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Hypochondriasis - Wikipedia
https://en.wikipedia.org/wiki/Hypochondriasis
Hypochondriasis
From Wikipedia, the free encyclopedia
For the anatomical term, see Hypochondrium.
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| Hypochondriasis | |
|---|---|
| Classification and external resources | |
| Specialty | psychiatry |
| ICD-10 | F45.2 |
| ICD-9-CM | 300.7 |
| MedlinePlus | 001236 |
| MeSH | D006998 |
Often, hypochondria persists even after a physician has evaluated a person and reassured them that their concerns about symptoms do not have an underlying medical basis or, if there is a medical illness, their concerns are far in excess of what is appropriate for the level of disease. Many hypochondriacs focus on a particular symptom as the catalyst of their worrying, such as gastro-intestinal problems, palpitations, or muscle fatigue. To qualify for the diagnosis of hypochondria the symptoms must have been experienced for at least 6 months.[3]
The DSM-IV-TR defines this disorder, "Hypochondriasis", as a somatoform disorder[4] and one study has shown it to affect about 3% of the visitors to primary care settings.[5] The newly published DSM-5 replaces the diagnosis of hypochondriasis with the diagnoses of "Somatic Symptom Disorder" and "Illness Anxiety Disorder".[6]
Hypochondria is often characterized by fears that minor bodily or mental symptoms may indicate a serious illness, constant self-examination and self-diagnosis, and a preoccupation with one's body. Many individuals with hypochondriasis express doubt and disbelief in the doctors' diagnosis, and report that doctors’ reassurance about an absence of a serious medical condition is unconvincing, or short-lasting. Additionally, many hypochondriacs experience elevated blood pressure, stress, and anxiety in the presence of doctors or while occupying a medical facility, a condition known as "white coat syndrome". Many hypochondriacs require constant reassurance, either from doctors, family, or friends, and the disorder can become a disabling torment for the individual with hypochondriasis, as well as his or her family and friends.[7] Some hypochondriacal individuals completely avoid any reminder of illness, whereas others frequently visit medical facilities, sometimes obsessively. Other victims of this disease will never speak about it.[citation needed]
Contents
Characteristics
Hypochondriasis is categorized as a somatic amplification disorder—a disorder of "perception and cognition"[1]—that involves a hyper-vigilance of situation of the body or mind and a tendency to react to the initial perceptions in a negative manner that is further debilitating. Hypochondriasis manifests in many ways. Some people have numerous intrusive thoughts and physical sensations that push them to check with family, friends, and physicians. For example, a person who has a minor cough may think that they have tuberculosis.[8] Or sounds produced by organs in the body, such as those made by the intestines, might be seen as a sign of a very serious illness to patients dealing with hypochondriasis.[citation needed]Other people are so afraid of any reminder of illness that they will avoid medical professionals for a seemingly minor problem, sometimes to the point of becoming neglectful of their health when a serious condition may exist and go undiagnosed. Yet others live in despair and depression, certain that they have a life-threatening disease and no physician can help them. Some consider the disease as a punishment for past misdeeds.[9]
Hypochondriasis is often accompanied by other psychological disorders. Bipolar disorder, clinical depression, obsessive-compulsive disorder (OCD), phobias, and somatization disorder are the most common accompanying conditions in people with hypochondriasis, as well as a generalized anxiety disorder diagnosis at some point in their life.[10]
Many people with hypochondriasis experience a cycle of intrusive thoughts followed by compulsive checking, which is very similar to the symptoms of obsessive-compulsive disorder. However, while people with hypochondriasis are afraid of having an illness, patients with OCD worry about getting an illness or of transmitting an illness to others.[9] Although some people might have both, these are distinct conditions.[citation needed]
Patients with hypochondriasis often are not aware that depression and anxiety produce their own physical symptoms, and mistake these symptoms for manifestations of another mental or physical disorder or disease. For example, people with depression often experience changes in appetite and weight fluctuation, fatigue, decreased interest in sex and motivation in life overall. Intense anxiety is associated with rapid heartbeat, palpitations, sweating, muscle tension, stomach discomfort, dizziness, and numbness or tingling in certain parts of the body (hands, forehead, etc.).[citation needed]
In some cases, hypochondriasis responds well to antipsychotics, particularly the newer atypical antipsychotic medication.[11][12]
If a person is ill with a medical disease such as diabetes or arthritis, there will often be psychological consequences, such as depression. Some even report being suicidal. In the same way, someone with psychological issues such as depression or anxiety will sometimes experience physical manifestations of these affective fluctuations, often in the form of medically unexplained symptoms. Common symptoms include headaches; abdominal, back, joint, rectal, or urinary pain; nausea; fever and/or night sweats; itching; diarrhea; dizziness; or balance problems. Many people with hypochondriasis accompanied by medically unexplained symptoms feel they are not understood by their physicians, and are frustrated by their doctors’ repeated failure to provide symptom relief.[citation needed]
Diagnosis
The ICD-10 defines hypochondriasis as follows:- A. Either one of the following:
-
- A persistent belief, of at least six months' duration, of the presence of a maximum of two serious physical diseases (of which at least one must be specifically named by the patient).
- A persistent preoccupation with a presumed deformity or disfigurement (body dysmorphic disorder).
-
- B. Preoccupation with the belief and the symptoms causes persistent distress or interference with personal functioning in daily living, and leads the patient to seek medical treatment or investigations (or equivalent help from local healers).
- C. Persistent refusal to accept medical advice that there is no adequate physical cause for the symptoms or physical abnormality, except for short periods of up to a few weeks at a time immediately after or during medical investigations.
- D. Most commonly used exclusion criteria: not occurring only during any of the schizophrenia and related disorders (F20-F29, particularly F22) or any of the mood disorders (F30-F39).
A. Preoccupation with fears of having, or the idea that one has, a serious disease based on the person's misinterpretation of bodily symptoms.The newly published DSM-5 replaces the diagnosis of hypochondriasis with "illness anxiety disorder".[6]
B. The preoccupation persists despite appropriate medical evaluation and reassurance.
C. The belief in Criterion A is not of delusional intensity (as in Delusional Disorder, Somatic Type) and is not restricted to a circumscribed concern about appearance (as in Body Dysmorphic Disorder).
D. The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
E. The duration of the disturbance is at least 6 months.
F. The preoccupation is not better accounted for by Generalized Anxiety Disorder, Obsessive-Compulsive Disorder, Panic Disorder, a Major Depressive Episode, Separation Anxiety, or another Somatoform Disorder.
Cause
Hypochondria is currently considered a psychosomatic disorder, as in a mental illness with physical symptoms.[13] Cyberchondria is a colloquial term for hypochondria in individuals who have researched medical conditions on the Internet. The media and the Internet often contribute to hypochondria, as articles, TV shows and advertisements regarding serious illnesses such as cancer and multiple sclerosis often portray these diseases as being random, obscure and somewhat inevitable. Inaccurate portrayal of risk and the identification of non-specific symptoms as signs of serious illness contribute to exacerbating the hypochondriac’s fear that they actually have that illness.[citation needed]Major disease outbreaks or predicted pandemics can also contribute to hypochondria. Statistics regarding certain illnesses, such as cancer, will give hypochondriacs the illusion that they are more likely to develop the disease.[citation needed]
Overly protective caregivers and an excessive focus on minor health concerns have been implicated as a potential cause of hypochondriasis development.[14]
It is common for serious illnesses or deaths of family members or friends to trigger hypochondria in certain individuals. Similarly, when approaching the age of a parent's premature death from disease, many otherwise healthy, happy individuals fall prey to hypochondria. These individuals believe they are suffering from the same disease that caused their parent's death, sometimes causing panic attacks with corresponding symptoms.[citation needed]
Family studies of hypochondriasis do not show a genetic transmission of the disorder. Among relatives of people suffering from hypochondriasis only somatization disorder and generalized anxiety disorder were more common than in average families.[9] Other studies have shown that the first degree relatives of patients with OCD have a higher than expected frequency of a somatoform disorder (either hypochondriasis or body dysmorphic disorder).[15]
Treatment
Most research indicates that cognitive behavioral therapy (CBT) is an effective treatment for hypochondriasis.[16][17] Much of this research is limited by methodological issues.[17] A small amount of evidence suggests that selective serotonin reuptake inhibitors can also reduce symptoms, but further research is needed.[18]Etymology
Among the regions of the abdomen, the hypochondrium is the uppermost part. The word derives from the Greek term ὑποχόνδριος hypokhondrios, meaning "of the soft parts between the ribs and navel" from hypo ("under") and khondros, or cartilage (of the sternum). Hypochondria in Late Latin meant "the abdomen".[19]The term hypochondriasis for a state of disease without real cause reflected the ancient belief that the viscera of the hypochondria were the seat of melancholy and sources of the vapor that caused morbid feelings.[20] Until the early 18th century, the term referred to a "physical disease caused by imbalances in the region that was below your rib cage" (i.e., of the stomach or digestive system). For example, Robert Burton's The Anatomy of Melancholy (1621) blamed it "for everything from 'too much spittle' to 'rumbling in the guts'".[21]
Immanuel Kant discussed hypochondria in his 1798 book, Anthropology like this:
The disease of the hypochondriac consists in this: that certain bodily sensations do not so much indicate a really existing disease in the body as rather merely excite apprehensions of its existence: and human nature is so constituted – a trait which the animal lacks – that it is able to strengthen or make permanent local impressions simply by paying attention to them, whereas an abstraction – whether produced on purpose or by other diverting occupations – lessen these impressions, or even effaces them altogether.
- Anthropology by Immanuel Kant, 1798 Journal of Speculative Philosophy Vol. XVI edited by William Torrey Harris p. 395-396
See also
- Nosophobia
- Cyberchondria
- Mithridatism
- Munchausen syndrome
- Nocebo
- Psychosomatic medicine
- Sickness behavior
- Somatoform disorder
- Somatosensory amplification
- Medical students' disease
- Man flu
- Valetudinarian
- The Imaginary Invalid
Researchers find genetically engineered virus reduces desire to drink ...
www.dailymail.co.uk/.../Is-genetically-engineered-virus-answer-alcoholism...
Oct 25, 2016 - Researchers claim it could reduce desire to drink. Experts found ... That gene then drives the neurons to express a specific protein. After the ...
Could a genetically engineered VIRUS cure alcoholism? Researchers claim it could reduce desire to drink
- Experts found alcohol changes the way your brain processes information
- They also identified a way to ease changes and reduce the desire to drink
- The team discovered a genetically engineered virus as the solution
- Virus inhibits the 'go' neurons to reduce alcohol drinking levels
About 17 million adults and more than 850,000 adolescents had some problems with alcohol in the United States in 2012.
Long-term alcohol misuse could harm your liver, stomach, cardiovascular system and bones, as well as your brain.
Chronic
heavy alcohol drinking can lead to a problem that we scientists call
alcohol use disorder, which most people call alcohol abuse or
alcoholism.
Scroll down for videos
Long-term alcohol misuse could harm
your liver, stomach, cardiovascular system and bones, as well as your
brain. Chronic heavy alcohol drinking can lead to a problem that we
scientists call alcohol use disorder, which most people call alcohol
abuse or alcoholism
Whatever
name you use, it is a severe issue that affects millions of people and
their families and causes economic burdens to our society.
Quitting alcohol, like quitting any drug, is hard to do.
One reason may be that heavy drinking can actually change the brain.
Our
research team at Texas A&M University Health Science Center has
found that alcohol changes the way information is processed through
specific types of neurons in the brain, encouraging the brain to crave
more alcohol.
Over time, the more you drink, the more striking the change.
In
recent research we identified a way to mitigate these changes and
reduce the desire to drink using a genetically engineered virus.
Alcohol use disorders include alcohol abuse and alcohol dependence, and can be thought of as an addiction.
Addiction is a chronic brain disease. It causes abnormalities in the connections between neurons.
Heavy alcohol use can cause changes in a region of the brain, called the striatum.
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This
part of the brain processes all sensory information (what we see and
what we hear, for instance), and sends out orders to control
motivational or motor behavior.
The striatum, which is located in the forebrain, is a major target for addictive drugs and alcohol.
Drug
and alcohol intake can profoundly increase the level of dopamine, a
neurotransmitter associated with pleasure and motivation, in the
striatum.
Our research team
at Texas A&M University Health Science Center has found that
alcohol changes in how brain neurons process information. The neurons in
the striatum (pictured) have higher densities of dopamine receptors as
compared to neurons in other parts of the brain
The neurons in the striatum have higher densities of dopamine receptors as compared to neurons in other parts of the brain.
As a result, striatal neurons are more susceptible to changes in dopamine levels.
There are two main types of neurons in the striatum: D1 and D2.
While both receive sensory information from other parts of the brain, they have nearly opposite functions.
D1-neurons control 'go' actions, which encourage behavior.
D2-neurons, on the other hand, control 'no-go' actions, which inhibit behavior.
In the study, the team gave mice with
two bottles, one containing water and the other containing 20 percent
alcohol by volume, mixed with drinking water. Then mice were infected
with a genetically engineered virus that delivers a gene into the 'go'
or 'no-go' neurons
Think of D1-neurons like a green traffic light and D2-neurons like a red traffic light.
Dopamine affects these neurons in different ways.
It promotes D1-neuron activity, turning the green light on, and suppresses D2-neuron function, turning the red light off.
As a result, dopamine promotes 'go' and inhibits 'no-go' actions on reward behavior.
Alcohol, especially excessive amounts, can hijack this reward system because it increases dopamine levels in the striatum.
As
a result, your green traffic light is constantly switched on, and the
red traffic light doesn't light up to tell you to stop.
This is why heavy alcohol use pushes you to drink to excess more and more.
These brain changes last a very long time.
But can they be mitigated? That's what we want to find out.
We
started by presenting mice with two bottles, one containing water and
the other containing 20 percent alcohol by volume, mixed with drinking
water.
The bottle containing alcohol was available every other day, and the mice could freely decide which to drink from.
Gradually, most of animals developed a drinking habit.
We
then used a process called viral mediated gene transfer to manipulate
the 'go' or 'no-go' neurons in mice that had developed a drinking habit.
Mice were infected with a genetically engineered virus that delivers a gene into the 'go' or 'no-go' neurons.
That gene then drives the neurons to express a specific protein.
After the protein is expressed,
experts injected the mice with a chemical that recognizes and binds to
it. This binding inhibits or promotes activity in these neurons, letting
us turn the green light off (by inhibiting 'go' neurons) or turn the
red light (by exciting 'no-go' neurons) back on
After the protein is expressed, we injected the mice with a chemical that recognizes and binds to it.
This
binding can inhibit or promote activity in these neurons, letting us
turn the green light off (by inhibiting 'go' neurons) or turn the red
light (by exciting 'no-go' neurons) back on.
Then
we measured how much alcohol the mice were consuming after being
'infected,' and compared it with what they were drinking before.
We
found that either inhibiting the 'go' neurons or turning on the 'no-go'
neurons successfully reduced alcohol drinking levels and preference for
alcohol in the 'alcoholic' mice.
In
another experiment in this study, we found that directly delivering a
drug that excites the 'no-go' neuron into the striatum can also reduce
alcohol consumption.
Conversely,
in a previous experiment we found that directly delivering a drug that
inhibits the 'go' neuron has the same effect.
Both results may help the development of clinical treatment for alcoholism.
Most
people with an alcohol use disorder can benefit from treatment, which
can include a combination of medication, counseling and support groups.
Although
medications, such as Naltrexone, to help people stop drinking can be
effective, none of them can accurately target the specific neurons or
circuits that are responsible for alcohol consumption.
Employing viruses to deliver specific genes into neurons has been for disorders such as Parkinson's disease in humans.
Researchers found that either
inhibiting the 'go' neurons or turning on the 'no-go' neurons
successfully reduced alcohol drinking levels and preference for alcohol
in the 'alcoholic' mice
But
while we've demonstrated that this process can reduce the desire to
drink in mice, we're not yet at the point of using the same method in
humans.
Our
finding provides insight for clinical treatment in humans in the
future, but using a virus to treat alcoholism in humans is probably
still a long way off.
Yifeng Cheng, Ph.D. Candidate, Texas A&M University Health Science Center, Texas A&M University and Jun Wang, Assistant Professor of Neuroscience and Experimental Therapeutics, Texas A&M Health Science Center , Texas A&M University
This article was originally published on The Conversation. Read the original article.
This article was originally published on The Conversation. Read the original article.
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