Hedgehog's Dilemma

The hedgehog's dilemma, or sometimes the porcupine dilemma, is an analogy about the challenges of human intimacy. It describes a situation in which a group of hedgehogs all seek to become close to one another in order to share heat during cold weather. They must remain apart, however, as they cannot avoid hurting one another with their sharp spines. Though they all share the intention of a close reciprocal relationship, this may not occur, for reasons they cannot avoid.

 

From 'Studies in Pessimism' (Schopenhauer, p. 142);

''A number of porcupines huddled together for warmth on a cold day in winter; but, as they began to prick one another with their quills, they were obliged to disperse. However the cold drove them together again, when just the same thing happened. At last, after many turns of huddling and dispersing, they discovered that they would be best off by remaining at a little distance from one another.

 

In the same way the need of society drives the human porcupines together, only to be mutually repelled by the many prickly and disagreeable qualities of their nature. The moderate distance which they at last discover to be the only tolerable condition of intercourse, is the code of politeness and fine manners; and those who transgress it are roughly told - in the English phrase - to keep their distance. By this arrangement the mutual need of warmth is only very moderately satisfied; but then people do not get pricked. A man who has some heat in himself prefers to remain outside, where he will neither prick other people nor get pricked himself.''

                            

Both Schopenhauer and Freud have used this situation to describe what they feel is the state of individuals in relation to others in society. The hedgehog's dilemma suggests that despite goodwill, human intimacy cannot occur without substantial mutual harm, and what results is cautious behaviour and weak relationships.

 

The dilemma is also used to justify or explain introversion and isolationism. The concept originates from Arthur Schopenhauer's 'Parerga and Paralipomena'. It then entered the realm of psychology after the tale was discovered and adopted by Freud in 1921.

_____________________________________________________________________________________________________________________

Sometimes love can be a spiky situation.

The Matrix: Was Neo Psychotic?





Auditory Hallucinations

Psychosis is a mental health problem that can  stop the person from thinking clearly, telling the difference between reality and their imagination, and acting in a normal way.

Morpheus: What is "real"? How do you define "real"?

It is a loss of contact with reality that usually includes delusions and hallucinations. Delusions are false beliefs about what is taking place or who one is, such as thinking that someone is plotting against you or that the TV is sending you secret messages. Hallucinations are false perceptions, such as hearing, seeing, or feeling something that is not there. 

Neo: What did she tell you?

Morpheus: That I would find the One. 

Signs of Psychosis

The early stage of psychosis is marked by a difficulty in concentrating, depressed mood, sleep changes - sleeping too much or not enough, anxiety, suspiciousness, withdrawal from family and friends and on-going unusual thoughts and beliefs. While the later stages involve being confused and having impaired reality testing; that is, people are unable to distinguish personal, subjective experiences from the reality of the external world. This can progress onto delusions, hallucinations, disorganized speech (switching topics erratically), difficulty functioning, depression and even suicidal thoughts or actions.

 

Morpheus: I see it in your eyes. You have the look of a man who accepts what he sees because he is expecting to wake up. Ironically, that's not far from the truth.

Causes:


A Psychoactive Aetiology?

A number of medical problems can cause psychosis, including:

- Alcohol and certain illegal drugs (or blue and red pills?)

- Brain diseases, such as Parkinson's  
- Huntington's disease, and certain chromosomal disorders

- Brain tumours or cysts

- Dementia (including Alzheimer's disease)

- HIV and other infections that affect the brain

- Some prescription drugs, such as steroids and stimulants

- Some types of epilepsy

- Stroke

Symptoms:

Psychotic symptoms may include: disorganized thought and speech, false beliefs that are not based in reality (delusions), especially unfounded fear or suspicion, and thoughts that "jump" between unrelated topics (disordered thinking).

Neo: I thought it wasn't real

Morpheus: Your mind makes it real

Exams and tests:

Psychiatric evaluation and testing are used to diagnose the cause of the psychosis. Laboratory testing and brain scans may not be needed, but sometimes can help pinpoint the diagnosis. The type of tests may include; blood tests for abnormal electrolyte and hormone levels, blood tests for syphilis and other infections, drug screens, and sometimes an MRI of the brain.



''Yeah...ehmm...sorry about that''

Possible Complications:

Psychosis can prevent people from functioning normally and caring for themselves. If the condition is left untreated, people can sometimes harm themselves or others (or Trinity).



 Morpheus: You've been living in a dream world, Neo.

 

 

''Your 50 minutes are up young man''

 

Treatment often depends on the cause of the psychosis. It might involve drugs to control symptoms and talk therapy, which can help address the underlying cause of the psychosis.

For example the talking therapy cognitive behavioural therapy has proved successful in helping people with schizophrenia.  Hospitalization is an option for serious cases where a person might be dangerous to himself or others.



''Perhaps we are asking the wrong questions'' ~ Agent Brown 

 

Social support should also be addressed, so as to help support the person with psychosis, who may have social needs such as education, employment or accommodation.

 

 

 

 

 

  

 

 

Agent Smith: It seems that you've been living two lives. One life, you're Thomas A. Anderson, program writer for a respectable software company. You have a social security number, pay your taxes, and you... help your landlady carry out her garbage. The other life is lived in computers, where you go by the hacker alias "Neo" and are guilty of virtually every computer crime we have a law for. One of these lives has a future, and one of them does not.

''The need to prove who you are will vanish once you know who you are''
~ Pierre

 

 

 

 

Similar to Parkinson's Disease and Schizophrenia, dopamine levels are thought to be too high during psychosis, or better, there is a 'functional excess' of dopamine in the person's brain. This can affect memory, emotion, social behaviour and self-awareness.

Bizarre delusions are often experienced during psychosis.

Examples of psychotic delusions include the paranoid type - more likely to be associated with schizophrenia - and delusions of grandeur.



''Sure ye do''



Delusions of grandeur: clearly false but strongly held beliefs in having a special power or authority - the person with psychosis may, as examples, believe that they are a world leader, very rich, that they are able to bring dead people back to life, or that they can control the weather.

 

While the classic hallmarks of psychosis are hallucination and delusion, other symptoms persist in disorders such as schizophrenia - known as negative symptoms. That is, cognitive and motivational impairments, which can be disabling and do not respond to drug treatment.



I think he saw me...

 

 

Paranoid delusions: these may cause the person with psychosis to be unduly suspicious of individuals or organisations, believing them to be plotting to cause them harm. Such delusions can be very frightening and may result in unusual behaviour to avoid things - for example, staying out of a room with certain devices in it, believing them to be controlling thoughts, or locking up the front door with an excessive number of padlocks.

 

Similar to Eric Bui and colleagues examining Borderline Personality Disorder and Darth Vader (2010), it is interesting to compare a disorder with something relevant, in an attempt to try and identify with it. While one is the work of fiction and the other a real life debilitating disorder, slight overlap can be seen and the crude comparisons hopefully elucidate the disorder a little.

______________________________________________________________________________________________________________________
Freudenreich O, Weiss AP, Goff DC. Psychosis and schizophrenia. In: Stern TA, Rosenbaum JF, Fava M, Biederman J,    Rauch SL, eds. Massachusetts General Hospital Comprehensive Clinical Psychiatry. 1st ed. Philadelphia, Pa: Mosby Elsevier; 2008:chap 28.

 

Katherine Darton, Mind. Psychotic experiences. London, UK: Mind, 2011. Information published online, accessed November 21st, 2013.

MedlinePlus. Psychosis. Bethesda, MA, US: National Library of Medicine, National Institutes of Health, Department of Health and Human Services.

 

NHS Choices. Causes of psychosis. London, UK: National Health Service.

 

Van Os J, Kapur S. Schizophrenia. The Lancet, 2009, volume 374, number 9690, pages 635-645 (DOI: 10.1016/S0140-6736(09)60995-8).

WHO. Chapter V: Mental and behavioural disorders. In: International Statistical Classification of Diseases and Related Health Problems, 10th Revision (ICD-10). Geneva, Switzerland: World Health Organization, 2010.

______________________________________________________________________________________________________________________

''Minds that have withered into psychosis are far more terrifying than any character of fiction''
                                                                                                                                   ~ Christian Baloga

Neuroleptic-Induced Dystonia

Dystonia is a neurological movement disorder which may affect anyone at any age. It is characterised by involuntary muscle contractions which force certain parts of the body into abnormal, sometimes painful, movements or postures. Dystonia can affect any part of the body including the arms and legs, trunk, neck, eyelids, face, or vocal cords.



The disordered tonicity of muscles that occurs in dystonia can also be associated with neuroleptics, a dopamine antagonist drug. This secondary, or acquired dystonia, can be a problem encountered specifically with the use of antipsychotic medication (Hansen, 1997), as one side effect of these drugs is debilitating movement disorders known as extrapyramidal symptoms (Yamamoto & Inada, 2012). Drugs that decrease the effectiveness of neurotransmission are known as antagonists. Antipsychotic medication blocks dopamine receptors and this in turn can lead to the dystonic reactions.

With Parkinson’s, the disease is caused by cell death in the substantia nigra, which has dopamine producing functions. This loss of dopamine activity results in a decreased stimulation of the motor cortex which can lead to movement disruptions in the body. Similarly, the dopamine blockade effect of neuroleptic antagonists reduces the activity of transmitters in the synapse causing involuntary muscle contractions (Hansen, 1997). Therefore the severe disturbances of motor behaviour are often caused by the drug-induced dysfunction of the dopaminergic extrapyramidal system, which plays a vital role in movement control (Smelser & Baltes, 2001).

Extrapyramidal symptoms can be categorised as acute and tardive. Acute dystonia has a sudden onset and is often seen within the first five days of starting an antipsychotic course of treatment. Conversely, tardive begins after a long-term use of dopamine antagonist medication (Van Harten & Kahn, 1999).

Neuroleptic-Induced acute dystonia can result in abnormal positioning or spasm of muscles in the head, such as the eyes (oculogyric), neck (impaired swallowing), limbs, and trunk. Acute dystonic reactions generally disappear once the drug dose is lowered or there is complete cessation of the antipsychotic (Yamamodo & Inada, 2012). With tardive dystonia there is currently no established course of treatment, however administration of clozapine has been cited as the only drug helpful if it is tolerated by the patient.

__________________________________________________________________

''Life has many twists and turns.

But when it literally involves your body, then the above saying takes on a whole different meaning''

"This is (probably) why you're Fat"



If you just consume fewer calories you'll lose weight. Unfortunately not always.

Most of us think that we only put fat in our fat cells when we eat too much. Your fat cells are like rechargeable fuel cells, every time you eat, you store some fat. In between meals, fat comes out of your fat cells to provide the fuels for your muscles and organs. If you're naturally thin, it's because you have efficient fat cells. Fat goes in quickly and comes out easily. Your body doesn't need much fat because the small bit of fat you do have is a reliable source of fuel. If you're predisposed to be fat, it's because you have 'greedy fat cells'.

 

When you eat you tend to store calories as fat instead of burning them. And when your other tissues need those calories, the fat comes out slowly, if it comes out at all. So if you don't eat, you start to starve at the cellular level. So you do exactly what your body is telling you to do - you eat more. In other words,

 

You're not getting fat because you're eating more,

You're eating more because you're getting fat!

 

 

If your fat cells are slow to release fuel, your body actually works to make them bigger. And they keep on getting bigger until they can release the energy that your body needs. This could mean gaining a little weight or it could mean gaining a lot! It all depends on how slowly your fat-cells release their fat. Most of us aren't born with 'greedy fat-cells', but we can certainly make them that way. When you eat too many carbohydrates, you raise your blood sugar. Since high blood sugar is toxic, your body releases insulin to bring it down. But your body can only burn a little bit of sugar at a time. So what happens to the rest of it? Your storage sites for carbohydrates are limited and you've got unlimited storage places for fat. So the body just ends up converting the carbs in to fat. And after bringing down your blood sugar, your insulin does its other job, it tells your body to store fat.

Insulin stimulates an enzyme called lipoprotein-lipase which sends fat into the fat cells. So if insulin is elevated, this lipoprotein-lipase production is really activated and it sends fat 'like crazy' into the fat cells. So if you eat a lot of carbohydrates, your insulin goes up and you begin storing fat in the fat cells.

Intra-abdominal (visceral) fat is a major culprit for insidious
effects to a person's health including; cardiovascular
disease, type 2 diabetes and high blood pressure.

When you have a healthy metabolism, it only takes a little bit of insulin to bring your blood sugar down and then everything goes back to normal. But over time, that can change. Cells can become resistant to the effects of insulin, so when that happens, insulin is talking with the cells, but they're not listening! They don't do what they're supposed to do. And so your body does what it has to do, it starts producing more insulin. So you've reached a point where your insulin is high just to keep your sugar levels normal, even if your not eating any sugar. When that happens, your insulin is driving fat into the fat cells and you've reached this point where all of a sudden - Bam! You get fat.

And you get fat even though you're eating the same number of calories you always did. Because now you have greedy fat-cells. So you do what the ''experts'' tell you to do, you go on a low fat, low calorie diet so you can burn your own body fat for fuel. But there's just one little problem with this: if too many carbs are keeping your insulin high, the insulin is telling your body to store the fat instead of burning it. Now you're really starving inside!

So once again your body does what it has to do: it slows down your metabolism. You stop losing weight and you get tired. And people can end up being, in most cases, larger than they were when they started out - but now with a lower metabolic rate. And this can be extremely frustrating for many people.

For every pound of fat you put on, you gain 7 new miles of blood vessels!

So some people get fat and stay fat because they're living on foods that tell their body to store the calories in their fat cells - which just makes you hungrier. In some people the fat-cells and the other tissues become insulin resistant at about the same rate. The good news for them is that they don't gain weight, the bad news is that insulin resistance can kill you even if you're skinny.

The demanding of your pancreas that it produce ever greater amounts of insulin to keep your blood sugar normal, is ultimately going to cause 'beta-cell burnout'. So the pancreas is producing all it can produce and that's not enough anymore. When that happens, the beta-cells get damaged, they can't produce anymore and your blood sugar goes up and now you're becoming diabetic. And further, when your blood sugar goes out of control, it can damage your arteries and lead to heart disease.



It's not easy struggling with something that keeps you alive. But you can blame away, you are in charge of yourself. There's no one giant step that does it, it's a lot of little steps. And that doesn't just relate to putting the weight on, but also for getting rid of it. Human nature is very addictive and human nature is very flawed. It is extraordinary that it takes such a long time for the penny to drop with some people. But it shouldn't be a surprise as the seeds of it are really deep. All the problems of being overweight are remedial. But the younger you put it on the bigger you can go. And the further you let yourself go, the longer of a battle it is to get back (O'Shea, 2012).

~ (Fat Head, 2009)

________________________________________________________________________
''I found there was only one way to look thin: hang out with fat people'' ~ Rodney Dangerfield


First-Generation and Second-Generation Antipsychotics

Antipsychotic medication (or neuroleptics) are an effective treatment for people with schizophrenia. In 1952, Henri Laborit, a surgeon in Paris, was looking for a way to reduce surgical shock in his patients. Much of the shock came from the anaesthesia, and if he could find a way to use less, his patients could recover quicker. He knew that shock was a result of certain brain chemicals so he looked for a chemical to counteract these.

 

His administration of a drug called Chlorpromazine had a marked effect on his patients. Previously restrained and often violent patients could now make contact with others and be left without supervision. It seemed to have a calming effect without sedating his patients. It was then trialled for a number of psychiatric disorders. Some being successful, however there were side effects and drawbacks to the drug which were revealed in the passing years.

 

Following the introduction of first-generation (typical) antipsychotics (FGAs) in the early 1950s, there was a radical change in the therapeutic regimens for schizophrenia.

 

But, as noted, it soon became apparent that these antipsychotics produced serious side effects including extrapyramidal symptoms (EPS) - a distressing and debilitating movement disorder. The extrapyramidal system itself is a neural network that is part of the motor system.

 

Along with extrapyramidal symptoms, other side effects of FGAs included;

- Neuroleptic Malignant Syndrome (NMS), a rare, but life-threatening idiosyncratic reaction to the medication. The syndrome is characterised by muscle rigidity, fever and a sudden raised body temperature which can be fatal. Incidence rates range from 0.02 to 3%. 

- Drowsiness, dry mouth, weight gain, constipation, depression.

 

To prevent EPS, second-generation (a-typical) antipsychotics were developed. These newer medications differed from FGAs primarily on the basis of their reduced risk of inducing EPS (Yamamoto  & Inada, 2012).

 

Neuroleptics work via the blockade of dopamine receptors. Dopamine is one of several transmitters that act on the central nervous system, and numerous dopamine receptors have been found in the extrapyramidal system. Dopamine D2 receptors are those most strongly associated with the efficacy of antipsychotics.

 

Second-generation antipsychotics are effective against psychosis and, at therapeutic doses, seldom cause EPS. Their therapeutic effects are attributable to central antagonism of both serotonin and dopamine receptors, and also possibly to relatively loose binding to D2 receptors (Lehan, 2004).

 

Controversy still lingers over the efficacy of first and second generation antipsychotics. Second generation antipsychotics were seen as an advance in drug treatment 20 years ago when they were developed, as they had additional benefits and fewer adverse effects. However, the invention of second-generation drugs have been regarded by some as invention only, a clever manipulation by the drug industry for marketing purposes, and there is often selective publication of trials that can skew the evidence in favour of a drug preferred by the investigators. Leucht and colleagues (2008) compiled a meta-analysis titled, 'Second-generation versus first-generation antipsychotic drugs for schizophrenia'. There were 150 trials examined. In 95 of them, the second-generation antipsychotic was compared with the high-potency first-generation antipsychotic Haloperidol. The use of Haloperidol showed a bias in favour of the second-generation drugs. Because this first-generation drug is likely to be associated with a high rate of EPS. They also avoided comparison with a medium-potency FGA, because these drugs are just as efficacious as the second-generation drug.

 

Antipsychotic drugs differ in their potencies and have a wide range of adverse effects, with nothing that clearly distinguishes the two groups. The only second-generation antipsychotic that is better than other drugs in resisting schizophrenia is clozapine. Nevertheless, it is argued that second-generation drugs have no special a-typical characteristics, that they are no more effective, do not improve specific symptoms, are less cost effective, and have no clearly different side effects than first-generation drugs (The Lancet, 2009).

____________________________________________________________________________