<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hypokinesia and can you explain it in depth? [/INST] Hypokinesia is one of the classifications of movement disorders, and refers to decreased bodily movement. Hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Hypokinesia is a symptom of Parkinsons disease shown as muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases.
The other category of movement disorder is hyperkinesia that features an exaggeration of unwanted movement, such as twitching or writhing in Huntingtons disease or Tourette syndrome.

Spectrum of disorders
Hypokinesia describes a variety of more specific disorders:

Causes
The most common cause of Hypokinesia is Parkinsons disease, and conditions related to Parkinsons disease.
Other conditions may also cause slowness of movements. These include hypothyroidism and severe depression. These conditions need to be carefully ruled out, before a diagnosis of Parkinsonism is made.
The remainder of this article describes Hypokinesia associated with Parkinsons disease, and conditions related to Parkinsons disease.

Pathophysiology
Associated neurotransmitters
Dopamine
The main neurotransmitter thought to be involved in hypokinesia is dopamine. Essential to the basal ganglionic-thalamocortical loop, which processes motor function, dopamine depletion is common in these areas of hypokinesic patients. Bradykinesia is correlated with lateralized dopaminergic depletion in the substantia nigra. The dopamine pathway in the substantia nigra is essential to motor function, and commonly a lesion in this area correlates with displayed hypokinesia. Tremor and rigidity, however, seem to be only partially due to dopamine deficits in the substantia nigra, suggesting other processes are involved in motor control. Treatments for hypokinesia often either attempt to prevent dopamine degradation by MAO-B or increase the amount of neurotransmitter present in the system.GABA and glutamate
The inhibitory neurotransmitter GABA and the excitatory glutamate are found in many parts of the central nervous system, including in the motor pathways that involve hypokinesia. In one pathway, glutamate in the substantia nigra excites the release of GABA into the thalamus, which then inhibits the release of glutamate in the cortex and thereby reduces motor activity. If too much glutamate is initially in the substantia nigra, then through interaction with GABA in the thalamus and glutamate in the cortex, movements will be reduced or will not occur at all.Another direct pathway from the basal ganglia sends GABA inhibitory messages to the globus pallidus and substantia nigra, which then send GABA to the thalamus. In the indirect pathway, the basal ganglia send GABA to the globus pallidus which then sends it to the subthalamic nucleus, which then disinhibited sends glutamate to the output structures of the basal ganglia. Inhibition of GABA release could disrupt the feedback loop to the basal ganglia and produce hypokinesic movements.GABA and glutamate often interact with each other and with dopamine directly. In the basal ganglia, the nigrostriatal pathway is where GABA and dopamine are housed in the same neurons and released together.

Neurobiology
Hypokinetic symptoms arise from damage to the basal ganglia, which plays a role in producing force and computing the effort necessary to make a movement. Two possible neural pathways enable the basal ganglia to produce movement. When activated, the direct pathway sends sensory and motor information from the cerebral cortex to the first structure of the basal ganglia, the putamen. That information directly inhibits the globus pallidus internal and allows free movement. The indirect pathway, traveling through the putamen, globus pallidus external, and subthalamic nucleus, activates the globus pallidus internal threshold and inhibits the thalamus from communicating with the motor cortex, producing hypokinetic symptoms.

When levels of dopamine decrease, the normal wave-firing pattern of basal ganglia neural oscillations changes and the tendency for oscillations increases, particularly in the beta wave of the basal ganglia.  Recent research indicates, when oscillations fire simultaneously, processing is disrupted at the thalamus and cortex, affecting activities such as motor planning and sequence learning, as well as causing hypokinetic tremors.

Treatments
Dopaminergic drugs
Dopaminergic drugs are commonly used in the early stages of the hypokinesia to treat patients. With increased intake, though, they can become ineffective because of the development of noradrenergic lesions. While initially the dopaminergic drugs may be effective, these noradrenergic lesions are associated with hypokinesic gait disorder development later on.Some Parkinsons patients are unable to move during sleep, prompting the diagnosis of "nocturnal hypokinesia". Physicians have experienced success treating this sleep disorder with slow-release or night-time dopaminergic drugs, and in some cases, continuous stimulation by the dopamine agonist rotigotine. Despite improved mobility during sleep, many Parkinsons patients report an extremely uncomfortable sleeping experience even after dopaminergic treatments.

Deep brain stimulation
Once the reaction to dopaminergic drugs begins to fluctuate in Parkinsons patients, deep brain stimulation (DBS) of the subthalamic nucleus and internal globus pallidus is often used to treat hypokinesia. DBS, like dopaminergic drugs, initially provides relief, but chronic use causes worse hypokinesia and freezing of gait. Lower-frequency DBS in irregular patterns has been shown to be more effective and less detrimental in treatment.

Posteroventral pallidotomy (PVP) is a specific kind of DBS that destroys a small part of the globus pallidus by scarring the neural tissue, reducing brain activity and therefore tremors and rigidity. PVP is suspected to recalibrate basal ganglia activity in the thalamocortical pathway. PVP in the dominant hemisphere has been reported to disrupt executive function verbal processing abilities, and bilateral PVP may disturb processes of focused attention.Many akinesia patients also form a linguistic akinesia in which their ability to produce verbal movements mirrors their physical akinesia symptoms, especially after unsuccessful PVP. Patients are usually able to maintain normal levels of fluency, but often stop midsentence, unable to remember or produce a desired word. According to a study of Parkinsons patients with articulatory hypokinesia, subjects with faster rates of speech experienced more problems trying to produce conversational language than those who normally spoke at slower rates.

Methylphenidate
Methylphenidate, commonly used to treat ADHD, has been used in conjunction with levodopa to treat hypokinesia in the short term. The two work together to increase dopamine levels in the striatum and prefrontal cortex. Methylphenidate mainly inhibits dopamine and noradrenaline reuptake by blocking presynaptic transporters, and levodopa increases the amount of dopamine, generally improving hypokinesic gait. Some patients, however, have adverse reactions of nausea and headache to the treatment and the long-term effects of the drug treatment still need to be assessed.

Stem cells
New treatments include increasing the number of dopamine cells by transplanting stem cells into the basal ganglia or stimulating endogenous stem cell production and movement to the basal ganglia. The successful integration of stem cells can relieve hypokinetic symptoms and decrease the necessary dose of dopaminergic drugs. However, a variety of complications, including possible tumor formation, inappropriate cell migration, rejection of cells by the immune system, and cerebral hemorrhage are possible, causing many physicians to believe the risks outweigh the possible benefits.

NOP receptor antagonists
Another treatment, still in an experimental stage, is the administration of nociception FQ peptide (NOP) receptor antagonists. This treatment has been shown to reduce hypokinesia in animal studies when increasing nociception FQ in the substantia nigra and subthalamic nucleus. Low doses can be taken with dopaminergic treatment to decrease the amount of L-dopa needed, which can reduce its long-term side effects and improve motor performance.

Dance therapy
Dance therapy has also been shown to reduce hypokinesic movements and rigidity, though targeted more at the muscular aspects of the disorder than the neural activity.

Associations
Cognitive impairment
Bradykinesia has been shown to precede impairment of executive functions, working memory, and attention. These cognitive deficiencies can be tied to nonfunction of the basal ganglia and prefrontal cortex, which is also linked to the motor-dysfunction of hypokinesia. Tremor and rigidity have not had observable connections to cognitive impairments, supporting the idea that they are not as involved in the dopamine pathway in the basal ganglionic-thalamocortical loop. Dopaminergic treatments have shown improvement in cognitive functions associated with hypokinesia, suggesting they are also dependent on dopamine levels in the system.

Motor motivation
Often debated is whether the efficiency, vigor, and speed of movements in patients with hypokinesia are tied to motivation for rewarding and against punishing stimuli. The basal ganglia have been tied to the incentives behind movement, therefore suggesting a cost/benefit analysis of planned movement could be affected in hypokinesia. Rewards have not been shown to change the aspects of a hypokinesic individuals movement. In fact, the motor planning and control of a patient with hypokinesia is already as efficient as possible (as shown by slightly faster, but generally the same movement after deep brain stimulation of the subthalamic nucleus). This suggests that hypokinetic individuals simply have a narrower range of movement that does not increase relative to motivation.Other studies have come to the same conclusion about rewards and hypokinesia, but have shown that aversive stimuli can, in fact, reduce hypokinesic movement. Dopamine is either less involved or has a more complex role in the response to punishment than it does to rewards, as the hypodopaminergic striatum allows more movement in response to aversive stimuli.

Demographic differentiation
Gender
More men than women typically develop hypokinesia, which is reflected in young and middle-aged populations where females have displayed higher levels of nigrostriatal dopamine than males. In the elderly, however, this differentiation is not present </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tracheobronchial injury and can you explain it in depth? [/INST] Tracheobronchial injury is damage to the tracheobronchial tree (the airway structure involving the trachea and bronchi). It can result from blunt or penetrating trauma to the neck or chest, inhalation of harmful fumes or smoke, or aspiration of liquids or objects.Though rare, TBI is a serious condition; it may cause obstruction of the airway with resulting life-threatening respiratory insufficiency. Other injuries accompany TBI in about half of cases. Of those people with TBI who die, most do so before receiving emergency care, either from airway obstruction, exsanguination, or from injuries to other vital organs. Of those who do reach a hospital, the mortality rate may be as high as 30%.TBI is frequently difficult to diagnose and treat. Early diagnosis is important to prevent complications, which include stenosis (narrowing) of the airway, respiratory tract infection, and damage to the lung tissue. Diagnosis involves procedures such as bronchoscopy, radiography, and x-ray computed tomography to visualize the tracheobronchial tree. Signs and symptoms vary based on the location and severity of the injury; they commonly include dyspnea (difficulty breathing), dysphonia (a condition where the voice can be hoarse, weak, or excessively breathy), coughing, and abnormal breath sounds. In the emergency setting, tracheal intubation can be used to ensure that the airway remains open. In severe cases, surgery may be necessary to repair a TBI.

Signs and symptoms
Signs and symptoms vary depending on what part of the tracheobronchial tree is injured and how severely it is damaged. There are no direct signs of TBI, but certain signs suggest the injury and raise a clinicians suspicion that it has occurred. Many of the signs and symptoms are also present in injuries with similar injury mechanisms such as pneumothorax. Dyspnea and respiratory distress are found in 76–100% of people with TBI, and coughing up blood has been found in up to 25%. However, isolated TBI does not usually cause profuse bleeding; if such bleeding is observed it is likely to be due to another injury such as a ruptured large blood vessel. The patient may exhibit dysphonia or have diminished breath sounds, and rapid breathing is common. Coughing may be present, and stridor, an abnormal, high-pitched breath sound indicating obstruction of the upper airway can also occur.Damage to the airways can cause subcutaneous emphysema (air trapped in the subcutaneous tissue of the skin) in the abdomen, chest, neck, and head. Subcutaneous emphysema, present in up to 85% of people with TBI, is particularly indicative of the injury when it is only in the neck. Air is trapped in the chest cavity outside the lungs (pneumothorax) in about 70% of TBI. Especially strong evidence that TBI has occurred is failure of a pneumothorax to resolve even when a chest tube is placed to rid the chest cavity of the air; it shows that air is continually leaking into the chest cavity from the site of the tear. Air can also be trapped in the mediastinum, the center of the chest cavity (pneumomediastinum). If air escapes from a penetrating injury to the neck, a definite diagnosis of TBI can be made. Hammans sign, a sound of crackling that occurs in time with the heartbeat, may also accompany TBI.

Causes
Injuries to the tracheobronchial tree within the chest may occur due to penetrating forces such as gunshot wounds, but are more often the result of blunt trauma. TBI due blunt forces usually results from high-energy impacts such as falls from height and motor vehicle accidents; the injury is rare in low-impact mechanisms. Injuries of the trachea cause about 1% of traffic-related deaths. Other potential causes are falls from high places and injuries in which the chest is crushed. Explosions are another cause.Gunshot wounds are the commonest form of penetrating trauma that cause TBI. Less commonly, knife wounds and shrapnel from motor vehicle accidents can also penetrate the airways. Most injuries to the trachea occur in the neck, because the airways within the chest are deep and therefore well protected; however, up to a quarter of TBI resulting from penetrating trauma occurs within the chest. Injury to the cervical trachea usually affects the anterior (front) part of the trachea.Certain medical procedures can also injure the airways; these include tracheal intubation, bronchoscopy, and tracheotomy. The back of the trachea may be damaged during tracheotomy. TBI resulting from tracheal intubation (insertion of a tube into the trachea) is rare, and the mechanism by which it occurs is unclear. However, one likely mechanism involves an endotracheal tube catching in a fold of membrane and tearing it as it is advanced downward through the airway. When an endotracheal tube tears the trachea, it typically does so at the posterior (back) membranous wall. Unlike TBI that results from blunt trauma, most iatrogenic injuries to the airway involve longitudinal tears to the back of the trachea or tears on the side that pull the membranous part of the trachea away from the cartilage. Excessive pressure from the cuff of an endotracheal tube can reduce blood supply to the tissues of the trachea, leading to ischemia and potentially causing it to become ulcerated, infected, and, later, narrowed.The mucosal lining of the trachea may also be injured by inhalation of hot gases or harmful fumes such as chlorine gas. This can lead to edema (swelling), necrosis (death of the tissue), scar formation, and ultimately stenosis. However, TBI due to inhalation, foreign body aspiration, and medical procedures is uncommon.

Mechanism
The structures in the tracheobronchial tree are well protected, so it normally takes a large amount of force to injure them. In blunt trauma, TBI is usually the result of violent compression of the chest. Rapid hyperextension of the neck, usually resulting from vehicle crashes, can also injure the trachea, and trauma to the neck can crush the trachea against the vertebrae. A crush injury of the larynx or cervical trachea can occur in head-on collisions when the neck is hyperextended and strikes the steering wheel or dashboard; this has been called a "dashboard injury". The larynx and cervical trachea may also be injured in front-on collisions by the seat belt.Although the mechanism is not well understood, TBI due to blunt trauma is widely thought to be caused by any combination of three possible mechanisms: an increase in pressure within the airways, shearing, and pulling apart. The first type of injury, sometimes called an "explosive rupture", may occur when the chest is violently compressed, for example when a driver strikes the steering wheel in a vehicle accident or when the chest is crushed. The pressure in the airways, especially the larger airways (the trachea and bronchi), quickly rises as a result of the compression, because the glottis reflexively closes off the airways. When this pressure exceeds the elasticity of the tissues, they burst; thus the membranous part of the trachea is more commonly affected by this mechanism of injury than cartilaginous portions.The second mechanism may occur when the chest is suddenly decelerated, as occurs in vehicle accidents, producing a shearing force. The lungs are mobile in the chest cavity but their movement is more restricted near the hilum. Areas near the cricoid cartilage and carina are fixed to the thyroid cartilage and the pericardium respectively; thus if the airways move, they can tear at these points of fixation.The third mechanism occurs when the chest is compressed from front to back, causing it to widen from side to side. The lungs adhere to the chest wall because of the negative pressure between them and the pleural membranes lining the inside of the chest cavity; thus when the chest widens, they are pulled apart. This creates tension at the carina; the airway tears if this tensile force exceeds its elasticity. This mechanism may be the cause of injury when the chest is crushed. Most TBI are probably due to a combination of these three mechanisms.When airways are damaged, air can escape from them and be trapped in the surrounding tissues in the neck (subcutaneous emphysema) and mediastinum (pneumomediastinum); if it builds up to high enough pressures there, it can compress the airways. Massive air leaks from a ruptured airway can also compromise the circulation by preventing blood from returning to the heart from the head and lower body; this causes a potentially deadly reduction in the amount of blood the heart is able to pump out. Blood and other fluids can build up in the airways, and the injury can interfere with the patency of the airway and interfere with its continuity. However, even if the trachea is completely transected, the tissues surrounding it may hold it together enough for adequate air exchange to occur, at least at first.

Anatomy
The trachea and bronchi form the tracheobronchial tree. The trachea is situated between the lower end of the larynx and the center of the chest, where it splits into the two bronchi at a ridge called the carina. The trachea is stabilized and kept open by rings made of cartilage that surround the front and sides of the structure; these rings are not closed and do not surround the back, which is made of membrane. The bronchi split into smaller branches and then to bronchioles that supply air to the alveoli, the tiny air-filled sacs in the lungs responsible for absorbing oxygen. An arbitrary division can be made between the intrathoracic and cervical trachea at the thoracic inlet, an opening at the top of the thoracic cavity. Anatomical structures that surround and protect the tracheobronchial tree include the lungs, the esophagus, large blood vessels, the rib cage, the thoracic spine, and the sternum. Children have softer tracheas and a more elastic tracheobronchial trees than adults; this elasticity, which helps protect the structures from injury when they are compressed, may contribute to the lower incidence of TBI in children.

Diagnosis
Rapid diagnosis and treatment are important in the care of TBI; if the injury is not diagnosed shortly after the injury, the risk of complications is higher. Bronchoscopy is the most effective method to diagnose, locate, and determine the severity of TBI, and it is usually the only method that allows a definitive diagnosis. Diagnosis with a flexible bronchoscope, which allows the injury to be visualized directly, is the fastest and most reliable technique. In people with TBI, bronchoscopy may reveal that the airway is torn, or that the airways are blocked by blood, or that a bronchus has collapsed, obscuring more distal (lower) bronchi from view.Chest x-ray is the initial imaging technique used to diagnose TBI. The film may not have any signs in an otherwise asymptomatic patient. Indications of TBI seen on radiographs include deformity in the trachea or a defect in the tracheal wall. Radiography may also show cervical emphysema, air in the tissues of the neck. X-rays may also show accompanying injuries and signs such as fractures and subcutaneous emphysema. If subcutaneous emphysema occurs and the hyoid bone appears in an X-ray to be sitting unusually high in the throat, it may be an indication that the trachea has been severed. TBI is also suspected if an endotracheal tube appears in an X-ray to be out of place, or if its cuff appears to be more full than normal or to protrude through a tear in the airway. If a bronchus is torn all the way around, the lung may collapse outward toward the chest wall (rather than inward, as it usually does in pneumothorax) because it loses the attachment to the bronchus which normally holds it toward the center. In a person lying face-up, the lung collapses toward the diaphragm and the back. This sign, described in 1969, is called fallen lung sign and is pathognomonic of TBI (that is, it is diagnostic for TBI because it does not occur in other conditions); however it occurs only rarely. In as many as one in five cases, people with blunt trauma and TBI have no signs of the injury on chest X-ray. CT scanning detects over 90% of TBI resulting from blunt trauma, but neither X-ray nor CT are a replacement for bronchoscopy.At least 30% of TBI are not discovered at first; this number may be as high as 50%. In about 10% of cases, TBI has no specific signs either clinically or on chest radiography, and its detection may be further complicated by concurrent injuries, since TBI tends to occur after high-energy accidents. Weeks or months may go by before the injury is diagnosed, even though the injury is better known than it was in the past.

Classification
Lesions can be transverse, occurring between the rings of the trachea, longitudinal or spiral. They may occur along the membranous part of the trachea, the main bronchi, or both. In 8% of ruptures, lesions are complex, occurring in more than one location, with more than one type of lesion, or on both of the main bronchi and the trachea. Transverse tears are more common than longitudinal or complex ones. The laceration may completely transect the airway or it may go only partway around. Partial tears that do not go all the way around the circumference of the airway do not allow a lacerated airway to become completely detached; tears that encircle the whole airway can allow separation to occur. Lacerations may also be classified as complete or incomplete. In an incomplete lesion, a layer of tissue surrounding the bronchus remains intact and can keep the air in the airway, preventing it from leaking into the areas surrounding the airways. Incomplete lacerations may require closer scrutiny to detect and may not be diagnosed right away.Bronchial injuries are divided into those that are accompanied by a disruption of the pleura and those that are not; in the former, air can leak from the hole in the airway and a pneumothorax can form. The latter type is associated with more minor signs; pneumothorax is small if it occurs at all, and although function is lost in the part of the lung supplied by the injured bronchus, unaffected parts of the lungs may be able to compensate.Most TBI that results from blunt trauma occurs within the chest. The most common tracheal injury is a tear near the carina or in the membranous wall of the trachea. In blunt chest trauma, TBI occurs within 2.5 cm of the carina 40–80% of the time. The injury is more common in the right main bronchus than the left, possibly because the former is near vertebrae, which may injure it. Also, the aorta and other tissues in the mid chest that surround the left main bronchus may protect it. Another possibility is that people with left main bronchus injuries are more likely to also have other deadly injuries and therefore die before reaching hospital, making them less likely to be included in studies that determine rates of injuries.

Prevention
Vehicle occupants who wear seat belts have a lower incidence of TBI after a motor vehicle accident. However, if the strap is situated across the front of the neck (instead of the chest), this increases the risk of tracheal injury. Design of medical instruments can be modified to prevent iatrogenic TBI, and medical practitioners can use techniques that reduce the risk of injury with procedures such as tracheotomy.

Treatment
Treatment of TBI varies based on the location and severity of injury and whether the patient is stable or having trouble breathing, but ensuring that the airway is patent so that the patient can breathe is always of paramount importance. Ensuring an open airway and adequate ventilation may be difficult in people with TBI. Intubation, one method to secure the airway, may be used to bypass a disruption in the airway in order to send air to the lungs. If necessary, a tube can be placed into the uninjured bronchus, and a single lung can be ventilated. If there is a penetrating injury to the neck through which air is escaping, the trachea may be intubated through the wound. Multiple unsuccessful attempts at conventional (direct) laryngoscopy may threaten the airway, so alternative techniques to visualize the airway, such as fiberoptic or video laryngoscopy, may be employed to facilitate tracheal intubation. If the upper trachea is injured, an incision can be made in the trachea (tracheotomy) or the cricothyroid membrane (cricothyrotomy, or cricothyroidotomy) in order to ensure an open airway. However, cricothyrotomy may not be useful if the trachea is lacerated below the site of the artificial airway. Tracheotomy is used sparingly because it can cause complications such as infections and narrowing of the trachea and larynx. When it is impossible to establish a sufficient airway, or when complicated surgery must be performed, cardiopulmonary bypass may be used—blood is pumped out of the body, oxygenated by a machine, and pumped back in. If a pneumothorax occurs, a chest tube may be inserted into the pleural cavity to remove the air.

People with TBI are provided with supplemental oxygen and may need mechanical ventilation. Employment of certain measures such as Positive end-expiratory pressure (PEEP) and ventilation at higher-than-normal pressures may be helpful in maintaining adequate oxygenation. However, such measures can also increase leakage of air through a tear, and can stress the sutures in a tear that has been surgically repaired; therefore the lowest possible airway pressures that still maintain oxygenation are typically used. The use of high frequency ventilation has been reported. Mechanical ventilation can also cause pulmonary barotrauma when high pressure is required to ventilate the lungs. Techniques such as pulmonary toilet (removal of secretions), fluid management, and treatment of pneumonia are employed to improve pulmonary compliance (the elasticity of the lungs).While TBI may be managed without surgery, surgical repair of the tear is considered standard in the treatment of most TBI. It is required if a tear interferes with ventilation; if mediastinitis (inflammation of the tissues in the mid-chest) occurs; or if subcutaneous or mediastinal emphysema progresses rapidly; or if air leak or large pneumothorax is persistent despite chest tube placement. Other indications for surgery are a tear more than one third the circumference of the airway, tears with loss of tissue, and a need for positive pressure ventilation. Damaged tissue around a rupture (e.g. torn or scarred tissue) may be removed in order to obtain clean edges that can be surgically repaired. Debridement of damaged tissue can shorten the trachea by as much as 50%. Repair of extensive tears can include sewing a flap of tissue taken from the membranes surrounding the heart or lungs (the pericardium and pleura, respectively) over the sutures to protect them. When lung tissue is destroyed as a result of TBI complications, pneumonectomy or lobectomy (removal of a lung or of one lobe, respectively) may be required. Pneumonectomy is avoided whenever possible due to the high rate of death associated with the procedure. Surgery to repair a tear in the tracheobronchial tree can be successful even when it is performed months after the trauma, as can occur if the diagnosis of TBI is delayed. When airway stenosis results after delayed diagnosis, surgery is similar to that performed after early diagnosis: the stenotic section is removed and the cut airway is repaired.

Prognosis and complications
Most people with TBI who die do so within minutes of the injury, due to complications such as pneumothorax and insufficient airway and to other injuries that occurred at the same time. Most late deaths that occur in TBI are attributed to sepsis or multiple organ dysfunction syndrome (MODS). If the condition is not recognized and treated early, serious complications are more likely to occur; for example, pneumonia and bronchiectasis may occur as late complications. Years can pass before the condition is recognized. Some TBI are so small that they do not have significant clinical manifestations; they may never be noticed or diagnosed and may heal without intervention.If granulation tissue grows over the injured site, it can cause stenosis of the airway, after a week to a month. The granulation tissue must be surgically excised. Delayed diagnosis of a bronchial rupture increases risk of infection and lengthens hospital stay. People with a narrowed airway may develop dyspnea, coughing, wheezing, respiratory tract infection, and difficulty with clearing secretions. If the bronchiole is completely obstructed, atelectasis occurs: the alveoli of the lung collapse. Lung tissue distal to a completely obstructed bronchiole often does not become infected. Because it is filled with mucus, this tissue remains functional. When the secretions are removed, the affected portion of the lung is commonly able to function almost normally. However, infection is common in lungs distal to a partially obstructed bronchiole. Infected lung tissue distal to a stricture can be damaged, and wheezing and coughing may develop due to the narrowing. In addition to pneumonia, the stenosis may cause bronchiectasis, in which bronchi are dilated, to develop. Even after an airway with a stricture is restored to normal, the resulting loss of lung function may be permanent.Complications may also occur with treatment; for example, a granuloma can form at the suture site. Also, the sutured wound can tear again, as occurs when there is excessive pressure in the airways from ventilation. However, for people who do receive surgery soon after the injury to repair the lesion, outcome is usually good; the long-term outcome is good for over 90% of people who have TBI surgically repaired early in treatment. Even when surgery is performed years after the injury, the outlook is good, with low rates of death and disability and good chances of preserving lung function.

Epidemiology
Rupture of the trachea or bronchus is the most common type of blunt injury to the airway. It is difficult to determine the incidence of TBI: in as many as 30–80% of cases, death occurs before the person reaches a hospital, and these people may not be included in studies. On the other hand, some TBI are so small that they do not cause significant symptoms and are therefore never noticed. In addition, the injury sometimes is not associated with symptoms until complications develop later, further hindering estimation of the true incidence. However, autopsy studies have revealed TBI in 2.5–3.2% of people who died after trauma. Of all neck and chest traumas, including people that died immediately, TBI is estimated to occur in 0.5–2%. An estimated 0.5% of polytrauma patients treated in trauma centers have TBI. The incidence is estimated at 2% in blunt chest and neck trauma and 1–2% in penetrating chest trauma. Laryngotracheal injuries occur in 8% of patients with penetrating injury to the neck, and TBI occurs in 2.8% of blunt chest trauma deaths. In people with blunt trauma who do reach a hospital alive, reports have found incidences of 2.1% and 5.3%. Another study of blunt chest trauma revealed an incidence of only 0.3%, but a mortality rate of 67% (possibly due in part to associated injuries). The incidence of iatrogenic TBI (that caused by medical procedures) is rising, and the risk may be higher for women and the elderly. TBI results about once every 20,000 times someone is intubated through the mouth, but when intubation is performed emergently, the incidence may be as high as 15%.The mortality rate for people who reach a hospital alive was estimated at 30% in 1966; more recent estimates place this number at 9%. The number of people reaching a hospital alive has increased, perhaps due to improved prehospital care or specialized treatment centers. Of those who reach the hospital alive but then die, most do so within the first two hours of arrival. The sooner a TBI is diagnosed, the higher the mortality rate; this is likely due to other accompanying injuries that prove fatal.Accompanying injuries often play a key role in the outcome. Injuries that may accompany TBI include pulmonary contusion and laceration; and fractures of the sternum, ribs and clavicles. Spinal cord injury, facial trauma, traumatic aortic rupture, injuries to the abdomen, lung, and head are present in 40–100%. The most common accompanying injury is esophageal perforation or rupture (known as Boerhaave syndrome), which occurs in as many as 43% of the penetrating injuries to the neck that cause tracheal injury.

History
Throughout most of history, the mortality rate of TBI was thought to be 100%. However, in 1871 a healed TBI was noted in a duck that had been killed by a hunter, thus demonstrating that the injury could be survived, at least in the general sense. This report, made by Winslow, was the first record in the medical literature of a bronchus injury. In 1873, Seuvre made one of the earliest reports of TBI in the medical literature: a 74-year-old woman whose chest was crushed by a wagon wheel was found on autopsy to have an avulsion of the right bronchus. Long-term survival of the injury was unknown in humans until a report was made of a person who survived in 1927. In 1931, a report made by Nissen described successful removal of a lung in a 12-year-old girl who had had narrowing of the bronchus due to the injury. Repair of TBI was probably first attempted in 1945, when the first documented case of a successful suturing of a lacerated bronchus was made </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Phimosis and can you explain it in depth? [/INST] Phimosis (from Greek φίμωσις phimōsis muzzling.) is a condition in which the ridged band of the foreskin of the penis cannot stretch to allow it to be pulled back past the glans. A balloon-like swelling under the foreskin may occur with urination. In teenagers and adults, it may result in pain during an erection, but is otherwise not painful. Those affected are at greater risk of inflammation of the glans, known as balanitis, and other complications.In young children, it is normal not to be able to pull back the foreskin at all. Over 90% of cases resolve by the age of seven, although full retraction is still prevented by preputial adhesions in over half at this age. Occasionally, phimosis may be caused by an underlying condition such as scarring due to balanitis or balanitis xerotica obliterans. This can typically be diagnosed by seeing scarring of the opening of the foreskin.Also, other pathologies should be considered in the differential diagnosis, such as congenital megaprepuce. Typically, the condition resolves without treatment by the age of 18. Efforts to pull back the foreskin during the early years of a young males life should not be attempted. For those in whom the condition does not improve further, time can be given or a steroid cream may be used to attempt to loosen the tight skin. If this method, combined with stretching exercises, is not effective, then other treatments such as circumcision may be recommended. A potential complication of phimosis is paraphimosis, where the tight foreskin becomes trapped behind the glans.

Signs and symptoms
At birth, the inner layer of the foreskin is sealed to the glans penis. The foreskin is usually non-retractable in early childhood, and some males may reach the age of 18 before their foreskin can be fully retracted.Medical associations advise not to retract the foreskin of an infant, in order to prevent scarring.  Some argue that non-retractability may "be considered normal for males up to and including adolescence."  Hill states that full retractability of the foreskin may not be achieved until late childhood or early adulthood.  A Danish survey found that the mean age of first foreskin retraction is 10.4 years.Rickwood, as well as other authors, has suggested that true phimosis is over-diagnosed due to failure to distinguish between normal developmental non-retractability and a pathological condition. Some authors use the terms "physiologic" and "pathologic" to distinguish between these types of phimosis; others use the term "non-retractile foreskin" to distinguish this developmental condition from pathologic phimosis.In some cases a cause may not be clear, or it may be difficult to distinguish physiological phimosis from pathological phimosis if an infant appears to have discomfort while urinating or demonstrates obvious ballooning of the foreskin. However, ballooning does not indicate urinary obstruction.In women, a comparable condition is known as "clitoral phimosis", whereby the clitoral hood cannot be retracted, limiting exposure of the glans clitoridis.

Severity
Score 1: full retraction of foreskin, tight behind the glans.
Score 2: partial exposure of glans, prepuce (not congenital adhesions) limiting factor.
Score 3: partial retraction, meatus just visible.
Score 4: slight retraction, but some distance between tip and glans, i.e. neither meatus nor glans can be exposed.
Score 5: absolutely no retraction of the foreskin.

Cause
There are three mechanical conditions that prevent foreskin retraction:

The tip of the foreskin is too narrow to pass over the glans penis. This is normal in children and adolescents.

The inner surface of the foreskin is fused with the glans penis. This is normal in children and adolescents but abnormal in adults.

The frenulum is too short to allow complete retraction of the foreskin (a condition called frenulum breve).Pathological phimosis (as opposed to the natural non-retractability of the foreskin in childhood) is rare, and the causes are varied. Some cases may arise from balanitis (inflammation of the glans penis).Lichen sclerosus et atrophicus (thought to be the same condition as balanitis xerotica obliterans) is regarded as a common (or even the main) cause of pathological phimosis. This is a skin condition of unknown origin that causes a whitish ring of indurated tissue (a cicatrix) to form near the tip of the prepuce. This inelastic tissue prevents retraction.
Phimosis may occur after other types of chronic inflammation (such as balanoposthitis), repeated catheterization, or forcible foreskin retraction.Phimosis may also arise in untreated diabetics due to the presence of glucose in their urine giving rise to infection in the foreskin.Beaugé noted that unusual masturbation practices, such as thrusting against the bed or rubbing the foreskin forward may cause phimosis. Patients are advised to stop exacerbating masturbation techniques and are encouraged to masturbate by moving the foreskin up and down so as to mimic more closely the action of sexual intercourse. After giving this advice Beaugé noted not once did he have to recommend circumcision.Phimosis in older children and adults can vary in severity, with some able to retract their foreskin partially (relative phimosis), while others are completely unable to retract their foreskin, even when the penis is in a flaccid state (full phimosis).

Treatment
Physiologic phimosis, common in males 10 years of age and younger, is normal, and does not require intervention. Non-retractile foreskin usually becomes retractable during the course of puberty.If phimosis in older children or adults is not causing acute and severe problems, nonsurgical measures may be effective. Choice of treatment is often determined by whether circumcision is viewed as an option of last resort or as the preferred course.

Nonsurgical
Patients are advised to stop exacerbating masturbation techniques and are encouraged to masturbate by moving the foreskin up and down so as to mimic more closely the action of sexual intercourse. After giving this advice Beaugé noted not once did he have to recommend circumcision.
Topical steroid creams such as betamethasone, mometasone furoate and cortisone are effective in treating phimosis and should be considered before circumcision.  It is theorized that the steroids work by reducing the bodys inflammatory and immune responses, and also by thinning the skin.
Gently stretching of the foreskin can be accomplished manually. Skin that is under tension expands by growing additional cells. There are different ways to stretch the phimosis. If the opening of the foreskin is already large enough, the foreskin is rolled over two fingers and these are carefully pulled apart. If the opening is still too small, flesh tunnels can be used. These are inserted into the foreskin opening and should preferably be made of silicone so that they can be folded when inserted and so that they do not interfere when worn. The diameter is gradually increased until the foreskin can be retracted without difficulty. Even phimosis with a diameter of less than a millimetre can be stretched with these rings. Rings in different sizes are also available as stretching sets. Studies involving treating phimosis using topical steroids in conjunction with stretching exercises have reported success rates of up to 96%. However, other sources claim "wildly variable reported failure rates (5 – 33 %) and lack of follow-up to adulthood."

Surgical
Surgical methods range from the complete removal of the foreskin to more minor operations to relieve foreskin tightness:

Dorsal slit (superincision) is a single incision along the upper length of the foreskin from the tip to the corona, exposing the glans without removing any tissue.
Ventral slit (subincision) is an incision along the lower length of the foreskin from the tip of the frenulum to the base of the glans, removing the frenulum in the process. Often used when frenulum breve occurs alongside the phimosis.
Preputioplasty, in which a limited dorsal slit with transverse closure is made along the constricting band of skin, can be an effective alternative to circumcision. It has the advantage of only limited pain and a short healing duration relative to circumcision, while also avoiding cosmetic effects.
Circumcision is sometimes performed for phimosis, and is an effective treatment; however, this method has become less common as of 2012.While circumcision prevents phimosis, studies of the incidence of healthy infants circumcised for each prevented case of phimosis are inconsistent.

Prognosis
The most acute complication is paraphimosis. In this condition, the glans is swollen and painful, and the foreskin is immobilized by the swelling in a partially retracted position </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Ingrown nail and can you explain it in depth? [/INST] An ingrown nail, also known as onychocryptosis from Greek: ὄνυξ (onyx) nail and κρυπτός (kryptos) hidden, is a common form of nail disease. It is an often painful condition in which the nail grows so that it cuts into one or both sides of the paronychium or nail bed. While ingrown nails can occur in the nails of both the hands and the feet, they occur most commonly with the toenails (as opposed to fingernails), and for the most part are only problematic and painful on the big toe.
A common conception is that the nail enters into the paronychium, but an "ingrown toenail" can simply be overgrown toe skin. The condition starts first from a microbial inflammation of the paronychium, and then a granuloma, which results in a nail buried inside of the granuloma. A true ingrown toenail is caused by actual penetration of flesh by a sliver of toenail.

Signs and symptoms
Symptoms of an ingrown nail include pain along the margins of the nail (caused by hypergranulation that occurs around the aforementioned margins), worsening of pain when wearing tight footwear, and sensitivity to pressure of any kind, even the weight of bedsheets. Bumping of an affected toe can produce sharp and even excruciating pain as the tissue is punctured further by the nail. By the very nature of the condition, ingrown nails become easily infected unless special care is taken early to treat the condition by keeping the area clean. Signs of infection include redness and swelling of the area around the nail, drainage of pus and watery discharge tinged with blood. The main symptom is swelling at the base of the nail on the ingrowing side (though it may be both sides).
Onychocryptosis should not be confused with a similar nail disorder, convex nail, nor with other painful conditions such as involuted nails, nor with the presence of small corns, callus or debris down the nail sulci (grooves on either side).

Causes
The main contributor to onychocryptosis is footwear, particularly ill-fitting shoes with inadequate toe box room and tight stockings that apply pressure to the top or side of the foot. Other factors may include the damp atmosphere of enclosed shoes, which soften the nail-plate and cause swelling on the epidermal keratin (eventually increasing the convex arch permanently), genetics, trauma and disease. Improper cutting of the nail may cause the nail to cut into the side-fold skin from growth and impact, whether or not the nail is truly "ingrown". The nail bends inwards or upwards depending on the angle of its cut. If the cutting tool, such as scissors, is at an altitude in which the lower blade is closer to the toe than the upper blade, the toenail will tend to grow upwards from its base, and vice versa. The process is visible along the nail as it grows, appearing as a warp advancing to the end of the nail. The upper corners turn more easily than the center of the nail tip. Holding the tool at the same angle for all nails may induce these conditions; as the nail turns closer to the skin, it becomes harder to fit the lower blade in the right attitude under the nail. When cutting a nail, it is not just the correct angle that is important, but also how short it is cut. A shorter cut will bend the nail more, unless the cut is even on both top and bottom of the nail.

Causes may include:

Shoes causing a bunching of the toes in the developmental stages of the foot (frequently in people under 21), which can cause the nail to curl and dig into the skin. This is particularly the case in ill-fitting shoes that are too narrow or too short, but any toed shoes may cause an ingrown nail.
Poor nail care, including cutting the nail too short, rounded off at the tip or peeled off at the edges instead of being cut straight across.
Broken toenails.
Trauma to the nail plate or toe, which can occur by dropping objects on or stubbing the toenail, or by the nail protruding through the shoe (as during sports or other vigorous activity), can cause the flesh to become injured and the nail to grow irregularly and press into the flesh.
Predisposition, such as abnormally shaped nail beds, nail deformities caused by diseases or a genetic susceptibility, increases the chance of an ingrown nail, but the ingrowth cannot occur without pressure from a shoe.
A bacterial infection, treatable with antibiotics.One study compared patients with ingrown toenails to healthy controls and found no difference in the shape of toenails between those of patients and of the control group. The study suggested that treatment should not be based on the correction of a non-existent nail deformity. In some cases, however, there is nail deformity.Ingrown toenails are caused by weight-bearing (activities such as walking, running, etc.) in patients that have too much soft skin tissue on the sides of their nail. Weight bearing causes this excessive amount of skin to bulge up along the sides of the nail. The pressure on the skin around the nail results in the tissue being damaged, resulting in swelling, redness and infection. Many treatments are directed at the nail itself and often include partial or full removal of the healthy nail. However, failure to treat the cutaneous condition can result in a return of the ingrowth and a deformity or mutilation of the nail.

Prevention
The most common digit to become ingrown is the big toe, but ingrowth can occur on any nail. Ingrown nails can be avoided by cutting nails straight across; not along a curve, not too short and no shorter than the flesh around it. Footwear that is too small or too narrow, or with too shallow a "toe box", will exacerbate any underlying problem with a toenail. Sharp square corners may be uncomfortable and cause snagging on socks. Proper cutting leaves the leading edge of the nail free of the flesh, precluding it from growing into the toe. Filing of the corner is reasonable. Some nails require cutting of the corners far back to remove edges that dig into the flesh; this is often done as a partial wedge resection by a podiatrist. Ingrown toe nails can be caused by injury, commonly blunt trauma in which the flesh is pressed against the nail causing a small cut that swells. Injury to the nail can cause it to grow abnormally, making it wider or thicker than normal, or even bulged or crooked.

Management
The treatment of an ingrown toenail partly depends on its severity.

Conservative treatment
Mild to moderate cases are often treated conservatively with warm water and epsom salt soaks, antibacterial ointment and the use of dental floss. If conservative treatment of a minor ingrown toenail does not succeed, or if the ingrown toenail is severe, surgical treatment may be required. A "gutter splint" may be improvised by slicing a cotton-tipped wooden applicator diagonally to form a bevel and using this to insert a wisp of cotton from the applicator head under the nail to lift it from the underlying skin after a foot soak.

Nail bracing
Nail bracing is more conservative than surgery, but less widely used. Nail braces work by gently lifting the sides of the toenail and eventually retraining the nail to grow to a flatter shape over time. The total time needed for the nail to be reshaped is one full nail growth or about 18 months.  There are two main types of nail braces: adhesive and hooked. Adhesive nail braces are generally made of a thin strip of composite material that is glued to the top of the nail. The strip naturally tries to return to a flat state and lifts the edges of the nails in the process. Hooked nail braces consist of a hook (usually made of dental wire) placed under either side of the nail with some type of tensioning system pulling the hooks together.
Because of the curved shape of the nail, the tensioning device rests on the higher middle of the nail by applying upward pressure to the sides of the nail. In studies of diabetics, who need to avoid surgery when possible, nail bracing was found to be effective at providing immediate, as well as long-term, relief.

Surgery
Surgical treatment for an ingrown nail is carried out by a podiatrist, a foot and ankle specialist. This is typically an in-office procedure requiring local anesthesia and special surgical instruments. The surgical approach is the removal of the offending part of the nail plate known as a wedge resection. If the ingrown toenail recurs despite this treatment, destruction of the sides of the nail with chemicals or excision is done; this is known as a matrixectomy. Antibiotics may be used after the procedure but are not recommended, as they may delay healing. Surgical treatment for ingrown nails is more effective at preventing the nail from regrowing inwards compared to non-surgical treatments.

References
Further reading
Aksakal AB, Ozsoy E, Gürer M (2003). "Silicone gel sheeting for the management and prevention of onychocryptosis". Dermatol Surg. 29 (3): 261–4. doi:10.1046/j.1524-4725.2003.29061.x. PMID 12614420. S2CID 28708033.
Boll OF (1945). "Surgical correction of ingrowing toenails". J Natl Assoc Chiroprod. 35: 8–9.
Chapeskie H (2008). "Ingrown toenail or overgrown toe skin?". Canadian Family Physician. 54 (11): 1561–1562. PMC 2592332. PMID 19005128.
Kominsky SJ, Daniels MD (2000) </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Opisthotonus and can you explain it in depth? [/INST] Opisthotonus or opisthotonos (from Ancient Greek: ὄπισθεν, romanized: opisthen, lit. behind and τόνος, tonos, tension) is a state of severe hyperextension and spasticity in which an individuals head, neck and spinal column enter into a complete "bridging" or "arching" position.This extreme arched pose is an extrapyramidal effect and is caused by spasm of the axial muscles along the spinal column. It has been shown to occur naturally in birds, snakes suffering from advanced boid inclusion body disease, and placental mammals, among existing animals; it is observed in some articulated dinosaur fossils.

Causes
Opisthotonus is a symptom of some cases of severe cerebral palsy and traumatic brain injury or as a result of the severe muscular spasms associated with tetanus. It can be a feature of severe acute hydrocephalus, poisoning, and drowning.

Infants
Opisthotonus is more pronounced in infants </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Intussusception and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Facial nerve paralysis and can you explain it in depth? [/INST] Facial nerve paralysis is a common problem that involves the paralysis of any structures innervated by the facial nerve. The pathway of the facial nerve is long and relatively convoluted, so there are a number of causes that may result in facial nerve paralysis. The most common is Bells palsy, a disease of unknown cause that may only be diagnosed by exclusion of identifiable serious causes.

Signs and symptoms
Facial nerve paralysis is characterised by facial weakness, usually only in one side of the face, with other symptoms possibly including loss of taste, hyperacusis and decreased salivation and tear secretion. Other signs may be linked to the cause of the paralysis, such as vesicles in the ear, which may occur if the facial palsy is due to shingles. Symptoms may develop over several hours. : 1228  Acute facial pain radiating from the ear may precede the onset of other symptoms. : 2585

Causes
Bells palsy
Bells palsy is the most common cause of acute facial nerve paralysis. There is no known cause of Bells palsy, although it has been associated with herpes simplex infection. Bells palsy may develop over several days, and may last several months, in the majority of cases recovering spontaneously. It is typically diagnosed clinically, in patients with no risk factors for other causes, without vesicles in the ear, and with no other neurological signs. Recovery may be delayed in the elderly, or those with a complete paralysis. Bells palsy is often treated with corticosteroids.

Infection
Lyme disease, an infection caused by Borrelia burgdorferi bacteria and spread by ticks, can account for about 25% of cases of facial palsy in areas where Lyme disease is common. In the U.S., Lyme is most common in the New England and Mid-Atlantic states and parts of Wisconsin and Minnesota, but it is expanding into other areas. The first sign of about 80% of Lyme infections, typically one or two weeks after a tick bite, is usually an expanding rash that may be accompanied by headaches, body aches, fatigue, or fever. In up to 10-15% of Lyme infections, facial palsy appears several weeks later, and may be the first sign of infection that is noticed, as the Lyme rash typically does not itch and is not painful. Lyme disease is treated with antibiotics.Reactivation of herpes zoster virus, as well as being associated with Bells palsy, may also be a direct cause of facial nerve palsy. Reactivation of latent virus within the geniculate ganglion is associated with vesicles affecting the ear canal, and termed Ramsay Hunt syndrome type II. In addition to facial paralysis, symptoms may include ear pain and vesicles, sensorineural hearing loss, and vertigo. Management includes antiviral drugs and oral steroids.
Otitis media is an infection in the middle ear, which can spread to the facial nerve and inflame it, causing compression of the nerve in its canal. Antibiotics are used to control the otitis media, and other options include a wide myringotomy (an incision in the tympanic membrane) or decompression if the patient does not improve.
Chronic otitis media usually presents in an ear with chronic discharge (otorrhea), or hearing loss, with or without ear pain (otalgia). Once suspected, there should be immediate surgical exploration to determine if a cholesteatoma has formed as this must be removed if present.  Inflammation from the middle ear can spread to the canalis facialis of the temporal bone - through this canal travels the facial nerve together with the statoacoustisus nerve. In the case of inflammation the nerve is exposed to edema and subsequent high pressure, resulting in a periferic type palsy.

Trauma
In blunt trauma, the facial nerve is the most commonly injured cranial nerve. Physical trauma, especially fractures of the temporal bone, may also cause acute facial nerve paralysis. Understandably, the likelihood of facial paralysis after trauma depends on the location of the trauma. Most commonly, facial paralysis follows temporal bone fractures, though the likelihood depends on the type of fracture.
Transverse fractures in the horizontal plane present the highest likelihood of facial paralysis (40-50%). Patients may also present with blood behind the tympanic membrane, sensory deafness, and vertigo; the latter two symptoms due to damage to vestibulocochlear nerve and the inner ear. Longitudinal fracture in the vertical plane present a lower likelihood of paralysis (20%). Patients may present with blood coming out of the external auditory meatus), tympanic membrane tear, fracture of external auditory canal, and conductive hearing loss. In patients with mild injuries, management is the same as with Bells palsy – protect the eyes and wait. In patients with severe injury, progress is followed with nerve conduction studies. If nerve conduction studies show a large (>90%) change in nerve conduction, the nerve should be decompressed. The facial paralysis can follow immediately the trauma due to direct damage to the facial nerve, in such cases a surgical treatment may be attempted. In other cases the facial paralysis can occur a long time after the trauma due to oedema and inflammation. In those cases steroids can be a good help.

Tumors
A tumor compressing the facial nerve anywhere along its complex pathway can result in facial paralysis. Common culprits are facial neuromas, congenital cholesteatomas, hemangiomas, acoustic neuromas, parotid gland neoplasms, or metastases of other tumours.Often, since facial neoplasms have such an intimate relationship with the facial nerve, removing tumors in this region becomes perplexing as the physician is unsure how to manage the tumor without causing even more palsy. Typically, benign tumors should be removed in a fashion that preserves the facial nerve, while malignant tumors should always be resected along with large areas of tissue around them, including the facial nerve.  While this will inevitably lead to heightened paralysis, safe removal of a malignant neoplasm is worth the often treatable palsy that follows.  In the best case scenario, paralysis can be corrected with techniques including hypoglossal-facial nerve anastomosis, end-to-end nerve repair, cross facial nerve grafting, or muscle transfer/transposition techniques, such as the gracilis free muscle transfer.
Patients with facial nerve paralysis resulting from tumours usually present with a progressive, twitching paralysis, other neurological signs, or a recurrent Bells palsy-type presentation.
The latter should always be suspicious, as Bells palsy should not recur. A chronically discharging ear must be treated as a cholesteatoma until proven otherwise; hence, there must be immediate surgical exploration. Computed tomography (CT) or magnetic resonance (MR) imaging should be used to identify the location of the tumour, and it should be managed accordingly.
Other neoplastic causes include leptomeningeal carcinomatosis.

Stroke
Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus. The facial nucleus itself can be affected by infarcts of the pontine arteries. Unlike peripheral facial palsy, central facial palsy does not affect the forehead, because the forehead is served by nerves coming from both motor cortexes.

Other
Other causes may include:

Diabetes mellitus
Facial nerve paralysis, sometimes bilateral, is a common manifestation of sarcoidosis of the nervous system, neurosarcoidosis.
Bilateral facial nerve paralysis may occur in Guillain–Barré syndrome, an autoimmune condition of the peripheral nervous system.
Moebius syndrome is a bilateral facial paralysis resulting from the underdevelopment of the VII cranial nerve (facial nerve), which is present at birth. The VI cranial nerve, which controls lateral eye movement, is also affected, so people with Moebius syndrome cannot form facial expression or move their eyes from side to side. Moebius syndrome is extremely rare, and its cause or causes are not known.
Facial piercings, namely eyebrow piercings or tongue piercings, can in very rare cases cause damage to the facial nerve.

Diagnosis
A medical history and physical examination, including a neurological examination, are needed for diagnosis. The first step is to observe what parts of the face do not move normally when the person tries to smile, blink, or raise the eyebrows. If the forehead wrinkles normally, a diagnosis of central facial palsy is made, and the person should be evaluated for stroke. Otherwise, the diagnosis is peripheral facial palsy, and its cause needs to be identified, if possible. Ramsey Hunts syndrome causes pain and small blisters in the ear on the same side as the palsy. Otitis media, trauma, or post-surgical complications may alternatively become apparent from history and physical examination. If there is a history of trauma, or a tumour is suspected, a CT scan or MRI may be used to clarify its impact. Blood tests or x-rays may be ordered depending on suspected causes. The likelihood that the facial palsy is caused by Lyme disease should be estimated, based on recent history of outdoor activities in likely tick habitats during warmer months, recent history of rash or symptoms such as headache and fever, and whether the palsy affects both sides of the face (much more common in Lyme than in Bells palsy). If that likelihood is more than negligible, a serological test for Lyme disease should be performed. If the test is positive, the diagnosis is Lyme disease. If no cause is found, the diagnosis is Bells Palsy.

Classification
Facial nerve paralysis may be divided into supranuclear and infranuclear lesions </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Biliary sludge and can you explain it in depth? [/INST] Biliary sludge refers to a viscous mixture of small particles derived from bile. These sediments consist of cholesterol crystals, calcium salts, calcium bilirubinate, mucin, and other materials.

Signs and symptoms
Complications
Biliary sludge may cause complications such as biliary colic, acute cholecystitis, acute cholangitis, and acute pancreatitis.

Cause
Biliary sludge has been associated with pregnancy, rapid weight loss, total parenteral nutrition, drugs such as ceftriaxone and octreotide, solid organ transplantation, and gastric surgery. In many of these conditions, it is thought that the impairment in the contractility of the gallbladder leads to the formation of the sludge.

Pathophysiology
The pathophysiology of biliary sludge formation is likely related to gallbladder dysmotility </s>