<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hypoactive sexual desire disorder and can you explain it in depth? [/INST] Hypoactive sexual desire disorder (HSDD), hyposexuality or inhibited sexual desire (ISD) is sometimes considered a sexual dysfunction, and is characterized as a lack or absence of sexual fantasies and desire for sexual activity, as judged by a clinician. For this to be regarded as a disorder, it must cause marked distress or interpersonal difficulties and not be better accounted for by another mental disorder, a drug (legal or illegal), or some other medical condition. A person with ISD will not start, or respond to their partners desire for, sexual activity. HSDD affects approximately 10% of all pre-menopausal women in the United States, or about 6 million women.There are various subtypes. HSDD can be general (general lack of sexual desire) or situational (still has sexual desire, but lacks sexual desire for current partner), and it can be acquired (HSDD started after a period of normal sexual functioning) or lifelong (the person has always had no/low sexual desire.)
In the DSM-5, HSDD was split into male hypoactive sexual desire disorder and female sexual interest/arousal disorder. It was first included in the DSM-III under the name inhibited sexual desire disorder, but the name was changed in the DSM-III-R. Other terms used to describe the phenomenon include sexual aversion and sexual apathy. More informal or colloquial terms are frigidity and frigidness.

Causes
Low sexual desire alone is not equivalent to HSDD because of the requirement in HSDD that the low sexual desire causes marked distress and interpersonal difficulty and because of the requirement that the low desire is not better accounted for by another disorder in the DSM or by a general medical problem. It is therefore difficult to say exactly what causes HSDD. It is easier to describe, instead, some of the causes of low sexual desire.In men, though there are theoretically more types of HSDD/low sexual desire, typically men are only diagnosed with one of three subtypes.
Lifelong/generalised: The man has little or no desire for sexual stimulation (with a partner or alone) and never had.
Acquired/generalised: The man previously had sexual interest in his present partner, but lacks interest in sexual activity, partnered or solitary.
Acquired/situational: The man was previously sexually interested in his present partner but now lacks sexual interest in this partner but has desire for sexual stimulation (i.e. alone or with someone other than his present partner.)Though it can sometimes be difficult to distinguish between these types, they do not necessarily have the same cause. The cause of lifelong/generalized HSDD is unknown. In the case of acquired/generalized low sexual desire, possible causes include various medical/health problems, psychiatric problems, low levels of testosterone or high levels of prolactin. One theory suggests that sexual desire is controlled by a balance between inhibitory and excitatory factors. This is thought to be expressed via neurotransmitters in selective brain areas. A decrease in sexual desire may therefore be due to an imbalance between neurotransmitters with excitatory activity like dopamine and norepinephrine and neurotransmitters with inhibitory activity, like serotonin. Low sexual desire can also be a side effect of various medications. In the case of acquired/situational HSDD, possible causes include intimacy difficulty, relationship problems, sexual addiction, and chronic illness of the mans partner. The evidence for these is somewhat in question. Some claimed causes of low sexual desire are based on empirical evidence. However, some are based merely on clinical observation. In many cases, the cause of HSDD is simply unknown.Some factors are believed to be possible causes of HSDD in women. As with men, various medical problems, psychiatric problems (such as mood disorders), or increased amounts of prolactin can cause HSDD. Other hormones are believed to be involved as well. Additionally, factors such as relationship problems or stress are believed to be possible causes of reduced sexual desire in women. According to one recent study examining the affective responses and attentional capture of sexual stimuli in women with and without HSDD, women with HSDD do not appear to have a negative association to sexual stimuli, but rather a weaker positive association than women without HSDD.

Diagnosis
In the DSM-5, male hypoactive sexual desire disorder is characterized by "persistently or recurrently deficient (or absent) sexual/erotic thoughts or fantasies and desire for sexual activity", as judged by a clinician with consideration for the patients age and cultural context. Female sexual interest/arousal disorder is defined as a "lack of, or significantly reduced, sexual interest/arousal", manifesting as at least three of the following symptoms: no or little interest in sexual activity, no or few sexual thoughts, no or few attempts to initiate sexual activity or respond to partners initiation, no or little sexual pleasure/excitement in 75–100% of sexual experiences, no or little sexual interest in internal or external erotic stimuli, and no or few genital/nongenital sensations in 75–100% of sexual experiences.For both diagnoses, symptoms must persist for at least six months, cause clinically significant distress, and not be better explained by another condition. Simply having lower desire than ones partner is not sufficient for a diagnosis. Self-identification of a lifelong lack of sexual desire as asexuality precludes diagnosis.

Treatment
Counseling
HSDD, like many sexual dysfunctions, is something that people are treated for in the context of a relationship. Theoretically, one could be diagnosed with and treated for HSDD without being in a relationship. However, relationship status is the most predictive factor accounting for distress in women with low desire and distress is required for a diagnosis of HSDD. Therefore, it is common for both partners to be involved in therapy.
Typically, the therapist tries to find a psychological or biological cause of the HSDD. If the HSDD is organically caused, the clinician may try to treat it. If the clinician believes it is rooted in a psychological problem, he or she may recommend therapy. If not, treatment generally focuses more on relationship and communication issues, improved communication (verbal and nonverbal), working on non-sexual intimacy, or education about sexuality may all be possible parts of treatment. Sometimes problems occur because people have unrealistic perceptions about what normal sexuality is and are concerned that they do not compare well to that, and this is one reason why education can be important. If the clinician thinks that part of the problem is a result of stress, techniques may be recommended to more effectively deal with that. Also, it can be important to understand why the low level of sexual desire is a problem for the relationship because the two partners may associate different meanings with sex but not know it.In the case of men, the therapy may depend on the subtype of HSDD. Increasing the level of sexual desire of a man with lifelong/generalized HSDD is unlikely. Instead, the focus may be on helping the couple to adapt. In the case of acquired/generalized, it is likely that there is some biological reason the clinician can address. In the case of acquired/situational, some form of psychotherapy may be used, possibly with the man alone and possibly together with his partner.

Medication
Approved
Flibanserin was the first medication approved by FDA for the treatment of HSDD in pre-menopausal women. Its approval was controversial and a systematic review found its benefits to be marginal. The only other medication approved in the US for HSDD in pre-menopausal women is bremelanotide, in 2019.

Off-label
A few studies suggest that the antidepressant, bupropion, can improve sexual function in women who are not depressed, if they have HSDD. The same is true for the anxiolytic, buspirone, which is a 5-HT1A receptor agonist similarly to flibanserin.Testosterone supplementation is effective in the short term. However, its long-term safety is unclear.

History
The term "frigid" to describe sexual dysfunction derives from medieval and early modern canonical texts about witchcraft. It was thought that witches could put spells on men to make them incapable of erections. Only in the early nineteenth century were women first described as "frigid", and a vast literature exists on what was considered a serious problem if a woman did not desire sex with her husband. Many medical texts between 1800 and 1930 focused on womens frigidity, considering it a sexual pathology.The French psychoanalyst Princess Marie Bonaparte theorized about frigidity and considered herself to have it.  In the early versions of the DSM, there were only two sexual dysfunctions listed: frigidity (for women) and impotence (for men).
In 1970, Masters and Johnson published their book Human Sexual Inadequacy describing sexual dysfunctions, though these included only dysfunctions dealing with the function of genitals such as premature ejaculation and impotence for men, and anorgasmia and vaginismus for women. Prior to Masters and Johnsons research, female orgasm was assumed by some to originate primarily from vaginal, rather than clitoral, stimulation. Consequently, feminists have argued that "frigidity" was "defined by men as the failure of women to have vaginal orgasms".Following this book, sex therapy increased throughout the 1970s. Reports from sex-therapists about people with low sexual desire are reported from at least 1972, but labeling this as a specific disorder did not occur until 1977. In that year, sex therapists Helen Singer Kaplan and Harold Lief independently of each other proposed creating a specific category for people with low or no sexual desire. Lief named it "inhibited sexual desire", and Kaplan named it "hypoactive sexual desire". The primary motivation for this was that previous models for sex therapy assumed certain levels of sexual interest in ones partner and that problems were only caused by abnormal functioning/non-functioning of the genitals or performance anxiety but that therapies based on those problems were ineffective for people who did not sexually desire their partner. The following year, 1978, Lief and Kaplan together made a proposal to the APAs taskforce for sexual disorders for the DSM III, of which Kaplan and Lief were both members. The diagnosis of Inhibited Sexual Desire (ISD) was added to the DSM when the 3rd edition was published in 1980.For understanding this diagnosis, it is important to recognize the social context in which it was created. In some cultures, low sexual desire may be considered normal, and high sexual desire conversely problematic. For example, sexual desire may be lower in East Asian populations than Euro-Canadian/American populations. In other cultures, this may be reversed. Some cultures try hard to restrain sexual desire. Others try to excite it. Concepts of "normal" levels of sexual desire are culturally dependent and rarely value-neutral. In the 1970s, there were strong cultural messages that sex is good for you and "the more the better". Within this context, people who were habitually uninterested in sex, who in previous times may not have seen this as a problem, were more likely to feel that this was a situation that needed to be fixed. They may have felt alienated by dominant messages about sexuality and increasingly people went to sex-therapists complaining of low sexual desire. It was within this context that the diagnosis of ISD was created.In the revision of the DSM-III, published in 1987 (DSM-III-R), ISD was subdivided into two categories: Hypoactive Sexual Desire Disorder and Sexual Aversion Disorder (SAD). The former is a lack of interest in sex and the latter is a phobic aversion to sex. In addition to this subdivision, one reason for the change is that the committee involved in revising the psychosexual disorders for the DSM-III-R thought that the term "inhibited" suggests psychodynamic cause (i.e., that the conditions for sexual desire are present, but the person is, for some reason, inhibiting their own sexual interest). The term "hypoactive sexual desire" is more awkward, but more neutral with respect to the cause. The DSM-III-R estimated that about 20% of the population had HSDD. In the DSM-IV (1994), the criterion that the diagnosis requires "marked distress or interpersonal difficulty" was added.The DSM-5, published in 2013, split HSDD into male hypoactive sexual desire disorder and female sexual interest/arousal disorder. The distinction was made because men report more intense and frequent sexual desire than women. According to Lori Brotto, this classification is desirable compared to the DSM-IV classification system because: (1) it reflects the finding that desire and arousal tend to overlap (2) it differentiates between women who lack desire before the onset of activity, but who are receptive to initiation and or initiate sexual activity for reasons other than desire, and women who never experience sexual arousal (3) it takes the variability in sexual desire into account. Furthermore, the criterion that 6 symptoms be present for a diagnosis helps safeguard against pathologizing adaptive decreases in desire.

Criticism
General
HSDD, as currently defined by the DSM, has come under criticism of the social function of the diagnosis.

HSDD could be seen as part of a history of the medicalization of sexuality by the medical profession to define normal sexuality. It has also been examined within a "broader frame of historical interest in the problematization of sexual appetite".
HSDD has been criticized over pathologizing normal variations in sexuality because the parameters of normality are unclear. This lack of clarity is partly due to the fact that the terms "persistent" and "recurrent" do not have clear operational definitions.
HSDD may function to pathologize asexuals, though their lack of sexual desire may not be maladaptive. Because of this, some members of the asexual community lobbied the mental health community working on the DSM-5 to regard asexuality as a legitimate sexual orientation rather than a mental disorder.Other criticisms focus more on scientific and clinical issues.

HSDD is such a diverse group of conditions with many causes that it functions as little more than a starting place for clinicians to assess people.
The requirement that low sexual desire causes distress or interpersonal difficulty has been criticized. It has been claimed that it is not clinically useful because if it is not causing any problems, the person will not seek out a clinician. One could claim that this criterion (for all of the sexual dysfunctions, including HSDD) decreases the scientific validity of the diagnoses or is a cover-up for a lack of data on what constitutes normal sexual function.
The distress requirement is also criticized because the term "distress" lacks a clear definition.

NICE (UK) assessment
Hypoactive sexual desire disorder is not recognized as a disorder by the National Institute for Health and Care Excellence for the British National Health Service, with the judgement based on an article in the Journal of Medical Ethics that "Hypoactive sexual desire disorder is a typical example of a condition that was sponsored by industry to prepare the market for a specific treatment".

DSM-IV criteria
Prior to the publication of the DSM-5, the DSM-IV criteria were criticized on several grounds. It was suggested that a duration criterion should be added because lack of interest in sex over the past month is significantly more common than lack of interest lasting six months. Similarly, a frequency criterion (i.e., the symptoms of low desire be present in 75% or more of sexual encounters) has been suggested.The current framework for HSDD is based on a linear model of human sexual response, developed by Masters and Johnson and modified by Kaplan consisting of desire, arousal, orgasm. The sexual dysfunctions in the DSM are based around problems at any one or more of these stages. Many of the criticisms of the DSM-IV framework for sexual dysfunction in general, and HSDD in particular, claimed that this model ignored the differences between male and female sexuality. Several criticisms were based on the inadequacy of the DSM-IV framework for dealing with females sexual problems.
Increasingly, evidence shows that there are significant differences between male and female sexuality. Level of desire is highly variable from female to female and there are some females who are considered sexually functional who have no active desire for sex, but they can erotically respond well in contexts they find acceptable. This has been termed "responsive desire" as opposed to spontaneous desire.
The focus on merely the physiological ignores the social, economic and political factors including sexual violence and lack of access to sexual medicine or education throughout the world affecting females and their sexual health.
The focus on the physiological ignores the relationship context of sexuality despite the fact that this is often the cause of sexual problems.
The focus on discrepancy in desire between two partners may result in the partner with the lower level of desire being labeled as "dysfunctional," but the problem really sits with the difference between the two partners. However, within couples the assessment of desire tends to be relative. That is, individuals make judgments by comparing their levels of desire to that of their partner.
The sexual problems that females complain of often do not fit well into the DSM-IV framework for sexual dysfunctions.
The DSM-IV system of sub-typing may be more applicable to one sex than the other.
Research indicates a high degree of comorbidity between HSDD and female sexual arousal disorder. Therefore, a diagnosis combining the two (as the DSM-5 eventually did) might be more appropriate.

See also
Drugs and sexual desire
HypersexualityAsexuality
Sexual anhedonia
Sexual anorexia
Sexual arousal disorder

References
Further reading
Cryle, Peter; Moore, Alison (2011). Frigidity: An Intellectual History. Basingstoke: Palgrave Macmillan. ISBN 978-0-230-30345-4.
Cryle, Peter; Moore, Alison (May 2010). "Frigidity at the Fin-de-Siècle, a Slippery and Capacious Concept". Journal of the History of Sexuality. 19 (2): 243–61. doi:10.1353/sex.0.0096. PMID 20617591. S2CID 40019141.
Moore, Alison (November 2009). "Frigidity, Gender and Power in French Cultural History – From Jean Fauconney to Marie Bonaparte". French Cultural Studies. 20 (4): 331–49. doi:10.1177/0957155809344155. S2CID 145773398.
Moore, Alison (2009). "The Invention of the Unsexual: Situating Frigidity in the History of Sexuality and in Feminist Thought". French History and Civilization. 2: 181–92.
Montgomery, KA (Jun 2008). "Sexual Desire Disorders". Psychiatry (Edgmont). 5 (6): 50–55. PMC 2695750. PMID 19727285.
Basson, R; Leiblum, S; Brotto, L;  et al. (December 2003). "Definitions of womens sexual dysfunction reconsidered: advocating expansion and revision". Journal of Psychosomatic Obstetrics and Gynaecology. 24 (4): 221–9. doi:10.3109/01674820309074686. PMID 14702882. S2CID 4780569.
Warnock, JJ (2002). "Female hypoactive sexual desire disorder: epidemiology, diagnosis and treatment". CNS Drugs. 16 (11): 745–53. doi:10.2165/00023210-200216110-00003. PMID 12383030. S2CID 24669452.
Basson, R (10 May 2005). "Womens sexual dysfunction: revised and expanded definitions". Canadian Medical Association Journal. Canadian Medical Association </s>


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


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Postpartum bleeding and can you explain it in depth? [/INST] Postpartum bleeding or postpartum hemorrhage (PPH) is often defined as the loss of more than 500 ml or 1,000 ml of blood  following childbirth. Some have added the requirement that there also be signs or symptoms of low blood volume for the condition to exist. Signs and symptoms may initially include: an increased heart rate, feeling faint upon standing, and an increased breathing rate. As more blood is lost, the patient may feel cold, blood pressure may drop, and they may become restless or unconscious. The condition can occur up to six weeks following delivery.The most common cause is poor contraction of the uterus following childbirth. Not all of the placenta being delivered, a tear of the uterus, or poor blood clotting are other possible causes. It occurs more commonly in those who: already have a low amount of red blood, are Asian, with bigger or more than one baby, are obese or are older than 40 years of age. It also occurs more commonly following caesarean sections, those in whom medications are used to start labor, those requiring the use of a vacuum or forceps, and those who have an episiotomy.Prevention involves decreasing known risk factors including procedures associated with the condition, if possible, and giving the medication oxytocin to stimulate the uterus to contract shortly after the baby is born. Misoprostol may be used instead of oxytocin in resource-poor settings. Treatments may include: intravenous fluids, blood transfusions, and the medication ergotamine to cause further uterine contraction. Efforts to compress the uterus using the hands may be effective if other treatments do not work. The aorta may also be compressed by pressing on the abdomen. The World Health Organization has recommended the non-pneumatic anti-shock garment to help until other measures such as surgery can be carried out. Tranexamic acid has also been shown to reduce the risk of death, and has been recommended within three hours of delivery.In the developing world about 1.2% of deliveries are associated with PPH and when PPH occurred about 3% of women died. Globally it occurs about 8.7 million times and results in 44,000 to 86,000 deaths per year making it the leading cause of death during pregnancy. About 0.4 women per 100,000 deliveries die from PPH in the United Kingdom while about 150 women per 100,000 deliveries die in sub-Saharan Africa. Rates of death have decreased substantially since at least the late 1800s in the United Kingdom.

Definition
Depending on the source, primary postpartum bleeding is defined as blood loss in excess of 500 ml following vaginal delivery or 1000 ml following caesarean section in the first 24 hours following birth. Secondary postpartum bleeding is that which occurs after the first day and up to six weeks after childbirth.

Signs and symptoms
Symptoms generally include heavy bleeding from the vagina that doesnt slow or stop over time. Initially there may be an increased heart rate, feeling faint upon standing, and an increased respiratory rate. As more blood is lost, the patient may feel cold, blood pressure may drop, and they may become unconscious.Signs and symptoms of circulatory shock may also include blurry vision, cold and clammy skin, confusion, and feeling sleepy or weak.

Causes
Causes of postpartum hemorrhage are uterine atony, trauma, retained placenta or placental abnormalities, and coagulopathy, commonly referred to as the "four Ts":
Tone: uterine atony is the inability of the uterus to contract and may lead to continuous bleeding. Retained placental tissue and infection may contribute to uterine atony.  Uterine atony is the most common cause of postpartum hemorrhage.
Trauma: Injury to the birth canal which includes the uterus, cervix, vagina and the perineum which can happen even if the delivery is monitored properly. The bleeding is substantial as all these organs become more vascular during pregnancy.
Tissue: retention of tissue from the placenta or fetus as well as placental abnormalities such as placenta accreta and percreta may lead to bleeding.
Thrombin: a bleeding disorder occurs when there is a failure of clotting, such as with diseases known as coagulopathies.Other risk factors include obesity, fever during pregnancy, bleeding before delivery, and heart disease.

Prevention
Oxytocin is typically used right after the delivery of the baby to prevent PPH. Misoprostol may be used in areas where oxytocin is not available. Early clamping of the umbilical cord does not decrease risks and may cause anemia in the baby, and thus is usually not recommended.Active management of the third stage is a method of shortening the stage between when the baby is born and when the placenta is delivered. This stage is when the mother is at risk of having a PPH. Active management involves giving a drug which helps the uterus contract before delivering the placenta by a gentle but sustained pull on the umbilical cord whilst exerting upward pressure on the lower abdomen to support the uterus (controlled cord traction).Another method of active management which is not recommended now is fundal pressure during the delivery of the placenta. A review into this method found no research and advises controlled cord traction because fundal pressure can cause the mother unnecessary pain. Allowing the cord to drain appears to shorten the third stage and reduce blood loss but evidence around this subject is not strong enough to draw solid conclusions.Nipple stimulation and breastfeeding triggers the release of natural oxytocin in the body, therefore it is thought that encouraging the baby to suckle soon after birth may reduce the risk of PPH for the mother. A review looking into this did not find enough good research to say whether or not nipple stimulation did reduce PPH. More research is needed to answer this question.

Management
Uterine massage is a simple first line treatment as it helps the uterus to contract to reduce bleeding. Although the evidence around the effectiveness of uterine massage is inconclusive, it is common practice after the delivery of the placenta.

Medication
Intravenous oxytocin is the drug of choice for postpartum hemorrhage. Ergotamine may also be used.Oxytocin helps the uterus to contract quickly and the contractions to last for longer. It is the first line treatment for PPH when its cause is the uterus not contracting well. A combination of syntocinon and ergometrine is commonly used as part of active management of the third stage of labour. This is called syntometrine. Syntocinon alone lowers the risk of PPH. Based on limited research available it is unclear whether syntocinon or syntometrine is most effective in preventing PPH but adverse effects are worse with syntometrine making syntocinon a more attractive option. Ergometrine also has to be kept cool and in a dark place so that it is safe to use. It may reduce the risk of PPH by improving the tone of the uterus when compared with no treatment, however it must be used with caution due to its effects of raising blood pressure and worsening pain. More research would be useful in determining the best doses of ergometrine and syntocinon.Oxytocin requires refrigeration, which may not always be available, particularly in low-resourced settings. When oxytocin is not available, misoprostol can be used. Misoprostol does not need to be kept at a certain temperature and research into its effectiveness in reducing blood loss appears promising when compared with a placebo in a setting where it is not appropriate to use oxytocin. Misoprostol can cause unpleasant side effects such as very high body temperatures and shivering. Lower doses of misoprostol appear to be safer and cause less side effects.Giving oxytocin in a solution of saline into the umbilical vein is a method of administering the drug directly to the placental bed and uterus. However quality of evidence around this technique is poor and it is not recommended for routine use in the management of the third stage. More research is needed to ascertain whether this is an effective way of administering uterotonic drugs. As a way of treating a retained placenta, this method is not harmful and has shown low certainty evidence of effectiveness.Carbetocin compared with oxytocin produced a reduction in women who needed uterine massage and further uterotonic drugs for women having caesarean sections. There was no difference in rates of PPH in women having caesarean sections or women having vaginal deliveries when given carbetocin. Carbetocin appears to cause less adverse effects. More research is needed to find the cost effectiveness of using carbetocin.Tranexamic acid, a clot stabilizing medication, may also be used to reduce bleeding and blood transfusions in low-risk patients, however evidence as of 2015 was not strong. A 2017 trial found that it decreased the risk of death from bleeding from 1.9% to 1.5% in women with postpartum bleeding. The benefit was greater when the medication was given within three hours.In some countries, such as Japan, methylergometrine and other herbal remedies are given following the delivery of the placenta to prevent severe bleeding more than a day after the birth. However, there is not enough evidence to suggest that these methods are effective.

Surgery
Surgery may be used if medical management fails or in case of cervical lacerations or tear or uterine rupture. Methods used may include uterine artery ligation, ovarian artery ligation, internal iliac artery ligation, selective arterial embolization, B-lynch suture, and hysterectomy. Bleeding caused by traumatic causes should be managed by surgical repair. When there is bleeding due to uterine rupture a repair can be performed but most of the time a hysterectomy is needed.There is currently no reliable evidence from randomised clinical trials about the effectiveness or risks of mechanical and surgical methods of treating postpartum bleeding.

Medical devices
The World Health Organization recommends the use of a device called the non-pneumatic anti-shock garment (NASG) for use in delivery activities outside of a hospital setting, the aim being to improve shock in a mother with obstetrical bleeding long enough to reach a hospital. External aortic compression devices (EACD) may also be used.Uterine balloon tamponade (UBT) can improve postpartum bleeding. Inflating a Sengstaken–Blakemore tube in the uterus successfully treats atonic postpartum hemorrhage refractory to medical management in approximately 80% of cases. Such procedure is relatively simple, inexpensive and has low surgical morbidity. A Bakri balloon is a balloon tamponade specifically constructed for uterine postpartum hemorrhage. While effective, commercially available devices may be expensive for settings in which postpartum hemorrhage is most common. Low-cost devices, such as the ESM-UBT, have been shown to be effective without the need for operative intervention.

Protocol
Protocols to manage postpartum bleeding are recommended to ensure the rapid giving of blood products when needed. A detailed stepwise management protocol has been introduced by the California Maternity Quality Care Collaborative. It describes four stages of obstetrical hemorrhage after childbirth and its application reduces maternal mortality.
Stage 0: normal - treated with fundal massage and oxytocin.
Stage 1:  more than normal bleeding - establish large-bore intravenous access, assemble personnel, increase oxytocin, consider use of methergine, perform fundal massage, prepare 2 units of packed red blood cells.
Stage 2: bleeding continues - check coagulation status, assemble response team, move to operating room, place intrauterine balloon, administer additional uterotonics (misoprostol, carboprost tromethamine), consider: uterine artery embolization, dilatation and curettage, and laparotomy with uterine compression stitches or hysterectomy.
Stage 3: bleeding continues - activate massive transfusion protocol, mobilize additional personnel, recheck laboratory tests, perform laparotomy, consider hysterectomy.A Cochrane review suggests that active management (use of uterotonic drugs, cord clamping and controlled cord traction) during the third stage of labour may reduce severe bleeding and anemia. However, the review also found that active management increased the patients blood pressure, nausea, vomiting, and pain </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Autonomic dysreflexia and can you explain it in depth? [/INST] Autonomic dysreflexia (AD) is a potential medical emergency classically characterized by uncontrolled hypertension and bradycardia, although tachycardia is known to commonly occur. AD occurs most often in individuals with spinal cord injuries with lesions at or above the T6 spinal cord level, although it has been reported in patients with lesions as low as T10. Guillain–Barré syndrome may also cause autonomic dysreflexia.The uncontrolled hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache; However, severe hypertension may result in potentially life-threatening complications including seizure, intracranial bleed, or retinal detachment.AD is triggered by either noxious or non-noxious stimuli, resulting in sympathetic stimulation and hyperactivity. The most common causes include bladder or bowel over-distension, from urinary retention and fecal compaction, respectively. The resulting sympathetic surge transmits through intact peripheral nerves, resulting in systemic vasoconstriction below the level of the spinal cord lesion. The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system to inhibit the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion. This results in bradycardia, vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while there is piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow.Initial treatment involves sitting the patient upright, removing any constrictive clothing (including abdominal binders and support stockings), rechecking blood pressure frequently, and then checking for and removing the inciting issue, which may require urinary catheterization or bowel disimpaction. If systolic blood pressure remains elevated (over 150 mm Hg) after initial steps, fast-acting short-duration antihypertensives are considered, while other inciting causes must be investigated for the symptoms to resolve.Prevention of AD involves educating the patient, family and caregivers of the precipitating cause, if known, and how to avoid it, as well as other triggers. Since bladder and bowel are common causes, prevention involves routine bladder and bowel programs and urological follow-up for cystoscopy/urodynamic studies.

Signs and symptoms
This condition is distinct and usually episodic, with the people potentially experiencing remarkably high blood pressure, intense headaches, profuse sweating, facial erythema, goosebumps, nasal stuffiness, a "feeling of doom" or apprehension, and blurred vision. An elevation of 20 mm Hg over baseline systolic blood pressure, with a potential source below the neurological level of injury, meets the current definition of dysreflexia.

Complications
Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical problems like soft tissue pressure injuries or hemorrhoids. Long term therapy may include alpha blockers or calcium channel blockers.Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction, or cerebral hemorrhage. Additional organs that may be affected include the kidneys and retinas of the eyes.

Causes
The first episode of autonomic dysreflexia may occur weeks to years after spinal cord injury takes place, but most people at risk (80%) develop their first episode within the first year after injury. Early AD tends to be associated with less severe increases in blood pressure.One common causative factor may be an undetected urinary tract infection. The difficulty in assessing this may be complicated with the usage of indwelling or suprapubic catheters. Other causes include medication side effects and various disease processes. The use of stimulants such as cocaine and amphetamines which can result in urinary retention, and the use of CNS depressants and other psychoactive drugs can also lead to urinary retention and constipation thus leading to autonomic dysreflexia when in use over an extended period of time.

Pain
Current scientific literature suggests that noxious (painful) stimuli are the primary initiators of AD. (Note: Not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli in unaffected people, e.g. broken bones, may not result in AD, and may in fact even go unnoticed.)  However, different studies have found that activation of pain receptors in muscle and skin below the lesion in spinal cord injured individuals did not trigger AD. These studies suggests that not all noxious stimuli are reliable triggers of AD, and because non-noxious stimuli can also trigger AD, attribution of an episode of AD to noxious stimuli may cause clinicians to overlook underlying non-noxious triggers.  As a result, non-noxious trigger factors remain undetected, prolonging an episode of AD. They concluded that when deducing the potential causes of AD it is important to consider non-noxious sources of stimulation in addition to noxious triggers. Current assessment of autonomic dysreflexia in patients with known causative factors include palpation of the bladder and bowel and can also include bladder scan.

Mechanism
Supraspinal vasomotor neurons send projections to the intermediolateral cell column, which is composed of sympathetic preganglionic neurons (SPN) through the T1-L2 segments. The supraspinal neurons act on the SPN and its tonic firing, modulating its action on the peripheral sympathetic chain ganglia and the adrenal medulla. The sympathetic ganglia act directly on the blood vessels they innervate throughout the body, controlling vessel diameter and resistance, while the adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine. The descending autonomic pathways, which are responsible for the supraspinal communication with the SPN, are interrupted resulting in decreased sympathetic outflow below the level of the injury. In this circumstance, the SPN is controlled only by spinal influences. The first couple of weeks after a spinal injury, the decreased sympathetic outflow causes reduced blood pressure and sympathetic reflex. Eventually, synaptic reorganization and plasticity of SPN develops into an overly sensitive state, which results in abnormal reflex activation of SPN due to afferent stimuli, such as bowel or bladder distension. Reflex activation results in systemic vasoconstriction below the spinal cord disruption.  The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system, which inhibits the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion. This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while theres piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow.
The reason this issue is much more prominent for lesions at or above the T6 level is because the Splanchnic nerves emerge from the T5 level and below. Loss of brains control over T6 and below causes splanchnic arteries to reflexively vasoconstrict and since the Splanchnic arteries are the bodys largest reservoir for circulating blood, their vasocontriction dramatically affects the blood pressure of the body.

Diagnosis
The symptoms are usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, the various modest cardiac and neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension, and ambient temperature intolerance.  In autonomic dysreflexia, patients will experience hypertension, sweating, spasms (sometimes severe spasms) and erythema (more likely in upper extremities) and may experience headaches and blurred vision.  Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be quite severe.  Older patients with very incomplete spinal cord injuries and systolic hypertension without symptoms are usually experiencing essential hypertension, not autonomic dysreflexia. Aggressive treatment of these elderly patients with rapidly acting antihypertensive medications can have disastrous results.

Treatment
Proper treatment of autonomic dysreflexia involves administration of anti-hypertensives along with immediate determination and removal of the triggering stimuli </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Coronary vasospasm and can you explain it in depth? [/INST] Coronary vasospasm refers to when a coronary artery suddenly undergoes either complete or sub-total temporary occlusion.In 1959, Prinzmetal et al. described a type of chest pain resulting from coronary vasospasm, referring to it as a variant form of classical angina pectoris. Consequently, this angina has come to be reported and referred to in the literature as Prinzmetal angina. A subsequent study distinguished this type of angina from classical angina pectoris further by showing normal coronary arteries on cardiac catheterization. This finding is unlike the typical findings in classical angina pectoris, which usually shows atherosclerotic plaques on cardiac catheterization.When coronary vasospasm occurs, the occlusion temporarily produces ischemia. A wide array of symptoms or presentations can follow: ranging from asymptomatic myocardial ischemia, sometimes referred to as silent ischemia, to myocardial infarction and even sudden cardiac death.

Signs and symptoms
Coronary vasospasm classically produces chest pain at rest, also known as vasospastic angina. Chest pain is more common at certain times of the day, usually from late night to early morning. These episodes can be accompanied by nausea, vomiting, cold sweating, and even syncope. Coronary vasospasm is also associated with symptoms of fatigue and tiredness, dyspnea, and palpitations. These can sometimes be the primary presenting symptoms, but they can also occur in conjunction with chest pain.There are cases of coronary vasospasm that occur without any symptoms at all, leading to episodes of silent or asymptomatic myocardial ischemia.

Complications
Depending on how long the occlusion lasts, a spectrum of different myocardial ischemic syndromes can occur. Shorter episodes of occlusion can lead to what is referred to as silent myocardial ischemia due to its asymptomatic nature. These episodes can also be accompanied by arrhythmias. Longer episodes of occlusion can lead to stable or unstable angina, myocardial infarction, and sudden cardiac death.

Risk factors
Unlike classical angina pectoris, traditional cardiovascular risk factors are not thought to be significantly associated with coronary vasospasm. The exception to this is with smoking, which is known to be a modifiable risk factor for vasospastic angina.There are several risk factors that are thought to precipitate, or trigger, episodes of coronary vasospasm. Many of these factors work by exerting effects on the autonomic nervous system. One of the mechanisms through which this occurs is via increasing sympathetic nervous system activity. The resulting increased sympathetic outflow leads to vasoconstrictive effects on blood vessels. For example, cocaine use can trigger vasospasm in coronary arteries through its actions on adrenergic receptors causing vasoconstriction. Exercise, cold weather, physical activity or exertion, mental stress, hyperventilation are additional precipitating factors.

Pathophysiology
The exact pathophysiology behind coronary vasospasm has not been elucidated. Instead, a combination of different factors has been proposed to contribute to coronary vasospasm. In general, it is thought that an abnormality within a coronary artery causes it to become hyperreactive to vasoconstrictor stimuli. This abnormality can be located in one segment of the coronary artery, or it may be diffuse and present throughout the entire artery. If and when vasoconstrictor stimuli act upon the hyperreactive segment of the artery, then vasospasm can result. Ultimately, when large coronary arteries undergo vasospasm, this can lead to either complete or transient occlusion of blood flow within the artery. As a result, ischemia to the tissues served by the artery can occur. Symptoms due to ischemia can follow.Some of the factors that have been proposed to contribute to coronary vasospasm include the following:
Endothelial dysfunction
Certain vasodilatory agents exert their effects by working via the endothelium, the cells that make up the lining of blood vessels. Specifically, these agents work by enhancing the production of nitric oxide from endothelial nitric oxide synthase. Normally, nitric oxide then works to promote vasodilation in a blood vessel through its own mechanisms such as inhibiting the release of agents that cause vasoconstriction.
Endothelial dysfunction wherein there is a deficiency in the production of nitric oxide has been found to be associated with coronary vasospasm in some but not all cases. Vasodilatory agents with mechanisms dependent on a functional endothelial nitric oxide synthase can cause vasoconstriction instead in the setting of endothelial dysfunction, leading to coronary vasospasm.
Chronic inflammation
Various markers of low-grade chronic inflammation have been found in cases of coronary vasospasm.
In addition to this, one of the risk factors for coronary vasospasm is smoking. Chronic inflammation due to smoking has been shown to be damaging to endothelial cell function.
Oxidative Stress
Oxygen free radicals contribute to the pathogenesis of coronary vasospasm through their damaging effects on vascular endothelial cells and degrading nitric oxide, an important vasodilatory agent.
Smooth Muscle Hypercontractility
At a cellular level, pathways that lead to enhanced myosin light chain phosphorylation promote vasoconstriction. Increased activity of Rho-kinase leading to enhanced myosin light chain phosphorylation has been implicated in the pathogenesis of coronary vasospasm.

Diagnosis
There are no set criteria to diagnose coronary vasospasm. Thorough history taking by a clinician can assist in the diagnosis of coronary vasospasm. In cases where symptoms of chest pain are present, identifying features that distinguish episodes of vasospastic angina from traditional angina can aid in the diagnosis. Features such as chest pain at rest, a diurnal variation in tolerance for exercise with a reduction in tolerance for exercise in the morning, and responsiveness of chest pain to calcium channel blockers as opposed to beta blockers can be important clues.EKG can occasionally be used to diagnose episodes of coronary vasospasm. However, relying on EKG is not always possible due to the transient nature of coronary vasospasm episodes. Due to the challenge of capturing episodes of coronary vasospasm spontaneously, provocative testing to induce coronary vasospasm during coronary catheterization can be used to make the diagnosis </s>


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


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Eosinophilic pneumonia and can you explain it in depth? [/INST] Eosinophilic pneumonia is a disease in which an eosinophil, a type of white blood cell, accumulates in the lungs. These cells cause disruption of the normal air spaces (alveoli) where oxygen is extracted from the atmosphere. Several different kinds of eosinophilic pneumonia exist and can occur in any age group. The most common symptoms include cough, fever, difficulty breathing, and sweating at night. Eosinophilic pneumonia is diagnosed by a combination of characteristic symptoms, findings on a physical examination by a health provider, and the results of blood tests and X-rays. Prognosis is excellent once most eosinophilic pneumonia is recognized and treatment with corticosteroids is begun.

Classification
Eosinophilic pneumonia is divided into different categories depending upon whether its cause can be determined or not. Known causes include certain medications or environmental triggers, parasitic infections, and cancer. Eosinophilic pneumonia can also occur when the immune system attacks the lungs, a disease called eosinophilic granulomatosis with polyangiitis. When a cause cannot be found, the eosinophilic pneumonia is termed "idiopathic". Idiopathic eosinophilic pneumonia can also be divided into acute and chronic forms, depending on the symptoms a person is experiencing.

Signs and symptoms
Most types of eosinophilic pneumonia have similar signs and symptoms. Prominent and nearly universal signs and symptoms include cough, fever, difficulty breathing, and night sweats. Acute eosinophilic pneumonia typically follows a rapid course. Fever and cough may develop only one or two weeks before breathing difficulties progress to the point of respiratory failure requiring mechanical ventilation. Chronic eosinophilic pneumonia usually follows a slower course. Symptoms accumulate over several months and include fever, cough, difficulty breathing, wheezing, and weight loss. Individuals with chronic eosinophilic pneumonia are often misdiagnosed with asthma before the correct diagnosis is made.
Eosinophilic pneumonia due to medications or environmental exposures is similar and occurs after an exposure to a known offending agent. Eosinophilic pneumonia due to parasitic infections has a similar prodrome in addition to a host of different symptoms related to the variety of underlying parasites. Eosinophilic pneumonia in the setting of cancer often develops in the context of a known diagnosis of lung cancer, cervical cancer, or other certain types of cancer.

Pathophysiology
Eosinophilic pneumonia can develop in several different ways depending on the underlying cause of the disease. Eosinophils play a central role in defending the body against infection by parasites. Many diseases, such as asthma and eczema, are caused when eosinophils overreact to environmental triggers and release an excess of chemicals, e.g., cytokines and histamine. The common characteristic among different causes of eosinophilic pneumonia is eosinophil overreaction or dysfunction in the lungs.

Medications and environmental exposures
Medications, substance abuse, and environmental exposures may all trigger eosinophil dysfunction. Medications such as nonsteroidal anti-inflammatory drugs (e.g., ibuprofen), nitrofurantoin, phenytoin, L-tryptophan, daptomycin and ampicillin, and drugs of abuse such as inhaled heroin and cocaine may trigger an allergic response which results in eosinophilic pneumonia. Chemicals such as sulfites, aluminum silicate, and cigarette smoke can cause eosinophilic pneumonia when inhaled. A New York City firefighter developed eosinophilic pneumonia after inhalation of dust from the World Trade Center on September 11, 2001.

Parasitic infections
Parasites cause eosinophilic pneumonia in three different ways. Parasites can either invade the lungs, live in the lungs as part of their life cycle, or be spread to the lungs by the bloodstream. Eosinophils then migrate to the lungs in order to fight the parasites, and cause eosinophilic pneumonia when they release their contents. Important parasites that invade the lungs include Paragonimus lung flukes and the tapeworms Echinococcus and Taenia solium. Important parasites which inhabit the lungs as part of their normal life cycle include the worms (helminths) Ascaris lumbricoides, Strongyloides stercoralis and the hookworms Ancylostoma duodenale and Necator americanus. When eosinophilic pneumonia is caused by helminths, it is often called "Löfflers syndrome". The final group of parasites cause eosinophilic pneumonia when their eggs are carried into the lungs by the bloodstream. This can include Trichinella spiralis, Strongyloides stercoralis, Ascaris lumbricoides, the hookworms, and the schistosomes.

Acute and Chronic Eosinophilic Pneumonia
The causes for both acute and chronic eosinophilic pneumonia are unknown as of 2005. There is some suspicion that at least the acute form is the result of the bodys response to some unidentified environmental agent.

Diagnosis
Eosinophilic pneumonia is diagnosed in one of three circumstances: when a complete blood count reveals increased eosinophils and a chest X-ray or computed tomography identifies abnormalities in the lungs, when a biopsy identifies increased eosinophils in lung tissue, or when increased eosinophils are found in fluid obtained by a bronchoscopy (bronchoalveolar lavage fluid). Association with medication or cancer is usually apparent after review of a persons medical history. Specific parasitic infections are diagnosed after examining a persons exposure to common parasites and performing laboratory tests to look for likely causes. If no underlying cause is found, a diagnosis of acute or chronic eosinophilic pneumonia is made based upon the following criteria. Acute eosinophilic pneumonia is most likely with respiratory failure after an acute febrile illness of usually less than one week, changes in multiple areas and fluid in the area surrounding the lungs on a chest X-ray, and eosinophils comprising more than 25% of white blood cells in fluid obtained by bronchoalveolar lavage. Other typical laboratory abnormalities include an elevated white blood cell count, erythrocyte sedimentation rate, and immunoglobulin G level. Pulmonary function testing usually reveals a restrictive process with reduced diffusion capacity for carbon monoxide. Chronic eosinophilic pneumonia is most likely when the symptoms have been present for more than a month. Laboratory tests typical of chronic eosinophilic pneumonia include increased levels of eosinophils in the blood, a high erythrocyte sedimentation rate, iron deficiency anemia, and increased platelets. A chest X-ray can show abnormalities anywhere, but the most specific finding is increased shadow in the periphery of the lungs, away from the heart.

Differential diagnosis
This includes:

Asthma
Environmental allergic reaction
Granulomatosis with polyangiitis
Allergic bronchopulmonary aspergillosis
Churg–Strauss syndrome
Loefflers syndrome
Acute eosinophilic pneumonia
Chronic eosinophilic pneumonia (Carringtons disease)
Polyarteritis nodosa
Parasitic infections
Tropical pulmonary eosinophilia
Tuberculosis
Fungal infection
Sarcoidosis
Drug reaction with eosinophilia and systemic symptoms
Mastocytosis
Lymphoproliferative hypereosinophilic syndrome
Myeloproliferative hypereosinophilic syndrome

Treatment
When eosinophilic pneumonia is related to an illness such as cancer or parasitic infection, treatment of the underlying cause is effective in resolving the lung disease. When due to acute or chronic eosinophilic pneumonia, however, treatment with corticosteroids results in a rapid, dramatic resolution of symptoms over the course of one or two days. Either intravenous methylprednisolone or oral prednisone are most commonly used. In acute eosinophilic pneumonia, treatment is usually continued for a month after symptoms disappear and the X-ray returns to normal (usually four weeks total). In chronic eosinophilic pneumonia, treatment is usually continued for three months after symptoms disappear and the X-ray returns to normal (usually four months total). Inhaled steroids such as fluticasone have been used effectively when discontinuation of oral prednisone has resulted in relapse.
Because eosinophilic pneumonia affects the lungs, individuals develop difficulty breathing. If enough of the lungs are involved, it may not be possible for a person to breathe without support. Non-invasive machines such as a bilevel positive airway pressure machine may be used. Otherwise, placement of a breathing tube into the mouth may be necessary and a ventilator may be used to help the person breathe.

Prognosis
Eosinophilic pneumonia due to cancer or parasitic infection carries a prognosis related to the underlying illness. Acute and chronic eosinophilic pneumonia, however, have very little associated mortality as long as intensive care is available and treatment with corticosteroids is given </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Glycosuria and can you explain it in depth? [/INST] Glycosuria is the excretion of glucose into the urine. Ordinarily, urine contains no glucose because the kidneys are able to reabsorb all of the filtered glucose from the tubular fluid back into the bloodstream. Glycosuria is nearly always caused by elevated blood glucose levels, most commonly due to untreated diabetes mellitus. Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys (such as Fanconi syndrome), producing a condition termed renal glycosuria. Glycosuria leads to excessive water loss into the urine with resultant dehydration, a process called osmotic diuresis.
Alimentary glycosuria is a temporary condition, when a high amount of carbohydrate is taken, it is rapidly absorbed in some cases where a part of the stomach is surgically removed, the excessive glucose appears in urine producing glycosuria.

Follow-up
In a patient with glucosuria, diabetes is confirmed by measuring fasting or random plasma glucose and glycated hemoglobin(HbA1c).

Pathophysiology
Blood is filtered by millions of nephrons, the functional units that comprise the kidneys </s>


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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Ataxia and can you explain it in depth? [/INST] Ataxia is a neurological sign consisting of lack of voluntary coordination of muscle movements that can include gait abnormality, speech changes, and abnormalities in eye movements. Ataxia is a clinical manifestation indicating dysfunction of the parts of the nervous system that coordinate movement, such as the cerebellum. Ataxia can be limited to one side of the body, which is referred to as hemiataxia. Several possible causes exist for these patterns of neurological dysfunction. Dystaxia is a mild degree of ataxia. Friedreichs ataxia has gait abnormality as the most commonly presented symptom. The word is from Greek α- [a negative prefix] + -τάξις [order] = "lack of order".

Types
Cerebellar
The term cerebellar ataxia is used to indicate ataxia due to dysfunction of the cerebellum. The cerebellum is responsible for integrating a significant amount of neural information that is used to coordinate smoothly ongoing movements and to participate in motor planning. Although ataxia is not present with all cerebellar lesions, many conditions affecting the cerebellum do produce ataxia. People with cerebellar ataxia may have trouble regulating the force, range, direction, velocity, and rhythm of muscle contractions. This results in a characteristic type of irregular, uncoordinated movement that can manifest itself in many possible ways, such as asthenia, asynergy, delayed reaction time, and dyschronometria. Individuals with cerebellar ataxia could also display instability of gait, difficulty with eye movements, dysarthria, dysphagia, hypotonia, dysmetria, and dysdiadochokinesia. These deficits can vary depending on which cerebellar structures have been damaged, and whether the lesion is bi- or unilateral.People with cerebellar ataxia may initially present with poor balance, which could be demonstrated as an inability to stand on one leg or perform tandem gait. As the condition progresses, walking is characterized by a widened base and high stepping, as well as staggering and lurching from side to side. Turning is also problematic and could result in falls. As cerebellar ataxia becomes severe, great assistance and effort are needed to stand and walk. Dysarthria, an impairment with articulation, may also be present and is characterized by "scanning" speech that consists of slower rate, irregular rhythm, and variable volume. Also, slurring of speech, tremor of the voice, and ataxic respiration may occur. Cerebellar ataxia could result with incoordination of movement, particularly in the extremities. Overshooting (or hypermetria) occurs with finger-to-nose testing and heel to shin testing; thus, dysmetria is evident. Impairments with alternating movements (dysdiadochokinesia), as well as dysrhythmia, may also be displayed. Tremor of the head and trunk (titubation) may be seen in individuals with cerebellar ataxia.Dysmetria is thought to be caused by a deficit in the control of interaction torques in multijoint motion. Interaction torques are created at an associated joint when the primary joint is moved. For example, if a movement required reaching to touch a target in front of the body, flexion at the shoulder would create a torque at the elbow, while extension of the elbow would create a torque at the wrist. These torques increase as the speed of movement increases and must be compensated and adjusted for to create coordinated movement. This may, therefore, explain decreased coordination at higher movement velocities and accelerations.

Dysfunction of the vestibulocerebellum (flocculonodular lobe) impairs balance and the control of eye movements. This presents itself with postural instability, in which the person tends to separate his/her feet upon standing, to gain a wider base and to avoid titubation (bodily oscillations tending to be forward-backward ones). The instability is, therefore, worsened when standing with the feet together, regardless of whether the eyes are open or closed. This is a negative Rombergs test, or more accurately, it denotes the individuals inability to carry out the test, because the individual feels unstable even with open eyes.
Dysfunction of the spinocerebellum  (vermis and associated areas near the midline) presents itself with a wide-based "drunken sailor" gait (called truncal ataxia), characterised by uncertain starts and stops, lateral deviations, and unequal steps. As a result of this gait impairment, falling is a concern in patients with ataxia. Studies examining falls in this population show that 74–93% of patients have fallen at least once in the past year and up to 60% admit to fear of falling.
Dysfunction of the cerebrocerebellum (lateral hemispheres) presents as disturbances in carrying out voluntary, planned movements by the extremities (called appendicular ataxia). These include:
Intention tremor (coarse trembling, accentuated over the execution of voluntary movements, possibly involving the head and eyes, as well as the limbs and torso)
Peculiar writing abnormalities (large, unequal letters, irregular underlining)
A peculiar pattern of dysarthria (slurred speech, sometimes characterised by explosive variations in voice intensity despite a regular rhythm)
Inability to perform rapidly alternating movements, known as dysdiadochokinesia, occurs, and could involve rapidly switching from pronation to supination of the forearm. Movements become more irregular with increases of speed.
Inability to judge distances or ranges of movement happens. This dysmetria is often seen as undershooting, hypometria, or overshooting, hypermetria, the required distance or range to reach a target. This is sometimes seen when a patient is asked to reach out and touch someones finger or touch his or her own nose.
The rebound phenomenon, also known as the loss of the check reflex, is also sometimes seen in patients with cerebellar ataxia, for example, when  patients are flexing their elbows isometrically against a resistance. When the resistance is suddenly removed without warning, the patients arms may swing up and even strike themselves. With an intact check reflex, the patients check and activate the opposing triceps to slow and stop the movement.
Patients may exhibit a constellation of subtle to overt cognitive symptoms, which are gathered under the terminology of Schmahmanns syndrome.

Sensory
The term sensory ataxia is used to indicate ataxia due to loss of proprioception, the loss of sensitivity to the positions of joint and body parts. This is generally caused by dysfunction of the dorsal columns of the spinal cord, because they carry proprioceptive information up to the brain. In some cases, the cause of sensory ataxia may instead be dysfunction of the various parts of the brain that receive positional information, including the cerebellum, thalamus, and parietal lobes.Sensory ataxia presents itself with an unsteady "stomping" gait with heavy heel strikes, as well as a postural instability that is usually worsened when the lack of proprioceptive input cannot be compensated for by visual input, such as in poorly lit environments.Physicians can find evidence of sensory ataxia during physical examination by having patients stand with their feet together and eyes shut. In affected patients, this will cause the instability to worsen markedly, producing wide oscillations and possibly a fall; this is called a positive Rombergs test. Worsening of the finger-pointing test with the eyes closed is another feature of sensory ataxia. Also, when patients are standing with arms and hands extended toward the physician, if the eyes are closed, the patients fingers tend to "fall down" and then be restored to the horizontal extended position by sudden muscular contractions (the "ataxic hand").

Vestibular
The term vestibular ataxia is used to indicate ataxia due to dysfunction of the vestibular system, which in acute and unilateral cases is associated with prominent vertigo, nausea, and vomiting. In slow-onset, chronic bilateral cases of vestibular dysfunction, these characteristic manifestations may be absent, and dysequilibrium may be the sole presentation.

Causes
The three types of ataxia have overlapping causes, so can either coexist or occur in isolation. Cerebellar ataxia can have many causes despite normal neuroimaging.

Focal lesions
Any type of focal lesion of the central nervous system (such as stroke, brain tumor, multiple sclerosis, inflammatory [such as sarcoidosis], and "chronic lymphocytyc inflammation with pontine perivascular enhancement responsive to steroids syndrome" [CLIPPERS]) will cause the type of ataxia corresponding to the site of the lesion: cerebellar if in the cerebellum; sensory if in the dorsal spinal cord...to include cord compression by thickened ligamentum flavum or stenosis of the boney spinal canal...(and rarely in the thalamus or parietal lobe); or vestibular if in the vestibular system (including the vestibular areas of the cerebral cortex).

Exogenous substances (metabolic ataxia)
Exogenous substances that cause ataxia mainly do so because they have a depressant effect on central nervous system function. The most common example is ethanol (alcohol), which is capable of causing reversible cerebellar and vestibular ataxia. Chronic intake of ethanol causes atrophy of the cerebellum by oxidative and endoplasmic reticulum stresses induced by thiamine deficiency. Other examples include various prescription drugs (e.g. most antiepileptic drugs have cerebellar ataxia as a possible adverse effect), Lithium level over 1.5mEq/L, synthetic cannabinoid HU-211 ingestion and various other medical and recreational drugs (e.g. ketamine, PCP or dextromethorphan, all of which are NMDA receptor antagonists that produce a dissociative state at high doses). A further class of pharmaceuticals which can cause short term ataxia, especially in high doses, are benzodiazepines. Exposure to high levels of methylmercury, through consumption of fish with high mercury concentrations, is also a known cause of ataxia and other neurological disorders.

Radiation poisoning
Ataxia can be induced as a result of severe acute radiation poisoning with an absorbed dose of more than 30 grays.

Vitamin B12 deficiency
Vitamin B12 deficiency may cause, among several neurological abnormalities, overlapping cerebellar and sensory ataxia. Neuropsychological symptoms may include sense loss, difficulty in proprioception, poor balance, loss of sensation in the feet, changes in reflexs, dementia, and psychosis, can be reversible with treatment. Complications may include a neurological complex known as subacute combined degeneration of spinal cord, and other neurological disorders.

Hypothyroidism
Symptoms of neurological dysfunction may be the presenting feature in some patients with hypothyroidism. These include reversible cerebellar ataxia, dementia, peripheral neuropathy, psychosis and coma. Most of the neurological complications improve completely after thyroid hormone replacement therapy.

Causes of isolated sensory ataxia
Peripheral neuropathies may cause generalised or localised sensory ataxia (e.g. a limb only) depending on the extent of the neuropathic involvement. Spinal disorders of various types may cause sensory ataxia from the lesioned level below, when they involve the dorsal columns.

Non-hereditary cerebellar degeneration
Non-hereditary causes of cerebellar degeneration include chronic alcohol use disorder, head injury, paraneoplastic and non-paraneoplastic autoimmune ataxia, high altitude cerebral oedema, coeliac disease, normal pressure hydrocephalus and infectious or post-infectious cerebellitis.

Hereditary ataxias
Ataxia may depend on hereditary disorders consisting of degeneration of the cerebellum or of the spine; most cases feature both to some extent, and therefore present with overlapping cerebellar and sensory ataxia, even though one is often more evident than the other. Hereditary disorders causing ataxia include autosomal dominant ones such as spinocerebellar ataxia, episodic ataxia, and dentatorubropallidoluysian atrophy, as well as autosomal recessive disorders such as Friedreichs ataxia (sensory and cerebellar, with the former predominating) and Niemann Pick disease, ataxia-telangiectasia (sensory and cerebellar, with the latter predominating),autosomal recessive spinocerebellar ataxia-14 and abetalipoproteinaemia. An example of X-linked ataxic condition is the rare fragile X-associated tremor/ataxia syndrome or FXTAS.

Arnold–Chiari malformation (congenital ataxia)
Arnold–Chiari malformation is a malformation of the brain. It consists of a downward displacement of the cerebellar tonsils and the medulla through the foramen magnum, sometimes causing hydrocephalus as a result of obstruction of cerebrospinal fluid outflow.

Succinic semialdehyde dehydrogenase deficiency
Succinic semialdehyde dehydrogenase deficiency is an autosomal-recessive gene disorder where mutations in the ALDH5A1 gene results in the accumulation of gamma-Hydroxybutyric acid (GHB) in the body. GHB accumulates in the nervous system and can cause ataxia as well as other neurological dysfunction.

Wilsons disease
Wilsons disease is an autosomal-recessive gene disorder whereby an alteration of the ATP7B gene results in an inability to properly excrete copper from the body. Copper accumulates in the nervous system and liver and can cause ataxia as well as other neurological and organ impairments.

Gluten ataxia
Gluten ataxia is an autoimmune disease triggered by the ingestion of gluten. Early diagnosis and treatment with a gluten-free diet can improve ataxia and prevent its progression. The effectiveness of the treatment depends on the elapsed time from the onset of the ataxia until diagnosis, because the death of neurons in the cerebellum as a result of gluten exposure is irreversible. It accounts for 40% of ataxias of unknown origin and 15% of all ataxias. Less than 10% of people with gluten ataxia present any gastrointestinal symptom and only about 40% have intestinal damage. This entity is classified into primary auto-immune cerebellar ataxias (PACA).

Potassium pump
Malfunction of the sodium-potassium pump may be a factor in some ataxias. The Na+-K+ pump has been shown to control and set the intrinsic activity mode of cerebellar Purkinje neurons. This suggests that the pump might not simply be a homeostatic, "housekeeping" molecule for ionic gradients; but could be a computational element in the cerebellum and the brain. Indeed, an ouabain block of Na+-K+ pumps in the cerebellum of a live mouse results in it displaying ataxia and dystonia. Ataxia is observed for lower ouabain concentrations, dystonia is observed at higher ouabain concentrations.

Cerebellar ataxia associated with anti-GAD antibodies
Antibodies against the enzyme glutamic acid decarboxylase (GAD: enzyme changing glutamate into GABA) cause cerebellar deficits. The antibodies impair motor learning and cause behavioral deficits.
GAD antibodies related ataxia is part of the group called immune-mediated cerebellar ataxias. The antibodies induce a synaptopathy. The cerebellum is particularly vulnerable to autoimmune disorders. Cerebellar circuitry has capacities to compensate and restore function thanks to cerebellar reserve, gathering multiple forms of plasticity. LTDpathies gather immune disorders targeting long-term depression (LTD), a form of plasticity.

Diagnosis
Imaging studies - A CT scan or MRI of the brain might help determine potential causes. An MRI can sometimes show shrinkage of the cerebellum and other brain structures in people with ataxia. It may also show other treatable findings, such as a blood clot or benign tumour, that could be pressing on the cerebellum.
Lumbar puncture (spinal tap) - A needle is inserted into the lower back (lumbar region) between two lumbar vertebrae to obtain a sample of cerebrospinal fluid for testing.
Genetic testing - Determines whether the mutation that causes one of the hereditary ataxic conditions is present. Tests are available for many but not all of the hereditary ataxias.

Treatment
The treatment of ataxia and its effectiveness depend on the underlying cause. Treatment may limit or reduce the effects of ataxia, but it is unlikely to eliminate them entirely. Recovery tends to be better in individuals with a single focal injury (such as stroke or a benign tumour), compared to those who have a neurological degenerative condition. A review of the management of degenerative ataxia was published in 2009. A small number of rare conditions presenting with prominent cerebellar ataxia are amenable to specific treatment and recognition of these disorders is critical. Diseases include vitamin E deficiency, abetalipoproteinemia, cerebrotendinous xanthomatosis, Niemann–Pick type C disease, Refsums disease, glucose transporter type 1 deficiency, episodic ataxia type 2, gluten ataxia, glutamic acid decarboxylase ataxia. Novel therapies target the RNA defects associated with cerebellar disorders, using in particular anti-sense oligonucleotides.The movement disorders associated with ataxia can be managed by pharmacological treatments and through physical therapy and occupational therapy to reduce disability. Some drug treatments that have been used to control ataxia include: 5-hydroxytryptophan (5-HTP), idebenone, amantadine, physostigmine, L-carnitine or derivatives, trimethoprim/sulfamethoxazole, vigabatrin, phosphatidylcholine, acetazolamide, 4-aminopyridine, buspirone, and a combination of coenzyme Q10 and vitamin E.Physical therapy requires a focus on adapting activity and facilitating motor learning for retraining specific functional motor patterns. A recent systematic review suggested that physical therapy is effective, but there is only moderate evidence to support this conclusion. The most commonly used physical therapy interventions for cerebellar ataxia are vestibular habituation, Frenkel exercises, proprioceptive neuromuscular facilitation (PNF), and balance training; however, therapy is often highly individualized and gait and coordination training are large components of therapy.Current research suggests that, if a person is able to walk with or without a mobility aid, physical therapy should include an exercise program addressing five components: static balance, dynamic balance, trunk-limb coordination, stairs, and contracture prevention. Once the physical therapist determines that the individual is able to safely perform parts of the program independently, it is important that the individual be prescribed and regularly engage in a supplementary home exercise program that incorporates these components to further improve long term outcomes. These outcomes include balance tasks, gait, and individual activities of daily living. While the improvements are attributed primarily to changes in the brain and not just the hip or ankle joints, it is still unknown whether the improvements are due to adaptations in the cerebellum or compensation by other areas of the brain.Decomposition, simplification, or slowing of multijoint movement may also be an effective strategy that therapists may use to improve function in patients with ataxia. Training likely needs to be intense and focused—as indicated by one study performed with stroke patients experiencing limb ataxia who underwent intensive upper limb retraining. Their therapy consisted of constraint-induced movement therapy which resulted in improvements of their arm function. Treatment should likely include strategies to manage difficulties with everyday activities such as walking. Gait aids (such as a cane or walker) can be provided to decrease the risk of falls associated with impairment of balance or poor coordination. Severe ataxia may eventually lead to the need for a wheelchair </s>


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<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Rectal tenesmus and can you explain it in depth? [/INST] Rectal tenesmus is a feeling of incomplete defecation.  It is the sensation of inability or difficulty to empty the bowel at defecation, even if the bowel contents have already been evacuated. Tenesmus indicates the feeling of a residue, and is not always correlated with the actual presence of residual fecal matter in the rectum </s>