Diagnosis is primarily anecdotal, that is, it depends upon a good occupational history. Diagnosis of metal fume fever can be easily missed because the complaints are non-specific, resemble a number of other common illnesses, and presentation occurs typically 2–4 hours after the exposure. When respiratory symptoms are prominent, metal fume fever may be confused with acute bronchitis or pneumonia. The diagnosis is based primarily upon a history of exposure to metal oxide fumes. Cain and Fletcher (2010) report a case of metal fume fever that was diagnosed only by taking a full occupational history and by close collaboration between primary and secondary health care personnel.

Physical symptoms vary among persons exposed, depending largely upon the stage in the course of the syndrome during which examination occurs. Patients may present with wheezing or crackles in the lungs. They typically have an increased white blood cell count, and urine, blood plasma and skin zinc levels may (unsurprisingly) be elevated. Chest X-ray abnormalities may also be present.

An interesting feature of metal fume fever involves rapid adaptation to the development of the syndrome following repeated metal oxide exposure. Workers with a history of recurrent metal fume fever often develop a tolerance to the fumes. This tolerance, however, is transient, and only persists through the work week. After a weekend hiatus, the tolerance has usually disappeared. This phenomenon of tolerance is what led to the name "Monday Fever".

In 2006, approximately 700 metal fume exposures were reported to the United States Poison control center. The American Welding Society estimated that 2500 employees in the steel industry develop metal fume fever in the US each year and that the majority of the cases are not reported.

The current reference range for acceptable blood lead concentrations in healthy persons without excessive exposure to environmental sources of lead is less than 5 µg/dL for children. It was less than 25 µg/dL for adults. Previous to 2012 the value for children was 10 (µg/dl). The current biological exposure index (a level that should not be exceeded) for lead-exposed workers in the U.S. is 30 µg/dL in a random blood specimen.

In 2015, US HHS/CDC/NIOSH designated 5 µg/dL (five micrograms per deciliter) of whole blood, in a venous blood sample, as the reference blood lead level for adults. An elevated BLL is defined as a BLL ≥5 µg/dL. This case definition is used by the ABLES program, the Council of State and Territorial Epidemiologists (CSTE), and CDC’s National Notifiable Diseases Surveillance System (NNDSS). Previously (i.e. from 2009 until November 2015), the case definition for an elevated BLL was a BLL ≥10 µg/dL. The U.S. national BLL geometric mean among adults was 1.2 μg/dL in 2009–2010.

Blood lead concentrations in poisoning victims have ranged from 30->80 µg/dL in children exposed to lead paint in older houses, 77–104 µg/dL in persons working with pottery glazes, 90–137 µg/dL in individuals consuming contaminated herbal medicines, 109–139 µg/dL in indoor shooting range instructors and as high as 330 µg/dL in those drinking fruit juices from glazed earthenware containers.

Treatment of mild metal fume fever consists of bedrest, keeping the patient well hydrated, and symptomatic therapy (e.g. aspirin for headaches) as indicated. In the case of non-allergic acute lung injury, standard or recommended approaches to treatment have not been defined.

The consumption of large quantities of cow's milk, either before or immediately after exposure is a traditional remedy. However, the United Kingdom Health and Safety Executive challenges this advice, warning, "Don’t believe the stories about drinking milk before welding. It does not prevent you getting metal fume fever."

Diagnosis includes determining the clinical signs and the medical history, with inquiry into possible routes of exposure. Clinical toxicologists, medical specialists in the area of poisoning, may be involved in diagnosis and treatment.

The main tool in diagnosing and assessing the severity of lead poisoning is laboratory analysis of the blood lead level (BLL).

Blood film examination may reveal basophilic stippling of red blood cells (dots in red blood cells visible through a microscope), as well as the changes normally associated with iron-deficiency anemia (microcytosis and hypochromasia). However, basophilic stippling is also seen in unrelated conditions, such as megaloblastic anemia caused by vitamin B12 (colbalamin) and folate deficiencies.

Exposure to lead also can be evaluated by measuring erythrocyte protoporphyrin (EP) in blood samples. EP is a part of red blood cells known to increase when the amount of lead in the blood is high, with a delay of a few weeks. Thus EP levels in conjunction with blood lead levels can suggest the time period of exposure; if blood lead levels are high but EP is still normal, this finding suggests exposure was recent. However, the EP level alone is not sensitive enough to identify elevated blood lead levels below about 35 μg/dL. Due to this higher threshold for detection and the fact that EP levels also increase in iron deficiency, use of this method for detecting lead exposure has decreased.

Blood lead levels are an indicator mainly of recent or current lead exposure, not of total body burden. Lead in bones can be measured noninvasively by X-ray fluorescence; this may be the best measure of cumulative exposure and total body burden. However this method is not widely available and is mainly used for research rather than routine diagnosis. Another radiographic sign of elevated lead levels is the presence of radiodense lines called lead lines at the metaphysis in the long bones of growing children, especially around the knees. These lead lines, caused by increased calcification due to disrupted metabolism in the growing bones, become wider as the duration of lead exposure increases. X-rays may also reveal lead-containing foreign materials such as paint chips in the gastrointestinal tract.

Fecal lead content that is measured over the course of a few days may also be an accurate way to estimate the overall amount of childhood lead intake. This form of measurement may serve as a useful way to see the extent of oral lead exposure from all the diet and environmental sources of lead.

Lead poisoning shares symptoms with other conditions and may be easily missed. Conditions that present similarly and must be ruled out in diagnosing lead poisoning include carpal tunnel syndrome, Guillain–Barré syndrome, renal colic, appendicitis, encephalitis in adults, and viral gastroenteritis in children. Other differential diagnoses in children include constipation, abdominal colic, iron deficiency, subdural hematoma, neoplasms of the central nervous system, emotional and behavior disorders, and intellectual disability.

In cases of suspected copper poisoning, penicillamine is the drug of choice, and dimercaprol, a heavy metal chelating agent, is often administered. Vinegar is not recommended to be given, as it assists in solubilizing insoluble copper salts. The inflammatory symptoms are to be treated on general principles, as are the nervous ones.

There is some evidence that alpha-lipoic acid (ALA) may work as a milder chelator of tissue-bound copper. Alpha lipoic acid is also being researched for chelating other heavy metals, such as mercury.

OSHA has set safety standards for grinding and sharpening copper and copper alloy tools, which are often used in nonsparking applications. These standards are recorded in the Code of Federal Regulations 29 CFR 1910.134 and 1910.1000.

Note: The most important nonsparking copper alloy is beryllium copper, and can lead to beryllium poisoning.

This disease is diagnosed mainly by the appearance of well-demarcated rash and inflammation. Blood cultures are unreliable for diagnosis of the disease, but may be used to test for sepsis. Erysipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, and diffuse inflammatory carcinoma of the breast.

Erysipelas can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevation of the antistreptolysin O titer occurs after around 10 days of illness.

Owing to the non-specific nature of the presentation of symptoms, diagnosis of malaria in non-endemic areas requires a high degree of suspicion, which might be elicited by any of the following: recent travel history, enlarged spleen, fever, low number of platelets in the blood, and higher-than-normal levels of bilirubin in the blood combined with a normal level of white blood cells. Reports in 2016 and 2017 from countries were malaria is common suggest high levels of over diagnosis due to insufficient or inaccurate laboratory testing.

Malaria is usually confirmed by the microscopic examination of blood films or by antigen-based rapid diagnostic tests (RDT). In some areas, RDTs need to be able to distinguish whether the malaria symptoms are caused by "Plasmodium falciparum" or by other species of parasites since treatment strategies could differ for non-"P. falciparum" infections. Microscopy is the most commonly used method to detect the malarial parasite—about 165 million blood films were examined for malaria in 2010. Despite its widespread usage, diagnosis by microscopy suffers from two main drawbacks: many settings (especially rural) are not equipped to perform the test, and the accuracy of the results depends on both the skill of the person examining the blood film and the levels of the parasite in the blood. The sensitivity of blood films ranges from 75–90% in optimum conditions, to as low as 50%. Commercially available RDTs are often more accurate than blood films at predicting the presence of malaria parasites, but they are widely variable in diagnostic sensitivity and specificity depending on manufacturer, and are unable to tell how many parasites are present.

In regions where laboratory tests are readily available, malaria should be suspected, and tested for, in any unwell person who has been in an area where malaria is endemic. In areas that cannot afford laboratory diagnostic tests, it has become common to use only a history of fever as the indication to treat for malaria—thus the common teaching "fever equals malaria unless proven otherwise". A drawback of this practice is overdiagnosis of malaria and mismanagement of non-malarial fever, which wastes limited resources, erodes confidence in the health care system, and contributes to drug resistance. Although polymerase chain reaction-based tests have been developed, they are not widely used in areas where malaria is common as of 2012, due to their complexity.

Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin, or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal.

Because of the risk of reinfection, prophylactic antibiotics are sometimes used after resolution of the initial condition. However, this approach does not always stop reinfection.

Malaria is classified into either "severe" or "uncomplicated" by the World Health Organization (WHO). It is deemed severe when "any" of the following criteria are present, otherwise it is considered uncomplicated.

- Decreased consciousness

- Significant weakness such that the person is unable to walk

- Inability to feed

- Two or more convulsions

- Low blood pressure (less than 70 mmHg in adults and 50 mmHg in children)

- Breathing problems

- Circulatory shock

- Kidney failure or hemoglobin in the urine

- Bleeding problems, or hemoglobin less than 50 g/L (5 g/dL)

- Pulmonary oedema

- Blood glucose less than 2.2 mmol/L (40 mg/dL)

- Acidosis or lactate levels of greater than 5 mmol/L

- A parasite level in the blood of greater than 100,000 per microlitre (µL) in low-intensity transmission areas, or 250,000 per µL in high-intensity transmission areas

Cerebral malaria is defined as a severe "P. falciparum"-malaria presenting with neurological symptoms, including coma (with a Glasgow coma scale less than 11, or a Blantyre coma scale greater than 3), or with a coma that lasts longer than 30 minutes after a seizure.

Various types of malaria have been called by the names below:

Gueules cassées (broken faces) is a French expression for facially disfigured servicemen which originated in World War I. Colonel Yves Picot is said to have coined the term when he was refused passing a checkpoint to a party.

Trench warfare protected the bodies but left the heads exposed. Ironically, the introduction of the steel helmet in 1915 made head shots more 'survivable', but this reduction of mortality meant a mutilated life for thousands.

At the start of the war those wounded to the head were generally not considered able to survive and they would not usually be 'helped first'. This changed in the course of the war, as progress was made in medical practices like oral and maxillofacial surgery and most notably in the new field of plastic surgery. Surgeons conducted experiments with bone, cartilage and tissue transplants and the likes of Hippolyte Morestin, Harold Gillies and Léon Dufourmentel made enormous advances. Because of the experimental character of this surgery some chose to remain as they were and others could just not be helped yet. Some of the latter were helped by all kinds of new prosthetics to make them look more or less 'normal'.

Embouchure collapse caused by focal dystonia can be diagnosed medically; embouchure collapse caused by embouchure overuse, however, is generally speaking not considered to be a specifically medical issue. A difficulty in diagnosis is that when a brass player describes the symptoms to a doctor or dentist (as is often the case), the medical practitioner does not fully understand what the patient means. This is because brass players learn their embouchure by "feel," and therefore words have a limited ability to describe embouchure problems, especially if the person listening to the description is not a brass player and has a limited knowledge of the embouchure.

Also, in less severe cases, the player may only be able to feel what is wrong while playing. Many players with an embouchure problem will, once they have realized that it is more than a simple case of tired lips, wish to refrain from playing. The fact that around 24 muscles are employed in forming a brass embouchure, and that each will change slightly as a player struggles to play when experiencing embouchure problems, mean that what players describe as being wrong will have not only worsened their condition when they play, but will be different each time they do so.

In the severest cases, the pain caused by embouchure overuse can be felt even when not playing; in some cases, other symptoms will manifest, such as loss of tissue and damaged nerves. This, however, occurs only in the rarest and most extreme circumstances and usually signals the end of the player's career.

Chimney sweep's cancer, also called soot wart, is a squamous cell carcinoma of the skin of the scrotum. It has the distinction of being the first reported form of occupational cancer, and was initially identified by Percivall Pott in 1775. It was initially noticed as being prevalent amongst chimney sweeps.

There was a study on a three year old that was a carrier of the hemoglobin variant of Hopkins-2. The child had mild anemia and reticulocytosis, which is commonly seen in anemia. There were, however, no sickled cells found in the blood and they had no symptoms relating to sickle cell. There was also a reduced mean corpuscular volume (MCV), which is the average volume of red blood cell count.

Chimney sweeps' carcinoma is a squamous cell carcinoma of the skin of the scrotum. Warts caused by the irritation from soot particles, if not excised, developed into a scrotal cancer. This then invaded the dartos, enlarged the testicle, and proceeded up the spermatic cord into the abdomen where it proved fatal.

Hemoglobin Hopkins-2 (Hb Hop-2) is a mutation of the protein hemoglobin, which is responsible for the transportation of oxygen through the blood from the lungs to the musculature of the body in vertebrates. Generally, the mutation causes two abnormal α chains in the protein's structure. Within the chains, the mutation is the result of hemoglobin's histidine amino acid being replaced with aspartic acid in the protein's genetic sequence. This amino acid structure change occurs at residue 112. Additionally, within one of the mutated alpha chains, there are substitutes at 114 and 118, two points on the amino acid chain. This mutation can cause sickle cell anemia.

Following the initial discovery of hemoglobin, two researchers working at Johns Hopkins Hospital in the mid-twentieth century, Ernest W. Smith and J.V. Torbert, discovered the Hopkins-2 mutation of hemoglobin. Work by Harvey A. Itano and Elizabeth A. Robinson in 1960 confirmed Smith's and Torbert's finding and emphasized the importance of the alpha loci in the mutation. Later in the twentieth century, Samuel Charache, another Hopkins affiliated scientist and doctor, studied the physiological impacts of the variant on health. His findings suggest that the variant plays no effect clinically.

Cheilitis is inflammation of the lips. This inflammation may include the perioral skin (the skin around the mouth), the vermilion border, and/or the labial mucosa. The skin and the vermilion border are more commonly involved, as the mucosa is less affected by inflammatory and allergic reactions.

It is a general term, and there are many recognized types and different causes. Cheilitis can be either acute or chronic. Most cheilitis is caused by exogenous factors such as dryness (chapping) and acute sun exposure. Patch testing may identify allergens that cause cheilitis.

Also termed "lip dermatitis", eczematous cheilitis is a diverse group of disorders which often have an unknown cause. Chronic eczematous reactions account for the majority of chronic cheilitis cases.

It is divided into endogenous (due to an inherent characteristic of the individual), and exogenous (where it is caused by an external agent). The main cause of endogenous eczematous cheilitis is atopic cheilitis (atopic dermatitis), and the main causes of exogenous eczematous cheilitis is irritant contact cheilitis ("e.g.", caused by a lip-licking habit) and allergic contact cheilitis. The latter is characterized by a dryness, fissuring, edema, and crusting. It affects females more commonly than males, in a ratio of about 9:1.

The most common causes of allergic contact cheilitis is lip cosmetics, including lipsticks and lip balm, followed by toothpastes. A lipstick allergy can be difficult to diagnose in some cases as it is possible that cheilitis can develop without the person even wearing lipstick. Instead, small exposure such as kissing someone who is wearing lipstick is enough to cause the condition.

Allergy to Balsam of Peru can manifest as cheilitis. Allergies to metal, wood, or other components can cause cheilitis reactions in musicians, especially players of woodwind and brass instruments, "e.g.", the so-called "clarinetist's cheilitis", or "flutist's cheilitis". "Pigmented contact cheilitis" is one type of allergic cheilitis in which a brown-black discoloration of the lips develops. Patch testing is used to identify the substance triggering allergic contact cheilitis.

As stated above, sufferers of focal dystonia have virtually no possibility of recovery from embouchure collapse. Sufferers of embouchure overuse, however, have been known to recover. The simplest way of doing so is to refrain from playing for an extended period of time, possibly years, before attempting to play again. The exact amount of time needed and whether or not the player will have to completely relearn the use of the embouchure is a largely subjective issue and depends on the individual.

Philip Smith, former principal trumpeter of the New York Philharmonic, has suffered from focal dystonia, which was part of the reason for his retirement. However, Smith had managed to gradually redevelop control over his embouchure and is now playing again, as well as teaching trumpet in the University of Georgia.

"Jerusalem syndrome as a discrete form, uncompounded by previous mental illness." This describes the best-known type, whereby a previously mentally balanced person becomes psychotic after arriving in Jerusalem. The psychosis is characterised by an intense religious character and typically resolves to full recovery after a few weeks or after being removed from the locality. It shares some features with the diagnostic category of a "brief psychotic episode", although a distinct pattern of behaviors has been noted:

1. Anxiety, agitation, nervousness and tension, plus other unspecified reactions.

2. Declaration of the desire to split away from the group or the family and to tour Jerusalem alone. Tour guides aware of the Jerusalem syndrome and of the significance of such declarations may at this point refer the tourist to an institution for psychiatric evaluation in an attempt to preempt the subsequent stages of the syndrome. If unattended, these stages are usually unavoidable.

3. A need to be clean and pure: obsession with taking baths and showers; compulsive fingernail and toenail cutting.

4. Preparation, often with the aid of hotel bed-linen, of a long, ankle-length, toga-like gown, which is always white.

5. The need to shout psalms or verses from the Bible, or to sing hymns or spirituals loudly. Manifestations of this type serve as a warning to hotel personnel and tourist guides, who should then attempt to have the tourist taken for professional treatment. Failing this, the two last stages will develop.

6. A procession or march to one of Jerusalem's holy places, ex:The Western Wall.

7. Delivery of a sermon in a holy place. The sermon is typically based on a plea to humankind to adopt a more wholesome, moral, simple way of life. Such sermons are typically ill-prepared and disjointed.

8. Paranoid belief that a Jerusalem syndrome agency is after the individual, causing their symptoms of psychosis through poisoning and medicating.

Bar-El et al. reported 42 such cases over a period of 13 years, but in no case were they able to actually confirm that the condition was temporary.

During a period of 13 years (1980–1993) for which admissions to the Kfar Shaul Mental Health Centre in Jerusalem were analysed, it was reported that 1,200 tourists with severe, Jerusalem-themed mental problems were referred to this clinic. Of these, 470 were admitted to hospital. On average, 100 such tourists have been seen annually, 40 of them requiring admission to hospital. About three and a half million tourists visit Jerusalem each year. Kalian and Witztum note that as a proportion of the total numbers of tourists visiting the city, this is not significantly different from any other city.

Samuel Taylor Coleridge (21 October 1772–25 July 1834) was an English poet, critic, and philosopher who was, along with his friend William Wordsworth, one of the founders of the Romantic Movement in England and one of the Lake Poets. He wrote the poems "The Rime of the Ancient Mariner" and "Kubla Khan", as well as the prose "Biographia Literaria".

Coleridge was widely known to have been a regular user of opium as a relaxant, analgesic, antidepressant, and treatment for numerous health concerns. "Kubla Khan" was apparently written under the drug's influence, but the degree to which he used the drug as a creative enhancement is not clear. Although Coleridge largely kept his addiction as hidden as possible from those close to him, it became public knowledge with the 1822 publication of "Confessions of an English Opium Eater" by his close friend Thomas de Quincey. The "Confessions" painted a rather negative picture of Coleridge and his reputation suffered accordingly.

Where Coleridge first developed his opium habit is an issue of some scholarly dispute but it clearly dates from a fairly youthful period in his life. Coleridge’s own explanation is clearly laid out in a letter to Joseph Cottle;

However, most scholars agree that Coleridge had resorted to the use of Laudanum (the tincture form of opium) before this date, particularly during times of nervousness and stress. Because Laudanum was widely available and widely used as an analgesic as well as a general sedative, many people were given the drug for all sorts of medical and nervous complaints. Coleridge was probably given the drug numerous times in his youth during several bouts of rheumatic illness. Small medicinal dosages seldom lead to full-blown addiction but for Coleridge, who experienced the painful return of the symptoms many times in his life, it surely introduced him to the use of the drug much earlier than his story to Cottle admits.

Regardless of when and where Coleridge’s opium addiction began, it is clear that the more reliant on the drug he became, the more his work suffered, the less he was able to focus and concentrate, and the more strained his relations became. In fact, it is arguable that any analysis of Coleridge’s life must be done against the constant background of opium usage. But as important as the issue of opium is in Coleridge’s life, it is never a straightforward issue because he often hid it from public and familial view and at other times he exaggerated its importance to his work. In the 1816 publication of his major ‘opium’ poems Coleridge purposely drew a connection between his creative work and his opium usage. Desperate for some financial success with his poetry, Coleridge intentionally attempted to portray himself as a dreamy opium eater because he, perhaps rightly, believed that it would draw a morbid fascination to his work. Opium played an interesting role in the public image of Romantic literature. There was, for a long time, a kind of cult glamorization of the drug and a morose allure to stories of its usage for respectable members of the bourgeoisie who were titillated by such taboo subjects. It was with this in mind that Coleridge generated an image of himself as dreamy poet who created drug induced fantasies.

This dreamy image of himself began even before he was widely known to have been addicted to opium. In one of a series of biographical letters written to his friend Thomas Poole, Coleridge painted this picture of himself, a picture that would always endure. Coleridge writes:

This slothful image was one that endured even with some of Coleridge’s close friends and may have been consciously created by Coleridge in the earlier part of his career in order to draw attention away from his addiction. It was only later that Coleridge perceived an advantage to drawing attention not to himself as simply a slothful scholar but a dreamy opium eater.

The most popular story that connects Coleridge’s work with his opium usage was told by Coleridge in his well-known preface to the poem Kubla Khan. Coleridge wrote:

The sleep of this story is said by Coleridge to be a sleep of opium, and Kubla Khan may be read as an early poetic description of this drug experience. The fact that the poem is generally regarded as one of Coleridge's best is one of the reasons for the continuing interest and debate about the role that opium may have played in his creative output, and in Romanticism in general.

Coleridge, in his lucid moments, understood the problems with which he struggled better than most. In an 1814 letter to his friend John Morgan, Coleridge wrote about his difficulties.

In some respects, Coleridge's life bears a resemblance to that of a modern opiate addict. Unfortunately, as much as Coleridge had some grasp of his addictions and its results, as well as an unusually sharp sense of how this addiction might be treated, many of his closest friends and peers did not understand. The people who might have served him best, like Southey and Wordsworth, were far too willing to maintain his image as slothful and selfish; this despite the professional help that he constantly bestowed upon them. Men like Robert Southey, naturally conservative in outlook were not forward looking enough to comprehend the possibility of Coleridge’s addiction being a largely physical dependence, despite the fact that Coleridge himself, as well as a growing number of professionals like his friend Gillman, were aware of the physical aspect of drug reliance. On more than one occasion Coleridge pointed to the fact that physical restraint might eventually lead to a cure, and on several occasions under the treatment of Dr. Gillman, he was led thus to the edge of freedom from the drug on which he had formed such a dependence. Southey wrote from the position of moral indignation and explicitly denied the physical aspect of the drug issue. Southey wrote to Cottle:

Juche (; ; ), usually left untranslated, or translated as "self-reliance", is the official state ideology of North Korea, described by the government as Kim Il-sung's "original, brilliant and revolutionary contribution to national and international thought". It postulates that "man is the master of his destiny", that the North Korean masses are to act as the "masters of the revolution and construction", and that by becoming self-reliant and strong a nation can achieve true socialism.

Kim Il-sung (1912–1994) developed the ideology, originally viewed as a variant of Marxism–Leninism until it became distinctly "Korean" in character, whilst incorporating the historical materialist ideas of Marxism–Leninism and strongly emphasising the individual, the nation state and its sovereignty. Consequently, "Juche" was adopted into a set of principles that the North Korean government has used to justify its policy decisions from the 1950s onwards. Such principles include moving the nation towards claimed ""jaju"" (independence), through the construction of ""jarip"" (national economy) and an emphasis upon ""jawi"" (self-defence), in order to establish socialism.

The Practice is firmly rooted in the ideals of sustainability through agricultural independence and a lack of dependency.

The "Juche" ideology has been criticized by many scholars and observers as a mechanism for sustaining the totalitarian rule of the North Korean regime, and justifying the country's heavy-handed isolationism and oppression of the North Korean people. It has also been described as a form of Korean ethnic nationalism, but one which promotes the Kim family as the saviours of the "Korean Race" and acts as a foundation of the subsequent personality cult surrounding them.

Treatment of tics present in conditions such as Tourette’s syndrome begins with patient, relative, teacher and peer education about the presentation of the tics. Sometimes, pharmacological treatment is unnecessary and tics can be reduced by behavioral therapy such as habit-reversal therapy and/or counseling. Often this route of treatment is difficult because it depends most heavily on patient compliance. Once pharmacological treatment is deemed most appropriate, lowest effective doses should be given first with gradual increases. The most effective drugs belong to the neuroleptic variety such as monoamine-depleting drugs and dopamine receptor-blocking drugs. Of the monoamine-depleting drugs, tetrabenazine is most powerful against tics and results in fewest side effects. A non-neuroleptic drug found to be safe and effective in treating tics is topiramate. Botulinum toxin injection in affected muscles can successfully treat tics; involuntary movements and vocalizations can be reduced, as well as life-threatening tics that have the potential of causing compressive myelopathy or radiculopathy. Surgical treatment for disabling Tourette’s syndrome has been proven effective in cases presenting with self-injury. Deep Brain Stimulation surgery targeting the globus pallidus, thalamus and other areas of the brain may be effective in treating involuntary and possibly life-threatening tics.