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June 10-11, 2019 | Edinburgh, Scotland
Central Nervous System and Therapeutics
2nd International Conference on
Journal of Neurology and Neurorehabilitation Research | Volume 4
allied
academies
Tardive Dyskenesia and Akathasia: A Dopamine system theory
Tamara C McGill Carter
The Chicago School of professional Psychology, USA
Statement of the Problem: Long term use of first-generation
anti-psychotics (FGAs) have been theorized in the formation
of motion disorders Tardive Dyskinesia and Akathasia and due
to the breakdown in the extra pyramidal system (EPS) located
in the Basal Ganglia (Lehne, 2013). The second-generation
anti-psychotics (SGAs) were sourced to be the “treatment” of
TD by blocking dopamine receptors with dopamine agonists
of the D2-D5 receptors while also being seen as the genesis
of AK. However, the blocking of the receptors in both motion
disorders is a theory known as the dopamine blockage theory,
despite the intermingle of other neurotransmitters such as
Serotonin and Norepineprine (Lieberman, Stroup, McEnvoy,
Swartz, Rosenheck, & Perkins, 2005).
The EP system includes theorized Dopamine and Serotonin
connections within the Basal Ganglia, the striatopallidongral
system, and other structures of the central nervous system
that contribute to the regulation of movement, including
brainstem nuclei and the cerebellum (Jibson, Marder, &
Hermann, 2018). One example of a classical disorder of
the pyramidal system is a stroke, resulting in paralysis of
an extremity. Cortiospinal lesions above the pyramidal
decussation typically result in paralysis of volitional
movements of the contralateral half of the body (Patterson,
McCahill, & Edwards, 2010). The pathophysiology of EPS
disorders has been disputed because some EPS disorders may
not involve lesions of the Basal ganglia. In addition, motions
associated with said disorders may not be involuntary
(Jibson, et al. 2018; Patterson, et al. 2010). Because of the
problems inherited in the concept of the EPS, caution must
be exercised in the classification of the EPS due the countless
symptoms that mimic other motion disorders as certain
neurotransmitters can create the actions of another.
Speaker Biography
Tamara C McGill Carter expertise is in Neuroanatomy and Neuroscience
with a focus on the intricate workings of the Limbic and Memory systems.
Her master’s thesis surrounds Human Memory and Encoding, detailing
the fundamental changes that creates as well as destroy memories. She is
currently is training in to become a licensed Neuropsychologist and is also
finishing her final year of the Chicago School of Professional Psychology’s
EducationalPsychologyandTechnologydoctorateprogram,duetograduate
by next summer. Her dissertation’s focus centers on Autism, Theory of
Mind, and Executive Functioning. Her expertise in neuroanatomy further
expanded while working with individuals with developmental disabilities/
delays at several Home Health Agencies, which created several projects
centering on how autism and developmental delays affect the brain.
She currently holds dual bachelor’s degrees in Psychology from Indiana
University Northwest in Gary and a Master of Arts degree from the Chicago
School of professional Psychology, the concentration focus being Trauma
and Crisis Intervention
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