Example Of Influence Of Music Therapy On The Patient With Rett Syndrome

Rebecca was a four-year-old girl whom was clinically diagnosed with Rett Syndrome (RT). Her case of RS was confirmed with genetic testing and analysis that was characterized by deletion of the MECP2 gene in exon 4. At the age of twelve months, Rebecca’s mother noticed her eye sight and pincer grip was excellent, as Rebecca would be able to specifically pick miniscule substances off of the floor. At this age, Rebecca appeared happy and content with self-entertainment, as well as encompassing interactions with other people around her. Rebecca was heavily vocal, great with babbling and was easily able to transfer objects from hand to hand.

Within several months after her initial year, she showed great interest in watching children’s television shows and DVD’s, she could hold other objects, such as drumsticks, and was even able to acknowledge pictures and accurately hold open a book. However, Rebecca’s mother noticed drastic changes, essentially over night. Rebecca completely lost her purposeful hand movements and gestures, as well as her ability to hold her bottles on her own. Initially, her mother associated these behaviors with “the terrible two’s” phase, as her daughter turned from being happy to being miserable. Rebecca refused to give her parent’s direct eye contact, preferred to be and play alone, and her hand movements began to manifest (Hackett, Morison & Pullen, 2013).

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At the age of four, Rebecca was referred for music therapy (MT) by her pediatrician, at the direct demand of her parents. Rebecca experiences 14 routine 30 minute MT sessions over the course of six months, as her parents observed behind a one-way mirror in a gallery above the room. Each session incorporated familiar songs to Rebecca followed by a period of improvisation that included verbal discussion and other forms of art secondary to musical activity. In this period, Rebecca was free to create her own music, beats and rhythms that were lead by her through eye contact and touch. Using this approach, Rebecca was able to make independent choices and establish “equal terms” with the relationship with her therapist. Repeated songs and rhythms were used to stimulate her voice output and increased her vocalization. The therapist wanted to encourage Rebecca to make independent choices by also using visual aids, objects, instruments and verbal cues or prompts (Hackett et al., 2013).

Each MT session performed by Hackett (2013) was video recorded and reviewed by a therapist in acknowledgment of two types of behavior: when Rebecca clearly picked up an instrument or object, the frequency of the holding the object and observations of Rebecca vocalizing, eye pointing contact or other forms of distinct interaction with her therapist. Her interaction frequency was counted during each session and plotted on statistical process control (SPC) charts to assess any patterns in trends over time.

A vital component to therapeutic work in MT with children who have RT is the growth of a trusting relationship with the therapist; this was strongly supported by the musical interaction with Rebecca, which ultimately encouraged performance and self-confidence. The use of familiar song at the beginning of ever session offered routine and established a meeting place, promoting interaction. Rebecca often responded to the therapist’s pause of songs, as well as his instructions to her singing. Rebecca would turn towards the sound of the therapist playing an instrument, the therapist would position beater closer to her, and she would chose to pick them up, improving her grip techniques. If Rebecca appeared anxious accompanied by heavier breathing patterns, the therapist would introduce warm, lower tones of music MT for Rebecca focused on enhancing motor skills (holding) and intentional communication through turn taking. The statistical results of Rebecca’s response to MT indicate a small, meaningful advancement in function (Hacket et al., 2013).

Literature Review

Rett Syndrome (RT) is a neurodevelopmental genetic disorder that affects between 1 and 10,000-22,000 females, representing the second most common cause of intellectual disability (Pidcock et al., 2016 & Gabel et al., 2015). RT also affects males in rare cases, although male RT patients typically manifest a wide range of symptoms including severe encephalopathy, mild mental retardation and dystonia apraxia (Liyanage et al., 2014). Early development appears normal within the first six months of life, followed by a period of harsh developmental arrest with deterioration of motor skills, cognitions, hand movements, gait abnormalities, deceleration of cranial growth and speech (Pidcock et al., 2016 & Lyst et al., 2015).

Genetic linkage studies have been able to map the location of the disease trait to Xq28 region of the X chromosome with mutations in three of the four exons of the MECP2 gene; this mutation is found in 90-95% of individuals with RT (Pidcock et al., 2016 & Liyanage et al., 2014). MECP2 is a key epigenetic modulator in the brain that controls gene expression and modulate chromatin architecture through binding to methylated DNA, as well as a regulator of RNA splicing, transcriptional repression and activation (De Felice et al., 2016 & Liyanage et al., 2014). It is important to note, however, that not all individuals who have an MECP2 mutation has Rett syndrome (Rett Syndrome, 2017). Scientists have also identified mutations in CDKL5 and FOXG1 genes in individuals who have congenital or atypical Rett Syndrome (Rett Syndrome, 2017). Although this is a genetic disorder, less than 1% of documented cases are inherited from one generation to the next (Rett Syndrome, 2017).

The MECP2 gene is frequently studied in mouse models. However, when interpreting results made from animal models, potential caveats should be kept in mind. MECP2 is the most studied protein that binds to methylated DNA through their methyl-binding domain (MBD) (Liyanage et al., 2014). MECP2 is a gene that ps ~ 76 kb in the long arm of Xq28 between interleukin-1 receptor associated kinase gene (IRAK1) and Red Opsin gene (RCP) (Liyanage et al., 2014).

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