Struggling to surf the stream of consciousness of an over-thinking mind.

The work is hard, the perks are few, the pay is terrible, and the product, when it’s finally finished, is pure joy.

Mary Lee Settle, on writing (via theparisreview)


Capgras and Fregoli Delusions

When people hear the words “psychiatric disorder,” they often think of depression, bipolar disorder, or schizophrenia. However, there are other psychiatric disorders that are not well-known, but are fascinating nonetheless. 

Have you ever thought that a close friend or family member, perhaps even your significant other, had been replaced by an imposter, a pretender? On the other end of the spectrum, perhaps you’ve thought that everybody around you was actually the same person assuming different disguises and playing different roles. If so, you may have an obscure psychological disorder.

Capgras Delusion

People suffering from this disorder believe that some of the people around them are imposters. They believe that familiar people and even pets have been replaced by imposters. They recognize the face of their family members or beloved pets, but they believe the real person has been replaced by an imposter. It is unknown exactly what causes Capgras Delusion, but it has been seen in people who suffer from other psychiatric disorders or have experienced a head trauma. It has been suggested that sufferers of Capgras Delusion have lost the connection between the area of the brain that recognize faces and the area that supplies an emotional response to the faces seen. Though the person recognizes the face as that of their wife, sister, or dog, they no longer have the emotional response usually connected to that face. Because of the lack of emotion, they may believe that the person cannot be who they think they are because if they were, the sufferer would have an emotional response to them. One sufferer of Capgras Delusion is profiled here on YouTube. Treatment for Capgras Delusion includes individual therapy that involves reframing and reality testing as well as antipsychotics and other drugs.

Fregoli Syndrome

This is similar to Capgras Delusion, but involves the sufferer believing that those around them are actually other people in disguise. When they see their wife, for example, they believe she is actually their doctor or some other person they know. This is named after Leopoldo Fregoli, who was an Italian actor known for his ability to quickly change appearance during stage performances. It was first described in 1927 in a paper in which the authors discussed a 27-year-old woman who was living in London. She believed she was being followed and persecuted by two actors she saw at the theatre often. She felt these people were taking the form of others she knew or had previously met. In a more recent case, the sufferer was a 21-year-old man who was schizophrenic. He believed that his daily facial cream attracted female students. He met a young woman on Facebook and wanted to have a relationship with her, but she was not interested. The man then developed the belief that when he was contacted by other women on Facebook, they were not who they appeared to be, but rather they were the first young woman in disguise. The man believed that this young woman was applying the same cream to her face to transform her appearance. Causes of Fregoli Syndrome are not entirely known, but it has been found in people taking the drug Levodopa. This is used to treat Parkinson’s Disease and dopamine responsive dystonia. Traumatic brain injuries are another possible cause. Treatment usually includes antipsychotic drugs. In some cases, antidepressants and anticonvulsants are prescribed.


Traumatic brain injury

Injury to the right frontal and left temporo-parietal areas can cause Fregoli syndrome. Research by Feinberg, et al. has shown that significant deficits in executive and memory functions follow shortly after damage in the right frontal or left temporoparietal areas. Tests performed on patients that have suffered from a brain injury revealed that basic attention ability and visuomotor processing speed are typically normal. However, these patients made many errors when they were called to participate in detailed attention tasks. Selective attention tests involving auditory targets were also performed, and brain-injured patients had many errors; this meant that they were deficient in their response regulation and inhibition.

Fusiform gyrus

Current research has shown that lesions in the right temporal lobe and the fusiform gyrus may contribute to DMSs. MRIs of patients exemplifying Fregoli symptoms have shown parahippocampal and hippocampal damage in the anterior fusiform gyrus, as well as the middle and inferior of the right temporal gyri. The inferior and medial of the right temporal gyri are the storage locations for long-term memory in retrieving information on visual recognition, specifically of faces; thus, damage to these intricate connections could be one of the leading factors in face misidentification disorders.

Recently, a face-specific area in the fusiform gyrus has been discovered and is close to the anterior fusiform gyrus. MRI studies performed by Hudson, et al. have shown lesions in the anterior fusiform gyrus, which is close to the face specific area (ventral fusiform cortex), may also be associated with Fregoli syndrome and other DMSs. Such damage may cause disruption in long-term visual memory and lead to improper associations of human faces.

On another note, our brains interpret visual scenes in two pathways: one is via the Parietal lobe-occipital dorsal pathway (visual spatial material is analyzed here), and the other is via the temporal-occipital ventral pathway (recognizes objects and faces). Thus, lesions in either structures or disruption of delicate connections may produce DMSs.

Abnormal P300

Delusional misidentification syndrome is thought to occur due to a dissociation between identification and recognition processes. The integration of information for further processing is referred to as working memory (WM). The P300 (P stands for positive voltage potential and the 300 for the 300-millisecond poststimulus) is an index of WM and is used during a WM test in DMS patients. In comparison to normal patients, DMS patients generally exhibit an attenuated amplitude of P300 at many abductions. These patients also exhibit prolonged latencies of P300 at all abductions. These implications suggest that DMSs are accompanied by abnormal WM, specifically affecting the prefrontal cortex (both outside and inside).

Sources: 1 2 3 4

All good poets of the past, almost without exception, were at least bilingual if not trilingual.

People are afraid of themselves, of their own reality; their feelings most of all. People talk about how great love is, but that’s bullshit. Love hurts. Feelings are disturbing. People are taught that pain is evil and dangerous. How can they deal with love if they’re afraid to feel? Pain is meant to wake us up. People try to hide their pain. But they’re wrong. Pain is something to carry, like a radio. You feel your strength in the experience of pain. It’s all in how you carry it. That’s what matters. Pain is a feeling. Your feelings are a part of you. Your own reality. If you feel ashamed of them, and hide them, you’re letting society destroy your reality. You should stand up for your right to feel your pain.

—Jim Morrison (via whiskeymystics-and-men)

People fear death even more than pain. It’s strange that they fear death. Life hurts a lot more than death. At the point of death, the pain is over. I guess it is a friend…

—Jim Morrison  (via mgkepp)

I’m a paradox. I want to be happy, but I think of things that make me sad. I’m lazy, yet I’m ambitious. I don’t like myself, but I also love who I am. I say I don’t care, but I really do. I crave attention, but reject it when it comes my way. I’m a conflicted contradiction. If I can’t figure myself out, there’s no way anyone else has.

—(via jessicachastains)

(Source: staaaaaaahp, via -5280)


Breakthrough program halts Huntington’s progression

Being sociable and exercising your mind and body can significantly slow down the progression of Huntington’s disease for those who are beginning to show symptoms according to a world-first study by Western Australian researchers.

The disorder, which affects muscle coordination and causes progressive mental and physical deterioration is a type of dementia, related to Alzheimer’s disease, and it is caused by a mutation in either one of an individual’s two copies of a gene called Huntingtin.

Currently researchers are trying to identify treatments to stop its progression and improve quality of life, while the search for a cure continues.

One promising study found the disease’s progression was significantly slowed down in mice given a physical and mental exercise program—this strategy forming the basis of a pilot study in Western Australia.

The Huntington’s Exercise Research Optimisation study recruited 20 patients in early to mid stages of Huntington’s disease to find out if a prolonged program of mental and physical rehabilitation would positively impact on features of the disease.

The program ran over 23 months and included gym-based exercises, home-based physical exercises and occupational therapy.

The pilot had remarkable results with participants deteriorating at a 50 per cent slower rate than a group who did not do the program—they also had noticeable improvements in body composition, muscular strength and perceptions of mental health.

In addition, participants showed mental improvement, which reached statistical significance for some aspects of cognitive function.

Researchers concluded the pilot study shows it’s possible to considerably impact on the progression of Huntington’s disease in a cohort of individuals at early-mid stages of the disease.

But they say larger studies are warranted to more clearly explain the program’s benefits.

Following the pilot’s success, researchers are recruiting for a new study with participants yet to be diagnosed as symptomatic.

This study will offer participants an ongoing multidisciplinary rehabilitation program as an adjunct to their normal pharmaceutical regime.

Edith Cowan University Professor and chief investigator Mel Ziman says the pilot shows quite distinctly that a program of physical and mental stimulation, as well as social stimulation, slows the onset of symptoms and the progression of the disease.

"Aerobic exercise is known to increase some chemicals in the brain—one called brain-derived neurotropic factor, which stimulates neurogenesis and we have to do quite a bit of exercise in this program to switch that on."

"There were very few other studies in humans and we were the world’s first to undertake such an all encompassing program in people and the aim is to improve their quality of life for a longer period of time, so they can maintain their independence."