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Makes melatonin during darkness; may play a role in producing drownsiness at night and other carcadian rhythms of the body. It has an antigonadotropic effect and may help prevent precocious (too early) puberty. Calcium deposits in this gland makes it visible in radiographs and CT images. |
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Uncertain function. One of many connections between the limbic system and the reticular formation of the brainstem. |
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Subthalamic Nucleus and zona incerta. Part of motor control system. |
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Anterior Division of Thalamus |
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Anterior Nucleus (principle relat nucleus for the limbic system) |
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Medial Division of Thalamus |
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Dorsomedical Nucleus (2-way connection to the prefrontal cortex; has inputs from the limbic system) |
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Lateral Division of Thalamus |
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9 named nuclei (including VPL&VPM); LD (limbic system), LP & Pulvinar (association cortex); VA & VL (motor); VPL&VPM (somatosensory); LGN (vision); MGN (hearing) |
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Lateral Geniculate Nucleus (LGN) |
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Medial Geniculate Nucleus (LGN) |
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Collections of nuclei embedded in the internal medullary lamina. Widespread connections within the CNS. Involved in sensory-motor integration with the limbic system. |
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Partially surrounds the thalamus. Neurons provide inhibitoy feedback to thalamic neurons. |
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[Anterior limb, genu, posterior limb]; contains thalamo-cortical, cortico-thalamic, cortico-pontine, corticobulbar, and cortico-spinal fibers. |
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Branches from the internal carotid (anterior choroidal) and posterior cerebral arteries. |
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Blood Supply to Internal Capsule |
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Branches from the anterior, middle, and posterior cerebral arteries. |
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[From the outer half of the optic cup] Lies on top of the retinal pigment epithilium layer of the choroid [from the inner half of the optic cup]. |
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Weak attachment between retina and the pigment epithilium that can become separated easily. |
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Photoreceptors, bipolar cells, ganglion cells, horizontal cells, and amacrine cells. |
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Function in very dim light (ex. moonlight) and DO NOT contribute to color vision nor vision in the daylight. |
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Come in three types "blue", "green", "red" and are based on wavelenghts of light to which they are most sensitive. |
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Lacking of "red" or "green" cones |
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About 2% of males lack these cones (sex-linked, recessive trait; genes are on the x chromosome). They have trouble differentiating between red and green colors; they are not really "color blind" |
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Absence of blue cones is a very rare condition (gene is on chromosome #7) |
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Only contains cones (very slim ones packed tightly together) and accounts for our best visual accuity. The center of our visual field falls on this area. |
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Two magnocellular layers (1&2-more sensitive to movement and contrast) and four parvocellular layers (3-6- more sensitive to color and form). Layers 1, 4, & 6 receive input from the contralateral eye (nasal retina). Layers 2, 3,& 5 receive information from the ipsilateral eye. |
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Broad band of fibers formed by geniculo-cortical projections. These projections are collected into a band of fibers before they terminate, on cortical neurons. This band is visible to the naked eye called line (stripe) of Gennari. |
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Another Name for the Primary Visual Cortex |
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Plays a role in orienting head/eyes toward visual stimuli, like movement. In humans, it is not involved in visual perception. However, in lower vertebrated it is the site for primary visual perception (ex. frogs). Temporal damage: Blind can still coordinate head/eye (can instinctivly avoid danger). |
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Responsible for pupillary light reflex. A light shone in one eye will constrict the pupil of both eyes (connected to Edinger-Westphal). |
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Thought to be the "master-clock" for circadian-rhythms of the body. Recent evidence implicates previously unknown light-sensitive retinal ganglion cells as the source of infor from the eyes about light/dark enviroment. |
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Arises from precentral gyrus, premotor cortex, & parietal lobe, including postcentral gyrus (some cortical cells). It travels through the posterior limb of the internal capsule, peduncles, pons, pyramids, lateral and ventral funiculi of the spinal cord (fascicles come together at pons and pyramids) and 90% cross over. Vulnerable to stroke because of small arteriole that can burst. Also projects to basal ganglia, thalamus, RF, & dorsal column nuclei (NG/NC-feedback loop for limb position) |
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Projects to the cranial nerve motor nuclei (trigeminal, facial, ambiguous, spinal accesory) and deals with muscles of the head. |
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Cortico-Ponto-Cerebellar Pathway |
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Connects the cerebral cortex with the cerebellum. Innervates pontine nuclei. |
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Primarily connected with prefrontal cortex and other association areas and involved with more cognitive functions and less directly in movement. |
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Motor functions of the basal ganglia. Receives efferents from cerebral cortex and substancia nigra. Projects efferents to globus pallidus and to thalamus. |
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Predominantly limbic system connections. |
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Internal and external. Gives rise to most efferents from the basal ganglia. |
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Part of motor circle becomes overactive in Parkinson's (normally surpressed) and it surpresses VPL & VPM (theoretically cause for parkinson's). |
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Contains dopamine producing cells to striatum (important because degeneration leads to Parkinson's disease). Early on can give precursor of dopamine to treat symptoms. Projects to caudate and putamen. |
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Would lession in case of Parkinson's but now we have deep brain stimulation. |
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Rubrospinal & Reticulospinal tract |
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Involved with adjustment of posture. |
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Involbed with maintenance of equilibrium and coordinating slow eye movements. |
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Intermediate Zone of Cerebellum |
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Involved with fine tunning limb movements during movements. |
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Lateral Hemispheres of Cerebellum |
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Involved with planning and programming of voluntary movements, particularly learned, skillfull movements that become more rapid, precise, and autonomic with practice. |
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Some cognitive functions. Problem solving related to word association tasks and spacial puzzles. Affective (mood) & autonomic functions. Cerebellar abnormalities have been found in the brains of people who had some psychological condition (ex. depression or schizophrenia). |
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Inherited, autosomal dominant, gene of chromosome 4 (excessive CAG-glutamine repeats). Begin to manifest between 30-50 years of age. Gradual changes in mood and personality, developing into dementia & psychiatric disturbances with death occuring 15-20 years after onset. Caused by degeneration of neurons, mostly in the striatum and especially in the caudate nucleus. Dissection of patient with huntingtons= no caudate left! No treatment or cure. |
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Involuntary, continuous, rapid movements of the face and tongue or distal limbs. |
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Involuntary, continuous, rapid movements of the face and tongue or distal limbs. |
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Develops arround 50-60 years of age. Involuntary tremor, shuffling gait, flexed posture, paucity & slowness of movement. Caused by degeneration of the dopaminergic nigrospinal cells in substancia nigra. Possibly caused by unknown environmental toxin, MPTP (in heroine), some pesticides, some have a genetic component. |
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Treatments of Parkinson's Disease |
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Taking L-Dopa (precursor of dopamine) which crosses blood-brain barrier. Medication works for a few years but substancia nigra cells continue to die. Too much L-Dopa leads to dyskenisia. Surgery: focal lessions of globus pallidus of VL of thalamus; deep brain stimulation (permanent electrodes placed in). Also, implantation of dopaminergic neurons derived from stem cells of embryonic SN cells. |
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