. In some cases, the decerebrate state may be a permanent condition, and individuals may require long-term care and support.
Hiccups can be caused by a variety of factors, including:
1. Overeating or drinking too quickly
2. Swallowing air or eating too much spicy or acidic food
3. Gastric distension (stomach expansion) due to eating or drinking too much
4. Irritation of the nerves that control breathing
5. Inflammation or injury to the diaphragm or other organs in the chest
6. Infections such as pneumonia or bronchitis
7. Neurological disorders such as multiple sclerosis, Parkinson's disease, or epilepsy
8. Inflammatory conditions such as laryngitis or sinusitis
9. Trauma to the chest or abdomen
10. Hormonal changes during pregnancy or menstruation.
Hiccups are usually a harmless and temporary condition, but they can be distressing and disruptive to daily activities. In rare cases, hiccups can persist for longer periods of time (more than 48 hours) and may indicate an underlying medical condition that needs attention.
There are several remedies and treatments for hiccups, including:
1. Breathing into a paper bag
2. Gargling with water
3. Drinking a glass of water quickly
4. Applying gentle pressure to the diaphragm
5. Using sugar or honey to soothe the throat and calm down the nerves
6. Trying relaxation techniques such as deep breathing or meditation
7. In severe cases, medications such as anticonvulsants or anesthetics may be prescribed to stop hiccups.
If you experience persistent or severe hiccups, it is important to seek medical attention to rule out any underlying conditions that may need treatment.
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.
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.
Types of Electric Injuries There are several types of electric injuries that can occur, including:
1. Electrical shock: This occurs when a person's body is exposed to an electric current, which can cause muscle contractions, nerve damage, and other systemic effects.
2. Electrical burns: These are burns caused by the heat generated by electrical currents flowing through the body. They can be superficial or deep, and may require surgical intervention.
3. Lightning strikes: This is a type of electric injury caused by direct exposure to lightning. It can cause a range of symptoms, including burns, cardiac arrest, and neurological damage.
4. Arc flash burns: These are burns caused by the intense heat generated when electrical currents flow through the body in an enclosed space. They can be severe and may require prolonged treatment.
Symptoms of Electric Injuries The symptoms of electric injuries can vary depending on the severity of the injury, but may include:
1. Muscle contractions or spasms
2. Numbness or tingling in the affected area
3. Burns or redness of the skin
4. Cardiac arrest or arrhythmias
5. Neurological damage or seizures
6. Respiratory distress or difficulty breathing
7. Weakness or fatigue
8. Dizziness or loss of consciousness
Treatment of Electric Injuries The treatment of electric injuries depends on the severity of the injury and may include:
1. Cardiopulmonary resuscitation (CPR) if the patient has cardiac arrest or is unresponsive
2. Burn care, including debridement and wound dressing
3. Electrolyte replacement to maintain fluid balance and prevent dehydration
4. Pain management with analgesics and sedatives
5. Physical therapy to restore strength and mobility
6. Monitoring of neurological function and seizure control
7. Psychological support to cope with the injury and its effects
Prevention of Electric Injuries Prevention of electric injuries is important, especially in workplaces where electrical hazards are present. Some measures for prevention include:
1. Proper training on electrical safety and equipment use
2. Regular inspection and maintenance of electrical equipment
3. Use of protective gear such as gloves, safety glasses, and hard hats
4. Avoiding direct contact with electrical sources
5. Use of ground fault circuit interrupters (GFCIs) to prevent electrical shock
6. Proper storage of electrical equipment when not in use
7. Emergency preparedness and response plans in place
In conclusion, electric injuries can be severe and potentially life-threatening. Prompt medical attention is essential for proper treatment and prevention of complications. It is important to be aware of the hazards of electricity and take measures to prevent electrical injuries in the workplace and at home. Proper training, equipment maintenance, and safety precautions can go a long way in preventing these types of injuries.
Peripheral Nervous System Diseases can result from a variety of causes, including:
1. Trauma or injury
2. Infections such as Lyme disease or HIV
3. Autoimmune disorders such as Guillain-Barré syndrome
4. Genetic mutations
5. Tumors or cysts
6. Toxins or poisoning
7. Vitamin deficiencies
8. Chronic diseases such as diabetes or alcoholism
Some common Peripheral Nervous System Diseases include:
1. Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
2. Multiple Sclerosis (MS) - an autoimmune disease that affects the CNS and PNS, causing a range of symptoms including numbness, weakness, and vision problems.
3. Peripheral Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
4. Guillain-Barré syndrome - an autoimmune disorder that causes muscle weakness and paralysis.
5. Charcot-Marie-Tooth disease - a group of inherited disorders that affect the nerves in the feet and legs, leading to muscle weakness and wasting.
6. Friedreich's ataxia - an inherited disorder that affects the nerves in the spine and limbs, leading to coordination problems and muscle weakness.
7. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) - an autoimmune disorder that causes inflammation of the nerves, leading to pain, numbness, and weakness in the affected areas.
8. Amyotrophic Lateral Sclerosis (ALS) - a progressive neurological disease that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness, atrophy, and paralysis.
9. Spinal Muscular Atrophy - an inherited disorder that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.
10. Muscular Dystrophy - a group of inherited disorders that affect the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.
It's important to note that this is not an exhaustive list and there may be other causes of muscle weakness. If you are experiencing persistent or severe muscle weakness, it is important to see a healthcare professional for proper evaluation and diagnosis.
Brachial plexus neuritis is a condition that affects the brachial plexus, a network of nerves that runs from the spine down to the shoulder and arm. It occurs when the nerves in this region become inflamed or damaged, leading to pain and weakness in the arm and hand.
The condition can be caused by a variety of factors, including injury, infection, or compression of the nerves. It is more common in young adults and may be associated with certain medical conditions, such as diabetes, thyroid disease, or Lyme disease.
Symptoms of brachial plexus neuritis may include pain, numbness, tingling, and weakness in the arm and hand. The condition can also cause difficulty with gripping or grasping objects, and may affect fine motor skills such as writing or buttoning a shirt.
Treatment for brachial plexus neuritis typically involves physical therapy, pain management, and addressing any underlying medical conditions. In some cases, surgery may be necessary to relieve compression or damage to the nerves. With appropriate treatment, most people with brachial plexus neuritis are able to recover significant function in their arm and hand over time.
There are several types of apnea that can occur during sleep, including:
1. Obstructive sleep apnea (OSA): This is the most common type of apnea and occurs when the airway is physically blocked by the tongue or other soft tissue in the throat, causing breathing to stop for short periods.
2. Central sleep apnea (CSA): This type of apnea occurs when the brain fails to send the proper signals to the muscles that control breathing, resulting in a pause in breathing.
3. Mixed sleep apnea (MSA): This type of apnea is a combination of OSA and CSA, where both central and obstructive factors contribute to the pauses in breathing.
4. Hypopneic apnea: This type of apnea is characterized by a decrease in breathing, but not a complete stop.
5. Hypercapnic apnea: This type of apnea is caused by an excessive buildup of carbon dioxide in the blood, which can lead to pauses in breathing.
The symptoms of apnea can vary depending on the type and severity of the condition, but may include:
* Pauses in breathing during sleep
* Waking up with a dry mouth or sore throat
* Morning headaches
* Difficulty concentrating or feeling tired during the day
* High blood pressure
* Heart disease
Treatment options for apnea depend on the underlying cause, but may include:
* Lifestyle changes, such as losing weight, avoiding alcohol and sedatives before bedtime, and sleeping on your side
* Oral appliances or devices that advance the position of the lower jaw and tongue
* Continuous positive airway pressure (CPAP) therapy, which involves wearing a mask during sleep to deliver a constant flow of air pressure into the airways
* Bi-level positive airway pressure (BiPAP) therapy, which involves two levels of air pressure: one for inhalation and another for exhalation
* Surgery to remove excess tissue in the throat or correct physical abnormalities that are contributing to the apnea.
Trauma to the nervous system can have a profound impact on an individual's quality of life, and can lead to a range of symptoms including:
* Dizziness and vertigo
* Memory loss and difficulty concentrating
* Mood changes such as anxiety, depression, or irritability
* Sleep disturbances
* Changes in sensation, such as numbness or tingling
* Weakness or paralysis of certain muscle groups
Trauma to the nervous system can also have long-lasting effects, and may lead to chronic conditions such as post-traumatic stress disorder (PTSD), chronic pain, and fibromyalgia.
Treatment for trauma to the nervous system will depend on the specific nature of the injury and the severity of the symptoms. Some common treatments include:
* Medication to manage symptoms such as pain, anxiety, or depression
* Physical therapy to help regain strength and mobility
* Occupational therapy to help with daily activities and improve function
* Cognitive-behavioral therapy (CBT) to address any emotional or psychological issues
* Alternative therapies such as acupuncture, massage, or meditation to help manage symptoms and promote relaxation.
It's important to seek medical attention if you experience any symptoms of trauma to the nervous system, as prompt treatment can help reduce the risk of long-term complications and improve outcomes.
There are different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
The main symptoms of Horner syndrome include:
1. Pain and numbness in the face and arm on one side of the body
2. Weakness or paralysis of the muscles on one side of the face, arm, and hand
3. Difficulty swallowing
4. Reduced sweating on one side of the body
5. Increased heart rate and blood pressure
6. Narrowing of the pupil (anisocoria)
7. Dilation of the unaffected pupil (paralysis of the parasympathetic nervous system)
8. Decreased reflexes
9. Loss of sensation in the skin over the chest and abdomen
10. Pale or clammy skin on one side of the body
The symptoms of Horner syndrome can be caused by a variety of factors, including:
1. Trauma to the thoracolumbar spine
2. Injury or tumor in the brainstem or spinal cord
3. Aneurysm or arteriovenous malformation (AVM) in the neck or chest
4. Multiple sclerosis, amyotrophic lateral sclerosis (ALS), or other neurodegenerative diseases
5. Inflammatory conditions such as sarcoidosis or tuberculosis
6. Infections such as meningitis or abscesses
7. Vasospasm or thrombosis of the blood vessels in the neck or chest.
The diagnosis of Horner syndrome is based on a combination of clinical findings, neuroimaging studies (such as MRI or CT scans), and laboratory tests to rule out other causes of the symptoms. Treatment of the condition depends on the underlying cause and may include surgery, medication, or other interventions. In some cases, Horner syndrome may be a sign of a more serious underlying condition that requires prompt medical attention.
Hypercapnia is a medical condition where there is an excessive amount of carbon dioxide (CO2) in the bloodstream. This can occur due to various reasons such as:
1. Respiratory failure: When the lungs are unable to remove enough CO2 from the body, leading to an accumulation of CO2 in the bloodstream.
2. Lung disease: Certain lung diseases such as chronic obstructive pulmonary disease (COPD) or pneumonia can cause hypercapnia by reducing the ability of the lungs to exchange gases.
3. Medication use: Certain medications, such as anesthetics and sedatives, can slow down breathing and lead to hypercapnia.
The symptoms of hypercapnia can vary depending on the severity of the condition, but may include:
4. Shortness of breath
6. Sleep disturbances
If left untreated, hypercapnia can lead to more severe complications such as:
1. Respiratory acidosis: When the body produces too much acid, leading to a drop in blood pH.
2. Cardiac arrhythmias: Abnormal heart rhythms can occur due to the increased CO2 levels in the bloodstream.
3. Seizures: In severe cases of hypercapnia, seizures can occur due to the changes in brain chemistry caused by the excessive CO2.
Treatment for hypercapnia typically involves addressing the underlying cause and managing symptoms through respiratory support and other therapies as needed. This may include:
1. Oxygen therapy: Administering oxygen through a mask or nasal tubes to help increase oxygen levels in the bloodstream and reduce CO2 levels.
2. Ventilation assistance: Using a machine to assist with breathing, such as a ventilator, to help remove excess CO2 from the lungs.
3. Carbon dioxide removal: Using a device to remove CO2 from the bloodstream, such as a dialysis machine.
4. Medication management: Adjusting medications that may be contributing to hypercapnia, such as anesthetics or sedatives.
5. Respiratory therapy: Providing breathing exercises and other techniques to help improve lung function and reduce symptoms.
It is important to seek medical attention if you suspect you or someone else may have hypercapnia, as early diagnosis and treatment can help prevent complications and improve outcomes.
There are several different types of spinal cord injuries that can occur, depending on the location and severity of the damage. These include:
1. Complete spinal cord injuries: In these cases, the spinal cord is completely severed, resulting in a loss of all sensation and function below the level of the injury.
2. Incomplete spinal cord injuries: In these cases, the spinal cord is only partially damaged, resulting in some remaining sensation and function below the level of the injury.
3. Brown-Sequard syndrome: This is a specific type of incomplete spinal cord injury that affects one side of the spinal cord, resulting in weakness or paralysis on one side of the body.
4. Conus medullaris syndrome: This is a type of incomplete spinal cord injury that affects the lower part of the spinal cord, resulting in weakness or paralysis in the legs and bladder dysfunction.
The symptoms of spinal cord injuries can vary depending on the location and severity of the injury. They may include:
* Loss of sensation in the arms, legs, or other parts of the body
* Weakness or paralysis in the arms, legs, or other parts of the body
* Difficulty walking or standing
* Difficulty with bowel and bladder function
* Numbness or tingling sensations
* Pain or pressure in the neck or back
Treatment for spinal cord injuries typically involves a combination of medical and rehabilitative therapies. Medical treatments may include:
* Immobilization of the spine to prevent further injury
* Medications to manage pain and inflammation
* Surgery to relieve compression or stabilize the spine
Rehabilitative therapies may include:
* Physical therapy to improve strength and mobility
* Occupational therapy to learn new ways of performing daily activities
* Speech therapy to improve communication skills
* Psychological counseling to cope with the emotional effects of the injury.
Overall, the prognosis for spinal cord injuries depends on the severity and location of the injury, as well as the age and overall health of the individual. While some individuals may experience significant recovery, others may experience long-term or permanent impairment. It is important to seek medical attention immediately if symptoms of a spinal cord injury are present.
There are several types of nerve compression syndromes, including:
1. Carpal tunnel syndrome: Compression of the median nerve in the wrist, commonly caused by repetitive motion or injury.
2. Tarsal tunnel syndrome: Compression of the posterior tibial nerve in the ankle, similar to carpal tunnel syndrome but affecting the lower leg.
3. Cubital tunnel syndrome: Compression of the ulnar nerve at the elbow, often caused by repetitive leaning or bending.
4. Thoracic outlet syndrome: Compression of the nerves and blood vessels that pass through the thoracic outlet (the space between the neck and shoulder), often caused by poor posture or injury.
5. Peripheral neuropathy: A broader term for damage to the peripheral nerves, often caused by diabetes, vitamin deficiencies, or other systemic conditions.
6. Meralgia paresthetica: Compression of the lateral femoral cutaneous nerve in the thigh, commonly caused by direct trauma or compression from a tight waistband or clothing.
7. Morton's neuroma: Compression of the plantar digital nerves between the toes, often caused by poorly fitting shoes or repetitive stress on the feet.
8. Neuralgia: A general term for pain or numbness caused by damage or irritation to a nerve, often associated with chronic conditions such as shingles or postherpetic neuralgia.
9. Trigeminal neuralgia: A condition characterized by recurring episodes of sudden, extreme pain in the face, often caused by compression or irritation of the trigeminal nerve.
10. Neuropathic pain: Pain that occurs as a result of damage or dysfunction of the nervous system, often accompanied by other symptoms such as numbness, tingling, or weakness.
There are several types of respiratory insufficiency, including:
1. Hypoxemic respiratory failure: This occurs when the lungs do not take in enough oxygen, resulting in low levels of oxygen in the bloodstream.
2. Hypercapnic respiratory failure: This occurs when the lungs are unable to remove enough carbon dioxide from the bloodstream, leading to high levels of carbon dioxide in the bloodstream.
3. Mixed respiratory failure: This occurs when both hypoxemic and hypercapnic respiratory failure occur simultaneously.
Treatment for respiratory insufficiency depends on the underlying cause and may include medications, oxygen therapy, mechanical ventilation, and other supportive care measures. In severe cases, lung transplantation may be necessary. It is important to seek medical attention if symptoms of respiratory insufficiency are present, as early intervention can improve outcomes and prevent complications.
Edward Waymouth Reid
Glen Lake Sanatorium
Central tendon of diaphragm
Root of the lung
Hubert von Luschka
List of medical mnemonics
Hypoxic ventilatory response
Lung cancer staging
Cervical spinal nerve 4
Interrupted aortic arch
Flat-chested kitten syndrome
Neurally adjusted ventilatory assist
Shortness of breath
Central sleep apnea
Local anesthetic nerve block
Index of anatomy articles
Central pattern generator
Ventral ramus of spinal nerve
Cervical magnetic stimulation of the phrenic nerves in bilateral diaphragm paralysis
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- The study aims were to assess the feasibility of recording EMGdi using a multipair oesophageal electrode catheter and examine whether diaphragm muscle and/or phrenic nerve function was compromised in AWD or CDH infants. (ersjournals.com)
- Measurement of airway and/or transdiaphragmatic pressures elicited by transcutaneous phrenic nerve stimulation allows diaphragm muscle function to be assessed directly and independently of volition 10 . (ersjournals.com)
- Phrenic nerve -- The nerve that controls the movement of the diaphragm muscle. (nih.gov)
Movement of the diaphragm1
- The phrenic nerves stimulate the movement of the diaphragm, a muscular membrane that causes the lungs to fill and empty. (scientificamerican.com)
- To examine these two hypotheses we studied five patients with isolated bilateral diaphragm paralysis using CMS and bilateral electrical phrenic stimulation (BES). (nih.gov)
- The phrenic nerve stimulation test , also called the phrenic nerve conduction study, uses electric or magnetic stimulation to the neck to measure the response of the phrenic nerve. (nm.org)
- A phrenic nerve that does not respond to stimulation can indicate the cause of paralysis of the diaphragm. (nm.org)
- Experiments on anesthetized, spinalized rats were conducted to determine the effects of systemic 5-hydroxytryptophan (5-HTP) administration on: (1) spontaneous phrenic nerve activity and (2) evoked phrenic responses to short latency, non-serotonergic synaptic inputs elicited by electrical stimulation of lateral funiculus. (nih.gov)
- His studies, which will use multiple cutting-edge techniques, including optogenetics, will aim to improve the efficiency of nerve transmission by developing phrenic sympathetic stimulation to healthy neuromuscular junctions. (nih.gov)
- Measurement of the diaphragm electromyogram (EMGdi) elicited by phrenic nerve stimulation could be useful to assess neonates suffering from respiratory distress due to diaphragm dysfunction, as observed in infants with abdominal wall defects (AWD) or congenital diaphragmatic hernia (CDH). (ersjournals.com)
- Diaphragm compound muscle action potentials elicited by magnetic phrenic nerve stimulation were recorded from 18 infants with surgically repaired AWD (n = 13) or CDH (n = 5), median (range) gestational age 36.5 (34-40) weeks. (ersjournals.com)
- Oesophageal EMG and magnetic stimulation of the phrenic nerves can be useful to assess phrenic nerve function in infants. (ersjournals.com)
- Our aims, therefore, were to assess the feasibility of recording the EMGdi elicited by magnetic stimulation of the phrenic nerves (MSPN) using an oesophageal electrode catheter in infants with AWD or CDH, and determine whether it was muscle and/or nerve function that was compromised in these patients. (ersjournals.com)
- Phrenic nerve stimulation was performed once the CDH and AWD infants no longer required either mechanical ventilation or continuous positive airways pressure. (ersjournals.com)
- Vagus nerve, which has many important jobs, including helping to control the digestive system . (clevelandclinic.org)
- This involves a complex neural pathway which includes the phrenic, vagus and the sympathetic pathways, it is usually self-limiting and resolves within a few minutes after onset. (scirp.org)
- The afferent limb includes the phrenic and vagus nerves and the sympathetic chain . (scirp.org)
- The brachial plexus (plexus brachialis) is a somatic nerve plexus formed by intercommunications among the ventral rami (roots) of the lower 4 cervical nerves (C5-C8) and the first thoracic nerve (T1). (medscape.com)
- A tumor, aortic aneurysm or cervical spondylosis can compress or damage the nerve. (clevelandclinic.org)
- Spinal cord lesions above the level of the third cervical segment sever the continuity of the bulbospinal respiratory pathways, which carry the descending rhythmic impulses needed to activate the phrenic motoneuron pool lying in the ventral gray matter between the third and fifth cervical segments. (jneurosci.org)
- The phrenic nerve fibers originate in the cervical spinal column (mostly C4) and travel through the cervical plexus to the diaphragm. (nih.gov)
- Las fibras del nervio frénico se originan en la médula espinal (principalmente a la altura de C4) y discurren a través de plexo cervical hasta el diafragma. (bvsalud.org)
- Reduced phrenic nerve conduction accompanies the reduced diaphragm force production observed in infants with CDH. (ersjournals.com)
- 5-Hydroxytryptophan (5-HTP) augments spontaneous and evoked phrenic motoneuron discharge in spinalized rats. (nih.gov)
- Your esophagus and several nerves and blood vessels run through openings in the diaphragm. (clevelandclinic.org)
- The diagnostic utility of inspiratory-expiratory radiography for the assessment of phrenic nerve palsy associated with brachial plexus injury. (mayo.edu)
- Phrenic nerve identification with cardiac multidetector computed tomography]. (bvsalud.org)
- The objectives of this study were to determine if the persistent increases in sympathetic nerve activity, known to be induced by acute intermittent hypoxia (AIH), are mediated through activation of the pituitary adenylate cyclase activating polypeptide (PACAP) signaling system. (bvsalud.org)
- Using PACAP receptor knockout mice, and pharmacological agents in Sprague Dawley rats, we measured blood pressure, heart rate, pH, PaCO2, and splanchnic sympathetic nerve activity, under anaesthesia, to demonstrate that the sympathetic response to AIH is mediated via the PAC1 receptor, in a cAMP-dependent manner. (bvsalud.org)
- These individuals' injuries have led to abnormal function of their phrenic nerve, which controls the diaphragm. (nih.gov)
- Abnormal phrenic nerve and/or respiratory muscle function can impair antenatal lung growth 6 and delay or prevent weaning and extubation from mechanical ventilation 7 . (ersjournals.com)
- Since the phrenic nerves come out of the protective spinal cord at the back of the neck, and Vader may have suffered serious burn damage there, we might theorize that severe heat damage destroyed the nerves and caused a partial paralysis. (scientificamerican.com)
- The typical spinal nerve root results from the confluence of the ventral nerve rootlets originating in the anterior horn cells of the spinal cord and the dorsal nerve rootlets that join the spinal ganglion in the region of the intervertebral foramen. (medscape.com)
- The central mediators are thought to be the medulla oblongata and reticular formation of the brainstem interacting with phrenic nerve nuclei and hypothalamus, and non-specific areas in the spinal cord between C3 and C5 , and the phrenic nerve with accessory neural connections to the glottis forming the efferent limb. (scirp.org)
- 5-HTP augmented spontaneous phrenic activity and allowed expression of a second, longer latency evoked response. (nih.gov)
- One AWD patient had prolonged phrenic nerve latency (PNL) bilaterally (left 9.31 ms, right 9.49 ms) and two CDH patients had prolonged PNL on the affected side (10.1 ms and 10.08 ms). There was no difference in left and right Tw P di in either group. (ersjournals.com)
- In addition, the phrenic nerve latency (PNL) and compound muscle action potential (CMAP) amplitude are reproducible as the catheter can be positioned accurately at the electrically active centre of the diaphragm 13 . (ersjournals.com)
Peripheral Nerve Surgery2
- The brachial plexus supplies all of the cutaneous innervation of the upper limb, except for the area of the axilla (which is supplied by the supraclavicular nerve) and the dorsal scapula area, which is supplied by cutaneous branches of the dorsal rami. (medscape.com)
- The spinal nerves that form the brachial plexus run in an inferior and anterior direction within the sulci formed by these structures. (medscape.com)
- The anterior division of the lower trunk forms the medial cord, which gives off the medial pectoral nerve (C8, T1), the medial brachial cutaneous nerve (T1), and the medial antebrachial cutaneous nerve (C8, T1). (medscape.com)
- The lower 2 nerve roots of the brachial plexus, C8 and T1, are most commonly (90%) involved, producing pain and paresthesias in the ulnar nerve distribution. (slideshare.net)
- Characterization of elbow flexion torque after nerve reconstruction of patients with traumatic brachial plexus injury. (mayo.edu)
- the forgotten nerve in head and neck surgery. (nih.gov)
- The ventral rami of spinal nerves C5 to T1 are referred to as the "roots" of the plexus. (medscape.com)
- Vitals laryngeal nerve (RLN) and the inferior thyroid artery. (who.int)
- As I have extremely tight and irritated muscles on my left side, does anyone have experience or knowledge with phrenic nerve being caught up in ES? (livingwitheagle.org)
- The suprascapular nerve contributes sensory fibers to the shoulder joint and provides motor innervation to the supraspinatus and infraspinatus muscles. (medscape.com)
- The diaphragmatic sphincter is composed of striated muscles that also exhibit tone and contracts due to the excitatory nerves. (nature.com)
- It appeared that a rough budgetary estimate of the cost of the units required for the phrenic stimulator and booster heart experiments would be approximately $50,000. (nih.gov)
- The most common conditions include hernias and nerve damage from surgery or an accident. (clevelandclinic.org)
- Crowe CS, Shin AY , Pulos N. Iatrogenic Nerve Injuries of the Upper Extremity: A Critical Analysis Review. (mayo.edu)
- Phrenic nerve, which controls the diaphragm's movement. (clevelandclinic.org)
- Our results suggest that spinal serotonin increases the efficacy of synaptic inputs to phrenic motoneurons. (nih.gov)
- Nerve damage can result from cancer , autoimmune diseases or trauma. (clevelandclinic.org)
- Several nerves, soft tissues and blood vessels pass through the diaphragm. (clevelandclinic.org)
- Factors Associated with Poorer Outcomes from Triceps Motor Branch to Anterior Axillary Nerve Transfer: A Case-Control Study. (mayo.edu)