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Sunday, December 25

  1. page Tourette's Syndrome edited Introduction What is Tourette’s syndrome? It states in the DSM-5 that the syndrome is diagno…

    What is Tourette’s syndrome?
    It states in the DSM-5 that the syndrome is diagnosed when the individual has presented multiple motor and one or more vocal tics for at least a year. The disorder must present itself before the age of eighteen in order to be diagnosed as Tourette’s syndrome. In order to be considered a tic due to Tourette’s syndrome, the tic cannot be a side affect of substance abuse or another medical condition. [1] Tics due to the syndrome tend to affect the face, neck, shoulders, and voice. [3] Breakthroughs and new insights into the neural circuits and structures of the brain, specifically the basal ganglia, have made it possible for doctors and researchers a like to have a better understanding of the neurophysiological causes of Tourette’s syndrome.
    Key Terms
    Caudate – Part of the striatum, receives input from the cortex and projects to the globus pallidus.
    CSTC pathways - Abbreviation for cortico-striato-thalamo-cortical pathway, the direct and indirect pathways fall within this category
    Direct Pathway – Pathway within the basal ganglia which facilitates movement through the release of neurons from tonic inhibition
    Globus Pallidus (external segment) – Part of the indirect pathway
    Globus Pallidus (internal segment) – Part of the direct pathway
    Indirect Pathway – Pathway within the basal ganglia, which modulates the direct pathway
    Midline Nuclei of the thalamus – Projects through out the cerebral cortex [7]
    Premotor Cortex – The part of the brain that influences motor behavior through its connections within the primary motor cortex. It also has axons that project into corticospinal pathways and influences the motor neurons of the brainstem and spinal cord. [6]
    Primary Motor Cortex – Found in the precentral gyrus of the cerebral cortex, necessary for voluntary movement. Receives input from basal ganglia, and the cerebellum from pathways through the thalamus, as well as somatosensory input [6]
    Somatosensory Cortex – Processes sensory information received from the sensory receptors of the body (i.e. joint receptors, subcutaneous receptors, etc) [6]
    Putamen – Part of the striatum, receives input from the cortex and projects to the globus pallidus
    Sensori-motor cortex – Consist of the Primary Motor and Primary somatosensory cortex
    Striatum – Sometimes referred to as the neostriatum, contains the caudate and the putamen.
    Substantia nigra pars compacta – contains dopaminergic synapses that project to the caudate and putamen to excite/inhibit depending on the receptors.
    Substantia nigra pars reticulata – Sends output from the basal ganglia to the thalamus [6]
    Supplementary motor area – Aids in the control of complex movement [4]
    Thalamus – Modulates sensory input, relays information from the cerebellum and the basal ganglia to the cortex [7]
    Tic – a sudden, rapid, recurrent, non-rhythmic motor movement or vocalization. [1]
    VA/VL complex – Combination of the ventral anterior and ventral lateral nuclei of the thalamus, gives feedback to basal ganglia output
    Functional Anatomy
    Basal Ganglia
    The Basal Ganglia is divided into five functional parts: The striatum, pallidum, thalamus, substhalamic nucleus, and the substantia nigra [Figure 1]. The striatum is the area of the basal ganglia that receives the input. The information coming into the striatum comes from all areas of cerebral cortex and parts of the thalamus. The striatum can be further broken down into two parts: the caudate and the putamen. The caudate tends to receive input from the frontal, parietal, temporal, and occipital lobes as well as the premotor cortex and supplementary motor areas. The putamen receives input from the primary motor and primary somatosensory cortex. The medium spiny neurons of the caudate and putamen then project to the internal segment of the globus pallidus [Figure 2a]. The spiny neurons have an inhibitory affect on the tonically active inhibitory neurons in the internal segment of the globus pallidus [Figure 2a]. [6] These neurons then project into the VA/VL complex of the thalamus. The substantia nigra pars compacta has an excitatory affect on the caudate/putamen through the release of dopamine to the D1 receptors of the caudate and putamen. [4,6]
    {ch18f3.jpg} The “direct pathway” [Figure 3a] of the basal ganglia acts to release the motor neurons from tonic inhibition. In the “indirect patheway”, the medium spiny neurons project to the external segment of the globus pallidus. The “indirect pathway” [Figure 3b], on the other hand, serves to increase tonic inhibition. The neurons from the external segment of the globus pallidus then project to the subthalamic nuceleus. The subthalamic nucleus, receiving both excitatory input from the cortex and inhibitory input from the external segment of the globus pallidus, then projects to the internal segment of the globus pallidus, which in turn makes any changes that need to be made to the “direct pathway”. [6]
    Tourette’s and the CSTC pathways
    The CSTC pathways are the pathways that project information from certain areas of the cortex, through the striatum, and after traveling through the globus pallidus reaches the VA/VL complex of the thalamus. From there, information is projected back to the cortex. These pathways, both direct and indirect as discussed in the previous section, help elicit and modulate movement. The pathophysiology of Tourette’s syndrome can be traced to the sensorimotor CTSC circuits. As discussed before, these pathways project from the sensori-motor, primary motor, and supplementary motor areasto the matrisomal portions of the putamen and the head of the caudate nucleus. [2] These sites then project to parts of the globus pallidus and the pars reticulata of the substantia nigra. From there, the information travels from the basal ganglia to the ventral-lateral and midline nuclei of the thalamus, and from the thalamus information is projected back to the cortex. Researchers believe that the development and function of these pathways play an important role in the initiation and performance of tics and compulsions. [2] One way researcher’s have begun to look at Tourette’s syndrome is as a syndrome in which major CTSC loops have been disinhibited. [2] In one study, researchers found that Tourette’s syndrome can be attributed to the combination of excessive motor pathway activity and reduced control of the CSTC circuit. [3] Studies have also shown that the release of glutamate in both the internal and external segments of the globus pallidus as well as the substantia nigra are different in people who have Tourrette’s syndrome as opposed to those who do not. [2]
    Being that Tourette Syndrome is a complex disorder that has both psychological and physiological base, there is no cure. Still, for many people the disorder can make day-to-day life difficult due to the constant disruptions. People affected by the order may seek pharmaceutical intervention. Dopamine agonists have been tested and proven to have an inhibitory affect on tics. [2] It’s important to note that medication can only cure the symptoms, not the disorder itself. Medication is usually employed if a specific tic can be significantly reduced. Treatments that focus on the behavioral aspect of the syndrome have become more popular and well accepted. Comprehensive Behavioral Intervention for Tics (CBIT) aims to focus on reversing the habits of the patient that seem to been tic inducing. Strategies like discussing what situations seem to be more tic inducing than others, are employed by the therapist in the hopes to help lessen the severity of the tic. [8]
    As research has found, the basal ganglia play an important role in the facilitation of wanted movement and the inhibition of unwanted movement. It comes as no surprise that breakthroughs in research about Tourette’s syndrome can be attributed to the dysfunction of the basal ganglia. Tics arise due to the inability of the direct and indirect pathways to inhibit unwanted movement. Medications have been found to be affective in treating the symptoms of Tourette's Syndrome, but behavioral therapy has been found to be most affective form of treatment.
    Suggested Readings and Websites:
    This website gives a helpful overview of how Tourette’s Syndrome manifests itself, prevalence, causes, and conditions that also tend to occur along with it.
    This website provides resources and helpful articles to parents with school-age children dealing with Tourette’s syndrome.
    Passing for Normal: A Memoir of Compulsion by Amy S. Wilensky
    This book offers the reader the perspective of what it’s like to live with a commonly misunderstood disorder.
    Tourette's syndrome--tics, obsessions, compulsions : developmental psychopathology and clinical care by James F. Leckman
    This book offers a variety of articles covering both the physiological and psychological aspects of Tourette’s syndrome and ways to treat it.
    Content Quiz
    1.) The CTSC pathway is the:
    a.) cortico-striato-thyro-cortical pathway
    b.) cortico-striato-thalamo-cortical pathway
    c.) cerebro-striato-thyro-cortical pathway
    d.) cerebro-striato-thalamo-cortical pathway
    2.) The basal ganglia consists of the striatum, the subthalamic nucleus, and the substantia nigra:
    a.) True
    b.) False
    3.) The basal ganglia deals primarily with repetitive motor planning:
    a.) True
    b.) False
    4.) The cortex has an excitatory affect on the external segment of the globus pallidus.
    a.) True
    b.) False
    5.) Tourette’s syndrome is caused by two separate factors: either excessive motor pathway activity or reduced control within the CSTC pathways.
    a.) True
    b.) False
    6.) The external segment of the globus pallidus:
    a.) plays a role in the indirect pathway
    b.) plays a role in the direct pathway
    c.) has an inhibitory affect to the subthalamic nucleus
    d.) sends excitatory input on the subthalamic nucleus
    e.) A&C
    f.) A&D
    g.) B&C
    h.) B&D
    Essay: You have a patient who comes in exhibiting three different motor tics and two vocal tics, with only one motor tic and one vocal tic persisting for over a year. At this stage, can you definitively diagnose the patient with Tourette’s syndrome? Explain what is going on in neurologically within the patient that would cause them to have these involuntary movements.
    1.) B
    2.) B: The striatum only includes the
    3.) B: the basal ganglia is also included in the regulation of emotions
    4.) A
    5.) B: Research has found that Tourette’s syndrome is caused by a combination of the two factors.
    6.) E
    Media Sources
    Figure 1
    Figure 2
    Figure 3
    Video 1
    <iframe width="560" height="315" src="" frameborder="0" allowfullscreen></iframe>
    1. Diagnostic and Statistical Manual of Mental Disorders: DSM-5. 5th ed. Arlington, VA: American Psychiatric Association, 2013. Print.
    2. Leckman, J.F. & Cohen, D.J. (1999). Tourette’s Syndrome: Tics, Obsessions, Compulsions. New York, NY: John Wiley & Sons, Inc.
    3. Wang Z., Maia T. V., Marsh R., Colibazzi T., Gerber A., Peterson B. S. (2011). The neural circuits that generate tics in Tourette’s syndrome. Am. J. Psychiatry 168 1326–1337. 10.1176/appi.ajp.2011.09111692
    4. Byrne, J. H. and Dafny, N. (eds.), Neuroscience Online: An Electronic Textbook for the Neurosciences
    Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston (UTHealth)
    © 1997, all rights reserved.
    5.Ji G-J, Liao W, Yu Y, Miao H-H, Feng Y-X, Wang K, Feng J-H and Zang Y-F (2016) Globus Pallidus Interna in Tourette Syndrome: Decreased Local Activity and Disrupted Functional Connectivity. Front. Neuroanat. 10:93. doi: 10.3389/fnana.2016.00093
    6. Purves D, Augustine GJ, Fitzpatrick D, et al., Neuroscience. 2nd ed. Sunderland, MA: Sinauer Associates; 2001.
    7. Rand Swenson, DC, MD, PhD, Review of Clinical and Functional Neuroscience.
    Dartmouth Medical School
    © Swenson 2006
    8. Tourette’s Syndrome.
    Center for Disease Control and Prevention

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Thursday, December 22

  1. page Saccades I edited ... {Sup. C location.jpg} Another important str…
    {Sup. C location.jpg}
    Another important structure for the control of saccadic eye movements is the superior colliculus (SC). The superior colliculus sits just under the thalamus as with the other members of the midbrain (mesencephalon).
    that was stimulated.Thestimulated. However, some research shows that the SC maps the distance between two points in the visual field than the amplitude of the saccade necessary to cover that distance (Bergeron and Guitton 2003).The rostral portion
    {superior colliculus.png}
    The key to understanding the control of saccadic eye movement is to understand how the superior colliculus is able to influence the nuclei that innervate the eye muscles. There are several specific neurons that are important for the production of a saccadic eye movement: The excitatory burst neuron, the cell body of which is in the horizontal gaze center in the paramedian pontine reticular formation (PPRF). The excitatory burst neuron is ultimately the link between the SC and the nuclei that have control over the eye muscles because it excites the ipsilateral abducens nucleus, thereby exciting the ipsilateral lateral rectus. Also,through this mechanism, a conjugate gaze can be maintained throughout the movement because the abducens and oculomotor nuclei are linked via the medial longitudinal fasciculus which allows for simultaneous contraction of the lateral rectus in one eye and the medial rectus in the other causing the eyes to turn in the same direction. It is also important to note that the PPRF inhibits the contralateral abducens nucleus through an inhibitory burst neuron so that the eyes will turn in the desired direction, or the direction of the stimulus in the case of a reflexive saccade. Also in the PPRF are long lead burst neurons which are responsible for aiding in the excitation of the excitatory burst neuron and is excited by the superior colliculus. Additionally influencing the excitatory burst neuron is the omnipause which is located in the nucleus of the dorsal raphe. The omnipause neuron is responsible for providing tonic inhibition on the excitatory burst neuron, so that the eyes are not jumping around when they should not be performing a saccade. While the omnipause neuron helps to the eyes stay fixed on a new location and inhibits the production of a saccade, the tonic neuron actively sends input to the abducens nucleus to keep the eyes in their location. The tonic neuron is located in the nucleus prepositus hypoglossi and participates in keeping the eyes at a new location after a saccade by changing their firing rate. The tonic neurons fire a some given rate when an individual is foveating on a fixation point. After a saccade is performed the tonic neuron's firing rate on the abducens nucleus changes in order to keep the eyes fixed on a new location.
    Burr, D. C., Morrone, M. C. & Ross, J. Selective suppression of the magnocellular visual pathway during saccadic eye movements. Nature 371, 511–513 (1994).
    Bergeron, A., Matsuo, S., & Guitton, D. (2003). Superior colliculus encodes distance to target, not saccade amplitude, in multi-step gaze shifts. Nature Neuroscience, 6(4), 404-413.
    Jarbus, A. L., & Yarbus, A. L. (1967). Eye movements and vision. New York: Plenum Press.

    Kunimatsu, J., & Tanaka, M. (2016). Striatal dopamine modulates timing of self-initiated saccades. Neuroscience, 337(1), 131-142.
    Purves D, Augustine GJ, Fitzpatrick D, Hall WC, LaMantia A-S, White LE, editors. Neuroscience. 2nd ed. Sunderland, MA: Sinauer Associates (2001)
    Robinson, F. R., & Fuchs, A. F. (2001). The Role of the Cerebellum in Voluntary Eye Movements. Annual Review of Neuroscience, 981-1004. Retrieved December 20, 2016.
    Ramat, S., Leigh, R. J., Zee, D. S., & Optican, L. M. (2006). What clinical disorders tell us about the neural control of saccadic eye movements. Oxford: Oxford University Press. doi:10.1093/brain/awl309
    Squire, L. R. (2003). Fundamental neuroscience. San Diego, CA: Academic.
    Jarbus, A. L., & Yarbus, A. L. (1967). Eye movements and vision. New York: Plenum Press.
    Purves D, Augustine GJ, Fitzpatrick D, Hall WC, LaMantia A-S, White LE, editors. Neuroscience. 2nd ed. Sunderland, MA: Sinauer Associates (2001)

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Wednesday, December 21

  1. page Prosopagnosia II edited ... What is Prosopagnosia? Prosopagnosia is a condition characterized by the inability to recogni…
    What is Prosopagnosia?
    Prosopagnosia is a condition characterized by the inability to recognize faces, due to impairments in the visual processing and visual association areas of the brain. These impairments can be present at birth as congenital or developmental prosopagnosia. In the case of congenital prosopagnosia the brain’s visual processing centers associated with visual recognition of faces does not develop properly. Prosopagnosia can also be present later in life in the form of acquired prosopagnosia which can be caused by traumatic brain injuries, neurological diseases and other various factors. [4] Most researchers agree that prosopagnosia is connected to dysfunctions in the fusiform gyrus of the brain, however the way in which the fusiform gyrus causes theses difficulties is still under investigation. [7] It is estimated that Developmental or congenital prosopagnosia is prevalent in 2 to 2.9% of the world’s population. [4] There are still a lot of unanswered questions about prosopagnosia and so more research is needed to deepen our understanding of this complicated disorder.
    {tumblr_mq5tpeqUQN1rn6pqko1_500.jpg} (

    Anatomical Structures and Neural Pathways Associated with Prosopagnosia
    In order for the brain to recognize faces, the following structures and neurological processes must be working correctly:
    retina and eitheractivate cone cells. Axons from the cone cells will hyperpolarize or depolarize cone cells,the bipolar cells depending on whether theybipolar cells are on or off center, which will then influencecenter bipolar cells.
    {eyes.png} Figure 1: Visual Processing
    Fusiform Gyrus (

    {Hippocampus.png} Figure
    of the Hippocampus(

    Fusiform Gyrus:
    The fusiform gyrus is a section of the inferior occipitotemporal cortex located on the ventral surface of the brain. It is found in between the hippocampal gyrus and the inferior temporal gyrus and is a part of the ventral stream or the “what” pathway of the brain. Within the fusiform gyrus there is a specific anatomical region known as the FFA or the fusiform face area which is most active when your visual system is analyzing faces. [10]
    Research on acquired Prosopagnosia is still under way, as the above hypotheses are not valid for every case of acquired prosopagnosia.
    Signs of Prosopagnosia
    {nofaces.jpg} (developmental
    Patients with Prosopagnosia will not only have difficulty recognizing faces, but they will have trouble with social situations. When people with prosopagnosia interact with others it can be difficult for them to engage as they have to constantly figure out, without using facial information, who it is they are talking to. This can be difficult for them and so they tend to be less social for fear of embarrassing themselves in front of their peers when addressing them. In addition to withdrawing from people and social situations, they may feel guilty about not being able to recognize people even though they have met many times beforehand. This can cause a lot of anxiety and frustration for people with prosopagnosia.
    TreatmentThere is currently no cure for prosopagnosia and so generally treatment involves giving them some tangible strategies in order to help them deal with their symptoms. Patients can learn how to rely on auditory information and gait patterns of those they are trying to remember. Additionally, memorizing clothing and hair styles of those closest to the person with prosopagnosia can help them to remember who they are interacting with. In addition, semantic information, or the context in which people have met or are used to seeing each other, can be helpful in recognizing others. [8]
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Tuesday, December 20

  1. page Saccades I edited ... Input & Output pathways (ne…
    Input & Output pathways (neuronal connections)
    little girl.jpg} Image from Alfred Yarbus'study mapping eye movements by tracking them. The individual dots are locations that the eyes saccade between when "searching" the figure while the lines aremovementsShows the path of travel that the eyes took.saccades searching a face
    There are two primary pathways that are means of eliciting a saccade, reflexive and voluntary movement. In the case of a reflexive horizontal saccadic eye movement, some stimulus must reach the superior colliculus and cause a region other than the rostral region (associated with the fovea) to become excited. If the stimulus is visual, then a stimulus excited photo receptors on the retina and the information will travel along the optic tracts directly to the superior colliculus where it excites a part of the colliculus that is different from the foveal region. When the activity in the SC shifts to the region associated with the stimulus, output signals from the SC cease their excitation the omnipause neuron, and increase excitation of the long-lead burst neuron. The collective affect of this is the disinhibition and excitation of the excitatory burst neuron, which in turn excites the ipsilateral abducens nucleus. The abducens then excites the ipsilateral lateral rectus and excites the contralateral oculomotor nuclei through the medial longitudinal fasiculus; the oculomotor nuclei then excites the medial rectus so to produce the saccade with conjugate gaze.
    In the case of a voluntary saccades, the visual information from M type ganglion cells travels through the “where” pathway in the dorsal stream ultimately projecting to the lateral inferior parietal cortex. This information is constantly happening anytime an individual is looking around. However, after being processed, the information is also being sent from the dorsal stream to the frontal eye fields, which is a part of the cortex
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