<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 Neurogenic shock and explain in detail? [/INST] Neurogenic shock is a distributive type of shock resulting in hypotension (low blood pressure), often with bradycardia (slowed heart rate), caused by disruption of autonomic nervous system pathways. It can occur after damage to the central nervous system, such as spinal cord injury and traumatic brain injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting from loss of sympathetic tone, which in turn causes blood pooling within the extremities rather than being available to circulate throughout the body. The slowed heart rate results from a vagal response unopposed by a sympathetic nervous system (SNS) response.  Such cardiovascular instability is exacerbated by hypoxia, or treatment with endotracheal or endobronchial suction used to prevent pulmonary aspiration.Neurogenic shock is a potentially devastating complication, leading to organ dysfunction and death if not promptly recognized and treated.It is not to be confused with spinal shock, which is not circulatory in nature.

Signs and symptoms
Instantaneous hypotension due to sudden, massive vasodilation and decrease in blood oxygen saturation
Warm, flushed skin due to vasodilation and inability to constrict blood vessels.
Priapism, also due to vasodilation
The patient will be unable to mount a tachycardic response, and often becomes bradycardic
If the injury is below cervical vertebrae C5, the patient will exhibit diaphragmatic breathing due to loss of nervous control of the intercostal muscles (which are required for thoracic breathing).
If the injury is above C3, the patient will go into respiratory arrest immediately following the injury, due to loss of nervous control of the diaphragm.

Causes
Neurogenic shock can result from severe central nervous system damage (brain injury, cervical or high thoracic spinal cord). In simple terms, the trauma causes a sudden loss of background SNS stimulation to the blood vessels. This causes them to relax (vasodilation) resulting in a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance).
Neurogenic shock results from damage to the spinal cord above the level of the 6th thoracic vertebra.  It is found in about half of people who have a spinal cord injury within the first 24 hours, and usually persists for one to three weeks.Neurogenic shock may be caused by severe brain injury. However, in case of increased intracranial pressure, according to the Cushing triad, blood pressure will be increased (unless decreased from hypovolemia), respirations will be irregular and bradycardia will also be a feature.

Pathophysiology
Neurogenic shock is diagnosed based on a persons symptoms and blood pressure levels.
Neurogenic shocks presentation includes:- warm and pink skin
- labored breathing
- low blood pressure
- dizziness
- anxiety
- history of trauma to head or upper spine.
- if the injury is to the head or neck, hoarseness or difficulty swallowing may occur.
Symptoms of neurogenic shock are differentiated from other forms of shock by the lack of signs of the compensatory mechanisms triggered by the SNS, usual in other forms of shock. This SNS response is effected via release of epinephrine and norepinephrine, and signs of these neurotransmitters activity are typically absent  where shock is of neurogenic origin. Those signs - in non-neurogenic shock -  would include: tachycardia (increased heart rate), tachypnea (increased breath rate), sweating, and adaptive vasoconstriction, which serves in other forms of shock to shunt blood away from the extremities and to the vital organs.
In neurogenic shock, the body loses its ability to activate the SNS so that only parasympathetic tone remains.  The resulting loss of sympathetic tone, which plays a major role in other forms of shock, is responsible for the unique and atypical features mentioned above.<ref name=incidence>Mallek JT; Inaba K;  et al </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 Megalencephalic leukoencephalopathy with subcortical cysts and explain in detail? [/INST] Megalencephalic leukoencephalopathy with subcortical cysts (MLC, or Van der Knaap disease) is a form of hereditary CNS demyelinating disease.  It belongs to a group of disorders called leukodystrophies. It is characterized by early-onset enlargement of the head (macrocephaly) as well as delayed-onset neurological deterioration to include spasticity, epilepsy, and lack of muscular coordination. MLC does not appear to be a disease that is fatal at birth or early in life despite its symptoms, although the number of patients throughout history known to have the disease is fairly limited.It belongs to a group of disorders called leukodystrophies. A series of cases with megalencephalic leukodystrophy were described by the Indian neurologist Bhim Sen Singhal (1933-) in 1991. However, it is sometimes referred to as Van der Knaap disease after the Dutch neurologist Marjo van der Knaap who described another series of cases with clinical and radiological features in 1995.There are three types of Megalencephalic leukoencephalopathy distinguished by the affected gene: Type 1 caused by autosomal recessive mutations on the MLC1 gene, Type 2A an autosomal recessive mutation on the HEPACAM gene, and Type 2B an autosomal dominant mutation on the HEPACAM gene.

Signs and Symptoms
Head
Macrocephaly
The disease is characterized by megalencephaly, the enlargement of the brain, which is followed by an increase in the size of the actual head.
Central Nervous System
Megalencephaly
The M in MLC stands for “megalencephaly”, the enlargement of the brain
Ataxia
Slow, progressive and early-onset cerebellar ataxia has been noted in many patients
Spasticity
Patients with MLC often have muscle spasms
Seizures
Delay in motor development
 Mild mental retardation
Diffuse swelling of cerebral white matter
 Large subcortical cysts in frontal and temporal lobes
Patients develop cysts on the tips of the temporal and subcortical area
Diffuse spongiform leukoencephalopathy
Vacuolizing myelinopathy
The protective myelin sheath on neurons pulls away from their cells forming small holes in nerve fibers – in turn affecting coordination and walking ability.

Genetics
It is associated with MLC1. The MLC1 gene is located in chromosome 22q13.33 and is in the genomic coordinates 22:50,059,390 – 50,085874. The gene contains 12 exons and that contain a start codon in exon 2 and an untranslated region in the 3’ end. The MLC1 gene product is a 377 amino acid protein highly expressed in the brain. The disease is caused by a homozygous or compound heterozygous mutation in the gene, MLC1. Previous research indicates that deficiency of cell surface protein expression of the MLC1 gene is the basis for the disorder. The mutant protein is expressed in intracellular compartments reducing the membrane surface expression when compared to the wild type.

Diagnosis
Diagnosis of Megalencephalic leukoencephalopathy with subcortical cysts is made with a combination of physical and clinical evaluations </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 Pilotto syndrome 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 Sphingolipidoses 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 Wasting and explain in detail? [/INST] In medicine, wasting, also known as wasting syndrome, refers to the process by which a debilitating disease causes muscle and fat tissue to "waste" away </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 Seal finger 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 Palindromic rheumatism and explain in detail? [/INST] Palindromic rheumatism (PR) is a syndrome characterised by recurrent, self-resolving inflammatory attacks in and around the joints, consists of arthritis or periarticular soft tissue inflammation. The course is often acute onset, with sudden and rapidly developing attacks or flares. There is pain, redness, swelling, and disability of one or multiple joints. The interval between recurrent palindromic attacks and the length of an attack is extremely variable from few hours to days. Attacks may become more frequent with time but there is no joint damage after attacks. It is thought to be an autoimmune disease, possibly an abortive form of rheumatoid arthritis.

Presentation
The exact prevalence of palindromic rheumatism in general population is unknown, and this condition is often considered a rare disease by nonrheumatologists. However, recent Canadian study showed that the incidence of PR in a cohort of incident arthritis was one case of PR for every 1.8 cases of rheumatoid arthritis (RA). The incidence of PR is less than that of RA but is not as rare as that was thought to be.
Palindromic rheumatism is a syndrome presented with inflammatory para-arthritis (soft tissue rheumatism) and inflammatory arthritis both of which cause sudden inflammation in one or several joints or soft tissue around joints. The flares usually present with  mono- or oligo-articular involvement, which have onset over hours and last a few hours to a few days, and then go away completely. However episodes of recurrence form a pattern, with symptom-free periods between attacks lasting for weeks to months. The most commonly involved joints were knees, metacarpophalangeals and proximal interphalangeals.  Constitutionally, there may or may not be a fever, and swelling of the joints. The soft tissues are involved with swelling of the periarticular tissues, especially heel pads and finger pads. Nodules may be found in the subcutaneous tissues. The frequency of attacks may be variable over the course but there is no joint damage after attacks.It typically affects people between the ages of 20 and 50. One study showed an average age of onset of 49.A population cohort study in Taiwan suggested that patients with PR had an increased risk of developing rheumatoid arthritis, systemic lupus erythematosus, Sjogrens syndrome, systemic sclerosis, and polymyositis.

Causes
Palindromic rheumatism is a disease of unknown cause. It has been suggested that it is an abortive form of rheumatoid arthritis (RA), since anti-cyclic citrullinated peptide antibodies (anti-CCP) and antikeratin antibodies (AKA) are present in a high proportion of patients, as is the case in rheumatoid arthritis. Unlike RA and some other forms of arthritis, palindromic rheumatism affects men and women equally. Palindromic rheumatism is frequently the presentation for Whipple disease which is caused by the infectious agent Tropheryma whipplei (formerly T. whippelii).

Diagnosis
Due to the symptoms of palindromic arthritis and the nature of the attacks, diagnosis can be difficult or take a long time. The symptoms can be similar to many other forms of arthritis or other autoimmune diseases </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 Craniometaphyseal dysplasia 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 Lymphocytic choriomeningitis and explain in detail? [/INST] Lymphocytic choriomeningitis (LCM) is a rodent-borne viral infectious disease that presents as aseptic meningitis, encephalitis or meningoencephalitis. Its causative agent is lymphocytic choriomeningitis mammarenavirus (LCMV), a member of the family Arenaviridae. The name was coined by Charles Armstrong in 1934.Lymphocytic choriomeningitis (LCM) is "a viral infection of the membranes surrounding the brain and spinal cord and of the cerebrospinal fluid". The name is based on the tendency of an individual to have abnormally high levels of lymphocytes during infection.  Choriomeningitis is "cerebral meningitis in which there is marked cellular infiltration of the meninges, often with a lymphocytic infiltration of the choroid plexuses".

Signs and symptoms
LCMV infection manifests itself in a wide range of clinical symptoms, and may even be asymptomatic for immunocompetent individuals. Onset typically occurs between one or two weeks after exposure to the virus and is followed by a biphasic febrile illness.  During the initial or prodromal phase, which may last up to a week, common symptoms include fever, lack of appetite, headache, muscle aches, malaise, nausea, and/or vomiting.  Less frequent symptoms include a sore throat and cough, as well as joint, chest, and parotid pain.  The onset of the second phase occurs several days after recovery, and consists of symptoms of meningitis or encephalitis.  Pathological findings during the first stage consist of leukopenia and thrombocytopenia.  During the second phase, typical findings include elevated protein levels, increased leukocyte count, or a decrease in glucose levels of the cerebrospinal fluid).Occasionally, a patient improves for a few days, then relapses with aseptic meningitis, or very rarely, meningoencephalitis.
Patients with meningitis may have a stiff neck, fever, headache, myalgia, nausea and malaise. In some occasions, meningitis occurs without a prodromal syndrome. Meningoencephalitis is characterized by more profound neurological signs such as confusion, drowsiness, sensory abnormalities and motor signs. Under reported complications include myelitis, Guillain–Barré-type syndrome, cranial nerve palsies, transient or permanent hydrocephalus, sensorineural hearing loss, orchitis, arthritis and parotitis. LCMV infections have also been associated with pancreatitis, pneumonitis, myocarditis and pericarditis. The entire illness usually lasts 1 to 3 weeks, nonetheless, temporary or permanent neurological damage is possible in all central nervous system infections, especially in cases of meningoencephalitis. Chronic infections have not been reported in humans and deaths rarely occur.

Cause
Virus biology
There are several strains of LCM virus, among which the most widely used are LCMV Armstrong and LCMV Clone 13. Armstrong is the original virus strain which was isolated from the brain by Charles Armstrong in 1934. It triggers a vigorous cytotoxic T lymphocytes(CTL) response and thus, it is cleared rapidly by the host. This is referred to as acute (Armstrong) LCMV infection. On the other hand, Clone 13 is a variant of the Armstrong viral strain, isolated from the spleen and is consequently tropic for visceral organs. It was first isolated from mice which sustained a persistent LCMV infection from birth. This variant potentiates a less vigorous CTL response in the immune system, and thus can ultimately persist in the host organism indefinitely. The latter is referred to as chronic (Clone 13) LCMV infection.LCMV is a spherical enveloped virus with a diameter between 60 and 300 nm. The helical nucleocapsid contains an RNA genome consisting of two negative single-stranded RNA segments. The negative RNA strand, complementary to the necessary mRNA strand, indicates that it must first be transcribed into a positive mRNA strand before it can be translated into the required proteins. The L strand is ambisense RNA, encoding multiple proteins in opposite directions, separated by an intergenic region. It is approximately 7.2 kb in size and encodes a high-molecular-mass protein (L; 200 kDa) and an 11 kDa small polypeptide Z with unknown function and a ring finger motif. The viral RNA-dependent RNA polymerase is encoded by the L protein which contains conserved characteristic motifs throughout all the RNA-dependent, RNA-polymerases.  The S strand is ambisense and approximately 3.4 kb in size. It encodes the two main structural proteins: nucleo-protein (NP) (63 kDa) and glycoprotein precursor complex (GPC) (75kDa). The latter undergoes posttranslational cleavage at two separate steps: first in the endoplasmic reticulum, where following translation on the membrane, the stable signal peptide region is cleaved by signal peptidase (SPase); notably, this signal peptide is retained, in contrast to other viruses. The second cleavage occurs at the Golgi apparatus, where GP1-GP2, having been trafficked to the Golgi, is cleaved into separate mature viral glycoproteins, GP1 and GP2 (with cleavage mediated by SK1-/PS1 or MTBPS1). The spikes present on the virion envelope are dictated by tetramer formation of GP-1 and GP-2.When LCMV attacks a cell, the process of replication starts by attachment of the virus to host receptors through its surface glycoproteins. It is then endocytosed into a vesicle inside the host cell and creates a fusion of the virus and vesicle membranes. The ribonucleocapsid is then released in the cytoplasm. The RNA-dependent, RNA-polymerase brought along with the virus initially binds to a promoter on the L and S segments and begins transcription from negative-stranded to a positive-stranded mRNA. The formation of a strong hairpin sequence at the end of each gene terminates transcription. The mRNA strands are capped by the RNA-dependent, RNA-polymerase in the cytoplasm and are then subsequently translated into the four proteins essential for LCMV assembly. The ribonucleocapsid interacts with the Z matrix protein and buds on the cell membrane, releasing the virion out from the infected cell.
The first arenavirus, Lymphocytic choriomeningitis mammarenavirus (LCMV), was isolated in 1933 by Charles Armstrong during a study of an epidemic in St. Louis. Although not the cause of the outbreak, LCMV was found to be a cause of nonbacterial or aseptic meningitis.In 1996, Peter Doherty and Rolf Zinkernagel shared the Nobel Prize in Medicine and Physiology, for their work with LCMV which led to a fundamental understanding of the adaptive immune response, MHC restriction. In the 1970s, studies concerning the importance of MHC locus were done exclusively in transplantation and tumor rejection. Taking this into consideration, Doherty and Zinkernagel were working on the response of mice to virus infections. They observed that T-cell receptors must recognise a complex of foreign antigen and an MHC antigen in order to destroy infected cells. Their key experiment involved harvesting of splenocytes containing LCMV-specific cytotoxic T lymphocytes(CTL) from an infected mouse strain A. These were then mixed in vitro with virus infected fibroblasts or macrophages from two different mouse strains, A and B. By the method of Cr-release cytotoxicity assay, thereby tagging the CTL with chromium-51 (Cr-51), the CTL destruction of infected cells was quantified by release of Cr-51. The results showed that CTL killed only the infected cells from strain A, and they did not lyse uninfected cells or infected cells from strain B. They concluded that these virus specific CTLs only lyse cells carrying the same molecules of the major histocompatibility site (MHC) as the CTLs themselves. Thus, the virus-specific CTLs are "MHC-restricted". This discovery lead to a greater understanding of an important aspect of the immune system.

Spread
LCMV is naturally spread by the common house mouse, Mus musculus. Once infected, these mice can become chronically infected by maintaining virus in their blood or persistently shedding virus in their urine.
Chronically infected female mice usually transmit infection to their offspring (vertical transmission), which in turn become chronically infected. Other modes of mouse-to-mouse transmission include nasal secretions, milk from infected dams, bites, and during social grooming within mouse communities. Airborne transmission also occurs.The virus seems to be relatively resistant to drying and therefore humans can become infected by inhaling infectious aerosolized particles of rodent urine, feces, or saliva, by ingesting food contaminated with virus, by contamination of mucous membranes with infected body fluids, or by directly exposing cuts or other open wounds to virus-infected blood.  The only documented cases of transmission from animals have occurred between humans and mice or hamsters.Cases of lymphocytic choriomeningitis have been reported in North and South America, Europe, Australia, and Japan, particularly during the 1900s. However, infection may occur wherever an infected rodent host population exists. LCMV occurs worldwide and its natural host, the rodent, has become established on all continents, except Antarctica.Seroprevalence is approximately 5% (0.7–4.7%) of the US population. It tends to be more common among lower socio-economic groupings, probably reflecting more frequent and direct contacts with mice.  However, obtaining an accurate sense of prevalence by geographic region is difficult due to underreporting.

Congenital infection
Lymphocytic choriomeningitis is a particular concern in obstetrics, as vertical transmission is known to occur. For immunocompetent mothers, there is no significant threat, but the virus has damaging effects upon the fetus.  If infection occurs during the first trimester, LCMV results in an increased risk of spontaneous abortion. Later congenital infection may lead to malformations such as intracranial calcifications, hydrocephalus, microcephaly or macrocephaly, intellectual disabilities, and seizures. Other findings include chorioretinal scars, and optic atrophy. Chorioretinitis, which is followed by chorioretinal scarring, is the most common ocular lesion. Mortality among infants is approximately 30%.  Among the survivors, two-thirds have lasting neurologic abnormalities.Other ocular defects including optic atrophy, microphthalmia, vitreitis, leukokoria and cataracts can also be seen. Most of the infants in one case series were of normal birth weight, although 30% were underweight. Aspiration pneumonia can be a fatal complication. Infants who survive may have severe neurological defects including epilepsy, impaired coordination, visual loss or blindness, spastic diplegia or quadriparesis/quadriplegia, delayed development and intellectual disability. Less severe cases with isolated cerebellar hypoplasia and symptoms of ataxia and jitteriness have been reported occasionally. There have also been rare cases with evidence of chorioretinitis but without neurological signs. Systemic signs seem to be rare, but hepatosplenomegaly, thrombocytopenia and hyperbilirubinemia have been documented in a few cases, and skin blisters were reported in one infant.If a woman has come into contact with a rodent during pregnancy and LCM symptoms are manifested, a blood test is available to determine previous or current infection.  A history of infection does not pose a risk for future pregnancies.

Organ donation
Patients infected in solid organ transplants have developed a severe fatal illness, starting within weeks of the transplant. In all reported cases, the initial symptoms included fever, lethargy, anorexia and leukopenia, and quickly progressed to multisystem organ failure, hepatic insufficiency or severe hepatitis, dysfunction of the transplanted organ, coagulopathy, hypoxia, multiple bacteremias and shock. Localized rash and diarrhea were also seen in some patients. Nearly all cases have been fatal.In May 2005, four solid-organ transplant recipients contracted an illness that was later diagnosed as lymphocytic choriomeningitis. All received organs from a common donor, and within a month of transplantation, three of the four recipients had died as a result of the viral infection. Epidemiologic investigation traced the source to a pet hamster that the organ donor had recently purchased from a Rhode Island pet store. Similar cases occurred in Massachusetts in 2008, and Australia in 2013. There is not a LCMV infection test that is approved by the Food and Drug Administration for organ donor screening.  The Morbidity and Mortality Weekly Report advises health-care providers to "consider LCMV infection in patients with aseptic meningitis and encephalitis and in organ transplant recipients with unexplained fever, hepatitis, or multisystem organ failure."

Diagnosis
Current or previous infection can be detected through a blood test. However, some authors note that such complement-fixation tests are insensitive and should not be used for diagnosis. Dr. Clare A. Dykewicz, et al. state,

Infection with LCMV should be considered in the differential diagnosis of any compatible, severe viral infection or aseptic meningitis, especially when there is a history of occupational exposure to laboratory rodents. Timeliness of diagnosis is important not only in expediting treatment of infected persons, but also in preventing further LCMV transmission to other workers and animals.Clinical diagnosis of LCM can be made by the history of prodrome symptoms and by considering the period of time before the onset of meningitis symptoms, typically 15–21 days for LCM.Pathological diagnosis of congenital infection is performed using either an immunofluorescent antibody (IFA) test or an enzyme immunoassay to detect specific antibody in blood or cerebrospinal fluid.  A PCR assay has been recently developed which may be used in the future for prenatal diagnosis; however, the virus is not always present in the blood or CSF when the affected child is born." Diagnoses is subject to methodological shortcomings in regard to specificity and sensitivity of assays used. For this reason, LCMV may be more common than is realized.Another detection assay is the reverse transcription polymerase chain reaction (RT-PCR) tests which may detect nucleic acids in the blood and cerebrospinal fluid.(CSF) Virus isolation is not used for diagnosis in most cases but it can be isolated from the blood or nasopharyngeal fluid early in the course of the disease, or from CSF in patients with meningitis. LCMV can be grown in a variety of cell lines including BHK21, L and Vero cells, and it may be identified with immuno-fluorescence. A diagnosis can also be made by the intracerebral inoculation of blood or CSF into mice.

Prevention
LCMV is susceptible to most detergents and disinfectants including 1% sodium hypochlorite, 70%
ethanol, 2% glutaraldehyde and formaldehyde. The effectiveness of infection quickly declines below pH 5.5 and above pH 8.5. In addition, LCMV can also be inactivated by heat, ultraviolet light or gamma irradiation.Studies have indicated that human infection of the virus occurs primarily during the fall and winter months, presumably due to the movement of mice indoors. Several measures can be taken to prevent exposure to LCM from wild rodents in the home. A checklist of precautions is provided by the Centers for Disease Control and Prevention, providing tips for sealing the home to keep rodents out, using traps to eliminate existing rodents, and maintaining a clean, healthy home. New technology reflects a growing trend for more humane means of eliminating rodents.  Products include devices that emit ultrasonic sound that allegedly irritates mice and drives them away, and more swift, painless means of death such as mini electrocution or gas chambers.  However, the traditional snap trap remains an economic and popular option.

Treatment
Treatment is symptomatic and supportive. Children with hydrocephalus often need a ventriculoperitoneal shunt. Nucleoside analog ribavirin is used in some cases due to the inhibitory effect the agent has in vitro on arenaviruses. However, there is not sufficient evidence for efficacy in humans to support routine use. The only survivor of a transplant-associated LCMV infection was treated with ribavirin and simultaneous tapering of the immunosuppressive medications. Early and intravenous ribavirin treatment is required for maximal efficacy, and it can produce considerable side effects. Ribavirin has not been evaluated yet in controlled clinical trials.Use of ribavirin during pregnancy is generally not recommended, as some studies indicate the possibility of teratogenic effects. If aseptic meningitis, encephalitis, or meningoencephalitis develops in consequence to LCMV, hospitalization and supportive treatment may be required.  In some circumstances, anti-inflammatory drugs may also be considered. In general, mortality is less than one percent.

Prognosis
Lymphocytic choriomeningitis is not a commonly reported infection in humans, though most infections are mild and are often never diagnosed. Serological surveys suggest that approximately 1–5% of the population in the U.S. and Europe has antibodies to LCMV. The prevalence varies with the living conditions and exposure to mice, and it has been higher in the past due to lower standards of living. The island of Vir in Croatia is one of the biggest described endemic places of origin of LCMV in the world, with IFA testing having found LCMV antibodies in 36% of the population. Individuals with the highest risk of infection are laboratory personnel who handle rodents or infected cells. Temperature and time of year is also a critical factor that contributes to the number of LCMV infections, particularly during fall and winter when mice tend to move indoors. Approximately 10–20% of the cases in immunocompetent individuals are thought to progress to neurological disease, mainly as aseptic meningitis. The overall case fatality rate is less than 1% and people with complications, including meningitis, almost always recover completely. Rare cases of meningoencephalitis have also been reported. More severe disease is likely to occur in people who are immunosuppressed.More than 50 infants with congenital LCMV infection have been reported worldwide. The probability that a woman will become infected after being exposed to rodents, the frequency with which LCMV crosses the placenta, and the likelihood of clinical signs among these infants are still poorly understood. In one study, antibodies to LCMV were detected in 0.8% of normal infants, 2.7% of infants with neurological signs and 30% of infants with hydrocephalus. In Argentina, no congenital LCMV infections were reported among 288 healthy mothers and their infants. However, one study found that two of 95 children in a home for people with severe mental disabilities had been infected with this virus. The prognosis for severely affected infants appears to be poor. In one series, 35% of infants diagnosed with congenital infections had died by the age of 21 months.Transplant-acquired lymphocytic choriomeningitis proves to have a very high morbidity and mortality rate. In the three clusters reported in the U.S. from 2005 to 2010, nine of the ten infected recipients died. One donor had been infected from a recently acquired pet hamster while the sources of the virus in the other cases were unknown.

Epidemiology
LCMV has been isolated from fleas, ticks, cockroaches, Culicoides and Aedes mosquitoes. Ticks, lice and mosquitoes have been shown to transmit this virus mechanically in the laboratory. The presence of LCMV in laboratories may cause serious long-term repercussions to worker safety. In 1989, an outbreak among humans occurred in a US cancer research institute that studied the effects of various therapeutic and diagnostic agents in animal models. Such agents had been developed in the animal care facility, which periodically screened sentinel animals for extraneous infection. Due to an oversight, no sentinel animals were monitored from August 1988 to March 1989.  When testing resumed, LCMV antibodies were found in the oldest sentinel hamsters. Several workers reported symptoms consistent with LCMV infection, leading to an investigation. Blood samples were obtained and tested for LCMV antibodies. Of the 82 workers that were tested, seven had definite serologic evidence of past LCMV infection, and two were hospitalized for an acute febrile illness.  All seven reported direct contact with the animals at the institute.An additional hazard associated with LCMV in laboratories misleading experimental results. Interference with research may involve:

[Inhibition of] tumor induction due to polyoma virus, and mammary tumor virus in the mouse, and [interference] with transplantable leukaemia in the guinea pig and the mouse. Infection is associated with depression of cellular immunity in the mouse. Rejection of cutaneous grafts or transplantable tumors may be delayed. In addition, infection will increase the sensitivity of the mouse to ectromelia virus and to bacterial endotoxins.Reported outbreaks have decreased, perhaps due to improved biohazard management in laboratories. However, it is possible that sporadic cases have been overlooked because of the wide range of clinical presentations. Clare A. Dykewicz, et al. recommend vigilant screening laboratory animals to be used in research facilities either through serum samples or cell line aliquots, as well as ensuring adequate ventilation in housing areas and use of appropriate sanitation products. Other practices to reduce cross-contamination in rodents include washing hands or changing gloves between animal care activities, thoroughly decontaminating cages before reusing them, and avoiding housing healthy rodents in the vicinity of potentially infected rodents.

Other animals
Although the house mouse (Mus musculus) is the primary reservoir host for LCMV, it is also often found in the wood mouse (Apodemus sylvaticus) and the yellow-necked mouse (Apodemus flavicollis). Hamster populations can act as reservoir hosts. Other rodents including guinea pigs, rats and chinchillas can be infected but do not appear to maintain the virus. LCMV has been shown to cause illness in New World primates such as macaques, marmosets and tamarins. Infections have also been reported in rabbits, dogs and pigs. After experimental inoculation, the incubation period in adult mice is 5 to 6 days. Congenitally or neonatally infected mice and hamsters do not become symptomatic for several months or longer.

Mice
A study conducted by John Hotchin and Heribert Weigand, of the New York State Department of Health, concluded, "The age of the mouse when first exposed to the virus determines its immune response."  If LCMV infection occurs in utero or within the first few hours of life, during the immunologically unresponsive period, the mouse will develop immune tolerance.  The virus will continue to proliferate for an indefinite time.  However, if a mouse is infected after the neonatal period, when the immune system is responsive, the immune response is active.  This immunological conflict can result in one of three ways; immunological paralysis, significant or complete suppression of virus with immunity to reinfection, or death.  Mice that are infected after the neonatal period often pass through a "runt" stage, which may last for several weeks.  Clinical symptoms include excitability, weight loss, and severe retardation of growth and hair development. In general, as the period of time between birth and inoculation decreases, less disease and mortality occurs.Post mortem lesions in mice show signs of hepatomegaly, splenomegaly, lymphadenopathy, and swollen or shrunken and pitted kidneys due to glomerulonephritis. Histological findings in persistently infected mice often show chronic glomerulonephritis. In these mice, and some hamsters, vasculitis and lymphocytic infiltrates in many organs and tissues including the liver, spleen, lung, kidneys, pancreas, blood vessels, meninges and brain are present.

Hamsters
Pathogenesis occurs in the same manner in hamsters as in mice. Symptoms in hamsters are highly variable, and typically indicate that the pet has been infected and shedding the virus for several months.  Early signs may include inactivity, loss of appetite, and a rough coat.  As the disease progresses, the animal may experience weight loss, hunched posture, inflammation around the eyes, and eventually death.  Alternatively, some infected hamsters may be asymptomatic.

Rats
Experimental intracerebral infection of suckling rats results in microcephaly, retinitis and the destruction of several brain regions, leading to permanent abnormalities of movement, coordination, vision and behavior.

Primates
LCMV causes callitrichid hepatitis in New World primates. The onset of the infection is nonspecific and may include fever, anorexia, dyspnea, weakness and lethargy. Jaundice is characteristic and petechial hemorrhages may develop. Prostration and death usually follow.Necropsy lesions in primates with callitrichid hepatitis show signs of jaundice, hepatomegaly, splenomegaly, and subcutaneous and intramuscular hemorrhages. Pleural and pericardial effusion, sometimes sanguineous, has also been reported. On histology, multifocal necrosis with acidophilic bodies and mild inflammatory infiltrates are typically found in the liver.

Diagnosis
As in humans, the sensitivity of testing methods for rodents contributes to the accuracy of diagnosis.  LCMV is typically identified through serology. However, in an endemically infected colony, more practical methods include MAP (mouse antibody production) and PCR testing. Another means of diagnosis is introducing a known naïve adult mouse to the suspect rodent colony. The introduced mouse will seroconvert, allowing use of immunofluorescence antibody (IFA), MFIA or ELISA to detect antibodies.

Treatment
Immunosuppressive therapy has been effective in halting the disease for laboratory animals.

Morbidity and mortality
LCMV infections are focal Estimates of its prevalence in wild mouse populations range from 0% to 60%, with an average prevalence of 9%. The incidence of LCMV in pet rodents is unknown, yet very few human cases have been associated with exposure to pets. In the transplant-associated cases linked to a pet hamster in 2005, two other hamsters and a guinea pig at the pet shop, and approximately 4% of the hamsters at the distributor, were also infected. Morbidity and mortality rates vary with the species of animal and its age at infection, as well as the strain of the virus and route of exposure. Neonatally and congenitally infected mice remain asymptomatic for many months, but the onset of glomerulonephritis reduces overall life expectancy. The morbidity rate in naturally infected post-neonatal mice is unknown; however, subclinical disease may be the most common form, as few natural outbreaks have been reported. In hamsters, approximately half of all congenitally infected animals clear the virus when they are approximately three months old and remain healthy; the remaining animals develop chronic disease. Hamsters infected as adults usually remain asymptomatic. Callitrichid hepatitis is reported to be highly fatal in naturally infected marmosets and tamarins in zoos. Since 1980, 12 outbreaks with 57 deaths have been reported in the U.S. In experimentally infected rhesusmacaques, three of four animals became fatally ill when inoculation was by the intravenous route. In contrast, inoculation by the intragastric route usually led to asymptomatic infections, with occasional disease and few deaths.

In pets
Pet rodents are not known to be natural reservoirs for lymphocytic choriomeningitis virus.  However, pets can become vectors if they are exposed to wild house mice in a breeding facility, pet store, or home. Such infections are rare. To date, (January 2017) documented infections in humans have occurred only after introduction to infected mice, guinea pigs, and hamsters, with the majority of cases transmitted by mice. LCMV infection in other animals, including zoo animals, may be possible.In choosing a pet, the CDC advises looking for general indications of health both in the prospective pet and others in the facility.  The rodent of choice should be lively and alert, have a glossy coat, breathe normally and have no discharge from eyes or nose.  If one of the animals in the facility looks ill, the others may have been exposed, and none of the rodents at that location should be purchased.Serologic testing is not recommended for pet rodents, as it has been unreliable in detecting antibodies in animals with active infections.  For laboratory purposes, immunohistochemistry staining of tissues and virus isolation are used for more accurate testing, but this is unnecessary for the general house pet.  The greatest risk of infection to humans occurs shortly after purchase of a pet, so that exposure to the virus, if present, has likely already occurred to existing pet owners.  Continued ownership poses negligible additional risk.The National Center for Infectious Disease suggests the following precautions to reduce the risk of LCMV infection:

Wash hands with soap and water after handling pet rodents; use waterless alcohol-based hand rubs when soap is not available.
Keep rodent cages clean and free of soiled bedding.
Clean the cage in a well-ventilated area or outside.
Wash hands thoroughly with soap and water after cleaning up pet droppings.  Closely supervise young children, especially those less than five years old, when cleaning cages, and make sure they wash their hands immediately after handling rodents and rodent caging or bedding.
Do not kiss pet rodents or hold them close to your face.Rodent owners who no longer wish to keep their pet should consult a veterinarian.  Pets should not be released into the wild for humane, legal, and ecological reasons.  After a rodent has been purchased, it should not be returned to the pet store as it may have been exposed to LCMV through house mice.

Research
LCM is the archetypal arenavirus, and was instrumental in research which uncovered the major pathogenetic mechanisms of all arenaviruses.The field of viral immunology will continue to be uncovered by the model system of LCMV. Specifically, the study of persistent viral infections as well as vaccine development, represent two essential areas. LCMV is already identified as the best model to examine the difference between acute and persistent infection in its natural host Mus musculus, the common house mouse. Conveniently, the mouse is also the most widely used genetic model for mammalian genetics. A major phenotypic difference results from only two nucleotide differences between acute LCMV, also known as Armstrong LCMV, and one of its variant, Clone 13, which leads to persistent LCMV infection.  One of the nucleotide mutations is in the process of glycoprotein formation and affects tropism. The second base pair mutation affects the polymerase which influences replicative capacity. The mechanism by which these mutations cause acute versus chronic LCMV infection is not understood.
An important aspect of the present modern society is the thorough understanding of the burden of cancer. In many ways, this disease mirrors persistent viral infection, in the way that it evades and progresses despite the immune systems effort to eliminate it. The LCMV model will be a great path towards advancements in cancer studies.  Furthermore, LCMV has been a widely used model system for understanding T cell memory and vaccine synthesis. It was the original model when first studied focused on CD-8 T cells response towards LCMV infection. In addition, a better understanding of CD-4 T cell memory is also a result of studies with LCMV and will continue to contribute to a more efficient mechanism of vaccine formation. Specifically, LCMV has been recently used to quantify the efficiency of a new hydrogen peroxide-based vaccine formation mechanism. The future enhancement of the field of vaccinology will greatly depend on the LCMV model system.LCMV is a prototype of more severe hemorrhagic fever viruses, especially Lassa virus with the greatest prevalence in sub-Saharan Africa. However, other strains of this virus (Junin and Machupo viruses) are present in parts of South America and other strains continue to significantly affect the southern African population. Since the modern society continue to become a more inter-connected world, the spread of these virus strains will continue to pose a severe threat around the globe. Understanding the biology of the LCMV model virus will help in advancing the understanding of this important class of viruses and more specifically will give insight into the biology of the Lassa virus which proves to be a growing threat around the world. Furthermore, the United States National Institute for Allergy and Infectious Diseases (NIAID) has appointed the family of arenaviridae to be "Category A Priority Pathogens". This translates to the highest level of importance for the high potential for morbidity and mortality from an infectious agent which is relatively easy to produce and transmit.

Footnotes
References
ICTVdB-The Universal Virus Database, version 4. [2]
Centers for Disease Control and Prevention. Lymphocytic Choriomeningitis Fact Sheet
CBWInfo (1999). "Safety Precautions for Lymphocytic Choriomeningitis Casualties". Archived from the original on 14 May 2006. Retrieved 11 May 2006.
"Rodent virus now linked to six deaths—PetSmart in Rhode Island testing animals for rare disease". NBC News. Microsoft. Associated Press. 25 May 2005. Retrieved 11 May 2006.
"Australian scientists discover new virus". The Age. Fairfax. Australian Associated Press. 22 April 2007. Retrieved 22 April 2007.
Marrie TJ, Saron MF (January 1998). "Seroprevalence of lymphocytic choriomeningitis virus in Nova Scotia". Am. J. Trop. Med. Hyg. 58 (1): 47–9. doi:10.4269/ajtmh.1998.58.47. PMID 9452291.
Bauers, Sandy.  "House vs. Mouse: The Latest Ideas in Humanely Showing Our Disease-Ridden Fall Visitors the Door." Philadelphia Inquirer 10 Nov. 2006: n.p. Web.
"choriomeningitis." The American Heritage Medical Dictionary. 2009. Web.
Craighead, John E. MD. Pathology and Pathogenesis of Human Viral Disease. San Diego, California: Academic, 2000. Print.
Lasker, Jill S. "Lymphocytic choriomeningitis." The Gale Encyclopedia of Medicine.  2nd ed. 2002. Web.
"Lymphocytic Choriomeningitis Virus (LCMV)." Centers for Disease Control and Prevention. CDC, n.d. Web. 22 Sept. 2009
"Lymphocytic Choriomeningitis Virus." Charles River.  Charles River Laboratories International, Inc, 2009.  Web.  28 Oct 2009.
"Prevent LCMV from wild rodents." CDC Special Pathogens Branch. CDC. n.d. pdf. 22 Sept. 2009. https://web.archive.org/web/20130810131242/http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/lcmv/prevent.pdf
United States. National Center for Infectious Diseases. Lymphocytic Choriomeningitis Virus from Pet Rodents. CDC, n.d. Web. 22 Sept. 2009.
---. Lymphocytic Choriomeningitis Virus (LCMV) and Pregnancy: Facts and Prevention. CDC, 5 Oct. 2005. Web. 22 Sept. 2009.
United States. Special Pathogens Branch, Centers for Disease Control and Prevention. Information for Pet Owners: Reducing the Risk of Becoming Infected with LCMV from Pet Rodents. CDC. 6 Sept. 2005. Web. 26 Sept. 2009.
---. Lymphocytic choriomeningitis. CDC. 11 October 2007. Web. 26 Sept. 2009.
Vilches, Jose MD ed. Pam Mouser, MD. "Lymphocytic Choriomeningitis." Animal Disease Diagnostic Laboratory.  Animal Disease Diagnostic Laboratory, Purdue University, 2007.  Web. 23 September 2009.
Lee, KJ; Novella, IS; Teng, MN; Oldstone, MBA; de la Torre, JC (2000). "NP and L Proteins of Lymphocytic Choriomeningitis Virus (LCMV) Are Sufficient for Efficient Transcription and Replication of LCMV Genomic RNA Analog". Journal of Virology. 74 (8): 3470–7. doi:10.1128/jvi.74.8.3470-3477.2000. PMC 111854. PMID 10729120.
Swiss Institute of Bioinformatics. Viral Zone "Arenaviridae"
Zhou, X; Ramachaundran, S; Mann, M; Popkin, DL (2012). "Role of Lymphocytic Choriomeningitis virus(LCMV) in understanding viral immunology: Past, Present and Future" </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 Erotomania and explain in detail? [/INST] Erotomania, also known as de Clérambaults Syndrome, named after French psychiatrist Gaëtan Gatian de Clérambault, is listed in the DSM-5 as a subtype of a delusional disorder. It is a relatively uncommon paranoid condition that is characterized by an individuals delusions of another person being infatuated with them. This disorder is most often seen (though not exclusively) in female patients who are shy, dependent and sexually inexperienced. The object of the delusion is typically a male who is unattainable due to high social or financial status, marriage or uninterest. The object of obsession may also be imaginary, deceased or someone the patient has never met. Delusions of reference are common, as the erotomanic individual often perceives that they are being sent messages from the secret admirer through innocuous events such as seeing license plates from specific states, but has no proof. Commonly, the onset of erotomania is sudden, and the course is chronic.

Presentation
Erotomania is more common in women, but men are more likely to exhibit violent and stalker-like behaviors. The core symptom of the disorder is that the individual holds an unshakable belief that another person is secretly in love with them. In some cases, the person with the condition may believe several people at once are "secret admirers". Most commonly, the individual has delusions of being loved by an unattainable person who is usually an acquaintance or someone the person has never met. They may also experience other types of delusions concurrently with erotomania, such as delusions of reference, wherein the perceived admirer secretly communicates their love by subtle methods such as body posture, arrangement of household objects, colors, license plates on cars from specific states, and other seemingly innocuous acts (or, if the person is a public figure, through clues in the media). Some delusions may be extreme such as the conception, birth, and kidnapping of children that never existed. The delusional objects may be replaced by others over time, and some may be chronic in fixed forms. Denial is characteristic with this disorder as the patients do not accept the fact that their object of delusion may be married, unavailable, or uninterested. The phantom lover may also be imaginary or deceased.
Erotomania has two forms: primary and secondary. Primary erotomania is also commonly referred to as de Clerambaults syndrome and Old Maids Insanity and it exists alone without comorbidities, has a sudden onset and a chronic outcome. The secondary form is found along with mental disorders like paranoid schizophrenia, often includes persecutory delusions, hallucinations, and grandiose ideas, and has a more gradual onset. Patients with a "fixed" condition are more seriously ill with constant delusions and are less responsive to treatment. These individuals are usually timid, dependent women that are often sexually inexperienced. In those with a more mild, recurrent condition, delusions are shorter-lived and the disorder can exist undetected by others for years. Problematic behaviors include actions like calling, sending letters and gifts, making unannounced house visits and other persistent stalking behaviors.

Cause
Erotomania may present as a primary mental disorder, or as a symptom of another psychiatric illness. With secondary erotomania, the erotomanic delusions are due to other mental disorders such as bipolar I disorder or schizophrenia. Symptoms may also be precipitated by alcoholism and the use of antidepressants. There may be a potential genetic component involved as family histories of first degree relatives with histories of psychiatric disorders are common. Sigmund Freud explained erotomania as a defense mechanism to ward off homosexual impulses which can lead to strong feelings of paranoia, denial, displacement and projection. Similarly, it has been explained as a way to cope with severe loneliness or ego deficit following a major loss. Erotomania may also be linked to unsatiated urges dealing with homosexuality or narcissism. Some research shows brain abnormalities occurring in patients with erotomania such as heightened temporal lobe asymmetry and greater volumes of lateral ventricles than those with no mental disorders.

Treatment
Prognosis differs from person to person, and the ideal treatment is not completely understood. Treatment for this disorder gains the best results when tailored specifically for each individual. To date, the mainline pharmacological treatments have been pimozide (a typical antipsychotic which was also approved for treating Tourettes Syndrome), and atypical antipsychotics like risperidone and clozapine. Non-pharmacologic treatments that have shown some degree of efficacy are electroconvulsive therapy (ECT), supportive psychotherapy, family and environment therapy, rehousing, risk management and treating underlying disorders in cases of secondary erotomania. ECT may provide temporary remission of delusional beliefs; antipsychotics help attenuate delusions and reduce agitation or associated dangerous behaviors, and SSRIs may be used to treat secondary depression. In delusional disorder there is some evidence that pimozide has superior efficacy compared with other antipsychotics. Psychosocial psychiatric interventions can enhance the quality of life through allowing some social functioning, and treating comorbid disorders is a priority for secondary erotomania. Family therapy, adjustment of socio-environmental factors, and replacing delusions with something positive may be beneficial to all. In most cases, harsh confrontation should be avoided. Structured risk assessment helps to manage risky behaviors in those individuals more likely to engage in actions that include violence, stalking, and crime. For particularly troublesome cases, neuroleptics and enforced separation may be moderately effective.

History
Early references to the condition can be found in the work of Hippocrates, Freud (1911), G.G. de Clérambault (1942), Erasistratus, Plutarch and Galen. Parisian physician, Bartholomy Pardoux (1545-1611) covered the topics of nymphomania and erotomania. In 1623, erotomania was referred to in a treatise by Jacques Ferrand (Maladie damour ou Mélancolie érotique) and has been called "erotic paranoia" and "erotic self-referent delusion" until the common usage of the terms erotomania and de Clérambaults syndrome. In 1971 and 1977, M.V. Seeman referred to the disorder as "phantom lover syndrome" and "psychotic erotic transference reaction and delusional loving". Emil Kraepelin and Bernard also wrote of erotomania and more recently, Winokur, Kendler, and Munro have contributed to knowledge on the disorder.G. E. Berrios and N. Kennedy outlined in Erotomania: a conceptual history (2002) several periods of history through which the definition of erotomania has changed considerably:

Classical times – early eighteenth century: General disease caused by unrequited love
Early eighteenth-beginning of nineteenth century: Practise of excess physical love (akin to nymphomania or satyriasis)
Early nineteenth century – beginning twentieth century: Unrequited love as a form of mental disease
Early twentieth century – present: Delusional belief of "being loved by someone else"In one case, erotomania was reported in a patient who had undergone surgery for a ruptured cerebral aneurysm.

Well-known cases
In his paper that described the syndrome, de Clérambault referenced a patient he had counselled who was obsessed with British monarch George V. She had stood outside Buckingham Palace for hours at a time, believing that the king was communicating his desire for her by moving the curtains.Parallels were drawn between this and a 2011 case where the body of a homeless American man was found on a secluded island in St James Park, within sight of Buckingham Palace. The man had sent hundreds of "strange and offensive" packages to Queen Elizabeth II over the previous fifteen years.The attempted assassination of United States president Ronald Reagan by John Hinckley Jr. has been reported to have been driven by an erotomaniac fixation on actress Jodie Foster, whom Hinckley was attempting to impress.
Late-night TV entertainer David Letterman and former astronaut Story Musgrave were both stalked by Margaret Mary Ray, who had erotomania.Michael David Barrett allegedly had erotomania, stalking ESPN correspondent Erin Andrews across the country, trying to see her and taking lewd videos.Many cases of obsession or stalking can be linked to erotomania but do not always necessarily go hand in hand.

In media
Nurse Betty (2000)
A main character in Orange Is the New Black, Lorna Morello, exhibits erotomanic behavior towards a man she has delusions of being engaged to.
He Loves Me... He Loves Me Not (2002)
A 2011 episode (Series 5, Episode 3) of the British TV series Lewis features a character with erotomania, referred to in the show as de Clérambaults syndrome.
Enduring Love (1997)
Criminal Minds Season 1, Episode 5: Broken Mirror.
Doc Martin Season 6, Episode 3: The Tameness of a Wolf

See also
Further reading
Remington GJ, Jeffries JJ (1994). "Erotomanic delusions and electroconvulsive therapy: a case series". J Clin Psychiatry. 55 (7): 306–8. PMID 8071292.
Anderson CA, Camp J, Filley CM (1998). "Erotomania after aneurysmal subarachnoid hemorrhage: case report and literature review". J Neuropsychiatry Clin Neurosci. 10 (3): 330–7. doi:10.1176/jnp.10.3.330. PMID 9706541.{{cite journal}}:  CS1 maint: multiple names: authors list (link)
Frank Bruni, Behind the Jokes, a Life Of Pain and Delusion; For Letterman Stalker, Mental Illness Was Family Curse and Scarring Legacy, New York Times, November 22, 1998
Foster, David & Levinson, Arlene. Suicide on a railroad track ends a celebrity-stalkers inner agony Archived 2011-06-14 at the Wayback Machine., Associated Press, October 11, 1998
Berrios GE, Kennedy N (2002). "Erotomania: a conceptual history". Hist Psychiatry. 13 (52): 381–400. doi:10.1177/0957154X0201305202. PMID 12638595. S2CID 24663481.
Helen K. Gediman (14 December 2016). Stalker, Hacker, Voyeur, Spy: A Psychoanalytic Study of Erotomania, Voyeurism, Surveillance, and Invasions of Privacy. Karnac Books. pp. 21–34. ISBN 978-1-78181-706-3.

References
Notes
Bibliography
Anderson CA, Camp J, Filley CM (1998). "Erotomania after aneurysmal subarachnoid hemorrhage: case report and literature review". J Neuropsychiatry Clin Neurosci. 10 (3): 330–70. doi:10.1176/jnp.10.3.330. PMID 9706541.{{cite journal}}:  CS1 maint: multiple names: authors list (link)
Berrios GE, Kennedy N (2002). "Erotomania: a conceptual history". History of Psychiatry. 13 (52): 381–400. doi:10.1177/0957154X0201305202. PMID 12638595. S2CID 24663481.
Helen K. Gediman (14 December 2016). Stalker, Hacker, Voyeur, Spy: A Psychoanalytic Study of Erotomania, Voyeurism, Surveillance, and Invasions of Privacy. Karnac Books. pp. 21–34. ISBN 978-1-78181-706-3.
Jordan H.W., Lockert E.W., Johnson-Warren M., Cabell C., Cooke T., Greer W., Howe G. (2006). "Erotomania revisisted: Thirty-four years later". Journal of the National Medical Association. 98 (5): 787–93. PMC 2569288. PMID 16749657.{{cite journal}}:  CS1 maint: multiple names: authors list (link)
Kelly B.D. (2005). "Erotomania: Epidemiology and management". CNS Drugs. 19 (8): 657–669. doi:10.2165/00023210-200519080-00002. PMID 16097848.
McDonnell, Margaux, and Mike McPadden. "9 Stalkers That Make Us Glad Were Not Famous." CrimeFeed, 12 Nov. 2013, crimefeed.com/2013/10/9-stalkers-that-make-us-glad-were-not-famous/.
Oliveira C., Alves S., Ferreira C., Agostinho C., Avelino M.J. (2016). "Erotomania-A review of De Clerambaults Syndrome". The Journal of the European Psychiatric Association. 33: S664.{{cite journal}}:  CS1 maint: multiple names: authors list (link)
Seeman M.V. (2016). "Erotomania and recommendations for treatment". Psychiatric Quarterly </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 Neuroglycopenia and explain in detail? [/INST] Neuroglycopenia is a shortage of glucose (glycopenia) in the brain, usually due to hypoglycemia. Glycopenia affects the function of neurons, and alters brain function and behavior. Prolonged or recurrent neuroglycopenia can result in loss of consciousness, damage to the brain, and eventual death.

Signs and symptoms
Abnormal mentation, impaired judgment
Nonspecific dysphoria, anxiety, moodiness, depression, crying, fear of dying, suicidal thoughts
Negativism, irritability, belligerence, combativeness, rage
Personality change, emotional lability
Fatigue, weakness, apathy, lethargy, daydreaming
Confusion, amnesia, dizziness, delirium
Staring, "glassy" look, blurred vision, double vision
Automatic behavior
Difficulty speaking, slurred speech
Ataxia, incoordination, sometimes mistaken for "drunkenness"
Focal or general motor deficit, paralysis, hemiparesis
Paresthesia, headache
Stupor, coma, abnormal breathing
Generalized or focal seizures
Plasma glucose 20 mg/dL (1.1 mmol/L) or lowerNot all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms. Specific manifestations vary by age and by the severity of the hypoglycemia. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person do tend to be similar from episode to episode.
In the large majority of cases, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.

Metabolic responses
Most neurons have the ability to use other fuels besides glucose (e.g. lactic acid, ketones) </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 Pneumoperitoneum and explain in detail? [/INST] Pneumoperitoneum is pneumatosis (abnormal presence of air or other gas) in the peritoneal cavity, a potential space within the abdominal cavity. The most common cause is a perforated abdominal organ, generally from a perforated peptic ulcer, although any part of the bowel may perforate from a benign ulcer, tumor or abdominal trauma. A perforated appendix seldom causes a pneumoperitoneum.
Spontaneous pneumoperitoneum is a rare case that is not caused by an abdominal organ rupture. This is also called an idiopathic spontaneous pneumoperitoneum when the cause is not known.
In the mid-twentieth century, an "artificial" pneumoperitoneum was sometimes intentionally administered as a treatment for a hiatal hernia.  This was achieved by insufflating the abdomen with carbon dioxide.  The practice is currently used by surgical teams in order to aid in performing laparoscopic surgery.

Causes
Perforated duodenal ulcer – The most common cause of rupture in the abdomen. Especially of the anterior aspect of the first part of the duodenum.
Perforated peptic ulcer
Bowel obstruction
Ruptured diverticulum
Penetrating trauma
Ruptured inflammatory bowel disease (e.g., megacolon)
Necrotising enterocolitis/pneumatosis coli
Bowel cancer
Ischemic bowel
Steroids
After laparotomy
After laparoscopy
Breakdown of a surgical anastomosis
Bowel injury after endoscopy
Peritoneal dialysis (PD), although the prevalence of pneumoperitoneum is estimated to be less than 4% among people with PD in a more recent study in the United Kingdom.
Vaginal insufflation (air enters via the fallopian tubes; e.g., water-skiing, oral sex)
Colonic or peritoneal infection
From chest (e.g., bronchopleural fistula)
Non-invasive PAP (positive airway pressure) can force air down duodenum as well as down trachea.

Spontaneous pneumoperitoneum
A spontaneous pneumoperitoneum is a rare case that is not caused by an abdominal organ rupture. This is also called an idiopathic spontaneous pneumoperitoneum when the cause is not known </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 Larynx and explain in detail? [/INST] The larynx (), commonly called the voice box, is an organ in the top of the neck involved in breathing, producing sound and protecting the trachea against food aspiration. The opening of larynx into pharynx known as the laryngeal inlet is about 4–5 centimeters in diameter. The larynx houses the vocal cords, and manipulates pitch and volume, which is essential for phonation. It is situated just below where the tract of the pharynx splits into the trachea and the esophagus. The word ʻlarynxʼ (plural ʻlaryngesʼ) comes from the Ancient Greek word  lárunx ʻlarynx, gullet, throat.ʼ

Structure
The triangle-shaped larynx consists largely of cartilages that are attached to one another, and to surrounding structures, by muscles or by fibrous and elastic tissue components. The larynx is lined by a ciliated columnar epithelium except for the vocal folds. The cavity of the larynx extends from its triangle-shaped inlet, to the epiglottis, and to the circular outlet at the lower border of the cricoid cartilage, where it is continuous with the lumen of the trachea. The mucous membrane lining the larynx forms two pairs of lateral folds that project inward into its cavity. The upper folds are called the vestibular folds. They are also sometimes called the false vocal cords for the rather obvious reason that they play no part in vocalization. The lower pair of folds are known as the vocal cords, which produce sounds needed for speech and other vocalizations. The slit-like space between the left and right vocal cords, called the rima glottidis, is the narrowest part of the larynx. The vocal cords and the rima glottidis are together designated as the glottis. The laryngeal cavity above the vestibular folds is called the vestibule. The very middle portion of the cavity between the vestibular folds and the vocal cords is the ventricle of the larynx, or laryngeal ventricle. The infraglottic cavity is the open space below the glottis.

Location
In adult humans, the larynx is found in the anterior neck at the level of the cervical vertebrae C3–C6. It connects the inferior part of the pharynx (hypopharynx) with the trachea. The laryngeal skeleton consists of nine cartilages: three single (epiglottic, thyroid and cricoid) and three paired (arytenoid, corniculate, and cuneiform). The hyoid bone is not part of the larynx, though the larynx is suspended from the hyoid. The larynx extends vertically from the tip of the epiglottis to the inferior border of the cricoid cartilage. Its interior can be divided in supraglottis, glottis and subglottis.

Cartilages
There are nine cartilages, three unpaired and three paired (3 pairs=6), that support the mammalian larynx and form its skeleton.
Unpaired cartilages:

Thyroid cartilage: This forms the Adams apple (also called the laryngeal prominence). It is usually larger in males than in females. The thyrohyoid membrane is a ligament associated with the thyroid cartilage that connects it with the hyoid bone. It supports the front portion of the larynx.
Cricoid cartilage: A ring of hyaline cartilage that forms the inferior wall of the larynx. It is attached to the top of the trachea. The median cricothyroid ligament connects the cricoid cartilage to the thyroid cartilage.
Epiglottis: A large, spoon-shaped piece of elastic cartilage. During swallowing, the pharynx and larynx rise. Elevation of the pharynx widens it to receive food and drink; elevation of the larynx causes the epiglottis to move down and form a lid over the glottis, closing it off.Paired cartilages:

Arytenoid cartilages: Of the paired cartilages, the arytenoid cartilages are the most important because they influence the position and tension of the vocal cords. These are triangular pieces of mostly hyaline cartilage located at the posterosuperior border of the cricoid cartilage.
Corniculate cartilages: Horn-shaped pieces of elastic cartilage located at the apex of each arytenoid cartilage.
Cuneiform cartilages: Club-shaped pieces of elastic cartilage located anterior to the corniculate cartilages.

Muscles
The muscles of the larynx are divided into intrinsic and extrinsic muscles. The extrinsic muscles act on the region and pass between the larynx and parts around it but have their origin elsewhere; the intrinsic muscles are confined entirely within the larynx and have their origin and insertion there.The intrinsic muscles are divided into respiratory and the phonatory muscles (the muscles of phonation). The respiratory muscles move the vocal cords apart and serve breathing. The phonatory muscles move the vocal cords together and serve the production of voice. The main respiratory muscles are the posterior cricoarytenoid muscles. The phonatory muscles are divided into adductors (lateral cricoarytenoid muscles, arytenoid muscles) and tensors (cricothyroid muscles, thyroarytenoid muscles).

Intrinsic
The intrinsic laryngeal muscles are responsible for controlling sound production.

Cricothyroid muscle lengthen and tense the vocal cords.
Posterior cricoarytenoid muscles abduct and externally rotate the arytenoid cartilages, resulting in abducted vocal cords.
Lateral cricoarytenoid muscles adduct and internally rotate the arytenoid cartilages, increase medial compression.
Transverse arytenoid muscle adduct the arytenoid cartilages, resulting in adducted vocal cords.
Oblique arytenoid muscles narrow the laryngeal inlet by constricting the distance between the arytenoid cartilages.
Thyroarytenoid muscles narrow the laryngeal inlet, shortening the vocal cords, and lowering voice pitch. The internal thyroarytenoid is the portion of the thyroarytenoid that vibrates to produce sound.Notably the only muscle capable of separating the vocal cords for normal breathing is the posterior cricoarytenoid.  If this muscle is incapacitated on both sides, the inability to pull the vocal cords apart (abduct) will cause difficulty breathing. Bilateral injury to the recurrent laryngeal nerve would cause this condition.  It is also worth noting that all muscles are innervated by the recurrent laryngeal branch of the vagus except the cricothyroid muscle, which is innervated by the external laryngeal branch of the superior laryngeal nerve (a branch of the vagus).
Additionally, intrinsic laryngeal muscles present a constitutive Ca2+-buffering profile that predicts their better ability to handle calcium changes in comparison to other muscles. This profile is in agreement with their function as very fast muscles with a well-developed capacity for prolonged work. Studies suggests that mechanisms involved in the prompt sequestering of Ca2+ (sarcoplasmic reticulum Ca2+-reuptake proteins, plasma membrane pumps, and cytosolic Ca2+-buffering proteins) are particularly elevated in laryngeal muscles, indicating their importance for the myofiber function and protection against disease, such as Duchenne muscular dystrophy. Furthermore, different levels of Orai1 in rat intrinsic laryngeal muscles and extraocular muscles over the limb muscle suggests a role for store operated calcium entry channels in those muscles functional properties and signaling mechanisms.

Extrinsic
The extrinsic laryngeal muscles support and position the larynx within the mid-cervical cereal region.
thumb|Extrinsic laryngeal muscles

Sternothyroid muscles depress the larynx. (Innervated by ansa cervicalis)
Omohyoid muscles depress the larynx. (Ansa cervicalis)
Sternohyoid muscles depress the larynx. (Ansa cervicalis)
Inferior constrictor muscles. (CN X)
Thyrohyoid muscles elevates the larynx. (C1)
Digastric elevates the larynx. (CN V3, CN VII)
Stylohyoid elevates the larynx. (CN VII)
Mylohyoid elevates the larynx. (CN V3)
Geniohyoid elevates the larynx. (C1)
Hyoglossus elevates the larynx. (CN XII)
Genioglossus elevates the larynx. (CN XII)

Nerve supply
The larynx is innervated by branches of the vagus nerve on each side. Sensory innervation to the glottis and laryngeal vestibule is by the internal branch of the superior laryngeal nerve. The external branch of the superior laryngeal nerve innervates the cricothyroid muscle.  Motor innervation to all other muscles of the larynx and sensory innervation to the subglottis is by the recurrent laryngeal nerve. While the sensory input described above is (general) visceral sensation (diffuse, poorly localized), the vocal cords also receives general somatic sensory innervation (proprioceptive and touch) by the superior laryngeal nerve.
Injury to the external branch of the superior laryngeal nerve causes weakened phonation because the vocal cords cannot be tightened. Injury to one of the recurrent laryngeal nerves produces hoarseness, if both are damaged the voice may or may not be preserved, but breathing becomes difficult.

Development
In newborn infants, the larynx is initially at the level of the C2–C3 vertebrae, and is further forward and higher relative to its position in the adult body. The larynx descends as the child grows.

Laryngeal cavity
The laryngeal cavity (cavity of the larynx) extends from the laryngeal inlet downwards to the lower border of the cricoid cartilage where it is continuous with that of the trachea.It is divided into two parts by the projection of the vocal folds, between which is a narrow triangular opening, the rima glottidis.
The portion of the cavity of the larynx above the vocal folds is called the laryngeal vestibule; it is wide and triangular in shape, its base or anterior wall presenting, however, about its center the backward projection of the tubercle of the epiglottis.
It contains the vestibular folds, and between these and the vocal folds are the laryngeal ventricles.
The portion below the vocal folds is called the infraglottic cavity. It is at first of an elliptical form, but lower down it widens out, assumes a circular form, and is continuous with the tube of the trachea.

Function
Sound generation
Sound is generated in the larynx, and that is where pitch and volume are manipulated. The strength of expiration from the lungs also contributes to loudness.
Manipulation of the larynx is used to generate a source sound with a particular fundamental frequency, or pitch.  This source sound is altered as it travels through the vocal tract, configured differently based on the position of the tongue, lips, mouth, and pharynx.  The process of altering a source sound as it passes through the filter of the vocal tract creates the many different vowel and consonant sounds of the worlds languages as well as tone, certain realizations of stress and other types of linguistic prosody. The larynx also has a similar function to the lungs in creating pressure differences required for sound production; a constricted larynx can be raised or lowered affecting the volume of the oral cavity as necessary in glottalic consonants.
The vocal cords can be held close together (by adducting the arytenoid cartilages) so that they vibrate (see phonation). The muscles attached to the arytenoid cartilages control the degree of opening. Vocal cord length and tension can be controlled by rocking the thyroid cartilage forward and backward on the cricoid cartilage (either directly by contracting the cricothyroids or indirectly by changing the vertical position of the larynx), by manipulating the tension of the muscles within the vocal cords, and by moving the arytenoids forward or backward. This causes the pitch produced during phonation to rise or fall. In most males the vocal cords are longer and have a greater mass than most females vocal cords, producing a lower pitch.
The vocal apparatus consists of two pairs of folds, the vestibular folds (false vocal cords) and the true vocal cords. The vestibular folds are covered by respiratory epithelium, while the vocal cords are covered by stratified squamous epithelium. The vestibular folds are not responsible for sound production, but rather for resonance. The exceptions to this are found in Tibetan chanting and Kargyraa, a style of Tuvan throat singing. Both make use of the vestibular folds to create an undertone. These false vocal cords do not contain muscle, while the true vocal cords do have skeletal muscle.

Other
The most important role of the larynx is its protective function, the prevention of foreign objects from entering the lungs by coughing and other reflexive actions.  A cough is initiated by a deep inhalation through the vocal cords, followed by the elevation of the larynx and the tight adduction (closing) of the vocal cords.  The forced expiration that follows, assisted by tissue recoil and the muscles of expiration, blows the vocal cords apart, and the high pressure expels the irritating object out of the throat.  Throat clearing is less violent than coughing, but is a similar increased respiratory effort countered by the tightening of the laryngeal musculature.  Both coughing and throat clearing are predictable and necessary actions because they clear the respiratory passageway, but both place the vocal cords under significant strain.Another important role of the larynx is abdominal fixation, a kind of Valsalva maneuver in which the lungs are filled with air in order to stiffen the thorax so that forces applied for lifting can be translated down to the legs.  This is achieved by a deep inhalation followed by the adduction of the vocal cords.  Grunting while lifting heavy objects is the result of some air escaping through the adducted vocal cords ready for phonation.Abduction of the vocal cords is important during physical exertion.  The vocal cords are separated by about 8 mm (0.31 in) during normal respiration, but this width is doubled during forced respiration.During swallowing, elevation of the posterior portion of the tongue levers (inverts) the epiglottis over the glottis opening to prevent swallowed material from entering the larynx which leads to the lungs, and provides a path for a food or liquid bolus to "slide" into the esophagus; the hyo-laryngeal complex is also pulled upwards to assist this process. Stimulation of the larynx by aspirated food or liquid produces a strong cough reflex to protect the lungs.
In addition, intrinsic laryngeal muscles are spared from some muscle wasting disorders, such as Duchenne muscular dystrophy,  may facilitate the development of novel strategies for the prevention and treatment of muscle wasting in a variety of clinical scenarios. ILM have a calcium regulation system profile suggestive of a better ability to handle calcium changes in comparison to other muscles, and this may provide a mechanistic insight for their unique pathophysiological properties

Clinical significance
Disorders
There are several things that can cause a larynx to not function properly. Some symptoms are hoarseness, loss of voice, pain in the throat or ears, and breathing difficulties.

Acute laryngitis is the sudden inflammation and swelling of the larynx. It is caused by the common cold or by excessive shouting. It is not serious. Chronic laryngitis is caused by smoking, dust, frequent yelling, or prolonged exposure to polluted air. It is much more serious than acute laryngitis.
Presbylarynx is a condition in which age-related atrophy of the soft tissues of the larynx results in weak voice and restricted vocal range and stamina. Bowing of the anterior portion of the vocal colds is found on laryngoscopy.
Ulcers may be caused by the prolonged presence of an endotracheal tube.
Polyps and vocal cord nodules are small bumps caused by prolonged exposure to tobacco smoke and vocal misuse, respectively.
Two related types of cancer of the larynx, namely squamous cell carcinoma and verrucous carcinoma, are strongly associated with repeated exposure to cigarette smoke and alcohol.
Vocal cord paresis is weakness of one or both vocal cords that can greatly impact daily life.
Idiopathic laryngeal spasm.
Laryngopharyngeal reflux is a condition in which acid from the stomach irritates and burns the larynx. Similar damage can occur with gastroesophageal reflux disease (GERD).
Laryngomalacia is a very common condition of infancy, in which the soft, immature cartilage of the upper larynx collapses inward during inhalation, causing airway obstruction.
Laryngeal perichondritis, the inflammation of the perichondrium of laryngeal cartilages, causing airway obstruction.
Laryngeal paralysis is a condition seen in some mammals (including dogs) in which the larynx no longer opens as wide as required for the passage of air, and impedes respiration. In mild cases it can lead to exaggerated or "raspy" breathing or panting, and in serious cases can pose a considerable need for treatment.
Duchenne muscular dystrophy, intrinsic laryngeal muscles (ILM) are spared from the lack of dystrophin and may serve as a useful model to study the mechanisms of muscle sparing in neuromuscular diseases. Dystrophic ILM presented a significant increase in the expression of calcium-binding proteins. The increase of calcium-binding proteins in dystrophic ILM may permit better maintenance of calcium homeostasis, with the consequent absence of myonecrosis. The results further support the concept that abnormal calcium buffering is involved in these neuromuscular diseases.

Treatments
Patients who have lost the use of their larynx are typically prescribed the use of an electrolarynx device.  Larynx transplants are a rare procedure.  The worlds first successful operation took place in 1998 at the Cleveland Clinic, and the second took place in October 2010 at the University of California Davis Medical Center in Sacramento.

Other animals
Pioneering work on the structure and evolution of the larynx was carried out in the 1920s by the British comparative anatomist Victor Negus, culminating in his monumental work The Mechanism of the Larynx (1929). Negus, however, pointed out that the descent of the larynx reflected the reshaping and descent of the human tongue into the pharynx. This process is not complete until age six to eight years </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 Hallermann–Streiff syndrome and explain in detail? [/INST] Hallermann–Streiff syndrome is a congenital disorder that affects growth, cranial development, hair-growth, and dental development. There are fewer than 200 people with the syndrome worldwide. One notable organization that is supporting people with Hallermann–Streiff syndrome is the Germany-based "Schattenkinder e.V".

Presentation
Patients with this syndrome are shorter than the average person and may not develop hair in many places, including in the facial, leg and pubic areas. Patients also have eye problems including reduced eye size, bilateral cataracts and glaucoma. The syndrome can be associated with sleep apnea. The physical characteristics of the syndrome can result in difficult intubation by medical professionals. Intelligence is usually normal.

Cause
The genetic cause of Hallermann–Streiff syndrome has not been conclusively determined. It is most likely due to a de novo mutation, and it may be associated with the GJA1 gene.

Diagnosis
Diagnosis is based on the physical characteristics and symptoms </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 Portal vein thrombosis and explain in detail? [/INST] Portal vein thrombosis (PVT) is a vascular disease of the liver that occurs when a blood clot occurs in the hepatic portal vein, which can lead to increased pressure in the portal vein system and reduced blood supply to the liver. The mortality rate is approximately 1 in 10.An equivalent clot in the vasculature that exits the liver carrying deoxygenated blood to the right atrium via the inferior vena cava, is known as hepatic vein thrombosis or Budd-Chiari syndrome.

Signs and symptoms
Portal vein thrombosis causes upper abdominal pain, possibly accompanied by nausea and an enlarged liver and/or spleen; the abdomen may be filled with fluid (ascites). A persistent fever may result from the generalized inflammation. While abdominal pain may come and go if the thrombus forms suddenly, long-standing clot build-up can also develop without causing symptoms, leading to portal hypertension before it is diagnosed.Other symptoms can develop based on the cause. For example, if portal vein thrombosis develops due to liver cirrhosis, bleeding or other signs of liver disease may be present. If portal vein thrombosis develops due to pylephlebitis, signs of infection such as fever, chills, or night sweats may be present.

Causes
Slowed blood flow due to underlying cirrhosis or congestive heart failure is often implicated. The prevalence of PVT in patients with cirrhosis is unclear, with a wide variety of incidence claimed by various researchers (estimated to be 1 in 100 by some while others believe it affects nearly 1 in 4).Thrombophilia (including inherited conditions such as factor V Leiden deficiency, protein C or S deficiency, or antiphospholipid antibody syndrome) is another common cause. Nearly one-third of patients have a myeloproliferative disorder (e.g. polycythemia vera or primary thrombocytosis), most commonly due to a Janus kinase 2 (JAK2) gene mutation. Oral contraceptive use or pregnancy are other non-inherited tendencies for thrombosis.Alternatively, the portal vein may be injured as a result of pancreatitis, diverticulitis, cholangiocarcinoma, hepatocellular carcinoma (HCC), or abdominal surgery/trauma. Red flags for cancerous growth as a cause are elevated alpha fetoprotein levels, portal vein diameter greater than 2.3 cm, pulsatility on Doppler ultrasound imaging, or hyperintense hepatic arterial phase (HAP) on CT scan with contrast.PVT is also a known complication of surgical removal of the spleen. During the last several years, myeloproliferative neoplasms (MPNs) have emerged as a leading systemic cause of splanchnic vein thromboses (which include PVT).

Mechanism
The main portal vein is formed by the union of the splenic vein and superior mesenteric vein (SMV). It is responsible for approximately three-fourths of the liver’s blood flow, transported from much of the gastrointestinal system as well as the pancreas, gallbladder, and spleen. Cirrhosis alters bleeding pathways thus patients are simultaneously at risk of uncontrolled bleeding and forming clots. A long-standing hindrance in flow as in chronic PVT, also known as portal cavernoma, can cause an increase in the hepatic venous pressure gradient (portal hypertension) and increased blood flow through subsidiary veins. This may lead to ascites or bleeding from varices.An infected thrombus may become septic, known as pylephlebitis; if blood cultures are positive for growth at this time, the most common organism is Bacteroides.

Diagnosis
The diagnosis of portal vein thrombosis is usually made with imaging confirming a clot in the portal vein; ultrasound is the least invasive method and the addition of Doppler technique shows a filling defect in blood flow </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 Coronary occlusion and explain in detail? [/INST]  </s>