Neuroscience Study Guide 2

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amygdala

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The amygdalae (singular: amygdala; also corpus amygdaloideum) (Latin, from Greek αμυγδαλή, amygdalē, 'almond', 'tonsil', listed in the Gray's Anatomy as the nucleus amygdalæ)[1] are almond-shaped groups of nuclei located deep within the medial temporal lobes of the brain in complex vertebrates, including humans.[2] Shown in research to perform a primary role in the processing and memory of emotional reactions, the amygdalae are considered part of the limbic system.[3]

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Anton’s syndrome

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Anton–Babinski syndrome is a rare symptom of brain damage occurring in the occipital lobe. People who suffer from it are "cortically blind", but affirm, often quite adamantly and in the face of clear evidence of their blindness, that they are capable of seeing. Failure to see is dismissed by the sufferer through confabulation. It is named after Gabriel Anton and Joseph Babinski.

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achromatopsia

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Achromatopsia (ACHM), is a medical syndrome that exhibits symptoms relating to at least five separate individual diseases. Although the term may refer to acquired disorders such as color agnosia and cerebral achromatopsia, it typically refers to an autosomal recessive congenital color vision disorder, the inability to perceive color AND to achieve satisfactory visual acuity at high light levels (typically exterior daylight). The syndrome is also present in an incomplete form which is more properly defined as dyschromatopsia. The only estimate of its relative occurrence of 1:33,000 in the general population dates from the 1960s or earlier.

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agnosia

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Agnosia (a-gnosis, or loss of knowledge) is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss.[1] It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream.[2]

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akinetopsia

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Akinetopsia, also known as cerebral akinetopsia or motion blindness, is an extremely rare neuropsychological disorder in which a patient cannot perceive motion in their visual field, despite being able to see stationary objects without issue. For patients with akinetopsia, the world becomes devoid of motion. Most of what is known about akinetopsia was learned through the case study of one patient, LM. There is currently no effective treatment or cure for akinetopsia.

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apperceptive agnosia

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Apperceptive Agnosia is the visual disorder that renders a person unable to recognize objects. It is also known as visual space agnosia. Distinction between shapes is difficult, although other aspects of vision, such as ability to see detail and colour, remain intact. Recognition of, copying and discriminating between visual stimuli, even of different shapes, is problematic. Apperceptive agnosics cannot complete an object matching task. Because they are unable to recognize even simple shapes, Apperceptive agnosia is considered a problem in the early part of the visual processing system. As contrasted with patients diagnosed Associative agnosia, whom are able to recognize simple shapes and even copy complex shapes (drawing of an anchor, for example) but are unable to recognize what an object is.
In both cases, identification of objects is entirely based on inferences made by the person based on the colour, size, social, or contextual cues.
A variant of apperceptive agnosia is the inability to recognize objects outside of their normal rotation or orientation.

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apraxia, ideomotor apraxia

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Ideomotor Apraxia, often IMA, is a neurological disorder characterized by the inability to correctly imitate hand gestures and voluntarily pantomime tool use, e.g. pretend to brush one's hair. The ability to spontaneously use tools, such as brushing one's hair in the morning without being instructed to do so, may remain intact, but is often lost as well. The general concept of apraxia and the classification of ideomotor apraxia were developed in Germany in the late 19th and early 20th centuries by the work of Hugo Liepmann, Adolph Kussmaul, Arnold Pick, Paul Flechsig, Hermann Munk, Carl Nothnagel, Theodor Meynert, and linguist Heymann Steinthal, among others. Ideomotor apraxia was classified as “ideo-kinetic apraxia” by Liepmann due to the apparent dissociation of the idea of the action with its execution.[1] The classifications of the various subtypes are not well defined at present, however, owing to issues of diagnosis and pathophysiology. Ideomotor apraxia is hypothesized to result from a disruption of the system that relates stored tool use and gesture information with the state of the body to produce the proper motor output. This system is thought to be related to the areas of the brain most often seen to be damaged when ideomotor apraxia is present: the left parietal lobe and the premotor cortex. Little can be done at present to reverse the motor deficit seen in ideomotor apraxia, although the extent of dysfunction it induces is not entirely clear.

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basal ganglia

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The basal ganglia (or basal nuclei) are a group of nuclei in the brains of vertebrates. They are situated at the base of the forebrain and strongly connected with the cerebral cortex, thalamus and other areas. The basal ganglia are associated with a variety of functions, including motor control and learning. Currently popular theories implicate the basal ganglia primarily in action selection, that is, the decision of which of several possible behaviors to execute at a given time. Experimental studies show that the basal ganglia exert an inhibitory influence on a number of motor systems, and that a release of this inhibition permits a motor system to become active. The "behavior switching" that takes place within the basal ganglia is influenced by signals from many parts of the brain, including the prefrontal cortex, which is widely believed to play a key role in executive functions.
The main components of the basal ganglia are the striatum, pallidum, substantia nigra, and subthalamic nucleus. The largest component, the striatum, receives input from many brain areas but sends output only to other components of the basal ganglia. The pallidum receives its most important input from the striatum (either directly or indirectly), and sends inhibitory output to a number of motor-related areas, including the part of the thalamus that projects to the motor-related areas of the cortex. The substantia nigra consists of two parts, one that functions similarly to the pallidum, and another that provides the source of dopamine input to the striatum. The subthalamic nucleus receives input mainly from the striatum and cortex, and projects to the pallidum. Each of these areas has a complex internal anatomical and neurochemical organization.

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basilar membrane

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The basilar membrane within the cochlea of the inner ear is a stiff structural element that separates two liquid-filled tubes that run along the coil of the cochlea, the scala media and the scala tympani (see figure).

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blindsight

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Blindsight is a phenomenon in which people who are perceptually blind in a certain area of their visual field demonstrate some response to visual stimuli.[1][2] In Type 1 blindsight subjects have no awareness whatsoever of any stimuli, but yet are able to predict, at levels significantly above chance, aspects of a visual stimulus, such as location, or type of movement, often in a forced-response or guessing situation. Type 2 blindsight is when subjects have some awareness of, for example, movement within the blind area, but no visual percept. This may be caused by, for example, the person being aware of their eyes' tracking motion which will function normally. Blindsight is caused by injury to the part of the brain responsible for vision (see occipital lobe). Evidence for it can be indirectly observed in children as young as two months, although it is difficult to determine the type in a person who is not old enough to answer questions.[3]

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brain’s “bouncer”

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Efficiency variations in the filtering of relevant from irrelevant information could contribute to individual differences in working memory. A new functional imaging study suggests that the basal ganglia act as this filter because activity in this region before stimulus presentation was inversely correlated with unnecessary storage.

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cerebellar dysfunction

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Involving the part of the brain (cerebellum), which controls walking, balance, and coordination.

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cerebellum

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is a region of the brain that plays an important role in motor control. It is also involved in some cognitive functions such as attention and language, and probably in some emotional functions such as regulating fear and pleasure responses,[1] but it is its function in movement that is most clearly understood. The cerebellum does not initiate movement, but it contributes to coordination, precision, and accurate timing. It receives input from sensory systems and from other parts of the brain and spinal cord, and integrates these inputs to fine tune motor activity.[2] Because of this fine-tuning function, damage to the cerebellum does not cause paralysis, but instead produces disorders in fine movement, equilibrium, posture, and motor learning.[2]
In terms of anatomy, the cerebellum has the appearance of a separate structure attached to the bottom of the brain, tucked underneath the cerebral hemispheres. The surface of the cerebellum is covered with finely spaced parallel grooves, in striking contrast to the broad irregular convolutions of the cerebral cortex. These parallel grooves conceal the fact that the cerebellum is actually a continuous thin layer of neural tissue (the cerebellar cortex), tightly folded in the style of an accordion. Within this thin layer are several types of neurons with a highly regular arrangement, the most important being Purkinje cells and granule cells. This complex neural network gives rise to a massive signal-processing capability, but almost the entirety of its output is directed to a set of small deep cerebellar nuclei lying in the interior of the cerebellum.

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change detection task

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(for measuring short term visual memory)- Change detection is like a search task in which subjects search for the presence of a difference between the test array and a memory representation of the sample array. To explore this analogy, we compared a traditional change-detection task in which subjects looked for a difference between the sample and test arrays (analogous to a search for feature presence) with a task in which all or all-but-one of the items change and subjects look for a no-change item (“any-sameness” task; analogous to a search for feature absence). Just a RTs are slower and more set size-dependent when subjects search for the absence of a feature as when they search for the presence of a feature, we found that RTs were slower and increased more rapidly as set size increased in any-sameness task than in the traditional change-detection task. These results suggest that the presence of a change is like the presence of a unique feature, and can be detected by an unlimited-capacity process.

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cochlear implant

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(CI) is a surgically implanted electronic device that provides a sense of sound to a person who is profoundly deaf or severely hard of hearing. The cochlear implant is often referred to as a bionic ear.
As of April 2009, approximately 188,000 people worldwide had received cochlear implants;[1] in the United States, about 30,000 adults and over 30,000 children are recipients.[2] The vast majority are in developed countries due to the high cost of the device, surgery and post-implantation therapy. A small but growing segment of recipients have bilateral implants (one implant in each cochlea).[3]

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conditioning and extinction

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the use of a behavior's antecedent and/or its consequence to influence the occurrence and form of behavior. Operant conditioning is distinguished from classical conditioning (also called respondent conditioning) in that operant conditioning deals with the modification of "voluntary behavior" or operant behavior. Operant behavior "operates" on the environment and is maintained by its consequences, while classical conditioning deals with the conditioning of reflexive (reflex) behaviors which are elicited by antecedent conditions. Behaviors conditioned via a classical conditioning procedure are not maintained by consequences.[1] extinction is when tat conditioning disappears

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cone photoreceptors (S- M- and L-types)

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long, medium and short wavelength cones have been demonstrated to exist in human retina by photometric, psychophysical and molecular biological methods: L-cones (red) are known to be maximally sensitive to wavelengths peaking at 564nm, M-cones (green) at 533nm and S-cones (blue) at 437nm respectively (see spectra above Fig. 14a) (Gouras, 1984, for a review).

Normal human color vision depends on the three cone mechanisms. This adds an additional dimension to color vision over those of dichromatic mammals, creating reds and greens rather than just long wavelength (red) and short wavelength (blue). To do, this nature splits the long-wave system into two similar systems with slightly different spectral sensitivities with relatively similar opsins (Fig. 14b). One cone opsin is most sensitive to yellow-green and the other to yellow-red. This splits the brightest and yellow part of the visible spectrum into two color bands, one green and the other red. This red-green system works in parallel with that for blue-yellow.

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consolidation, reconsolidation

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Memory consolidation is a category of processes that stabilize a memory trace after the initial acquisition.[1] Consolidation is distinguished into two specific processes, synaptic consolidation, which occurs within the first few hours after learning, and system consolidation, where hippocampus-dependent memories become independent of the hippocampus over a period of weeks to years. Recently, a third process has become the focus of research, reconsolidation, in which previously consolidated memories can be made labile again through reactivation of the memory trace.

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constraint-induced therapy

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CI or CIMT) is a form of therapy that helps stroke and Central Nervous System damage victims regain the use of affected limbs.[1]
The focus of CI lies with forcing the patient to use the affected limb by restraining the unaffected one. The affected limb is then used intensively for either three or six hours a day for at least two weeks. As a result of the patient engaging in repetitive exercises with the affected limb, the brain grows new neural pathways.
CI was developed by Dr. Edward Taub of the University of Alabama at Birmingham. Taub argues that, after a stroke, the patient stops using the affected limb because they are discouraged by the difficulty. As a result, a process that Taub calls "learned non-use" sets in, furthering the deterioration. It is this process that CI seeks to reverse.
Practitioners say that stroke victims disabled for many years have recovered the use of their limbs using CI. The American Stroke Association has written that Taub's therapy is "at the forefront of a revolution" in what is regarded possible in terms of recovery for stroke survivors.[1]

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Suzanne Corkin

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Suzanne Corkin, Professor of Behavioral Neuroscience in the Department of Brain and Cognitive Sciences at MIT, is due to publish a book about HM in 2010.[7] memory consolidation