Schizophrenia

The real etiology of schizophrenia is still a dream despite massive studies on the involvement of the brain. Studies of the brain through neuroimaging have revealed that frontal cortex, temporal lobe, and sub cortical structures are involved. Some of abnormalities in the brain of schizophrenic patients include enlarged ventricles, reduced volume of frontal cortex, temporal lobe cortex, and sub cortical structures like hippocampus and amygdala. These abnormalities have been persistently reported in schizophrenic patients and this shows that they are not functioning inadequately.

Some of these abnormalities are present at the start and some even before the onset of psychosis and this is in support of neurodevelopment of theory of schizophrenia. The key neurotransmitter in schizophrenia is dopamine; however, there are others such as serotonin and glutamate which are also thought to play a role. Schizophrenia is an inherited condition, although genetic research has not come up with a clear conclusion on this matter may be because of the complexity of genetic involvement.

Despite the fact that brain abnormalities are still not very clear in schizophrenia, the evidence is continuously pilling and this is driving towards a complicated disease of the brain network that is affected by genetically mediated developmental abnormality. Introduction Neuropathologists have been involved in research on schizophrenia for about hundred years. Despite the length of the research, the neuropathogy of the disorder is still not clear.

Although they have made some steps in their quest since the beginning when they believed that it was a functional psychosis without structural basis, the main cause of the chronic disorder is still illusive. With the technological advancement in science, researchers have come to a common finding in patients diagnosed with schizophrenia and the common finding is brain abnormalities. These discoveries have made the researchers to wonder if the cause of schizophrenia is brain abnormalities and how the abnormalities arise.

Despite recovery of some brain abnormalities in patients suffering from schizophrenia, most scientists maintained that some of the abnormalities realized are quite slight and some of them are not common in all schizophrenic patients and to occur exclusively in people with schizophrenia. Although these patients have structural pathologies in their brains, the developed abnormalities do not coincide with the disease duration. Some of the abnormalities realized remain the same throughout the development of the disease (Bhogal, 2002).

Understanding of the abnormalities of the brain in schizophrenia is among the challenges currently facing the medical community. The numerous symptoms associated with schizophrenia points at the involvement of various regions of the brain or even a widespread of network or system. Conventional approaches of neurological disorders such as lesion studies or post mortem examinations have defied efforts to understand the brain pathology in schizophrenia. Just like other fields of medicine, luck and destiny have help make major steps in discoveries like dopamine theory and anti psychotics which are used in the management of the disorder.

Modern research in neuroscience such as neuroimaging has aided in improving the foundation knowledge of the disorder and has sustained the hope that complete understanding of the disorder will be realized in the future. In this paper, I am going to summarize the major brain abnormalities found in schizophrenia through neuroimaging (Haren, 2004). Just like other complicated diseases, there are numerous theories on schizophrenia as compared to facts. The initially neurodevelopment theory points at abnormalities in fetal brain development as the cause of the failure of brain functions in early adulthood.

A series of information such as increased rate of obstetric complications, minor physical abnormalities, neurologic mild signs, and slight behavioral abnormalities in children who later suffer from schizophrenia. This model is quite relevant to the development of schizophrenia in particular but also for other neuropsychiatric disorders (Bhogal, 2002). The major drawback of this model is that the prevalence of these signs in the non affected population is quite substantial therefore the positive predictive value in the development of schizophrenia is not convincing.

The disease usually begins at adolescent or early childhood and early adulthood and this indicates brain maturational problem during that time or before the appearance of psychosis. Excessive synaptic or dendritic pruning during the time of onset of the disorder has been suggested as one of the potential mechanism explaining the onset of psychosis in adolescent or in early childhood, although the biology underlying this stage is still not very clear (Lawrie & Abukmeil, 1998).

Neurodegenerative model is based on active biologic processes that may be going on during the prodromal period or the usually prolonged period of untreated psychosis. Development of the disorder is also linked to environmental factors such as illicit drug use and psychosocial stress which are considered as potential secondary triggers which may be accompanying the beginning and the start of schizophrenia. The initial researchers believed that schizophrenia is associated with brain pathology.

Emergence of imaging techniques such as magnetic resonance imaging (MRI) and computed tomography scanning (CTS) have seriously contributed to the detailed study of the brain. Through computed tomography brain abnormalities such as enlarged ventricles and reduced total brain volume have been reported in schizophrenic individuals and these findings were later confirmed by magnetic resonance imaging (Bhogal, 2002). Studies of the brain structures have also been made easy through improvement in segmentation techniques coupled with the use of MRI.

These techniques can be used to identify grey from white matter and measuring of their volume. These also contributed to a more focused investigations of specific regions of the brain such as temporal, frontal lobes, and subcortical structures. Some of the consistent findings in these regions include alteration in structures such as hippocampus, amygdala, superior temporal gyrus, and platinum temporale (Lawrie & Abukmeil, 1998).

Lateral temporal neocortical areas where primary auditory and auditory associations are located are the places of interest in schizophrenia since they are involved in thought processes. Most of the studies in the superior temporal gyrus in schizophrenic patients have always discovered reduced volumes of grey matter in the initial stages of the disorder together with those individuals who are genetically at risk of developing schizophrenia such as offspring of schizophrenic patients.

Other structures of the brain which have also been reported to be abnormally small in schizophrenic patients include medial temporal structures such as hippocampus, amygdala, and parahippocampus gyri. These structures are also reported to be altered in other psychiatric disorders like mood disorders and post traumatic stress disorder (Lawrie & Abukmeil, 1998). Injuries sustained at the time of birth such as anoxia may be associated to hippocampus reduction and this is possibly due to neurodevelopmental abnormality.

The finding is also common among concordant twins who had birth injuries. Medial temporal volume reductions have been discovered in people who are genetically at risk of developing schizophrenia. Reductions in the grey matter in the temporal regions of the brain have also been observed in people who are classified as having prodromal features of schizophrenia who have later on developed psychotic symptoms during the follow up (Haren, 2004). The highly developed region of the brain in man is the frontal lobe.

It is involved in the modulations of higher brain functions such as planning, attention, and working memory. Behavioral and cognitive deficits like lack of motivation, defects in executive functions, Wisconsin card score sorting test and spatial working memory points at frontal lobe functional abnormalities in schizophrenic patients (Lawrie, 1999). Decreased blood flow to the frontal lobe is a common finding in schizophrenia. Despite the fact that this finding is not consisted, it can also be attributed to the complex nature of the region, it has been observed though quite slight.

Basal ganglia which contain caudate, putamen, and globus pallidus are involved in information processing in the cortical and subcortical networks involved in integration of cognition, emotion, and motor function. These structures have been reported to be enlarged in patients using the conventional antipsychotics and this can lead to a conclusion that dopamine blockades causes an increase in volume of the above structures. Psychosis patients who have not used any antipsychotics are reported to have a smaller caudate volume which implies that caudate may be involved in the development of psychoses.

Thalamus acts as the regulatory board for sensory signals and has reciprocal connections to the frontal lobe. It has been suggested that the connections between these two structures are associated with schizophrenia. Thalamus is a bit difficult to measure using MRI, although the findings are inconsistent, smaller thalamus have always been reported in schizophrenic patients. Other anatomic abnormalities in schizophrenia include corpus callosum which is altered both in shape and structure therefore disruption in the integration between the hemispheres.

In most humans, brain functions are lateralized with the left cerebrum being dominantly involved in language. There are proposals that developmental abnormalities of language, peculiar functions of the human beings, and its lateralization which is genetically mediated may be one of the causes of schizophrenia (Bhogal, 2002). Temporal lobe findings of smaller superior temporal gyrus and hippocampus have been reported to be in the left cerebrum and loss of normal asymmetry of the left superior temporal gyrus being a bit larger that the right has been reported in patients suffering from schizophrenia (Staal et.

al, 2000). In the meta analysis study of laterality in schizophrenia, the researchers who were involved in this study concluded that there is a strong proof for decreased cerebral lateralization in schizophrenia more so in the language cortex. We can therefore summarize that structural imaging studies have discovered evidence of extensive anatomic alterations in the brain regions of schizophrenic patients.

The regions highly altered in these patients include those mediating higher mental functions like thought, cognition, effect, and language both early in the illness and those at risks of developing the disorder like children born to schizophrenic patients (Haren, 2004). Synapses and susceptibility genes Neuroimaging studies are in support of the possibility of neurodevelopmental abnormality in schizophrenia, neuronal, molecular, and neurochemical mechanisms underlying these brain abnormalities are not conclusive.

High profile neuropathologic studies have revealed losses in synapse density and relatively normal or elevated neuronal numbers in schizophrenia, which indicates that the main defect may be synapse integrity. This discovery has elicited search for genes that may be associated with synapse integrity by the use of DNA microarray techniques. Post mortem findings on the patients with schizophrenia revealed under expression of a family of synapse related genes (Bhogal, 2002). Genetic factors are the main factors listed as being associated with schizophrenia, however the exact genes involved in susceptibility is still a puzzle.

Although the initial studies on finding these genes was not successful, current studies have implicated several genes in the development of schizophrenia and some of the genes include dysbindin-1, neuregulin-1, d-amino acid oxidase, its activator DAOA, and the regulator of G protein signaling 4. Recent proposals indicated that synapses, especially glutamatergic ones might be the site of initial abnormalities in schizophrenia with downstream disruption of neural circuitry and subsequent effect on other neurotransmitters (Lawrie, 1999). Conclusions

It has become clear that the early scientists were right in their suspicion that the brain is involved in schizophrenia. This evidence cannot be disputed despite the fact that there is no comprehensive information on the etiology and pathophysiology of the disorder. The brain abnormalities in schizophrenia appear to be distributed in extensive areas supporting the fact that schizophrenia is a disorder associated with brain connections. We are still very far from understanding some of the major neuropsychiatric disorders such as Alzheimer’s disease.

The molecular, physiologic, and neurochemical mechanisms underlying schizophrenia continues to evade our findings. Recent research on the disorder acts as the foundations for future fundamental discoveries on the nature of schizophrenia. References: Bhogal, B. (2002). Physical Brain Abnormality a Possible Cause of Schizophrenia. Retrieved on May 6, 2010 from http://serendip. brynmawr. edu/bb/neuro/neuro02/web1/bbhogal. html Haren, N. E. M. (2004). Brain abnormalities in schizophrenia: longitudinal and genetic aspects.

Quebec: s. n. Lawrie, S. (Jan. 4, 1999). “Risk Of Schizophrenia Onset Linked To Brain Abnormalities. ” The Lancet. Lawrie, S. M. & Abukmeil, S. S. (1998). “Brain abnormality in schizophrenia. A systematic and quantitative review of volumetric magnetic resonance imaging studies. ” The British Journal of Psychiatry 172. Staal, G. S. et. al. (2000). “Structural Brain Abnormalities in Patients With Schizophrenia and Their Healthy Siblings. ” American Journal of Psychiatry, 157.

There has been a long term controversy over the legalization of Marijuana in the United State.

Some believe it should be legal in the United States because it could “create a source of additional tax revenues and police and courts would be freed up for more serious crimes”. Others believe it should be an illegal drug because of its health risks. Marijuana should remain illegal in the United States as a schedule I controlled substance due to the many physical and psychological effects it has on it’s users as well as the harmful effects it has on today’s society.Marijuana acts on the brains reward system which governs the response to pleasurable things. Users of marijuana seek the euphoric feeling or “high” caused by the drug. THC enters the body and creates the high the marijuana user seeks by stimulating brain cells to release dopamine, which is a chemical found in the brain. Marijuana has many effects on the body, both short and long, though there is limited research on the long lasting effects of marijuana use.

The acute effects present during intoxication may include but are not limited to impairments to the short memory, attention, judgment, coordination, balance and other cognitive functions.Smoking marijuana may also distort the user’s depth perception. The heart rate of a person during their intoxication increases as well as their blood pressure. Just seconds after inhaling marijuana smoke the persons bronchial passages enlarge and relax. Blood vessels in the eye expand which commonly makes the user’s eyes look red or bloodshot. Users begin to feel relaxed, have heightened sensory perception, and altered perception of time. A User may laugh and have an increase in appetite after smoking marijuana.

Large doses of marijuana sometimes lead to acute psychosis including hallucinations, delusions or a loss of sense of personal identity. Some users may have psychotic episodes such as anxiety, fear, distrust, panic and paranoia. After the euphoric feeling subsides or fades the person may feel depressed or tired. There is limited knowledge or information on the long term effects of smoking marijuana. Some studies suggest that effects on the brain can build up and deteriorate critical life skills over time. Effects often are worse for people with mental disorders, or simply by virtue of the normal aging process.Schizophrenia like disorders have been associated with the use of marijuana in vulnerable individuals.

Long term users may have sleep impairment or suffer from insomnia. Chronic abuse of marijuana increases the risk of chronic cough or bronchitis. Smoking Marijuana has the same, if not worse, respiratory problems as tobacco, such as frequent acute chest illness and a risk of lung infection. Using Marijuana has the potential to create cancer of the lungs and other parts of the reparatory tract because marijuana contains irritants and carcinogens up to 70% more than tobacco smoke.Some believe that marijuana may impair the ability to form new memories and focus which makes learning, doing complicated tasks, participating in athletics and driving difficult. The effects of marijuana use can last days or even weeks after the acute effects wear off, which mean a daily user is functioning at a reduced intellectual level most or all of the time. Contrary to popular belief marijuana is an addictive drug.

The use of marijuana has many harmful effects to the users but it also affects others who do not participate in the use of marijuana.The World Health Organization ranks the United States first among 17 European and North America countries for prevalent use of marijuana. In 2008, 2. 2 million Americans used marijuana for the first time and greater than half were under the age of 18. Because marijuana affects brain systems that are still maturing through young adulthood, its use by teens may have a negative effect on their development. 42% of United States high school graduates have tired marijuana. Marijuana smoking students compared to non-marijuana smoking students tend to have lower grades and a higher dropout rate.

It is easily assumed that while being under the influence of marijuana driving would become more difficult because of the loss of coordination, balance and the perception of depth. The National Highway Traffic Administration issued a report stating that 18% of motor vehicle driver’s deaths involved drugs other than alcohol. 6. 8% of drivers, mostly under the age of 35, involved in accidents tested positive for THC. There many questions about the use of marijuana while a woman is pregnant.Even low amounts of THC, when administered during the prenatal period, could have profound and long lasting consequences on the brain and behavior of the unborn child. Marijuana exposed children show gaps in problem solving, memory and ability to remain attentive in a classroom setting.

Marijuana also affects places of employment. In a study among postal workers, employees who tested positive for marijuana on a pre-employment urine drug test had 55% more industrial accidents, 85% more injuries and a 75% increase in absenteeism compared to those who tested negative for marijuana.There is a higher job turn over rate for people who choose to use marijuana and be employed. Employees who use marijuana tend to have more absences, tardiness, accidents and worker compensation claims. Marijuana use has adverse physical, mental, emotional and behavior effects. It causes students to perform poorly in school. Marijuana use affects many of it’s users at their place of employment due to being absent and causing more accidents in the work place making it unsafe for others.

Many children are born with defects and behavior problems due to the poor judgment of their mothers, who partook in the use of marijuana during the prenatal period. The roads in America are polluted with drivers under the influence of marijuana whose judgment and motor skills are impaired. Marijuana should remain illegal in the United States due to the harmful effects on its users as well as innocent bystanders.

Introduction

Non-behavioral tests became in use in the 1970’s with the development of the auditory brainstem response (ABR). The testing method became popular in the 1980’s and revolutionized audiometric testing methods. The method however had its weaknesses: it is often difficult to record and record near threshold levels, it provides limited information regarding the nature of hearing loss, it requires extensive multiple testing and interpretation of response are subjective (Cone-Wesson et al, 2002).

Another testing method that became popular was through otoacoustic emissions (OAE’s). In the 1990’s, OAE’s were utilized to asses frequency-specific responses of outer hair cells but the test can not be utilized to establish the degree of hearing loss (Batterjee and Dutt, 2005, p. 2).However, the test has proven its use in hearing screening for infants and its still is used extensively today due primarily to its high degree of objectivity in testing cochlear function. To address the limitations of ABR and OAE, a more comprehensive testing methodology was evolved and the result was the development of ASSR.

Though auditory steady-state response (ASSR) testing is still in its infancy, it has already shown itself to be a promising audiometric diagnostic and clinical tool. Acoustic reflexes or behavioral measures in audiometric testing may be problematic with patients who are unable to provide deliberate response to stimuli such as infants, mentally disabled and otherwise incapacitated, whether deliberate or not (Batterjee and Dutt, 2005). In these situations, there is a need for a dependable audiogram to reveal true hearing thresholds across various frequencies to facilitate diagnosis and treatment.

Delineating of Auditory Steady State Response

Auditory Evoked Potential (AEP) stimulates the brain to react to auditory stimuli that can either be transient or steady-sate in nature. Transient AEP’s such as ABR’s respond to stimuli momentarily and infrequently. The frequency of responses may also vary during testing with repetition. Steady-state AEP is a reaction to recurring stimuli that are sustained by a continuous amplitude and phase during testing. The result is a response whose waveform from the brain is identical to the waveform of the stimulus creating a cycle of stimulus and response explicit to the testing frequency or a steady-sate evoked potential (SSEP) known as ASSR (Hall, 2000).

Development

ASSR traces its development from the 40Hz event related potential (ERP) studies conducted in the 1980’s is a steady. 40Hz ERP is an example of steady-state response produced through stimulation at the rate of 40 times per second (Batterjee and Dutt, 2005, p. 4).  The method promised to be a dependable estimation tool to define low frequency hearing thresholds which was a limitation of ABR. The drawback to it however was its vulnerability to sleep and attention preconditions and undependable application to newborn testing (Hall, 2000).

            Researches in the 1990’s suggested the use of higher modulated audiometric systems. One of the main objectives was to develop steady-state response tools that can estimate frequency-specific hearing in infants which were estimated to be over 60 Hz (Batterjee and Dutt, 2005). Also, there were evolving studies on how to utilize multiple stimuli concurrently to both ears to streamline testing and assessment methods (John, 2003). These efforts led to the foundation of ASSR.

Strengths

The main benefit of ASSR system is its capacity to make a distinction of levels of hearing loss. Knowledge of hearing loss profundity is essential in treatment selection as well as technical aspects related to implants and other hearing aids. It can provide information for amplification needs of individuals in relation to their hearing capacity accurately (Picton et al, 2002).

Bringing together ASSR evaluations and behavioral analysis or methods can also facilitate the effectiveness of therapy or rehabilitation of patients ensuring them maximization of existing hearing capacity or applied tools. Efficiency in testing is also achieved since ASSR requires less time than ABR testing (Batterjee and Dutt, 2005, pp. 5-8). It also been applied in testing babies at birth hastening testing and treatment for infants improving chances for auditory function (Luts, Desloovere and Wouters, 2006).

            Furthermore, according to Batterjee and Dutt, ASSR does away with subjective interpretation of responses as well as satisfy the prescribed requirement of the Joint Commission on Infant Hearing (JCIH) and the American Speech and Hearing Association (ASHA) (2005, p.1-9).

Weaknesses

Recent studies have shown that ASSR’s are not as accurate as they have claimed to be and may differ significantly form actual behavioral thresholds (Pastor et al, 2003). It Ted Venema’s studies have also shown that ASSR’s for several carrier frequencies, in particular those at 30 dBHL, can be missing in individuals with normal-hearing (2004).

ASSR still needs further studies to define its use and implication to the field. Further studies should be done in particular with higher frequencies as well as studying external factors that can influence responses.

Multiple Stimuli Application

            As previously mentioned, multiple stimuli application became a focus of researches in 1990’s consequent to studies to explore steady-state response. Studies in multiple stimuli application aim to enhance threshold estimation (Lins & Picton, 1995).

            One of the challenges in dealing with multiple application stimulation or synchronized ASSR and behavioral threshold testing is the difficulty in identifying and observing different generators without signal-to-noise and multiple electrode use (Picton, 2002, pp. 25-26.)

Related Studies

According to a study of auditory steady-state responses to multiple simultaneous done by Lins and Picton, “steady-state responses can follow multiple simultaneous auditory stimuli” (1995, pp. 430-432). If the stimuli used is modulated at varying rates, exclusive responses can be exhibited and can de identified within frequency domain of the spectral component that is consistent or associated with the rate of modulation. Considering this, it points out that steady-state response can still be monitored even if there are multiple stimuli modulations (pp.425-428).

In another study focusing on multiple auditory steady-state responses to amplitude-modulated (AM) and frequency-modulated (FM) stimuli showed that reaction to AM occur later than FM responses. The study also experimented on different levels of modulation to study changes in response. It showed that resulting mixed modulation (MM) elicit independent response and that the most significant MM response was evident when the maximum frequency of MM is used right after the use of the maximum amplitude MM (John et al, 2001)

Implications

            Multiple stimuli testing can show relationship of not just stimuli but responses to advance cognitive studies as well as provide applications for improvement The application of multiple ASSR is an indication of the motivation to comprehensively study auditory responses not only as a clinical study but also to recognize the reality of people’s hearing experience. The understanding of the effects of multiple stimuli also expands current methods of audiometry and allows for the development of studies that can lead to improving methods today.

Observation and Recording

            Steady-state responses observation has allowed scientist the opportunity to study responses better than ABR. This has led to a better understanding of responses and stimuli and the requirementents for treatment of auditory conditions.

            Recording of the responses may vary subtly between single stimuli and multiple stimuli but the same basic methods are used. There is no significant difficulty in recording multiple responses since they can be tracked by their specific variations.

Basic Methods

            Recording parameters of ASSR have not yet been established but generally follow standards and principles previously utilized in ABR and OAE recording. Recording is done through the use of electrodes, differential amplification, signal averaging and filtering set lower than those used for ABR (Venema, 2004). The left hand side of Figure 1 shows that ASSR’s are elicited; it is characterized by strong responses and strong clustered vectors as well as uniform phases. On the other hand, if there is no ASSR response, as shown by the right hand side of Figure 1, the vectors are short and arbitrarily spread out.

            Increasing response using a differential amplifier can be done through the placement of electrodes that transmit varying voltages. Actual ASSR waveforms are measured in nanovolts which ease their observation as well allow for multiple methods for recording and presentation. ASSR’s utilizes single-channel vertical electrode montage that allows the testing of both ears separately without necessitating adjustment of electrodes on test subjects (Venema, 2004; Dimitrijevic, 2004).

Methods for Multiple Auditory Steady-State Response

The multiple auditory steady-state response (MASTER) techniques makes available the concurrent observation and assessment of four varying tonal frequencies in each ear (John & Picton, 2000). It makes use of 1 Hz-300 Hz filters to coincide with ASSPR spectral energy. The methodology allows for detailed evaluation of specific hearing thresholds of infants who failed newborn hearing screening test.

The stimuli specific responses are mapped individually and are used to identify specific responses in multiple auditory steady-state tests. The modulation, frequency and spectral components are used to consider and evaluate responses. A factor that can enlarge multiple-response recording time is the minute size of responses recorded at 500 and 4000 Hz but increasing intensities of stimuli can augment responses without influencing other responses (John et al, 2002).

Uses Auditory Steady State Response

            ASSR has a lot of potential and application in evaluating aided and unaided hearing thresholds. It promises to be an important tool for professionals in testing and allows for various applications to several fields of study (Venema, 2004). Integration and standardization of ASSR will enhance its addition to customary audiologic procedures (Batterjee and Dutt, 2005). But most of all, continuous studies and application of ASSR and applications will establish its importance in the field of Audiology.

Infant Hearing Screenings

            Studies done to compare ASSR and click-evoked ABR and behavioral hearing thresholds showed that broadness of the range in infants.  Dichotic multiple-stimulus ASSR technique provided an important diagnostic tool to asses the hearing-impaired children and provided implicit details for rehabilitation after neonatal hearing assessment (Luts, Desloovere and Wouters, 2006). In 1994, the UNHS stipulated that all infants diagnosed with impaired hearing must be ascertained before they reach the age of three months and to receive treatment by their sixth month. This is to highlight the need for opportune treatment and rehabilitation (Batterjee and Dutt, 2005).

Compared to ABR and OAE, ASSR is able to meet JCIH and ASHA standards regarding hearing assessment (Hall, 2000). ASSR has allowed for the development of specific rehabilitation programs for infants due to proper evaluation of degrees of hearing loss. Though ASSR may become unreliable and difficult to observe with low modulation rates, it still is the most suited in testing infants and also with adolescents and children with hearing and hearing aids (Lins & Picton, 1995; Picton et al, 2002)

Sleep Studies

ASSR has been utilized to study auditory steady state evoked potential (SSEP) both for natural and sedated sleep (Hall, 2000). The study showed that amplitude diminished considerably during sleep but consequent phase variability did not change considerably (Jerger et al, 1986). It suggested the use of phase variability of SSEP as a method to assess and estimate threshold sensitivity of patients.

According to Ted Venema (2004), ASSR’s can actually be more extensivelsy observed during sleep. He attributed this to the individual’s relaxed state that enhances ASSR documentation.

Schizophrenia Related Studies

            ASSR has also been used to schizophrenia, schizotypal personalities and similar disorders. Amplitude-modulated tones were utilized to assess steady state AEP use with individuals diagnosed with schizophrenia, schizoaffective disorders (Picton, 2002).

The consequent analysis of evoked magnetic fields showed the deficiency of steady-state responses to recurring stimuli which revealed neural synchronization irregularities that can affect perception and cognitive assimilation in patients (Lindsay & Norman, 1972; Picton, 2002).

Surgery Monitoring

ASSR does not involve voluntary response and has become a promising tool in monitoring patient health during surgery. It also has a promising application in monitoring brain function in comatose patients, the mentally disabled or in assessing anyone unable or unwilling to reveal actual hearing capacities (Venema, 2004).

ASSR monitoring acts as a safeguard to ensure proper anesthetic is applied to patients. ASSR checks ensure that patients are not in any distress even when they are not exhibiting any sign of consciousness.

Physiological Studies

            ASSR can also be utilized to study effects of extreme conditions to brain function or to ASSR itself. An evaluation of ASSR changes due to manipulated conditions can serve as reference for overall neural response changes.

For example, a study conducted by Lucertini, Verde and De Santis tried to evaluate ASSR variations after exposure to hypobaric hypoxia. Their study showed that exposure resulted to a phase shift in ASSR sinus wave after two exposures. Their study pointed out to the vulnerability of the central acoustic pathway to hypoxia and it was concluded that the auditory system organ functions can be significantly impaired by repeated exposure to hypoxic conditions (2002, pp.110-113). Further studies are being done today to study effects on other sensory preceptor organs as well as the effect of other extreme conditions.

Rehabilitation and Treatment

            Because of the greater specificity in hearing impairment that ASSR affords during assessment, treatment and rehabilitation can be made more specific for patients. This is critical not only to afford care but also to prevent further hearing loss of debilitation.

            ASSR has significantly contributed to the level of amplification in developing hearing aids (Picton et al, 2002) and understanding of sensory response systems during schizophrenic and psychotic attacks (Picton, 2002; Pastor et al, 2003)

Conclusions

            Auditory steady-state response has opened up new possibilities for the filed of Audiology as well as incorporation of principles in other fields of study. ASSR combined with established techniques and application of ABR and OAE can further develop the filed audiometric techniques and applications.

            ASSR method flexibility should also be tempered with the need to create standards and procedures for its use so that it can be utilized as a universal tool. One of the strengths of using ASSR is the variety of methodologies for its use however the prevailing methods should take in consideration diagnostic requirements and information for use in rehabilitation and treatment. ASSR has proven itself to be definitive but at the same time a flexible diagnostic and research tool.

The insight into human perception that ASSR affords us today is essential in developing a comprehensive understanding of not only human function but also experience as a whole. It has been shown that ASSR as an AEP evolved to be more responsive to clinical and research studies than ABR and OAE. The increasing application of ASSR not only expands Audiology but also our understanding of ASSR into everyday life. ASSR provides a new method of understanding response mechanisms as well as furthering the neurological studies that can enhance function and performance and ability.

            ASSR’s objectivity, frequency specificity and accuracy clinical assessment of pediatric, disabled and other special circumstanced patients has allowed for care and rehabilitation despite difficulties associated with these patients. It has allowed for the development of better treatment and rehabilitation programs to suit their specific conditions that would otherwise been impossible. It has allowed preventive protective care for the hearing impaired especially in infants and young children who could still recover hearing capacities.  Therefore, ASSR should be studied and developed because it has already shown that it is a useful tool to improve quality of life.

References

Batterjee, Rana and Dutt, Sunil Narayan (2005). Introduction to Auditory Steady-State Response: Will it Replace the ABR?. Pinpoint Medical Online Journal November/December Volume 14 Number 5. Retrieved September 30, 2006 from www.pinpointmedical.com/ent_news/article_archive/audiology/JF06_Auditory.pdf

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Luts, Heleen A, Desloovere, Christian B, Wouters, Jan (2006). Clinical Application of Dichotic Multiple-Stimulus Auditory Steady-State Responses in High-Risk Newborns and Young Children. Audiology & Neuro-Otology Volume 11 Number 1. pp. 24-37

Pastor, Maria A., Artieda, Julio, Arbizu, Javier, Valencia, Miguel and Masdeu, Jose C. (2003). Human Cerebral Activation During Steady-State Visual-Evoked Responses. Journal of Neuroscience Volume 23 Number 37. pp. 11621-11627.

Picton, Terence W. (2002). Source Analysis of Auditory Evoked Electromagnetic Fields. International Journal of Bioelectromagnetism Volume 4 Number. 2. pp. 225 – 228

Picton, Terence W.,   Dimitrijevic, Andrew, van Roon, Patricia,  John, M. Sasha,  Reed, Marilyn and Finkelstein, Heather (2002). Possible Roles for the Auditory Steady-State Response in Fitting Hearing Aids. Sound Foundation Through Early Amplification 2001 – Proceedings of the Second International Conference – Section II – Chapter 5.

Picton, Terence W., John, M. Sasha, Purcell, David W. and Plourde, Gilles (2003). Human Auditory Steady-State Responses: The Effects of Recording Technique and State of Arousal. Anesthesia Analgesia 2003 Volume 97. Cleveland, Ohio: International Anesthesia Research Society. pp. 1396-1402

Venema, Ted (2004). A Clinician’s Encounter with the Auditory Steady-State Response (ASSR). The Hearing Review May 2004. Retrieved September 30, 2006 from http://www.hearingreview.com/article.php?s=HR/2004/05&p=2

The Movie a Beautiful mind is about a genius mathematician, named John Nash. Unfortunately, enough for him his future is not as bright as his genius like capabilities. He attends Princeton as a graduate student who believes that his genius like abilities are at a higher-level than the rest of his class, not only them but his professors His monumental talents of code breaking in mid thought are one for the records.. When settling in to his single while glaring out the window to gaze at an interactive social scene Nashes imaginary roommate Charles appears.Charles is a very nice mine who is full of life and usually only appears when Nash is stressed. Nash does not attend class only for the pure reason that he feels it is of no help and only deter him. In turn Nash is approached by the head master who tells him before he works he must finish his thesis paper. Nash decides to work on something never thought about, an original theory. His original theory and it disproved the original theory of game theory. He added to the concept of governing dynamics. He was then forth appointed at MIT. He also works for pentagon and helps them break codes.On his second trip to the pentagon Nash runs into what he thinks is an agent and follows him to his headquarters where he gives Nash an implant which secretly ties him to his agency. Nash in the long run gets in over his head. His work for the secret agent intensifies when he is on a high speed chase only to see that the two men chasing them are killed by William Parcher, the secret agent Nash works for. He is then slowly but surely going insane leaving his wife Alicia to check Nash into a psychiatric hospital. Nash Then comes to the realization with the help of his wife that Parcher, Charles, and Marci are all a figment of his imagination.He gets out and quickly relapses by not taking his antipsychotic medication. After an altercation with his wife Nash realizes that he Marci is not real and this told Alicia that her husband is recovering at his own pace. He ages and then is assisted back into the real world by his wife Alicia. Although after he says by to his hallucinations they never leave him. He learns to ignore them. They don’t respect his wishes and stay with him until he is old and possibly when he dies. Although he goes crazy on occasions when let out of the house. He is able the control his psychotic episodes more than before.Nash incurs his psychosis late in life. Although it does not show what triggered it I am sure that his loneliness had a lot to do with the formation of scytzoprainia. Nashes first delusion was in a form of a roommate named Charles. This was a positive delusion who only helped Nash relieve stress. When Nash ends of smashing his head on the mirror because he is frustrated Charles takes him out of his element in an effort for Nash to be relieved of his stress. Another delusion was one that takes on the role of William Parcher, a secret government agent. He was a negative dellision as he made Nash believe that he works for him as a spy.Parcher was the negative side of Charles thoughts while working for the pentagon he became suspicious as to why they has him break codes. Parcher satisfied Nashe’s thoughts. He had Nash find codes in magazines, and newspapers and then mails his gatherings to Washington D. C. daily. With Parcher came thoughts of paranoia. ashes appearance was bad as he did not shower neither sleep or eat because of constant thoughts of paranoia. Nashes living conditions were good as well as for Alicia his wife they were able to afford a wife, who in turn had his child. His delusions caused Nash to miss work.Nash could not leave his house without thoughts of people following him. His third delusion came in the form of Charles niece whose mom was killed in an accident. He becomes entrenched in this lovely little girl who welcomes Nash with love. At his speech in Harvard Nash believes that soviets are after him but in actuality they are hospital faculty. Nash is medicated and eventually discharged from the hospital. He ends up relapses and at the peak of his relapse realizes years has passed but his dillision Marci has never aged. Thereforth he thanks Charles for being a good friend, say bye to Marci, and ignores Parcher.His realization that he must move forward and say good bye to things that are not real to his life was a pivotal move for Nash. His delusions Unfortunately do not respect Nashes wish. With age Nash learns to ignore his delusions, and eventually awarded Nobel Prize for his revolutionary work in game theory. This was a pivotal point in Nashes life and made him feel honored. John Nash has a series of symptoms that will be with him throughout the movie. He begins with seeing codes in mid air of solutions to problems. This is genius but is deviant as it is what gets Nash in trouble later on life.Although this is a unique gift, it is not normal and also a contributory part of his delusions. Without code breaking abilities he would not be needed to work for the pentagon. He will not be a called a beautiful mind as he will be simple, and possibly would not have schizophrenia. Nashes maladaptive behavior is seeing imaginary people. This is not normal for people to have imaginary friends. Early in the movie as Nash moves in to his dorm room he is met by his lively imaginary roommate named Charles. Charles usually helps Nash in stressful situations and keeps him relaxed.Later in the movie he meets Charles niece, Marci who then forth is with Charles everywhere he goes. William Parcher is another imaginary person that shows up after john has successfully broke codes for the pentagon. As John Nash wonders whether his second trip to the pentagon has to do with a Russion invasion. Parcher later confirms Nashes theory and has him work for him as a code breaker. Nash agrees not knowing the consequences, and in turn has an imaginary microchip implanted in his arm. He then has a rude awakening when his delusions of Russians chasing him are set into place.Russians chase him and Parcher only to be later killed by Parcher. His delusions and paranoia intensify when he finds that if he escapes from ties with Parcher he is by himself. Scared to die Nash continues to help Parcher. Nash suffered the most emotionally when he was wrong and unable to find solutions. When he lost a game of checkers with his fellow graduate school rival he trapped himself in his room for two days straight, with no food, and just did math problems. Later in the movie when let out from the mental hospital he irrationally did not take his medications because it was interfering with his genius like abilities of seeing codes.With his medication he would zone out and the delusions came back as it I shown when almost drowned his child. His unpredictable behavior was when he realized that he was going to lose the love of his life if he didn’t try to cope with his disorder. For the time being he snapped out of his zombie like ways and began to show signs of recovery. Nash is socially awkward, so it was surprising that he found someone who liked his attributes. In the beginning of the movie when the professor was speaking to the graduate class you could tell at that point that he was different.While everyone was interested in what the professor had to say with eye contact, Nash had his hands interlocked, and his head down. These symptoms are slowly deteriorating Nash and also his family as his wife is finding it impossible to control her husband’s sudden psychotic episodes. She does not know the new man but misses the man that she has once married. Nash consistently hides from her and is unable to reveal his secrets until finally she results to calling the psychiatric hospital. Nash comes home after being heavily medicated and seems heartless even more than before as he hold his baby with no compassion what so ever.It was as if his baby fell on the floor he would still be as if in a trance. He daily struggles with the delusions that will not leave him. Nashes Wife takes care of him as she gives him his daily medication feeds him and makes sure he is clothed. Nash is unable to get a job as he tries day in and day out to get a position but is unfortunately taking over by delusions. Nashes symptoms deter him in the worst way possible from living a normal live. In the end he gets a job at Princeton. He learns how to deal with his hallucinations. With old age his mental illness becomes more tolerable.Early in his life his delusions were not as detrimental, being that it served as more as an aid than a distraction. Charlie only appeared when Nash was stressed. He was more of a positive delusion. Nashes symptoms got worse with the arrival of government agent William Parched. Nash is influenced by Parcher and has one of two choices which are he can either work for Parcher or die. He goes to MIT several times for a teaching position and fails miserably. His delusions get the best of him and he looks deranged yelling at his delusions.While in school he does not attend any of his classes because he believes that classes only make you dumber. The headmaster tells him that he should do a thesis because Nash has not showed up to class, or do any of the assignments. Nash spends time writing mathematical solutions on the windows in his dorms. Nash finds it hard to meet girl. He is blunt and doesn’t sensor his sexual thoughts when talking to the girl he meets at the pool hall. He also spends most of his leisure time with Charlie not knowing that Charlie is not real. Since Charlie is nice to him he is out of touch with reality not know what it’s like to have a real friend.Nash is not as financially privileged like most but claims that he is well balanced. This false diagnosis of him is what sets Nash outside from being normal His first grade teacher thought otherwise, as she said that he had 2 helpings of brain, but half a helping of heart. He say’s in the movie that people do not like him and neither does he like people. He does not even introduce himself when meeting part of his graduate class. I would think if you don’t put yourself out their then no one will want to get to know you. This uneven balance should deter Nash’s life in the future.His behavior became irrational, when he told his wife that there was an organization out for his demise. He would relatively spend a portion of his day driving to a so called secret house mailing letters to Washington d. c saying that he was part of a secret organization. There after he was admitted to McLean Hospital and after he was relieved he thought it was in his best notion to quit work at MIT. In the “Beautiful mind” not much of Nashes background life was mentioned, but from what was said was that he was a genius with no heart. This has a great deal to do with why Nash turned out the way he did.Living with a society that highly depends of friends you must adapt to forms of sociability. It seems to me that as a young man Nash did not have many friends and kept to himself. His friend was math. In a society where people got out relieving stress it seemed to me that Nash did not. He believed that he had a normal life. In his eyes he saw it as normal because there was nobody to talk to. There was one to tell him that most of society is not as committed to logic as he was. It seemed that he had bottled up stress for so long that it finally erupted when he was put into a social setting.Nash might have though himself to be perfectly fine, but what he does was not normal to society. All he did was find solutions for everything and when your solution based you’re imbalanced to the rest of society. The only leisure time Nash had was with a fictional depiction of a friend. This is not normal for someone in college to have an imaginary friend. He wrote solutions and formed a formula for a mug on the windows of his dorm. This will be looked at as maladaptive deviancy. Later when working for Parcher he had hundreds of magazines and newspapers of codes in his office.Nashes background has a great deal to do with the person he became. The onset of abnormal behavior could have easily been analyzed and suppressed so that in the future his psychosis could not have been as server as it was. John Nash is paranoid schizophrenic. The symptoms that Nash experienced were that of hallucinations, and disorganized Speech. After the imaginary wild speed chase where he is almost supposedly killed his paranoia increased. After his fake assignment brought upon by William Parcher to look for patterns in newspapers and find codes Nash becomes paranoid, and thinks Russians are looking for him.It is only during the time of his speech at Harvard when Alicia calls the psychiatric clinic. While giving the speech Nash is incoherent and not making any sense. The psychiatric faculty gets Nash off stage and Nash in turn believes that he is being chased by soviet spies. While incarcerated Nash cuts his arm to find the implant that he received at the pentagon. He obvisously did not find an implant as they were part of his delusions After Alicia retrieved all the letters from the secret mailbox and showed Nash, he then knew that everything that he thought was real was just a figment of his imagination.He then agreed to get help and take antipsychotic medication. He was released after shock therapy and went home with Alicia and their baby girl. The adverse affects of the medication Nash was taking caused a decrease in sexual and emotional relationship with his wife. The worst effect was that it caused him to lose his genius like abilities of seeing codes. He then decides to stop taking his medication which ultimately causes a relapse in which he almost drowns his daughter while baiting her. Alicia returns in shock from what she saw in the shed of the reoccurrence of the code finding newspapers Parcher made Nash do.His only response was that Charles was watching the baby. Alicia runs to the phone to call the hospital and Parcher appears telling Nash to kill his wife. Parcher points a gun at his wife then Nash lunges to supposedly save his wife. His wife is scared and runs away then is stopped by Nash in front of her car. He has an epiphany that Marci is a hallucination because she never gets old. He then says buy to the hallucinations forever, but they don’t seem to get the point. They still followed him regardless coming and going when they pleased.As an old man he arrives at Princeton for a job. He is giving one by Martin Henson and old graduate school rival/ buddy. He ends up fighting with his hallucinations in front of the school and is encouraged to try again by his wife. He eventually keeps calm and is able to work out side of the library and audit classes. In time he comes to his rightful duties of teaching. Nashes paranoid schizophrenia is so obvious. All the symptoms are perfectly linked as Nash had problems meeting girls. His behavior when approaching women is undesirable for a guy to have when meeting women.His body mannerisms are not normal as he does not show any eye contact with a bad poster when talking to women. This type of behavior is common with people who have schizophrenia. Lucky for Nash he found a wife who shared some of his weird ways and loved for his personality. Later on as schizophrenia worsened he was unable to have a stable relationship with his wife. Another prognosis was increased suspiciousness. His suspicions were that the soviets were after him. He hid out in his room unable to eat sleep in an attempt to not be found. He also thought himself to be smarter than everyone else in college.He lost a game at table checkers which had him in shock. Nash also had cognitive skills. This is also a symptom of paranoid schizophrenia. When he realizes Marci never ages is a great example. This something that other subtypes of schizophrenia lack, this is paranoid schizophrenia is the most desirable. The treatment I would use for Nash is long term institutionalization. Since there are adverse effects to using medication and it is affecting his ability to have any emotional or social connectives. I would use medication when worst comes to worst and his schizophrenia is as bad as it gets.I would leave him in the psychiatric institution until I am sure he is ready to go back into society. When Nash is released from the institution I would try to movie to a less industrialized country, such as India.

The levels of expressed emotion are not as high there as in the U. S. , so this will mean that there will be a faster recovery than in the same place that he has been living. If he moves this also means new faces which alluding bad memories from affecting Nashes recover Process. Family therapy is another great approach to help relieve Nashes schizophrenic episodes. This can better tellAlicia what to expect when dealing with Nash, and how to help him in the recovery process. I will also Keep Nash involved in community work where he can best be distracted from his problem. Then when I am sure that he is ready to enter into society I will make sure he has something productive to do. The last form of treatment when all fails is I will use the second generation antipsychotic medication. This is not as strong as narcoleptics but has a higher level of recovery. I will either proscribe Nash haldol, or thorazine. I will proscribe him a low dose in and eventually he will want to be weaned of medication.I will love to treat Nash to the best of my ability making sure he has all of his attributes and has a chance of normal living. Most hospitals unfortunately over medicate and do not know how to deal with patients in a relapsed state. This does tot cure the problem it only suppresses it for the time being. While Nash is being institutionalized I will make sure a therapist see’s him every day with enlightenment on his disorder encouraging him that it will get better in time. All people need during their time of suffering is a support system.It seems hard to convince them they believe everything is delusions being that they think that you don’t believe that they see and hear things. They in time will understand that they are delusional. I will make sure the psychiatrist seeing Nash is persistent. I would temporarily recommend that Nash moves to a new a town. A town that is not as industrialized, which will contain low levels of sociability. This in return gives chance a better chance of recovery. Being thrown into a situation that requires you to be socially proactive could lead to the possibility of a relapse.He can slowly be adjusted to having guests. I will ask that Nashes wife brings one guest at a time. The guest has to be positive and understand Nashes circumstances. As he gets used to this guest in an ample amount of time you can increase the number of guests and eventually Nash will adjust. After a couple mounts of rest I would advise that Nash be put back to work. This will focus Nashes energy on something productive. He could even take on hobbies, and have leisure time. He can play chess for fun. With most people with schizophrenia they lose interest real quick and this and this sets them back.If they are reluctant give them a break but then reasserts the fact that they must got out and keep active in order to face their disorder. The Movie the beautiful mind is a depiction of someone who suffers from the illness paranoid schizophrenia. This depiction of schizophrenia is close to the DSM-1VTR definition but leaves out surprising parts of this disease. This mental disorder onset is mostly in the tees. With quick detection of this sickness in time it will be fixed. I hope I enlightened you on schizophrenia. Nash in real life beat his disease and currently does not take medications.He believes that there are adverse effects of taking medication and should only be taking as a last resort. Paranoid Schizophrenia affects many and should be taking seriously. From watching this movie I learned to treat everyone no matter, race gender or disability as they treat you. That I am blessed for what I have a saddened at what others doesn’t have.

Works Cited

1. Abnormal Psychology by James N. Butcher, Susan Mineka, Jim M. Hooley
2. http://www. oppapers. com/essays/Symptoms-Schizophrenia-Seen-A-Beautiful-Mind/56167
3.  http://en. wikipedia. org/wiki/Schizophrenia
4. http://www. schizophrenia. com/szparanoid. htm

The schizophrenia theory is reinforced by the biological standard of psychiatry and remains the leading model of mental illness within the mental health service. Genetic factors commonly have accounted for an appraised 81–85% of the variance in liability to developing schizophrenia. Twin studies provide a benchmark approximation of heritability by which molecular genetic studies can guesstimate the degree of the contributions from either a particular poly-morphism or a GCTA pattern to the global genetic variance in schizophrenia liability, also offering evidence of the degree to which schizophrenia and other psychotic disorders may be co-heritable.

In a preliminary way, last century’s changes in the rate or scale of environmental risk factors for schizophrenia have decreased the relative importance of environmental relative to genetic factors in schizophrenia liability (Kläning, 2106). On a May 3rd, 2013 an official press release from the leader of the DSM-5 Task Force, conceded that “despite four decades of determined effort, researchers have failed to identify any genetic variants that cause severe psychopathology” (Fosse, Joseph, Richardson, 2015).

In 2014, the Schizophrenia Working Group of the Psychiatric Genomics Consortium issued outcomes from the biggest genetic study of schizophrenia to date, broadcasting that 108 statistically substantial single nucleotide polymorphisms (SNPs) together could report for only 3.4% of variation on the liability scale.

Given the long history of disappointments to replicate early findings in molecular genetics searches, it is premature to resolve that even this low level of explained variance does not represent false positives. Most essentially, the lack of direct genetic confirmation of anything close to the high heritability estimates from twin studies has led to the view that there is a missing heritability problem for schizophrenia as well as for other mental disorders overall.

Environment

The extreme concordance for schizophrenia in monozygotic (MZ) twins is usually understood as verification of genetic influence. Some who study twins through lineage or population strategies have concluded that MZ twins nurtured apart (MZA) share fundamentally no environmental influences, and the MZA connection is a direct approximation of heritability.

Few researchers, specifically those focused on schizophrenia, have taken advantage of the fact that MZ twins propose a special opportunity to study prenatal influences. The placenta is a diagnostically important element of prenatal environment: “It is a physical and physiological link between mother and child, and it exhibits variations with regard to membrane type, size, shape, and circulation which may be important in themselves or may affect the nutrition of the embryo or the transport of drugs, toxins, and other agents which can influence brain development” (Davis; Phelps, 1995).

Genetics

The statement that genetics plays a role in the etiology of schizophrenia is recognized by all researchers in the field. There is substantial debates, however, regarding both the degree of that role and its defined nature; recent attention in linkage analysis and molecular genetics has amplified such debates. Theories regarding the genetics of schizophrenia range from monogenic to polygenic.

The genes may possibly be dominant or recessive, at a single locus or several loci, have adaptable levels of penetrance and produce variable levels of disease expressivity. The genes may theoretically code for neurochemical (e.g., dopamine) abnormalities which could produce the symptoms of schizophrenia directly. Or they may control specific events in neurodevelopment, such as the proliferation and migration of neurons, which could produce the symptoms more indirectly.

Discussion

The schizophrenia hypothesis and the criteria for diagnosis are built into diagnostic manuals and provide mental health professionals with a structure, consistency, understanding and a standard from which they can provide clinical interventions and study their role and interventions. Yet, acceptance of genetic causes for schizophrenia is abhorrence to a person-centered, evidence-based and recovery-orientated mental health service.

The concern of accepting a genetic cause for schizophrenia is the conviction that the symptoms and behavior are genetically encoded. If schizophrenia has a genetic base, then the frequency of schizophrenia will be greater amongst family members and/or relatives than it would be in the general populace. Looking at the principles that monozygotic or identical twins share, 100% of their genes are First-degree.

Relatives such as parents, fraternal twins, children, siblings share 50% of genes, second-degree relatives such as grandparents, aunts/uncles, half-siblings, niece/nephew, grandchildren share 25% of their genes and third-degree relatives such as great grandparents, great aunts/uncles, cousins, great-grandchildren share 12.5% of genes.

These philosophies dictate that the closer the relationship to the relative with schizophrenia the higher the risk of developing schizophrenia. It doesn’t appear to be an unvarying rate of frequency in the studies that are being conducted and the practical differences makes it’s dif?cult to compare and appeal firm unequivocal conclusions about the nature of hereditary transmissions of schizophrenia. One of the purest conclusions that can be sketched from the findings of family studies, however, is that they uniformly support an environment argument for schizophrenia.

THE WALKING DEAD SYNDROME English 150 Instructor: S. Jone November 7, 2011 The Walking Dead Syndrome Introduction The Walking Dead syndrome is considered a rare disease. I believe everyone in this existence has a purpose on this vast place we call earth. However, there are people diagnosed with a syndrome who believe they have no soul or convinced themselves they are dead. The “Walking Dead Syndrome” is also commonly known as “Cotard’s Syndrome”. In this paper, I will refer this syndrome as “Cotard’s syndrome”.

Cotard’s syndrome is linked with other mental illnesses which could explain a person’s state of mind of feeling non-existent in society. I will further discuss eight aspects of this syndrome: defining the Walking Dead Syndrome, defining mental illness, description of several mental illnesses associated with this syndrome, classifications of Cotard’s syndrome, analysis of patients, diagnosis of syndrome, and types of treatments available for patients. Defining Walking Dead Syndrome or Cotard’s Syndrome

Many people I discussed this topic with never heard of the “Walking Dead Syndrome”. The Walking Dead Syndrome was first created by French neurologist, Jules Cotard, hence, named the “Cotard’s Syndrome”. He was a French neurologist who first described this psychiatric condition. First reference to the syndrome was made in the year 1880, when Jules Cotard gave a lecture in Paris. In this lecture, he described various degrees of the syndrome, while he said that a person who resorts to despair and self-hatred begins in the early stages of this disorder.

With deterioration, the person might go to the extent of denying the very existence of himself or herself. There are detached from the sense of existence of self (“Cotard Syndrome” 2010). Patients portray themselves similar to the concept of “zombies”. Hollywood has portrayed horror and science fiction based movies on “zombies” or the “walking dead”. In the movies, zombies are typically mean and fond of human flesh, they groan and cannot talk, have incredible strength, and display rotting flesh.

A zombie is physically identical to a normal human being, but completely lacks conscious experience. If we suddenly lost our minds, or consciousness our bodies might continue to run on for a while, our hearts might continue to beat, we might breathe while asleep and digest food. But without the contribution made by minds, behavior could not show characteristically human features. In the Urban Dictionary, 1999-2011, a zombie is defined “as deceased human being who has partially returned to life due to undeterminable causes.

The brain retains base facilities, namely gross motor function. In its near-mindless state, it grasps no remains of emotion, personality, or sensation of pain. In rare cases, some of the reanimated have reflexively preformed routine activities from their past lives”. The people diagnosed with Walking Dead Syndrome have similar portrayals including not having internal organs and smelling of rotting flesh. A hypothetical analogy can be explained when most of us have woken up after a really good night out.

Our first drive in the morning was motivated by a desire for food and coffee. If we as a society experience a chemical or radiological contamination, we might be experiencing the hangover from hell. Our higher thought would be destroyed, the neural system would be degraded, and leave just the body running on its primary functions. Defining Mental Illness Since the beginning of man, I think there has been mental illness, and chemical imbalance generates a huge part, and some people just do not have the ability to use parts of their brain for reason and logic.

According to to Sorrentino, Wilk, and Newmaster (2009), a mental illness can be: “caused by a combination of genetic, biological, personality, and environmental factors, is a disturbance in a person’s ability to cope with or adjust to stress; the person’s thinking, mood, and behaviours are affected, and functioning is impaired …mental illnesses affect people of all ages, culture, and educational and income levels. The onset of most mental illnesses occurs during adolescence and young adulthood” (p. 641). Most mental illnesses are brought on by the stresses of life, money, property, and consumption.

Having a mental illness varies from person to person and if you cannot go about your day as you normally would due to a condition then it is a mental illness. An example would be having an “anxiety disorder”, and if you cannot leave your house anymore due to petrifying fear, then there is clearly a problem. Unless of course you cannot recognize that you are having problems and you are posing a threat to yourself or others, then you can be forcibly placed under the guidance of a psychologist. Mental illness can be contributed to either biological, psychological, and environmental factors.

The biological factors can be attributed to genetics or “mental disorders tend to run in families, suggesting a hereditary factor…the number of close relatives a person has who suffer from depression or other mood disorders is the best predictor of the likelihood that the individual will develop a mood disorder” (Boyd, Johnson, Bee, 2009, p. 385). In addition, psychological aspects can be contributed to emotional, physical, or sexual abuse, and the environmental causes can be defined as a person living in poverty or substance abuse. Mental Illnesses Associated with Cotard’s Syndrome

People diagnosed with the “Cotard’s Syndrome” have been treated for a mental illness or combination of bi-polar, delusions, schizophrenia, and schizoaffective disorder, to name a few. The major mental illnesses are painful, pervasive, disruptive and usually disabling. Firstly, a “bi-polar disorder” is defined as “a brain disorder that causes unusual shifts in a person’s mood, energy, and ability to function” (Sorrentino, Wilk, Newsmaster, 2009, p. 651). Whereas, “delusions” are the “false beliefs that are firmly held” (Purse, 2011). An example is a person who has grandeur delusions or has paranoid tendencies.

In the grandiose subtype, the person is convinced that he has some great talent or has made some important discovery, they have an inflated sense of self-worth. In addition, their delusions center on their own importance, such as believing that they have done or created something of extreme value or think they have a “special mission”. There is reference to another type of delusion known as “nihilistic delusions”. This type of delusion describes a person “focused on the individual’s body, including loss of body parts, being dead, or not existing at all” (Debruyne, Portzky, Peremans, & Audenaert, 2011).

Furthermore, Cotard syndrome created a new type of depression which “is described as anxious melancholia, ideas of damnation or rejection, insensitivity to pain, delusions or nonexistence concerning one’s own body, and delusions of immorality” (Debruyne, Portzky, Peremans, & Audenaert, 2011). This type of delusion is a major attribute of Cotard’s syndrome. Thirdly, “schizophrenia” which “is an extremely complex mental health disorder characterized by delusions, hallucinations, disturbances in thinking, and withdrawal from social activity” (Sorrentino, Wilk, Newsmaster, 2009, p. 55). News and entertainment media tend to link mental illnesses including schizophrenia to criminal violence. Most people with schizophrenia, however, are not violent toward others but are withdrawn and prefer to be left alone. Lastly, “schizoaffective disorder” is described as a “person having symptoms of both schizophrenic and bipolar disorder” (Purse, 2006). Some disorders will cause parts of the brain to stop performing their normal functions. These can leave people out of control and disoriented (not knowing what they themselves are doing). Classifications of Cotard’s Syndrome

In its early stages, Cotard’s syndrome is characterized by vague feeling of anxiety with a varying time p from weeks to years. This anxious state gradually augments and can result in nihilistic delusions where denial of life or denial of body parts are the prominent features. The patient loses sense of reality. Despite the delusion of being dead, these patients show an increased tendency to automutilation (self harm) or suicidal behaviour. (Debruyne, Portzky, Peremans, and Audenaert, 2011). A case studying involving 100 patients, in Debruyne, Portzky, Van den Eynde, and Audenaert, (2009) reveal three types of Cotard’s syndrome.

The first is a form of “psychotic depression” in which anxiety, melanchonlia, delusions of guilt, and auditory hallucinations are the more prominent features. The second class is “Cotard’s syndrome Type I”, which is associated with hypochondriac and nihilistic delusions. The third type is “Cotard’s syndrome Type II”, which includes anxiety, depression, delusions of immortality, nihilistic delusions and suicidal behaviour are characteristic features”. However, in Debruyne, Portzky, Peremans, and Audenaert, 2011, a case study conducted in 1999, identified three stages of Cotard’s syndrome.

The first stage, germination stage, is characterized by important hypochondriac cenesthopathy and depressive mood. A diagnosis of Cotard’s syndrome cannot be made in this stage yet. In the blooming stage, the characteristic features of Cotard’s syndrome (nihilistic delusions, delusions of immorality together with anxiety and negativism) are seen. The last stage, the chronic stage is differentiated in two forms: one with persistent emotional disturbances (depressive type) and the second where depressive symptoms are less prominent (paranoid type) (as cited by Yamman, 1999).

The two classifications described above have assisted in diagnosing of Cotard’s syndrome. The similar features displayed are nihilistic delusions, depressive mood, and anxiety. Analysis This syndrome does not affect a specific category of people. A study of 100 patients, revealed that “Cotard’s syndrome was diagnosed in 2 of 349 patients…taking into account only severely depressed older adult patients. In addition, the average of age of person studied was 52 years of age, however, the study also suggested that Cotard’s was occasionally described in children and adolescents (Debruyne, Portzky, Van den Eynde, Audenaert, 2009).

Furthermore, according to Wani et al. , (2008), “this syndrome is typically related to depression and is mostly found in middle-aged or older people. In the analysis the following results were displayed: “depressive mood (89%), nihilistic delusions (69%), anxiety (65%), delusions of guilt (63%), delusions of immortality (55%), hypochondriac delusions (58%)” (Debruyne, Portzky, Peremans, and Audenaert, 2011). Diagnosis The diagnosis reveals a psychological and neurological aspect of Cotard’s syndrome. The “depersonalization phenomenon” as described in Debruyne, Portzky, Van den Eynde, and Audenaert, 2009, is referred to using German erminology leib (body for me) and korper (body as such), korper becomes more prominent than leib and the body less associated with the self (leib), depersonalization onset can then occur. However, in depersonalization, the patient feels as if he or she is dead (in difference of affect), whereas in Cotard’s syndrome, the patient is convinced that he or she is dead (lack of feeling). Cotard’s syndrome is often associated with parietal lobe lesions. Compared with controls, patients with Cotard’s syndrome have more brain atrophy in general and more median frontal lobe atrophy in particular.

Cotard’s syndrome may be associated with multifocal brain atrophy and medial frontal lobe disease. Neurological assessments were performed and findings resulted in patients affected by “parietal brain dysfunction” and structural brain abnormalities. Recent discoveries have indicated that Cotard’s syndrome was associated with multifocal brain atrophy and interhemispheric fissure enlargement. The interhemispheric fissure enlargement means “parietal lobe lesions” (Joseph and O’Leary, 2011) or bending in the frontal and occipital regions and this abnormality also been observed in schizophrenic patients.

Others have described and enlargement of the third and lateral ventricles. In one patient, the patient was diagnosed with a schizophrenia disorder and a left sided hypoperfusion in the temporal, parietal and frontal lobes. The medical term of hypoperfusion is defined as a “decreased blood flow through an organ” (Meriam-Webster, 2011). In addition, the patient experienced improvements of the inferior frontal and left hypoperfusion and there was evidence of decreased hyperprofusion of the left temporal lobe…” (cited in Debruyne, Portzky, Van den Eynde, and Audenaert, 2009).

Treatments There are several methods utilized to treat mental health struggles. A patient can seek professional assistance by psychology or psychiatry therapy and/or the utilization of medication. If you lived in the 16th century with any undefined mental disorder, you were considered as “possessed by the Devil” and cast away to some godforsaken monastery dungeon in which monks would constantly pray for and exorcise you. The Catholic Church they used a methodical guidebook to describe all behavioral aspects and associations of witchcraft, satanism, etc. nd utilized this upon people who were suffered with mental or behavioral maladies, and it was not commonly understood in the Medieval and Renaissance periods. In the medieval ages, they were burned because they thought demons haunted the mentally ill. In later years, we willfully experimented on them, cutting into their bodies and brains to “fix them”, this was called, trepanation. The “evidence of trepanation has been found in prehistoric human remains from Neolithic times onward.

Cave paintings indicate that people believed the practice would cure epileptic seizures, migraines, and mental disorders” (Wikipedia, 2011). It is really disgusting and is the major reason that even today it is to some a badge of humiliation instead of just an illness. Complete recovery may occur spontaneously and suddenly as onset of Cotard’s syndrome. There are several reports of successful pharmacological treatment of Cotard’s syndrome. Electroconvulsive Therapy (ECT) is considered an important treatment option in Cotard’s syndrome.

It is noted, in Debruyne, Portzky, Van den Eynde, Audenaert, 2009, that young patients use of mood stabilizers should be considered because Cotard’s syndrome in this population is often part of a bipolar disorder. Successful treatment with ECT and the patient with underlying major depressive disorder resulted in recovery of left and right temporal hypoprofussion and normalization of profusion in the frontal cortex was reported after treatment with antidepressants (Debruyne, Portzky, Peremans, and Audenaert, 2011). Please be aware that people who have true mental illnesses do suffer.

They want more than anything to be able to feel and function like other people and they will actively seek help. The reality is that certain medications and treatments help those who are suffering from these conditions. Conclusion Mental illness is not a modern invention. The mentally ill have been recognized in one form or another by every culture we have a record of. How they were perceived and what their value is what has largely changed. Some people do not retreat into their minds as much as they are supposed to, while others spend all their time there.

What we eat and breathe and drink affects our health and our brain, and a healthy individual’s brain tends to have more to work with and develop all the right chemicals and nerve sheaths. A good parent with their strong sense of empathy realizes that their child is a thinking, growing human being and will always need that light touch that points them in the “right direction” and prevent them from getting “lost”. The right nature and nurturing are essential for a healthy development. Some cases of these disorders I believe could be a simple lack of the ingredients to solve this chemical imbalance.

Given that our brain is constantly changing accordingly with the times, a chronic chemical imbalance quickly becomes more than just that, as the brain has grown and changed around this shortcoming. The kind of understanding you wish people had for those with mental disorders would be a universal understanding for all if people would look into themselves and observe their own thoughts and behaviors. We are our best test subjects since we have full access to all the “data”, and by observing ourselves totally (mentally, developmentally, chemically) we can apply our understanding to others and learn from the experience.

People need to care about how people’s minds work in general, understanding “you guys” would come with the turf, and communication with our angry neighbors would be much more effective since we’d all see where everyone is coming from. Philosophers have long contemplated human happiness, and how to live a “good” life, in harmony with our own nature. The problem is that humans do not really know what makes them happy, and what they think will, or will not, and instead they find contempt and superficial pleasures they believe will satisfy them.

As a result, some people will not live a good and peaceful life that satisfies the majority of people. The fact is not everyone needs medication, but there are those who do. Some need it temporarily, some for a lifetime. Some simply need therapy, and some benefit from dietary changes. I believe understanding is the highest ideal we should seek to attain. Understanding and being honest with ourselves about ourselves and applying our own understanding to others may help us see that we are not as different as we’d like to believe.

I believe that sense of commonality with all human beings can generate empathy, compassion and ultimately peace in all of us. It is when we categorize each other, ourselves, and place value on those categories then we breed hatred, ignorance and fear. References Boyd, D. , Johnson, Paul, Bee, Helen (2009). Lifep Development. (4th Canadian Edition). Toronto: Pearsons Canada Inc. Cotard Syndrome. (2010). Disorders Central. Retrieved October 10, 2011, from http://www. disorderscentral. com/cotard-syndrome. html Debruyne, H. , Portzky, M. Peremans, K. , ; Audenaert, K. , (2011). Mind and Brain The Journal of Psychiatry. Retrieved October 6, 2011, from http://content. yudu. com/Library/A1t5r8/MindampBraintheJourn/resources/73. htm Debruyne, H. , Portzky, M. , Van den Eynde, F. , ; Audenaert, K. (2009). Cotard’s Syndrome: A Review. Current Psychiatry Reports. Retrieved October 6, 2011, from University of Calgary On-line Resources: http://www. springerlink. com. ezproxy. lib. ucalgary. ca/content/f43j790n7161432m/ Hypoperfusion. (2011). Merriam-Webster Dictionary.

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