<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Absence seizure and explain in detail? [/INST] Absence seizures are one of several kinds of generalized seizures. These seizures are sometimes referred to as petit mal seizures (from the French for "little illness", a term dating from the late 18th century). Absence seizures are characterized by a brief loss and return of consciousness, generally not followed by a period of lethargy (i.e. without a notable postictal state). Absence seizure is very common in children. It affects both sides of the brain.

Epidemiology
Absence seizures affect between 0.7 and 4.6 per 100,000 in the general population and 6% to 8% in children younger than 15 years. Childhood absence seizures account for 10% to 17% of all absence seizures. Onset is between 4 and 10 years and peaks at 5 to 7 years. It is more common in girls than in boys.

Etiology
An absence seizure is specifically caused by multifactorial inheritance. The voltage-gated T-type calcium channel is regulated by GABRG2, GABRG3, and CACNA1A2 genes. Inheritance of these genes is involved in etiology of absence seizure. The factors that trigger an absence seizure are lack of sleep and compliance, drinking alcohol, and benzodiazepine withdrawal, and use of medication that reduces the threshold of seizure such as Isoniazid, antipsychotics.

Signs and symptoms
The clinical manifestations of absence seizures vary significantly among patients. Impairment of consciousness is the essential symptom, and may be the only clinical symptom, but this can be combined with other manifestations.  The hallmark of the absence seizures is abrupt and sudden-onset impairment of consciousness, interruption of ongoing activities, a blank stare, possibly a brief upward rotation of the eyes. If the patient is speaking, speech is slowed or interrupted; if walking, they stand transfixed; if eating, the food will stop on its way to the mouth. Usually, the patient will be unresponsive when addressed. In some cases, attacks are aborted when the patient is called.  The attack lasts from a few seconds to half a minute and evaporates as rapidly as it commenced. Absence seizures generally are not followed by a period of disorientation or lethargy (postictal state), in contrast to the majority of seizure disorders.
Absence with impairment of consciousness only as per the above description.
Absence with mild clonic components.  Here the onset of the attack is indistinguishable from the above, but clonic components may occur in the eyelids, at the corner of the mouth, or in other muscle groups which may vary in severity from almost imperceptible movements to generalised myoclonic jerks. Objects held in the hand may be dropped.
Absence with atonic components.  Here there may be a diminution in tone of muscles subserving posture as well as in the limbs leading to dropping of the head, occasionally slumping of the trunk, dropping of the arms, and relaxation of the grip.  Rarely tone is sufficiently diminished to cause this person to fall.
Absence with tonic components.  Here during the attack tonic muscular contraction may occur, leading to increase in muscle tone which may affect the extensor muscles or the flexor muscles symmetrically or asymmetrically.  If the patient is standing, the head may be drawn backward and the trunk may arch. This may lead to retropulsion, which may cause eyelids to twitch rapidly; eyes may jerk upwards or the patients head may rock back and forth slowly, as if nodding. The head may tonically draw to one or another side.
Absence with automatisms.  Purposeful or quasi-purposeful movements occurring in the absence of awareness during an absence attack are frequent and may range from lip licking and swallowing to clothes fumbling or aimless walking.  If spoken to, the patient may grunt, and when touched or tickled may rub the site.  Automatisms are quite elaborate and may consist of combinations of the above described movements or may be so simple as to be missed by casual observation.
Absence with autonomic components.  These may be pallor, and less frequently flushing, sweating, dilatation of pupils and incontinence of urine.Mixed forms of absence frequently occur.
These seizures can happen a few times a day or in some cases, hundreds of times a day, to the point that the person cannot concentrate in school or in other situations requiring sustained, concentrated attention.

Risk factors
Typical absences are easily induced by hyperventilation (over-breathing) in more than 90% of people with typical absences. This is a reliable test for the diagnosis of absence seizures: a patient suspected of typical absences should be asked to hyperventilate for three minutes, counting breaths. During hyperventilation, the oxygen and carbon dioxide level will become abnormal. This results in weakening of electrical signal which leads to a reduction in the seizure threshold. Intermittent photic stimulation may precipitate or facilitate absence seizures; eyelid myoclonia is a common clinical feature.A specific mechanism difference exists in absence seizures in that T-type Ca++ channels are believed to be involved. Ethosuximide is specific for these channels and thus it is not effective for treating other types of seizures. Valproate and gabapentin (among others) have multiple mechanisms of action including blockade of T-type Ca++ channels, and are useful in treating multiple seizure types. Gabapentin can aggravate absence seizures.

Pathophysiology
The corticothalamic cortical circuit plays an important role in the pathophysiology of absence seizure. Some of the neurons are important in their occurrence. They are

Cortical glutamatergic neurons
Thalamic relay neurons
Neurons of thalamic nucleus reticularisAbnormal oscillatory rhythms develop in the thalamic nucleus reticularis. This causes inhibition of GABAergic neurotransmission and excitation of glutamate neurotransmission. Abnormal oscillatory spikes are produced by the low threshold T-type calcium channel. This explains how inheritance of gene code for T-type calcium channel leads to an absence seizure. Antiepileptic drugs such as Gabapentin, Tiagabine and Vigabatrin cause inhibition of GABA results in exacerbation of absence seizures.

Diagnosis
The primary diagnostic test for absence seizures is electroencephalography (EEG). However, brain scans such as by an MRI can help rule out other diseases, such as a stroke or a brain tumor.During EEG, hyperventilation can be used to provoke these seizures. Ambulatory EEG monitoring over 24 hours can quantify the number of seizures per day and their most likely times of occurrence.Absence seizures are brief (usually less than 20 seconds) generalized epileptic seizures of sudden onset and termination. When someone experiences an absence seizure they are often unaware of their episode. Those most susceptible to this are children, and the first episode usually occurs between 4–12 years old. It is very rare that someone older will experience their first absence seizure. Episodes of absence seizures can often be mistaken for inattentiveness when misdiagnosed, and can occur 50–100 times a day. They can be so difficult to detect that some people may go months or years before being given a proper diagnosis. There are no known before or after effects of absence seizures.Absence seizures have two essential components:
Clinical - the impairment of consciousness (absence)
EEG - the EEG shows generalized spike-and-slow wave dischargesAbsence seizures are broadly divided into typical and atypical types:

Typical absence seizures usually occur in the context of idiopathic generalised epilepsies and an EEG shows fast >2.5 Hz generalised spike-wave discharges.  The prefix "typical" is to differentiate them from atypical absences rather than to characterise them as "classical" or characteristic of any particular syndrome.
Atypical absence seizures:
Occur only in the context of mainly severe symptomatic or cryptogenic epilepsies of children with learning difficulties who also have frequent seizures of other types, such as atonic, tonic and myoclonic.
Have slower onset and termination and changes in tone are more pronounced.
Have particular ictal characteristics: EEG is of slow (less than 2.5 Hz) spike and slow wave. The discharge is heterogeneous, often asymmetrical and may include irregular spike and slow wave complexes, fast and other paroxysmal activity. Background interictal EEG is usually abnormal.

Syndromes
Absence seizure syndromes are childhood absence epilepsy, epilepsy with myoclonic absences, juvenile absence epilepsy and juvenile myoclonic epilepsy. Other proposed syndromes are Jeavons syndrome (eyelid myoclonia with absences), and genetic generalised epilepsy with phantom absences.
Absence seizures are also known to occur to patients with porphyria and can be triggered by stress or other porphyrin-inducing factors.

Treatment
Treatment of patients with absence seizures only is mainly with ethosuximide or valproic acid, which are of equal efficacy controlling absences in around 75% of patients. Lamotrigine monotherapy is less effective, controlling absences in around 50% of patients.  This summary has been recently confirmed by Glauser et al. (2010), who studied the effects of ethosuximide, valproic acid, and lamotrigine in children with newly diagnosed childhood absence epilepsy. Drug dosages were incrementally increased until the child was free of seizures, the maximal allowable dose was reached, or a criterion indicating treatment failure was met. The primary outcome was freedom from treatment failure after 16 weeks of therapy; the secondary outcome was attentional dysfunction. After 16 weeks of therapy, the freedom-from-failure rates for ethosuximide and valproic acid were similar and were higher than the rate for lamotrigine. There were no significant differences between the three drugs with regard to discontinuation because of adverse events. Attentional dysfunction was more common with valproic acid than with ethosuximide.
If monotherapy fails or unacceptable adverse reactions appear, replacement of one by another of the three antiepileptic drugs is the alternative </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Meckels diverticulum and explain in detail? [/INST] A Meckels diverticulum, a true congenital diverticulum, is a slight bulge in the small intestine present at birth and a vestigial remnant of the omphalomesenteric duct (also called the vitelline duct or yolk stalk). It is the most common malformation of the gastrointestinal tract and is present in approximately 2% of the population, with males more frequently experiencing symptoms.
Meckels diverticulum was first explained by Fabricius Hildanus in the sixteenth century and later named after Johann Friedrich Meckel, who described the embryological origin of this type of diverticulum in 1809.

Signs and symptoms
The majority of people with a Meckels diverticulum are asymptomatic. An asymptomatic Meckels diverticulum is called a silent Meckels diverticulum. If symptoms do occur, they typically appear before the age of two years. The most common presenting symptom is painless rectal bleeding such as melaena-like black offensive stools, followed by intestinal obstruction, volvulus and intussusception. Occasionally, Meckels diverticulitis may present with all the features of acute appendicitis. Also, severe pain in the epigastric region is experienced by the person along with bloating in the epigastric and umbilical regions. At times, the symptoms are so painful that they may cause sleepless nights with acute pain felt in the foregut region, specifically in the epigastric and umbilical regions. In some cases, bleeding occurs without warning and may stop spontaneously. The symptoms can be extremely painful, often mistaken as just stomach pain resulting from not eating or constipation. Rarely, a Meckels diverticulum containing ectopic pancreatic tissue can present with abdominal pain and increased serum amylase levels, mimicking acute pancreatitis.

Complications
The lifetime risk for a person with Meckels diverticulum to develop certain complications is about 4–6%. Gastrointestinal bleeding, peritonitis or intestinal obstruction may occur in 15–30% of symptomatic people (Table 1). Only 6.4% of all complications require surgical treatment, and untreated Meckels diverticulum has a mortality rate of 2.5–15%.Table 1 – Complications of Meckels Diverticulum:

Bleeding
Bleeding of the diverticulum is most common in young children, especially in males who are less than 2 years of age. Symptoms may include bright red blood in stools (hematochezia), weakness, abdominal tenderness or pain, and even anaemia in some cases.Bleeding may be caused by:

Ectopic gastric or pancreatic mucosa:Where diverticulum contains embryonic remnants of mucosa of other tissue types.
Secretion of gastric acid or alkaline pancreatic juice from the ectopic mucosa leads to ulceration in the adjacent ileal mucosa i.e. peptic or pancreatic ulcer.
Pain, bleeding or perforation of the bowel at the diverticulum may result.
Mechanical stimulation may also cause erosion and ulceration.Gastrointestinal bleeding may be self-limiting but chronic bleeding may lead to iron deficiency anaemia.The appearance of stools may indicate the nature of the bleeding:

Tarry stools: Alteration of blood produced by slow bowel transit due to minor bleeding in upper gastrointestinal tract
Bright red blood stools: Brisk bleeding
Stools with blood streak: Anal fissure
"Currant jelly" stools: Ischaemia of the intestine leads to copious mucus production and may indicate that one part of the bowel invaginates into another intussusception.

Diverticulitis
Inflammation of the diverticulum can mimic symptoms of appendicitis, i.e., periumbilical tenderness and intermittent crampy abdominal pain. Perforation of the inflamed diverticulum can result in peritonitis. Diverticulitis can also cause adhesions, leading to intestinal obstruction.Diverticulitis may result from:

Association with the mesodiverticular band attaching to the diverticulum tip where torsion has occurred, causing inflammation and ischaemia.
Peptic ulceration resulting from ectopic gastric mucosa of the diverticulum
Following perforation by trauma or ingested foreign material e.g. stalk of vegetable, seeds or fish/chicken bone that become lodged in Meckels diverticulum.
Luminal obstruction due to tumors, enterolith, foreign body, causing stasis or bacterial infection.
Association with acute appendicitis

Intestinal obstruction
Symptoms: Vomiting, abdominal pain and severe or complete constipation.
The vitelline vessels remnant that connects the diverticulum to the umbilicus may form a fibrous or twisting band (volvulus), trapping the small intestine and causing obstruction. Localised periumbilical pain may be experienced in the right lower quadrant (like appendicitis).
"Incarceration": when a Meckels diverticulum is constricted in an inguinal hernia, forming a Littré hernia that obstructs the intestine.
Chronic diverticulitis causing stricture
Strangulation of the diverticulum in the obturator foramen.
Tumors e.g. carcinoma: direct spread of an adenocarcinoma arising in the diverticulum may lead to obstruction
Lithiasis, stones that are formed in Meckels diverticulum can:Extrude into the terminal ileum, leading to obstruction
Induce local inflammation and intussusception.The diverticulum itself or tumour within it may cause intussusception. For example, from the ileum to the colon, causing obstruction. Symptoms of this include "currant jelly" stools and a palpable lump in the lower abdomen. This occurs when the diverticulum inverts into the lumen of the ileum, due to either:An active peristaltic mechanism of the diverticulum that attempts to remove irritating factors
A passive process such as the transit of food

Umbilical anomalies
Anomalies between the diverticulum and umbilicus may include the presence of fibrous cord, cyst, fistula, or sinus, leading to:
Infection or excoriation of periumbilical skin, resulting in a discharging sinus
Recurrent infection and healing of sinus
Abscess formation in the abdominal wall
Fibrous cord increases the risk of volvulus formation and internal herniation

Neoplasm
Tumors in Meckels diverticulum may cause bleeding, acute abdominal pain, gastrointestinal obstruction, perforation or intussusception.
Benign tumors:Leiomyoma
Lipoma
Vascular and neuromuscular hamartomaMalignant tumors:Carcinoids: most common, 44%
Mesenchymal tumors: Leiomyosarcoma, peripheral nerve sheath and gastrointestinal stromal tumors, 35%
Adenocarcinoma, 16%
Desmoplastic small round cell tumor

Other complications
A diverticulum inside a Meckels diverticulum (daughter diverticula)
Stones and phytobezoar (a bezoar of vegetable fibers) in Meckels diverticulum
Vesicodiverticular fistula

Pathophysiology
The omphalomesenteric duct (omphaloenteric duct, vitelline duct, or yolk stalk) normally connects the embryonic midgut to the yolk sac ventrally, providing nutrients to the midgut during embryonic development. The vitelline duct narrows progressively and disappears between the 5th and 8th weeks of gestation.In Meckels diverticulum, the proximal part of vitelline duct fails to regress and involute, which remains as a remnant of variable length and location. The solitary diverticulum lies on the antimesenteric border of the ileum (opposite to the mesenteric attachment) and extends into the umbilical cord of the embryo. The left and right vitelline arteries originate from the primitive dorsal aorta, and travel with the vitelline duct. The right becomes the superior mesenteric artery that supplies a terminal branch to the diverticulum, while the left involutes. Having its own blood supply, Meckels diverticulum is susceptible to obstruction or infection.
Meckels diverticulum is located in the distal ileum, usually within 60–100 cm (2 feet) of the ileocecal valve. This blind segment or small pouch is about 3–6 cm (2 inch) long and may have a greater lumen diameter than that of the ileum. It runs antimesenterically and has its own blood supply. It is a remnant of the connection from the yolk sac to the small intestine present during embryonic development. It is a true diverticulum, consisting of all 3 layers of the bowel wall which are mucosa, submucosa and muscularis propria.As the vitelline duct is made up of pluripotent cell lining, Meckels diverticulum may harbor abnormal tissues, containing embryonic remnants of other tissue types. Jejunal, duodenal mucosa or Brunners tissue were each found in 2% of ectopic cases. Heterotopic rests of gastric mucosa and pancreatic tissue are seen in 60% and 6% of cases respectively. Heterotopic means the displacement of an organ from its normal anatomic location. Inflammation of this Meckels diverticulum may mimic appendicitis. Therefore, during appendectomy, ileum should be checked for the presence of Meckels diverticulum, if it is found to be present it should be removed along with appendix.A memory aid is the rule of 2s:
2% (of the population)
2 feet (proximal to the ileocecal valve)
2 inches (in length)
2 types of common ectopic tissue (gastric and pancreatic)
2 years is the most common age at clinical presentation
2:1 male:female ratioHowever, the exact values for the above criteria range from 0.2–5 (for example, prevalence is probably 0.2–4%).It can also be present as an indirect hernia, typically on the right side, where it is known as a "Hernia of Littré". A case report of strangulated umbilical hernia with Meckels diverticulum has also been published in the literature. Furthermore, it can be attached to the umbilical region by the vitelline ligament, with the possibility of vitelline cysts, or even a patent vitelline canal forming a vitelline fistula when the umbilical cord is cut. Torsions of intestine around the intestinal stalk may also occur, leading to obstruction, ischemia, and necrosis.

Diagnosis
A technetium-99m (99mTc) pertechnetate scan, also called Meckel scan or nuclear scintigraphy scan, is the investigation of choice to diagnose Meckels diverticula in children. This scan detects gastric mucosa; since approximately 50% of symptomatic Meckels diverticula have ectopic gastric or pancreatic cells contained within them, this is displayed as a spot on the scan distant from the stomach itself. In children, this scan is highly accurate and noninvasive, with 95% specificity and 85% sensitivity; however, in adults the test is only 9% specific and 62% sensitive.
Patients with these misplaced gastric cells may experience peptic ulcers as a consequence. Therefore, other tests such as colonoscopy and screenings for bleeding disorders should be performed, and angiography can assist in determining the location and severity of bleeding </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Foreign body in alimentary tract and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Adhesive capsulitis of the shoulder and explain in detail? [/INST] Adhesive capsulitis, also known as frozen shoulder, is a condition associated with shoulder pain and stiffness. It is a common shoulder ailment that is marked by pain and a loss of range of motion, particularly in external rotation. There is a loss of the ability to move the shoulder, both voluntarily and by others, in multiple directions. The shoulder itself, however, does not generally hurt significantly when touched. Muscle loss around the shoulder may also occur. Onset is gradual over weeks to months. Complications can include fracture of the humerus or biceps tendon rupture.The cause in most cases is unknown. The condition can also occur after injury or surgery to the shoulder. Risk factors include diabetes and thyroid disease. The underlying mechanism involves inflammation and scarring. The diagnosis is generally based on a persons symptoms and a physical exam. The diagnosis may be supported by an MRI. Adhesive capsulitis has been linked to diabetes and hypothyroidism, according to research. Adhesive capsulitis was five times more common in diabetic patients than in the control group, according to a meta-analysis published in 2016.The condition often resolves itself over time without intervention but this may take several years. While a number of treatments, such as NSAIDs, physical therapy, steroids, and injecting the shoulder at high pressure, may be tried, it is unclear what is best. Surgery may be suggested for those who do not get better after a few months. About 4% of people are affected. It is more common in people 40–60 years of age and in women.

Signs and symptoms
Symptoms include shoulder pain and limited range of motion although these symptoms are common in many shoulder conditions. An important symptom of adhesive capsulitis is the severity of stiffness that often makes it nearly impossible to carry out simple arm movements. Pain due to frozen shoulder is usually dull or aching and may be worse at night and with any motion.The symptoms of primary frozen shoulder have been described as having three or four stages. Sometimes a prodromal stage is described that can be present up to three months prior to the shoulder freezing. During this stage people describe sharp pain at end ranges of motion, achy pain at rest, and sleep disturbances.

Stage one: The "freezing" or painful stage, which may last from six weeks to nine months, and in which the patient has a slow onset of pain. As the pain worsens, the shoulder loses motion.
Stage two: The "frozen" or adhesive stage is marked by a slow improvement in pain but the stiffness remains. This stage generally lasts from four to twelve months.
Stage three: The "thawing" or recovery, when shoulder motion slowly returns toward normal. This generally lasts from 5 to 26 months.Physical exam findings include restricted range of motion in all planes of movement in both active and passive range of motion. This contrasts with conditions such as shoulder impingement syndrome or rotator cuff tendinitis in which the active range of motion is restricted but passive range of motion is normal. Some exam maneuvers of the shoulder may be impossible due to pain.

Causes
The causes of adhesive capsulitis are incompletely understood; however, there are several factors associated with higher risk. Risk factors for secondary adhesive capsulitis include injury or surgery leading to prolonged immobility. Risk factors for primary, or idiopathic adhesive capsulitis include many systemic diseases, such as diabetes mellitus, stroke, lung disease, connective tissue diseases, thyroid disease, heart disease, autoimmune disease, and Dupuytrens contracture. Both type 1 diabetes and type 2 diabetes are risk factors for the condition.

Primary
Primary adhesive capsulitis, also known as idiopathic adhesive capsulitis, occurs with no known trigger. It is more likely to develop in the non-dominant arm.

Secondary
Adhesive capsulitis is called secondary when it develops after an injury or surgery to the shoulder.

Pathophysiology
The underlying pathophysiology is incompletely understood, but is generally accepted to have both inflammatory and fibrotic components. The hardening of the shoulder joint capsule is central to the disease process. This is the result of scar tissue (adhesions) around the joint capsule. There also may be a reduction in synovial fluid, which normally helps the shoulder joint, a ball and socket joint, move by lubricating the gap between the humerus and the socket in the shoulder blade. In the painful stage (stage I), there is evidence of inflammatory cytokines in the joint fluid. Later stages are characterized by dense collagenous tissue in the joint capsule.Under the microscope, the appearance of the affected shoulder joint capsule tissue is similar to the appearance of the tissue that restricts finger movement in Dupuytrens contracture.

Diagnosis
Adhesive capsulitis can be diagnosed by history and physical exam. It is often a diagnosis of exclusion, as other causes of shoulder pain and stiffness must first be ruled out. On physical exam, adhesive capsulitis can be diagnosed if limits of the active range of motion are the same or similar to the limits to the passive range of motion. The movement that is most severely inhibited is external rotation of the shoulder.Imaging studies are not required for diagnosis, but may be used to rule out other causes of pain. Radiographs will often be normal, but imaging features of adhesive capsulitis can be seen on ultrasound or non-contrast MRI. Ultrasound and MRI can help in diagnosis by assessing the coracohumeral ligament, with a width of greater than 3 mm being  60% sensitive and 95% specific for the diagnosis. Shoulders with adhesive capsulitis also characteristically fibrose and thicken at the axillary pouch and "rotator interval", best seen as a dark signal on T1 sequences with edema and inflammation on T2 sequences. A finding on ultrasound associated with adhesive capsulitis is hypoechoic material surrounding the long head of the biceps tendon at the rotator interval, reflecting fibrosis. In the painful stage, such hypoechoic material may demonstrate increased vascularity with Doppler ultrasound.Grey-scale ultrasound can play a key role in timely diagnosis of adhesive capsulitis due to its high sensitivity and specificity. It is also widely available, convenient, and cost efficient. Thickening in the coracohumeral ligament, inferior capsule/ axillary recess capsule, and rotator interval abnormality, as well as restriction in range of motion in the shoulder can be detected using ultrasound. The range of motion is prohibited due to scapulohumeral rhythm changes occurring in the shoulder joint. The altered scapular kinematics can restrict anterior and posterior tilting, downward rotation and depression as well as external rotation. All of these restrictions lead the scapula to be excessively upwardly rotated. The restriction of the scapular posterior tilt is due to tightness in the lower serratus anterior, anterior capsule and the pectoralis minor. Downward rotation and depression are restricted due to the tightness of the rhomboids, upper trapezius and the superior capsule. Respective sensitivity values were 64.4, 82.1, 82.6, and 94.3, and respective specificity levels were 88.9, 95.7, 93.9, and 90.9.

Management
Management of this disorder focuses on restoring joint movement and reducing shoulder pain, involving medications, occupational therapy, physical therapy, or surgery. Treatment may continue for months; there is no strong evidence to favor any particular approach. The main treatment for adhesive capsulitis is a trial of conservative therapies, including analgesia, exercise, physiotherapy, oral nonsteroidal anti-inflammation drugs, and intra-articular corticosteroid injections.Medications such as NSAIDs can be used for pain control. Corticosteroids are used in some cases either through local injection or systemically. In the short term, intra-articular corticosteroid injections were more effective in pain alleviation. Unfortunately, this pain reduction was not long-lasting. In both the short and long term, intra-articular corticosteroid injections improved passive range of motion (ROM). Oral steroids may provide short-term benefits in range of movement and pain but have side effects such as hyperglycemia. Steroid injections compared to physical therapy have a similar effect in improving shoulder function and decreasing pain. The benefits of steroid injections appear to be short-term. The results of this study imply that using an IA corticosteroid early in individuals with frozen shoulder who have had it for less than a year had a better prognosis. To increase the chances of recovery, this treatment should be combined with a home exercise program. Oral corticosteroids should not be used consistently to treat adhesive capsulitis because of the dangers associated with long-term use and the lack of long-term benefit.The role for occupational therapy (OT) in adhesive capsulitis is dependent on restrictions on daily activities, pain, and limitations the person is experiencing; an occupational therapist usually makes an initial evaluation. Pain and limited joint mobility are primary complaints that impact a persons daily life. OT will usually start by using a preparatory method, like physical agent modalities to be used as part of a comprehensive occupational therapy program. The occupational therapist may teach strengthening exercises and provide a home exercise program. The goal of OT would be for the client to resume meaningful functional daily activities.The role for physical therapy in adhesive capsulitis is not settled. Physical therapy is used as an initial treatment in adhesive capsulitis with the use of range of motion (ROM) exercises and manual therapy techniques to restore range and function. A low-dose corticosteroid injection and home exercise programs in those with symptoms for less than 6 months may be useful. There may be some benefit with manual therapy and stretching as part of a rehabilitation program, but, due to the time required, such use should be carefully considered. Physical therapists may utilize joint mobilization directly at the glenohumeral joint to decrease pain, increase function, and increase range of motion as another form of treatment. There are some studies that have shown that intensive passive stretching can promote healing. Additional interventions include modalities such as ultrasound, shortwave diathermy, laser therapy and electrical stimulation. Another osteopathic technique used to treat the shoulder is called the Spencer technique. Mobilization techniques and other therapeutic modalities are most commonly used by physical therapists; however, there is not strong evidence that these methods can change the course of the disease.If these measures are unsuccessful, more aggressive interventions such as surgery can be trialed.  Manipulation of the shoulder under general anesthesia to break up the adhesions is sometimes used. Hydrodilatation or distension arthrography is controversial. However, some studies show that arthrographic distension may play a positive role in reducing pain and improve range of movement and function. Surgery to cut the adhesions (capsular release) may be indicated in prolonged and severe cases; the procedure is usually performed by arthroscopy. Surgical evaluation of other problems with the shoulder, e.g., subacromial bursitis or rotator cuff tear, may be needed. Resistant adhesive capsulitis may respond to open release surgery. This technique allows the surgeon to find and correct the underlying cause of restricted glenohumeral movement such as contracture of coracohumeral ligament and rotator interval. Physical therapy may achieve improved results after surgical procedure and postoperative rehabilitation.Physical therapy is an effective procedure that provides essential exercises to improve range of motion. Patients who receive the proper training from an authorized physiotherapist can perform these exercises independently at home. The physiotherapy treatment for frozen shoulder will include manual therapy to mobilize the affected joints and release their muscles. "Pendulum stretch", "finger walk", "towel stretch", "armpit stretch" and "crossbody reach" are some essential mobility exercises specifically designed to improve the shoulder mobility of patients with frozen shoulders. There are also limited case reports of therapy utilizing vibration platforms obtaining fast results, not as a post-operative aid, but instead of surgery.Acupuncture has been found to decrease pain levels and improve shoulder function and range of motion, particularly in shoulder flexion </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Takayasus arteritis and explain in detail? [/INST] Takayasus arteritis (TA), also known as aortic arch syndrome, nonspecific aortoarteritis, and pulseless disease, is a form of large vessel granulomatous vasculitis with massive intimal fibrosis and vascular narrowing, most commonly affecting young or middle-aged women of Asian descent, though anyone can be affected. It mainly affects the aorta (the main blood vessel leaving the heart) and its branches, as well as the pulmonary arteries. Females are about 8–9 times more likely to be affected than males.Those with the disease often notice symptoms between 15 and 30 years of age. In the Western world, atherosclerosis is a more frequent cause of obstruction of the aortic arch vessels than Takayasus arteritis. Takayasus arteritis is similar to other forms of vasculitis, including giant cell arteritis which typically affects older individuals. Due to obstruction of the main branches of the aorta, including the left common carotid artery, the brachiocephalic artery, and the left subclavian artery, Takayasus arteritis can present as pulseless upper extremities (arms, hands, and wrists with weak or absent pulses on the physical examination) which may be why it is also commonly referred to as the "pulseless disease." Involvement of renal arteries may lead to a presentation of renovascular hypertension.

Sign and symptoms
Some people develop an initial "inflammatory phase" characterized by systemic illness with signs and symptoms of malaise, fever, night sweats, weight loss, joint pain, fatigue, and fainting. Fainting may result from subclavian steal syndrome or carotid sinus hypersensitivity. There is also often anemia and marked elevation of the ESR or C-reactive protein (nonspecific markers of inflammation). The initial "inflammatory phase" is often followed by a secondary "pulseless phase". The "pulseless phase" is characterized by vascular insufficiency from intimal narrowing of the vessels manifesting as arm or leg claudication, renal artery stenosis causing hypertension, and neurological manifestations due to decreased blood flow to the brain.Of note is the function of renal artery stenosis in the causation of high blood pressure: Normally perfused kidneys produce a proportionate amount of a substance called renin. Stenosis of the renal arteries causes hypoperfusion (decreased blood flow) of the juxtaglomerular apparatus, resulting in exaggerated secretion of renin, and high blood levels of aldosterone, eventually leading to water and salt retention and high blood pressure. The neurological symptoms of the disease vary depending on the degree; the nature of the blood vessel obstruction; and can range from lightheadedness to seizures (in severe cases). One rare, important feature of the Takayasus arteritis is ocular involvement in form of visual field defects, vision loss, or retinal hemorrhage. Some individuals with Takayasus arteritis may present with only late vascular changes, without a preceding systemic illness. In the late stage, weakness of the arterial walls may give rise to localized aneurysms. As with all aneurysms, the possibility of rupture and vascular bleeding is existent and requires monitoring. In view of the chronic process and good collateral development, Raynauds phenomenon or digital gangrene are very rare in Takayasu arteritis. A rare complication of this condition are coronary artery aneurysms.

Laser Doppler imaging by near-infrared digital holography can reveal characteristic blood flow waveforms in the central artery and vein of the retina in patients with vascular insufficiency who may exhibit a smooth systo-diastolic pulse in the central retinal artery. This technique enables non invasive functional microangiography by high-contrast measurement of endoluminal blood flow profiles in vessels in the posterior segment of the eye with a spatial resolution comparable to state-of-the-art indocyanine green angiography.

Pathophysiology
Although the cause of Takayasu arteritis is unknown, the condition is characterized by segmental and patchy granulomatous inflammation of the aorta and its major derivative branches. This inflammation leads to arterial stenosis, thrombosis, and aneurysms. There is irregular fibrosis of the blood vessels due to chronic vasculitis, leading to sometimes massive intimal fibrosis (fibrosis of the inner section of the blood vessels). Prominent narrowing due to inflammation, granuloma, and fibrosis is often seen in arterial studies such as magnetic resonance angiography (MRA), computed tomography angiography (CTA), or arterial angiography (DSA).

Genetics
The genetic contribution to the pathogenesis of Takayasus arteritis is supported by the genetic association with HLA-B∗52. A 2013 large collaborative study uncovered multiple additional susceptibility loci for this disease, increasing its number of genetic loci to five risk loci across the genome. About 200,000 genetic variants were genotyped in two ethnically divergent Takayasus arteritis cohorts from Turkey and North America by using a custom-designed genotyping platform (Immunochip). Additional genetic variants and the classical HLA alleles were imputed and analyzed. The study identified and confirmed two independent susceptibility loci within the HLA region (r2 < 0.2): HLA-B/MICA (rs12524487, OR = 3.29, p = 5.57 × 10-16) and HLA-DQB1/HLA-DRB1 (rs113452171, OR = 2.34, p = 3.74 × 10-9; and rs189754752, OR = 2.47, p = 4.22 × 10-9). In addition, a genetic association was identified and confirmed between Takayasus arteritis and the FCGR2A/FCGR3A locus on chromosome 1 (rs10919543, OR = 1.81, p = 5.89 × 10-12). The risk allele at this locus results in increased mRNA expression of FCGR2A. In addition, a genetic association between IL12B and Takayasu arteritis was established (rs56167332, OR = 1.54, p = 2.18 × 10-8). A fifth genetic locus for the disease in an intergenic region on chromosome 21q22 downstream of PSMG1 was revealed (P=4.39X10-7). A recent genome-wide association study (GWAS) identified genetic susceptibility loci for Takayasu arteritis with a genome-wide level of significance in IL6 (rs2069837) (odds ratio [OR] 2.07, P = 6.70 × 10(-9)), RPS9/LILRB3 (rs11666543) (OR 1.65, P = 2.34 × 10(-8)), and the intergenic locus on chromosome 21q22 (rs2836878) (OR 1.79, P = 3.62 × 10(-10)). The genetic susceptibility locus in RPS9/LILRB3 lies within the leukocyte receptor complex gene cluster on chromosome 19q13.4, and the disease risk variant in this locus correlates with reduced expression of multiple genes including the inhibitory leukocyte immunoglobulin-like receptor gene LILRB3 (P = 2.29 × 10(-8)). In addition, this study identified additional candidate susceptibility genes with suggestive levels of association (P < 1 × 10(-5)) including PCSK5, LILRA3, PPM1G/NRBP1, and PTK2B.Another gene associated with this condition is MLX (Max-like protein X)

Diagnosis
Diagnosis is based on the demonstration of vascular lesions in large and middle-sized vessels on angiography, CT scan, magnetic resonance angiography or FDG PET. Seeing abnormal diffuse arterial wall thickening, the macaroni sign, with ultrasound is highly suggestive of the condition. FDG PET can help in diagnosis of active inflammation not just in patients with active Takayasu arteritis prior to treatment but also in addition in relapsing patients receiving immunosuppressive agents.Contrast angiography has been the gold standard. The earliest detectable lesion is a local narrowing or irregularity of the lumen. This may develop into stenosis and occlusion. The characteristic finding is the presence of "skip lesions," where stenosis or aneurysms alternate with normal vessels. Angiography provides information on vessel anatomy and patency but does not provide information on the degree of inflammation in the wall.The age at onset helps to differentiate Takayasus arteritis from other types of large vessel vasculitis. For example, Takaysus arteritis has an age of onset of <40 years, while giant cell arteritis has an age of onset >60 years.Takayasu arteritis is not associated with ANCA, rheumatoid factor, ANA, and anticardiolipin antibodies.

Treatments
Most people with Takayasu’s arteritis respond to steroids such as prednisone. The usual starting dose is approximately 1 milligram per kilogram of body weight per day (for most people, this is approximately 60 milligrams a day). Because of the significant side effects of long-term high-dose prednisone use, the starting dose is tapered over several weeks to a dose that controls symptoms while limiting the side effects of steroids.Promising results are achieved with mycophenolate and tocilizumab. If treatment is not kept to a high standard, long-term damage or death can occur.Patients who do not respond to steroids may require revascularization, either via vascular bypass or angioplasty and stenting. Outcomes following revascularization vary depending on the severity of the underlying disease.

History
The first case of Takayasu’s arteritis was described in 1908 by Japanese ophthalmologist Mikito Takayasu at the Annual Meeting of the Japan Ophthalmology Society </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Depression in childhood and adolescence and explain in detail? [/INST] Depression is a mental disorder characterized by prolonged unhappiness or irritability, accompanied by a constellation of somatic and cognitive signs and symptoms such as fatigue, apathy, sleep problems, loss of appetite, loss of engagement; low self-regard or worthlessness; difficulty concentrating or indecisiveness; or recurrent thoughts of death or suicide. Depression in childhood and adolescence is similar to adult major depressive disorder, although young sufferers may exhibit increased irritability or behavioral dyscontrol instead of the more common sad, empty, or hopeless feelings seen with adults. Children who are under stress, experiencing loss, or have other underlying disorders are at a higher risk for depression. Childhood depression is often comorbid with mental disorders outside of other mood disorders; most commonly anxiety disorder and conduct disorder. Depression also tends to run in families. In a 2016 Cochrane review cognitive behavior therapy (CBT), third wave CBT and interpersonal therapy demonstrated small positive benefits in the prevention of depression. Psychologists have developed different treatments to assist children and adolescents suffering from depression, though the legitimacy of the diagnosis of childhood depression as a psychiatric disorder, as well as the efficacy of various methods of assessment and treatment, remains controversial.

Base rates and prevalence
About 8% of children and adolescents suffer from depression. In 2016, 51 percent of students (teens) who visited a counseling center reported having anxiety, followed by depression (41 percent), relationship concerns (34 percent) and suicidal ideation (20.5 percent). Many students reported experiencing multiple conditions at once. Research suggests that the prevalence of children with Major Depressive Disorder in Western cultures ranges from 1.9% to 3.4% among primary school children. Amongst teenagers, up to 9% meet criteria for depression in a given moment and approximately 20% experience depression sometime during adolescence. Studies have also found that among children diagnosed with a depressive episode, there is a 70% rate of recurrence within five years. Furthermore, 50% of children with depression will have a recurrence at least once during their adulthood. While there is no gender difference in depression rates up until age 15, after that age the rate among women doubles compared to men. However, in terms of recurrence rates and symptom severity there is no gender difference. In an attempt to explain these findings, one theory asserts that preadolescent women on average have more risk factors for depression when compared to men. These risk factors then combine with the typical stresses and challenges of adolescent development to trigger the onset of depression. Depression in youth and adolescence is associated with a wide array of outcomes that can come later in life for the affected individual. Some of these outcomes include poor physical and mental health, trouble functioning socially, and suicide.

Suicidal intent
Like their adult counterparts, children and adolescent depression sufferers are at an increased risk of attempting or committing suicide. Suicide is the third leading cause of death among 15-to-19-year-olds. Adolescent males may be at an even higher risk of suicidal behavior when also presenting with a conduct disorder. In the 1990s, the National Institute of Mental Health (NIMH) found that up to 7% of adolescents who develop major depressive disorder may commit suicide as young adults. Such statistics demonstrate the importance of interventions by family and friends, the importance of early diagnosis, and treatment by medical staff, in order to prevent suicide amongst at-risk youth. However, some data showed an opposite conclusion. Most depression symptoms are reported more frequently by females; such as sadness (reported by 85.1% of women and 54.3% of men) and crying (approximately 63.4% of women and 42.9% of men). Women have a higher probability to experience depression than men with the prevalences of 19.2% and 13.5% respectively.

Risk factor
Risk factors for adolescent depression include female sex, a family history of depression, a personal history of trauma, family conflict, minority sexual orientation, or having a chronic medical illness. There tends to be higher prevalence rates and more severe symptoms in adolescent girls when compared to adolescent boys. These higher rates are also applicable in older adolescents when compared to younger adolescents. This may be due to hormonal fluctuations may that make adolescent women to be more vulnerable to depression. The fact that increased prevalence of depression correlates with hormonal changes in women, particularly during puberty, suggests that female hormones may be a trigger for depression. The gender gap in depression between adolescent men and women is mostly due to young womens lower levels of positive thinking, need for approval, and self-focusing negative conditions. Frequent exposure to victimization or bullying was related to high risks of depression, ideation and suicide attempts compared to those not involved in bullying. Nicotine dependence is also associated with depression, anxiety, and poor dieting, mostly in young men.  Although causal direction has not been established, involvement in any sex or drug use is cause for concern. Children who develop major depression are more likely to have a family history of the disorder (often a parent who experienced depression at an early age) than patients with adolescent- or adult-onset depression. Adolescents with depression are also likely to have a family history of depression, though the correlation is not as high as it is for children.

Comorbidity
There is also a substantial comorbidity rate with depression in children with anxiety disorder, conduct disorder, and impaired social functioning. Particularly, there is a high comorbidity rate with anxiety, ranging from 15.9% to 75%. Conduct disorders also have a significant comorbidity with depression in children and adolescents with a rate of 23% in one longitudinal study. Beyond other clinical disorders, there is also an association between depression in childhood, poor psychosocial and academic outcomes, as well as a higher risk for substance abuse and suicide.The prevalence of psychiatric comorbidities during adolescence may vary by race and ethnicity.

Social causes
Adolescents are engaged in a search for identity and meaning in their lives. They have also been regarded as a unique group with a wide range of difficulties and problems in their transition to adulthood. Academic pressure, intrapersonal and interpersonal difficulties, death of loved ones, illnesses, and loss of relationships, have shown to be significant stressors in young people. While it is a normal part of development in adolescence to experience distressing and disabling emotions, there is an increasing incidence of mental illness globally. This is due mainly because of the breakdown in traditional social and family structures. Depression is usually a response to life events such as relationship issues, financial problems, physical illness, bereavement, etc. Some people can become depressed for no obvious reason and their suffering is just as real as those reacting from life events. Psychological makeup can also play a role in vulnerability to depression. People who have low self-esteem, constantly view themselves and the world with pessimism, or are readily overwhelmed by stress, may be especially prone to depression. Community surveys find that women are more likely than men to say they are under stress. Other studies suggest that women are more likely than men to become depressed in response to a stressful event. Women are also more likely to experience certain kinds of severe stress such as child sexual abuse, adult sexual assaults, and domestic violence.

Diagnosis
According to the DSM-IV, children must exhibit either a depressed mood or a loss of interest/pleasure in normal activities. These activities may include school, extracurricular activities, or peer interactions. Depressive moods in children can be expressed as being unusually irritable. These expressions may be displayed by "acting out," behaving recklessly, or reacting with anger/hostility. Children who do not have the cognitive or language development to properly express mood states can also exhibit their mood through physical complaints such as showing sad facial expressions (frowning) and poor eye contact. A child must also exhibit four other symptoms in order to be clinically diagnosed. However, according to the Omnigraphics Health References Series: Depression Sourcebook, Third Edition, a more calculated evaluation must be given by a medical or mental health professional such as a physiologist or psychiatrist. Following the bases of symptoms, signs include but are not limited to, an unusual change in sleep habits (for example, trouble sleeping or overly indulged sleeping hours); a significant amount of weight gain/loss by the lack or excessive eating; experiencing aches/pains for no apparent reason that can found; and an inability to concentrate on tasks or activities. If these symptoms are present for a period of two weeks or longer, it is safe to make the assumption that the child, or anybody else for that matter, is falling into major depression.

Assessment
It is recommended by the American Academy of Pediatrics that primary care providers screen children and adolescents for depression with validated screening tools, self-rated, or clinician-administered ones, once per year. However, there is no universally recommended screening tool and the clinician is free to choose from various validated ones based on personal preference. Once the screening tool indicates the potential presence of a depression, a thorough diagnostic assessment is recommended. In early 2016, the USPSTF released an updated recommendation for the screening of adolescents ages 12 to 18 years for major depressive disorder (MDD). Appropriate treatment and follow-up should be provided for adolescents who screen positive.

Correlation between adolescent depression and adulthood obesity
According to research conducted by Laura P. Richardson et al., major depression occurred in 7% of the cohort during early adolescence (11, 13, and 15 years of age) and 27% during late adolescence (18 and 21 years of age). At 26 years of age, 12% of study members were obese. After adjusting for each individuals baseline body mass index (calculated as the weight in kilograms divided by the square of height in meters), depressed late-adolescent girls were at a greater than 2-fold increased risk for obesity in adulthood compared with their non-depressed female peers (relative risk, 2.32; 95% confidence interval, 1.29-3.83). A dose-response relationship between the number of episodes of depression during adolescence and the risk for adult obesity was also observed in female subjects. The association was not observed for late adolescent boys or for early adolescent boys or girls.

Correlation between child depression and adolescent cardiac risks
According to research by RM Carney et al., any history of child depression influences the occurrence of adolescent cardiac risk factors, even if individuals no longer suffer from depression. They are much more likely to develop heart disease as adults.

Distinction from major depressive disorder in adults
While there are many similarities to adult depression, especially in expression of symptoms, there are many differences that create a distinction between the two diagnoses. Research has shown that when a childs age is younger at diagnosis, typically there will be a more noticeable difference in the expression of symptoms from the classic signs in adult depression. One major difference between the symptoms exhibited in adults and in children is that children have higher rates of internalization; therefore, symptoms of child depression are more difficult to recognize. One major cause of this difference is that many of the neurobiological effects in the brain of adults with depression are not fully developed until adulthood. Therefore, in a neurological sense children and adolescents express depression differently.

Treatment
Clinicians often divide treatment into three phases: In the acute phase, which usually lasts six to 12 weeks, the goal is to relieve symptoms. In the continuation phase, which can last for several more months, the goal is to maximize improvements. At this stage, clinicians may make adjustments to the dose of a medication. In the maintenance phase, the aim is to prevent relapse. Sometimes the dose of a drug is lowered at this stage, or psychotherapy carries more of the weight. Unique differences in life experience, temperament, and biology make treatment a complex matter; no single treatment is right for everyone. Psychotherapy and medications are commonly used treatment options. In some research, adolescents showed a preference for psychotherapy rather than antidepressant medication for treatment. For adolescents, cognitive behavioral therapy and interpersonal therapy have been empirically supported as effective treatment options. Studies have shown that a combination of psychotherapy and medication is the most effective treatment. Pediatric massage therapy may have an immediate effect on a childs emotional state at the time of the massage, but sustained effects on depression have not been identified.Treatment programs have been developed that help reduce the symptoms of depression. These treatments focus on immediate symptom reduction by concentrating on teaching children skills pertaining to primary and secondary control. While much research is still needed to confirm this treatment programs efficacy, one study showed it to be effective in children with mild or moderate depressive symptoms.Identification and treatment of concomitant parental depression is associated with improved responses to treatment in adolescents with depression as having a parent with depression may negatively affect a young persons response to therapy as well as their outlook on depression.

Talk therapy
There are a variety of common types of talk therapy. These can assist people to live more fully, help improve good feelings, and have a better life. Effective psychotherapy for children always includes parent involvement, teaching skills that are practiced at home or at school, and measures of progress that are tracked over time. In many types, men are encouraged to open up more emotionally and communicate their personal distress, while women are encouraged to be assertive of their own strengths. Often psychotherapy teaches coping skills while allowing the teens or children to explore feelings and events in a safe environment.Severe depression, low global functioning, higher scores on suicidality scales, co-existing anxiety, distorted thought processes and feelings of hopelessness are characteristics of adolescent depression that are associated with a poor response to psychotherapy. If there is concomitant family conflict then interpersonal therapy is more effective than cognitive therapy.
Talk therapy is one of the best forms of therapy, as the depressed person finds a solace in the one whom he/she is talking to. Through this means, the counselor is able to know and understood fully the mind of the depressed individual. Many people are depressed and simply needs the right person to talk to. This is where the talk therapy comes in as a very helpful solution to those who are in need of it.

Cognitive therapy
Cognitive therapy aims to change harmful ways of thinking and reframe negative thoughts in a more positive way. Aims of cognitive therapy include various steps of patient learning. During cognitive behavioral therapy, children and adolescents with depression work with therapists to learn about their diagnosis, how to identify and reshape negative thought patterns, and how to increase engagement in enjoyable activities. CBT-trained therapists work with individuals, families, and groups. The approach can be used to help anyone irrespective of ability, culture, race, gender, or sexual preference. It can be applied with or without concurrent psychopharmacological medication, depending on the severity or nature of each patients problem. The duration of cognitive-behavioral therapy varies, although it typically is thought of as one of the briefer psychotherapeutic treatments. Especially in research settings, duration of CBT is usually short, between 10 and 20 sessions. In routine clinical practice, duration varies depending on patient comorbidity, defined treatment goals, and the specific conditions of the health care system.

Behavioral therapy
Behavioral therapy helps change harmful ways of acting and gain control over behavior which is causing problems.

Interpersonal therapy
Interpersonal therapy helps one learn to relate better with others, express feelings, and develop better social skills. Interpersonal therapy helps the patient identify and cope through reoccurring conflicts within their relationships. Typically, the therapy will focus on one of the four specific problems, grief, social isolation, conflicts about roles and social expectations, or the effect of a major life change.

Family therapy
The principles of group dynamics are relevant to family therapists who must not only work with individuals, but with entire family systems. Family counseling can help families understand how a childs individual challenges may affect relations with parents and siblings and vice versa.Therapists strive to understand not just what the group members say, but how these ideas are communicated (process). Therapists can help families improve the way they relate and thus enhance their own capacity to deal with the content of their problems by focusing on the process of their discussions.  Virginia Satir expanded on the concept of how individuals behave and communicate in groups by describing several family roles that can serve to stabilize expected characteristic behavior patterns in a family. For instance, if one child is considered to be a "rebel child", a sibling may take on the role of the "good child" to alleviate some of the stress in the family. This concept of role reciprocity is helpful in understanding family dynamics because the complementary nature of roles makes behaviors more resistant to change. It is good to understand that most depression in children and adolescents begin right in the home. Parents are advised to treat their children properly and learn to fully understand their child/children, and also give them adequate attention, love, care and quick response to their useful needs. Parents and Guardians should detest ignoring their children or wards and give them attention because neglect can lead to shame, loss of self-confidence, frustration and finally depression.

Antidepressants
As of 2021, the FDA has approved the selective serotonin reuptake inhibitors (SSRIs) fluoxetine and escitalopram for the treatment of depression in adolescents but other SSRIS or serotonin norepinephrine reuptake inhibitors (SNRIs) are often used off label for treatment. Clinicians usually recommend one of these SSRIs as a first line treatment for depression in adolescence. These drugs act on the serotonin system that affects mood, arousal, anxiety, impulses, and aggression. SSRIs also appear to indirectly influence other neurotransmitter systems, including those involving norepinephrine and dopamine. Some possible adverse reactions of SSRIs include headache, gastrointestinal side effects, dry mouth, sedation or insomnia and activation. Activation refers to a state of psychomotor agitation that includes symptoms of insomnia, disinhibition and restlessness that may result in discontinuation of a medication. There is a rare risk of suicidal thoughts or behaviors with SSRIs especially when treatment is started or the dose is increased, with the rate being up to 0.7% as compared to placebo in early meta analyses of SSRIs in the treatment of adolescent depression. This led the FDA to issue a black box warning regarding this risk. Once remission is achieved, the medications are continued for at least 6 to 12 months and then there is consideration of discontinuing them. Early or premature discontinuation of medications, prior to 6 to 12 months of having achieved remission, is associated with an increased risk of relapse of the depression.The combination of psychotherapy with medications has been shown to be more effective for the treatment of depression in adolescence than medications alone.Other medications can be added to SSRIs if a partial response is achieved and further improvement is needed; these agents include lithium, bupropion and atypical antipsychotics. These options are medications that work in different ways. Bupropion (Wellbutrin) works through the neurotransmitters norepinephrine and dopamine, while mirtazapine (Remeron) affects transmission of norepinephrine and serotonin. The drugs venlafaxine (Effexor) and duloxetine (Cymbalta) work in part by simultaneously inhibiting the reuptake of serotonin and norepinephrine. The oldest drugs on the market are not prescribed often, but may be a good option for some women. These include tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs). TCAs may cause side effects like dry mouth, constipation, or dizziness. MAOIs can cause sedation, insomnia, dizziness, and weight gain. To avoid the risk of a rapid rise in blood pressure, people taking MAOIs must also avoid eating a substance called tyramine, found in yogurt, aged cheese, pickles, beer, and red wine. Some drug side effects subside with time, while others may lessen when a drug dose is lowered.

Research
Differences in the brains structure and function appear to be present in adolescents with depression though this may depend on age. Younger adolescents, mostly under the age of 18, with depression have shown greater white matter volume within frontal regions of the brain, greater cortical thickness in the anterior cingulate cortex and medial orbitofrontal cortex, as well as greater functional connectivity between cortico-limbic brain regions. Whereas older adolescents, mostly above the age of 18, appear to show lower cortical surface area in regions including the lingual, occipital gyri, as well as medial orbitofrontal and motor cortices.  Results such as these have led to the hypothesis that the biological causes of depression may in part be neurodevelopmental, with its biological underpinnings forming early on in brain development.

History
Although antidepressants were used by child and adolescent psychiatrists to treat major depressive disorder, they were not always used in young people with a comorbid conduct disorder because of the risks of overdose in such a population. Tricyclic antidepressant were the predominant antidepressants used at that time in this population. With the advent of selective serotonin re-uptake inhibitors (SSRIs), child and adolescent psychiatrists probably began prescribing more anti-depressants in the comorbid conduct disorder/major depressive group because of the lower risk of serious harm in overdose. This raises the possibility that more effective treatment of these young people might also improve their outcomes in adult life. Although treatment rates are becoming more stable, there is a trend that suggests that little progress has been made in narrowing the mental health treatment gap for adolescent depression. The FDA has also placed a black box warning on using antidepressants, leading doctors to be hesitant on prescribing them to adolescents.

Controversies
Throughout the development and research of this disorder, controversies have emerged over the legitimacy of depression in childhood and adolescence as a diagnosis, the proper measurement and validity of scales to diagnose, and the safety of particular treatments.

Legitimacy as a diagnosis
In early research of depression in children, there was debate as to whether or not children could clinically fit the criteria for major depressive disorder. However, since the 1970s, it has been accepted among the psychological community that depression in children can be clinically significant. The more pertinent controversy in psychology today centers around the clinical significance of sub-threshold mood disorders. This controversy stems from the debate regarding the definition of the specific criteria for a clinically significant depressed mood in relation to the cognitive and behavioral symptoms. Some psychologists argue that the effects of mood disorders in children and adolescents that exist (but do not fully meet the criteria for depression) do not have severe enough risks. Children in this area of severity, they argue, should receive some sort of treatment since the effects could still be severe. However, since there has yet to be enough research or scientific evidence to support that children that fall within the area just shy of a clinical diagnosis require treatment, other psychologists are hesitant to support the dispensation of treatment.

Diagnosis controversy
In order to diagnose a child with depression, different screening measures and reports have been developed to help clinicians make a proper decision. However, the accuracy and effectiveness of certain measures that help psychologists diagnose children have come into question. Due to absence of strong evidence that screening children and adolescents for depression leads to improved mental health outcomes, it has been questioned whether it causes more harm than benefit. Questions have also surfaced about the safety and effectiveness of antidepressant medications.

Measurement reliability
The effectiveness of dimensional child self-report checklists has been criticized. Although literature has documented strong psychometric properties, other studies have shown a poor specificity at the top end of scales, resulting in most children with high scores not meeting the diagnostic criteria for depression.  Another issue with reliability of measurement for diagnosis occurs in parent, teacher, and child reports </s>