Alzheimer’s has been proven to not be linked to any form of infection even though signs have been noted after times of stress and when an individual is particularly worried, but it’s felt it’s not specifically a trigger from these form of emotions. There has been opinion that certain deficiencies such as dietary or hormonal may have a bestowment to the progression of this disease, even though most doctors do not believe in this presumption. Also the fact that aluminium present in the diet is a resulting factor. It has been noted that any form of head injury earlier on in life may intensify the risk of Alzheimer’s disease (Cayton, Graham & Warner 2004).
Certain research has shown that the genes affiliated with Alzheimer’s may influence chemicals known as neurotransmitters; this allows the transmittal between nerve cells. One form of neurotransmitters, named acetylcholine, is known to be lacking in this form of disease.
Alternatively, abnormal genes may effectuate through the influence on the nerve growth factor. The genes might intermeddle, enhancing the augmentation of functioning nerve cells to reimburse the death of the other cells.
Foregoing experiments have focussed on a gene that creates a protein called apolipoprotein E (ApoE). There are three forms of ApoE – E2, E3 and E4. Every individual inherits an ApoE gene from each parent. Evidence has shown that individuals that inherit E4 gene have a considerable elevated risk of exhibiting Alzheimer’s.
Also identified have been abnormalities on three other genes – PS1 (presenilin type 1), PS2 and APP (amyloid precursor protein) has been identified as causes of the sparse inherited form, but the mechanism is still unclear.
There is no clear explanation of Alzheimer’s; continuous research is looking at these factors. Individuals at the prime of their intellectual powers can be diagnosed with it. People feeling anxious at their loss of stability and their identity and access to their personal memories. Brains shrink and the neurons modify their shape, exhibiting ‘tangles and plaques’ (Rose 2003).
Symptoms of Schizophrenia
Some symptoms of Schizophrenia are commonly having chaotic thinking patterns, and frequently endure delusions. These frequent delusions often compromise of “ideas of reference”, in which the individual endears great personal importance to objects or events. For example an individual suffering from schizophrenia may see neighbours talking and come to the conclusion that they are conspiring to kill them.
Through this illness you can frequently occur hallucinations. Delusions emerge from misconstrued elucidation of objective phenomena and events, but hallucinations appear in the distraction of external stimulus. A high percentage of Schizophrenic hallucinations consist of voices, normally saying something of personal pertinence to the individual. Suggestions were made by McGuigan (1966) that auditory hallucinations happen because sufferers misconceive their own inner speech for another’s voice. It was found that the individual’s larynx was frequently operative during the encounter of the auditory hallucinations. A magnitude of recent studies has clarified the interpretation of hallucinations (Frith, 1992).
Subsequently, there are sufferers of Schizophrenia whose demeanour is more extreme. The most customary behavioural abnormalities inhabit almost stationery for long periods of time. Others do strange grimaces whilst others continually repeat unusual gestures.
Positive symptoms
- hallucinations
- bizarre forms of behaviour (Schneider, 1959)
Negative symptoms
- absence of emotion and motivation
- language deficits
- general apathy
- avoidance of social activity (Slater & Roth, 1969).
Causes of Schizophrenia
The cause of Schizophrenia is still an unknown entity, many researches have begun to try and establish the facts. There are many conclusions and with frequent discrimination against these theories.
There are a variety of factors in the risks of Schizophrenia, these include:
- genetic susceptibility
- drug abuse (specifically from a young age)
- prenatal or birth complications
- seasonal variation of birth
- immigration status and ethnicity
- urban birth and upbringing
- social isolation/adverse events
- slightly higher rates in males
To some extent Schizophrenia is genetic. It’s of the understanding that it’s inherited albeit not being created by a single gene but the genes inhabit to be influential. Throughout continuous studies it has been recognised that Schizophrenia is confidently inheritable, one study being carried out by Gottesman (1991).
Up until 1978, theoretically it was known as a functional psychosis, conformably to Gershon & Reider (1992) due to the development of the CT scan, it was used to research the brains of inveterate Schizophrenias (by Johnstone et al. at the Clinical Research Centre in Middlesex, England). This exhibited an enhanced size of the lateral cerebral ventricles (the fluid spaces in between the brain) and additional x-ray attestation confirmed less brain tissue (specifically in the medical temporal lobe), this confirmed by technology. Also showing a weakened blood flow in the frontal coretex, signifying decreased neuronal activity and post-mortems have signified that specific groups on neurons correlated in an abnormal way or entangled differently compared to non-schizophrenics.
There are conclusions that there is a surplus neurotransmitter dopamine, but this evidence is inconclusive (Lavender 2000). There are no differences in the dopamine levels amidst drug free schizophrenics and normal individuals, neither is there any averment of increased levels of other metabolites exhibiting greater dopamine activity.
Arguably, the most unambiguous test of genetic influence is the adoption studies, because they show the more refined separation of genetic and environmental factors. The study of the twins has specifically been supplanted in favour of the genetic theory (Joseph, 2003).
A particular study carried out by Heston (1966) carried out a study of 47 adults born to schizophrenic mothers and disjoined within a period of 3 days. As children they had been brought up differently, but not specifically by the mother or her family. There were comparisons of their upbringings and their average age estimated at 36. Where there were signs of the mother being schizophrenic, five of the group were diagnosed and with other theorists became the conclusion that hereditary is a strong factor.
Yet a great deal is still unknown about schizophrenia and the brain, individuals are unsure if there are particular patterns of abnormal ‘wiring’, how the abnormalities congeal in the brain and relate to the known symptoms. There is still the unsure factor that schizophrenia may develop from the growth in the womb. There is an understanding that genes are involved, but the specific connection to brain abnormities is still an unknown entity.
Symptoms of Attention Deficit Hyperactivity Disorder (ADHD)
Adults and children of all ages can suffer from this disorder. Internationally identified, Attention Deficit Hyperactivity Disorder (ADHD) is a medical condition of brain dysfunction, in which causes problems prohibiting inappropriate behaviour and dominating impulses, so affecting behaviour, education and other difficulties. These specific areas have a tendency to evolve within early childhood and are more common within boys than girls, a ratio of 9:1.
The main symptoms are excessive inattentiveness and/or impulsiveness and hyperactivity. One of the main criteria with ADHD is that it is often instituted with other conditions, thus symptoms overlapping for example hyperkinesias or Asperger’s Syndrome or dyslexia. If a child does suffer from ADHD there is a tendency that the child will also experience other complex conditions, like excessive oppositionality and conduct disorder, anxiety and depression, learning difficulties, obsessions, co-ordination and speech and language difficulties. These conditions frequently cover the underlying ADHD.
Apparently no two children have the same symptoms of ADHD. They have various core symptoms, complications, environments and IQ’s, with indigenous personality characteristics, these with a varying tendency to the overall system pattern.
These specifically tend to differentiate into four groups:
- Children are recognised as being very active.
- Mainly impulsive diminished hyperactivity
- Children are recognised as being hyperactive or over-active and a form of dietary management may be tried. Though through a period of time this signs may deteriorate and issues arising may be verbal or emotional impulsiveness, then difficulties evolve like low self esteem and declined social skills.
- Predominantly inattentive ADHD
- Primarily none of the above but severe lack of concentration in school, general and life therefore unable to focus clearly.
- Masking of symptoms such as learning difficulties, low self esteem, poor social skills, conduct disorder and various other difficulties for the underlying core of ADHD. (Kewley 1999).
Causes of Attention Deficit Hyperactivity Disorder (ADHD)
There is continuous research and discussion into the magnitude that ADHD has a biological cause, which it can be inherited and the amplitude to which it has psychological and social roots. The evidence is strong for a largely biological illustration and is agreeable by many experts, specifically from Australia and North America, unfortunately not necessarily the UK. Opinion from society and professionals perceive a child’s behaviour is greatly stemming from direct psychological or social problems, in which it is believed to be entangled by poor parenting, environmental factors or teaching (Kewley 1999).
Though from the biological description these symptoms would be conjoined to differences in activity of the forebrain, an area located for concentration, time awareness and impulse control. It is believed that there is a malfunction in the brain neurochemical messengers’ that methodize these characteristics (Kewley 1999).
Many different factors have come into consideration; genetic factors, environmental factors, diet and social factors and continuously alternative theories are being propositioned such as the hunter -v- farmer, head injuries and neurodiversity but the research continues until it can establish the cause of ADHD, like many other diseases (Wikipedia accessed on 17th February 2009).
Conclusion
Primarily, now you have read this report there is a huge indication that after looking at all three of the psychological disorders, that professionals only partly know the causes of each of these illnesses.
Theorists are continuing their research to try and have a clearer understanding on how they develop obvious signs for society and professionals and being able to provide individuals who suffer from these illnesses a specific cause so they truly understand the depths of their illness.
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Referencing
Cayton, H., Dr Graham, N., and Dr Warner, J., (1997). Alzheimer’s at your fingertips. London: Class Publishing.
Frith, C.D. (1992). The cognitive neuropsychology of schizophrenia. Hove, UK: Psychology Press as cited in Eysenck, M., (2000). Psychology A Students Handbook. East Sussex: Psychology Press Ltd.
Gershon, E.S & Reider, R.O. (1992) Major Disorders of mind and brain. Scientific American. 267(3), 88-95). as cited in Gross, R., 2005. Psychology The Science of Mind and Behaviour. 5th Edition. London: Hodder Headline plc.
Gottesman, I.I. (1991) Schizophrenia Genesis. New York: W.H.Freeman. as cited in Gross, R., 2005. Psychology The Science of Mind and Behaviour. 5th Edition. London: Hodder Headline plc.
Heston, L.L. (1966) Psychiatric disorders in fosterhome-reared children of schizophrenic mothers. British Journal of Psychiatry, 122, 819-825. as cited in Gross, R., 2005. Psychology The Science of Mind and Behaviour. 5th Edition. London: Hodder Headline plc.
[Access on 17th February 2009]
Joseph, J. (2003) The Gene Illusion: Genetic research in psychiatry and psychology under the microscope. Ross-on-Wye: PCCS Books. as cited in Gross, R., 2005. Psychology The Science of Mind and Behaviour. 5th Edition. London: Hodder Headline plc.
Kewley, G.D. (1999). Attention Deficit Hyperactivity Disorder: Recognition, reality and resolution. Great Britain: David Fulton Publishers.
Lavender, T. (2000) Schizophrenia. In L. Champion & M. Power (eds) Adult Psychological Problems: An Introduction (2nd edition). Hove: Psychology Press. as cited in Gross, R., 2005. Psychology The Science of Mind and Behaviour. 5th Edition. London: Hodder Headline plc.
McGuigan, F.J. (1966). Covert oral behaviour and auditory hallucinations. Psychophysiology, 29, 96-109 as cited in Eysenck, M., (2000). Psychology A Students Handbook. East Sussex: Psychology Press Ltd.
Reveley, A., (2006). Your Guide to Schizophrenia. London: Hodder Headline
Rose, S. (2003) The Making of Memory: From Molecules to Mind (Revised edition). London:Vintage. as cited in Gross, R., 2005. Psychology The Science of Mind and Behaviour. 5th Edition. London: Hodder Headline plc.
Schneider, K. (1959) Clinical Psychopathology. New York: Grune & Stratton. as cited in Gross, R., 2005. Psychology The Science of Mind and Behaviour. 5th Edition. London: Hodder Headline plc.
Slater, E & Roth, M. (1969) Clinical Psychiatry (3rd edition). London, Balliere Tindall and Cassell. as cited in Gross, R., 2005. Psychology The Science of Mind and Behaviour. 5th Edition. London: Hodder Headline plc.
