Ch. 2: Functional Anatomy & Essential Neuropsychology Flashcards

1
Q

Brain Divisions

A
  • Forebrain (cerebral hemis and diencephalon)
  • Midbrain
  • Hindbrain- medulla, pons, cerebellum form connection between brain and spinal cord
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2
Q

Ventral-Dorsal Plane

A

Front- back direction in the cord but means inferior/superior in the brain

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3
Q

Rostral-Caudal Plane

A

Head-toes in cord but front-back in brain

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4
Q

Gray matter tracts

A

Cell bodies of neurons. Basic synaptic communication happens here,

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5
Q

White Matter tracts

A

provide communication in cortical areas and between cortical and subcortical areas over longer distances. Disconnection syndromes occur in response to WM damage disconnecting functional inputs and outputs.

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6
Q

Unimodal cortex

A

Processes information pertaining to a specific sensory modality. Prominent role in perception.

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7
Q

Polymodal cortex

A

Processes information from disparate modalities through Afferent connections. Role in higher order conceptual processes that are less dependent on concrete sensory information that on abstract features extracted from multiple inputs. (e.g., anterior temporal lobe, and inferior parietal lobule)

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8
Q

Orbitofrontal/ventromedial PFC

A

1/3 Frontal lobe region: emotion regulation, reward monitoring personality. Damage to OBFC=disinhibition; to VMD PFC= disordered reward/punishment processing and problems making perceptual or learning experiences with reqard value and emotional significance

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9
Q

Dorsolateral PFC

A

Cognitive-executive functions; damage produces dysexecutive syndromes, impairments in WM and poor attentional control of behavior. Layer 4 contains inputs from the thalamus. Layers II & III contain cortico-cortico connections. DLPFC, to perform complex abstract reasoning and problem-solving tasks, depends upon modulatory input that engages and disengages areas of cortex (the role played by input from subcortical re-entrant circuits that include the thalamus) as well as rich associations among adjacent and nonadjacent cortical regions for processing task demands (the role played by cortico-cortical connections).

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10
Q

Dorsomedial PFC

A

intentional and behavioral activation. akinetic mutism with damage- alaert and awake but cannot speak

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11
Q

Temporal Pole of Temporal lobe(Temporal)

A

polymodal convergence zone important for intersensory integration and semantic memory

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12
Q

Ventral temporal areas(Temporal)

A

object recognition and discrimination; bilateral damage- object or face agnosia

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13
Q

Posterior temporal region (Temporal)

A

Middle & Superior temporal sulci contain primary auditory areas & Wernicke’s area in language dominant hemisphere. Important for language comprehension and prosodic comp in the homologous non-dominant hemisphere

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14
Q

Superior parietal lobe (parietal)

A

sensorimotor integration, body schema, spatial processing

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15
Q

Temporoparietal junction (parietal)

A

Phonological and sound based processing. Language comprehension (left) and music comprehension (right)

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16
Q

Inferior parietal lobule (parietal)

A

complex spatial attention, integration of tactice sensation, self-awareness

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17
Q

Primary visual cortex (occipital)

A

around calcarine fissure & Visual association cortex. Complete damage here produces cortical blindness or (rarely) Anton’s syndrome- denial of cortical blindness or blindsight (detection of unconsciously perceived stimuli in the blind field). Partial damage- visual field defects that reflect the region of VC damaged.

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18
Q

Ventral visual pathway (occipital)

A

Connects occipital & Temporal association cortex and then to inferotemporal. Important for object and face recognition, item based memory and complex visual discrimination. processes structural and feature-based information important for the analysis and recognition of visual form such as faces and objects.
-Lesions here: produce perceptual disturbances and, in severe forms, disorders of recognition of familiar objects and/or faces, known as agnosias. When the disorder results from impairment inprocessing basic visual elements of objects (e.g., shape, depth, contour), it is APPERCEPTIVE in nature

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19
Q

Dorsal visual pathway

A

Projects to parieto-occipital association cortex via the superior temporal sulcus, preferentially processes spatial information and is likely involved in visuomotor interaction (e.g., reaching, manipulating objects).

  • Important for spatial vision and visuomotor integration.
  • Lesions here: impairments in spatial perception, attention and visuomotor processing (e.g., hemispatial neglect, impaired visual reaching)
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20
Q

Neocortex

A

Six-layer laminar structure, distinguishes it from the limbic cortex (archicortex) which has only 3

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21
Q

Functional System & Disconnection Syndromes

A

Interconnected group of cortical and subcortical structures that each contributes important components of a complex behavior or skill. Complex behaviors such as memory or language can be impaired by damage to the processors themselves or by damage to their connecting fibers. When damage affects a specific processor, the resulting deficit reflects a loss of that processor’s contribution to the complex behaviors supported by the system. When damage affects the interconnections among processors, a disconnection syndrome results. Disconnection syndromes occur when fiber damage causes functional processors to lose their ability to coordinate or communicate in performing a complex task or behavior.

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22
Q

Optic tracts

A

Retinal ganglion cells in each eye send their axons into the optic nerve, which projects posteriorly and comes together at the optic chiasm, where the optic tracts originate.

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23
Q

Geniculostriate visual Pathway

A

visual discrimination and form perception. Retinal ganglion–>optic nerve–>Optic Chiasm–> Lateral Geniculate Nucleus–> primary visual cortex (bA17)

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24
Q

Extrastriate/Tectopulvinar visual pathway

A
Small portion (10%) of fibers that dont terminate in the geniculostriate visual pathway. Pupilary light reflex, attention-directed, --> 
retinal ganglion-->optic nerve--> optic chiasm--?pretectal area and superior colliculus--> broad aras of parietal and frontal association cortex via relays in the pulvinar of thalamus
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25
Q

Neuroanatomy of memory

A

Severe disorders of memory (i.e. amnesic syndrome) can result from focal damage to:

  • medial temporal lobes
  • medial diencephalon or
  • basal forebrain (BF)

An understanding of the underlying circuitry provides a basis for considering these three regions not as discrete entities, but as parts of an integrated, distributed memory system.

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26
Q

Hippocampus

A

Dentate gyrus
Ammons horn
Subiculum
Most hippocampal cortical connections are with the adjacent parahipocampal cortex

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27
Q

Trisynaptic Circuit

A

Primary internal connections of the hippocampus:
Entorhinal cortex –> Dentate granule cells [synapse 1]–>
CA3 mossy fibers [synapse 2]–>
CA1 via schaffer collaterals [synapse 3]
CA! then projects to the subiculum –> Projects back to entorhinal cortex

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28
Q

Subiculum of the hippocampus

A

CA1 inputs: Major source of direct hippocampal cortical efferrent projections. Projects back to entorhinal cortex

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29
Q

Parahippocampal cortex

A

-Rhinal (entorhinal & perirhinal: receives anterior temporal “non-spatial” info)
-Pre-and parasubicular cortex
-Parahippocampal cortex (receives posterior medial “spatial” information
Perirhinal and parahipp receive a majority of the cortical inpu tto the temporal lobe memory circuit.
These connections come from unimodal and heteromodal association cortices and info from both sources is combined into 3D representations of experienced. stimuli.

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30
Q

Parahipocampal * Perirhinal streams of information

A

One view:
Parahippocampal= spatial
Perirhinal = non spatial info
These streams go into the hippocampus which then “binds them together to form and episode.
Another view:
Recent findings suggest that input from the parahippocampal cortex to the perirhinal cortex, as well as present “spatial” and “non-spatial” cortical connections to both the perirhinal and parahippocampal cortices, allows both structures access to non-spatial and spatial information from the cortex prior to their interaction with the hippocampus.

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31
Q

Segregated Cortical inputs to the hippocampus

A

Ventral stream: Unimodal (visual) cortex–>Perirhinal Cortex–> Lateral Entorhinal Cortex–> HC CA1 & 3

Dorsal Stream: Parietal & Frontal Association areas–> Parahippocampal cortex –> Medial entorhinal cortex

32
Q

3 main subcortical projections from the hippocampus to structures outside of the temporal lobe memory circuit

A

2/3 which involve the fornix, which divides into two pathways at the anterior commissure:

1) Fibers from CA1, CA3, and the subiculum project in the precommissural fornix to the lateral septal nucleus.
2) Subicular projections travel in the postcommissural fornix and terminate on the mammillary bodies or the anterior nucleus of the thalamus.
3) The hippocampus also projects to the amygdala, nucleus accumbens, other regions of the BF, and ventromedial hypothalamus.

33
Q

Medial Limbic Circuit (Circuit of Papez)

A

Explains how the hypothalamus and cortex coordinate emotion-cognition interaction.
hippocampus–> postcommissural fornix–>mamilary body + medial limbic circuit: Projection from the mammilar bodies to the anterior thalamic nucleus and subsequent thalamic projections to the cingulate gurys and cingulate projections via the cingulate bundle or cingulum which extend back to the hippocampus.

One of two limbic circuits subserving memory in the medial temporal lobe and diencephalon. The circuit is as follows: Hippocampus → mammillary bodies (via the fornix) → anterior thalamic nucleus (via the mammillothalamic tract) → cingulate gyrus → hippocampus (via cingulum and parahippocampal cortex). It must be damaged along with the lateral limbic circuit for dense amnesia to occur.

34
Q

Amygdala

A

Deep in the periamygdaloid and perirhinal cortices in the temporal lobe. Two main parts:

  • large basolateral group of nuclei (connects to limbic system, association cortex and DM thalamic nucleus)
  • smaller corticomedial segment - extensive connections extensive connections wit the BF, hypothalamus and brainstem.
35
Q

Similarities/Differences between Amygdala & Hipp circuits

A

Similar
-Strongly interconnected with frontal and temporal limbic cortex
-Both have indirect access to polymodal neocortical association areas
both project to BF and hypothalamys
-Both connect directly with each other
Different:
-Amygdala is paleocortex vs archicortex hipp
-Amygdala projects to DM thalamus vs Mammilary bodies of hypothalamus for hippocampus
-the amygdala relates to different portions of the BF (bed nucleus of the stria terminalis) than does the hippocampus (septal region).
-cholinergic inputs to the amygdala (nucleus basalis of Meynert [nbM]) are different from that of the hippocampus (diagonal band of Broca).
-unlike the hippocampus, the amygdala has strong connections with brainstem autonomic centers (nucleus of the solitary tract), providing a direct pathway for limbic–autonomic interaction.

36
Q

Lateral Limbic Circuit

A

Amygdala–> DMN Thalamus–> OBFC–> Uncinate fasciculus–>Amygdala

temporal lobe, diencephalon, and frontal lobe. The circuit is as follows: Amygdala → dorsomedial thalamic nucleus (via amygdalofugal pathway) → orbitofrontal lobe → amygdala (via uncinate fasciculus). It must be damaged along with the medial limbic circuit for dense amnesia to occur.

37
Q

Anatomy of Temporal Lobe Amnesia

A

The two-system theory of amnesia forms a core principle of understanding memory disorders from a functional systems perspective, and explains how amnesia can be caused by several different lesion profiles.
The basic principle is that amnesia occurs when both the lateral and medial limbic circuit are damaged (this principle explains most diencephalic and BF amnesias as well).

Thus, for example, lesions that interrupt both the fornix (disrupting Papez’s circuit) and the ventral amygdalofugal pathways (disrupting the lateral circuit) cause severe amnesia, whereas lesions restricted to either pathway alone cause less severe memory disturbance.

Many other combinations on this general theme are possible and have been documented in the literature.

Lesions that affect either the posteromedial or anteromedial aspect of the thalamus cause little memory disturbance; but severe amnesia, comparable to that associated with medial temporal ablations, occurs when both anterior and posterior medial thalamic regions are involved.

Finally, lesions that affect the frontal projections of both Papez’s circuit (anterior cingulate gyrus) and the lateral circuit (ventromedial frontal lobe) produce greater memory loss than lesions of either alone.

Six decades of primate lesion studies suggest (1) that structures within each memory system are highly interdependent, since damage to different parts of each system can cause apparently equivalent deficits; and (2) that each system can, to a large extent, carry on the function of the other, since lesions affecting only one system result in memory loss that is far less severe than if both systems are damaged. More recently, it has been shown that collateral damage to the perirhinal cortex was responsible for the memory deficits seen after amygdala lesions, and, in fact, extensive lesions of the perirhinal and parahippocampal cortices produce an amnesia equivalent to or worse than that produced by impairment of the two circuits described earlier, even when the hippocampus and amygdala are spared. This means that the perirhinal/parahippocampal cortex contributes to memory in its own right. Because both the amygdala and the perirhinal/parahippocampal cortex project to dorsomedial thalamus, the dual-system theory can be easily modified by substituting “perirhinal/parahippocampal cortex” for “amygdala” in Figure 4.2.

38
Q

Temporal Lobe Amnesia summary

A

1) Damage to cortical & Subcortical structures within the temporal lobe whether focal or extensive can result in amnesia
2) Amnesia most likely results from damage to both the hippocampally based medial limbic circuit or the amygdala based lateral limbic circuit.
3) Damage to individual elements of these circuits can all result in amnesia if both circuits are damaged
4) The hippocampus appears critical for episodic memory whereas the amygdala appears more directly involved in emotional aspects of cognition, including emotional memory and assigning emotional significance to stimuli

39
Q

Thalamus

A

Sensory relay nuclus
HIgher cognitive proc - alertness, BA and memory
-number of nuclear groups: Ventral-dorsal and anterior-posterior planes
=System of myelinated fiber tracks called the internal medullary lamina (IML)

40
Q

Internal Medullary Lamina of Thalamus

A

System of myelinated fiber tracks - memory relevant fibers of the mammillothalamic tract travel to anterior thalamic nuclie and the ventral amygdalofugal pathways travel on their way to dorsomedial thalamic nuclei

41
Q

DM Thalamic lesions

A

Associated with amnesia- lesions affecting the IML and mammillothalamic tract in particular. if IML and MM tract are spared then not associated with amnesia

42
Q

Midline Thalamic nuclei

A

connected to hippocampus and are consitently damaged in pateints with WK disease. Thalamic lesions may disconnect thalamic connections with the frontal lobes. It has also been proposed that restricted thalamic lesions in Wernicke-Korsakoff disease might disconnect dorsomedial-frontal connections important for imposing cognitive structure on semantic memories resident in posterior cortex.

43
Q

Basal Forebrain

A
  • Third major region essential for normal human memory. At the junction of the diencephalon and cerebral hemispheres: septal area, diagonal band of broca, NACC septi, olfactory tubercle, substantia innominata (containing NB of Meynert), bed nucleus of the stria terminalis and preoptic area.
  • Lesions in anterior communicating artery can create amnesia by damaging cholinergic regions in the BF which project to BOTH the medial and lateral limbic circuits.
  • Lesion size may not be as important as lesion location in producing amnesia (ie cholinergic disconnection with diencephalic & medial temporal lobe memory systems
44
Q

Neuroanatomy of language

A

There are extensive reciprocal connections with broad areas of visual, auditory, and motor cortex that enable functions key to language processing and that provide the substrate for understanding meaning, processing visual language stimuli (reading), performing meaningful actions (praxis), selecting morphemes for use in speech, establishing the intention to communicate, and using language pragmatically in everyday life.

  • For example, Broca’s area connects with other frontal lobe regions, including the prefrontal, premotor, and supplementary motor areas, and intact interconnections among these regions appear necessary for processing syntax and grammatical structure of language.
  • Wernicke’s area connects reciprocally with the supramarginal and angular gyri in the parietal lobe, a system important not only for language comprehension but also for writing and for mapping sounds to meaning (lexical semantics)
  • Connections with specific visual areas in the inferior temporal lobe critical to the recognition of word forms is one part of the substrate for grapheme-phoneme conversion, key to reading ability.
  • Callosal connections enable the language-nondominant hemisphere to participate in the language-processing network, thus integrating linguistic processing with prosodic information communicating the emotional aspects of speech.
45
Q

Prosody

A

The use of tone, pitch, rhythm, and other vocal intonation patterns to convey both meaning (e.g., marking specific states such as anger, sadness or mirth) in language.

  • primarily processed in the right hemisphere where focal lesions can produce prosodic syndromes (aprosodias) that bear striking similarity to their contralateral language based counterparts.
  • i.e., damage to the inferior right frontal lobe produces a deficit in expressing emotional prosody in speech that is analogous to Brocas aphasia
  • posterior temporal parietal lesions produce a deficit in prosodic comprehension with fluent production akin to Wernickes aphasia
46
Q

Alexia without agraphia

A

Left visual cortex damage produces right Inability to read sparing writing ability. Left visual cortex damage produces homonymous hemianopia extending anteriorly to affect the interhemispheric corssing fibers int he splenium of the corpus callosum. These lesions prevent info received appropriately in the right hemi/left visual field from accessing the perisylvian language areas in the left hemisphere.

47
Q

Color agnosia

A

color naming disturbances: Left visual cortex damage produces homonymous hemianopia extending anteriorly to affect the interhemispheric corssing fibers int he splenium of the corpus callosum. These lesions prevent info received appropriately in the right hemi/left visual field from accessing the perisylvian language areas in the left hemisphere.

48
Q

Optic aphasia

A

Cannot name a visually apprehended object but can demostrate its use bc more anterior callosal fibers connecting the intact visual areas to the left hemi praxis mechanisms are intact

49
Q

Pure word deafness

A

pateint cannot understand language but can identify non-verbal sounds (e.g. chriping bird or jingling keys)- white matter disconnection of fibers from left and right auditory receptive areas from Wernickes area in the left hemisphere.

50
Q

Neuroanatomy of Frontal/executive skills

A

Vast regions of the DLPFC have large granular layers (layer IV), suggesting strong and broadly distributed interactions with subcortical networks involving the thalamus.

Architectonically, frontal cortex also contains regions with large layers II and III, suggesting the presence of extensive cortico-cortical connectivity.

Such interactions allow modulation and volitional control to be exerted on perceptual, emotional, and action systems toward the completion of goal-directed action.

51
Q

Frontal-subcortical interactions: Cortico-striatal-pallidal-thalamo-cortical loops

A

Cortical-subcortical networks involved in BA and selection in an ovrall process called “selective engagement”. An essential feature of cortical-subcortical interaction in a variety of cognitive domains. Cortical activity is modulated by connections from cortex, through inhibitory and excitatory structures in the basal forebrain and thalamus, and back to cortex as a way of engaging a cortical region needed for task performance or of inhibiting another region whose function would interfere with processing or compete for output. The process of activating cortical regions for task performance is known as selective engagement.

52
Q

Selective engagement

A

Process by which some circuits are activated and some are inhibited by the frontal lobes to complete a goal. Involves Cortical-striatal-pallidal-thalamo-cortical loop

53
Q

Frontal lobe attention

A

Attention must be volitionally utilized in the service of ongoing goals, plans and cognitive demands that evolve over time. Interactions between frontal lobe and posterior perceptual systems balance attentional deploynmet and sensory tuning to result in the selection of appropriate stimuli for further processing. Any complex attentional act is a combination of top down and bottom up attentional processes.

54
Q

Top-down attention

A

frontal lobe regions engaged in volitional deployment of attention and in establishing behavioral priorities in the face of conflicting demands. Top down biases from parietal lobe providing visuomotor frames of reference and frontal lobe whic provide the substrate for working memory and goal setting are transmitted to colliculi, pulvinar and frontal eye fields. DORSAL FRONTOPARIETAL SYSTEM

55
Q

Posner & Rothbart 3 systems of attention

A

Three interconnected systems for attention: -orienting

  • alerting
  • executive aspects of attention
56
Q

orienting attention

A

(tuning perceptual systems to incoming stim for selection), dependent on acetylcholine, and superior colliculus, pulvinar thalamic nucleus, posterior temporoparietal cortex and frontal eye fields.

57
Q

Alerting attention

A

state of sensitivity to incoming stimuli modulated by norepinephrine and depends primarily on ascending sensory inputs from the thalamus

58
Q

executive aspects of attention-

A

monitoring and resolving conflicts among thoughts, feelings and behaviors. Primarily dependent on dopamine and involves key structures including the ACC and DLPFC

59
Q

Bottom up

A

-sensory signals arrive at frontal and parietal cortices having been preprocessed by superior colliculi and pulvinar providing bottom up information that is biased toward salient environmental stimuli. VENTRAL frontoparietal system is involved in target detection in the sensory environment

60
Q

Frontal Lobes & Working Memory

A
Functionally separate WM subsystems exist in DLPFC. Goldman Rakic studies populations of neurons that are silent during stimulation or response execution but are selectively active during the delay period of working memory tak and are thus responsible for keeping information active or online during thi stime. 
Dorsal PFC (arcuate sulcus BA 46) code spatial information
Ventral PFC (inferior PF convexity BA 12) are slectively active during object WM tasks.
61
Q

Neuroanatomy of WM

A

Two views- domain or process specificity. -dorsal (spatial)-ventral (object based) distinction reflects domain specificity (spatial vs object based) wheras others argue for process-specificity.
Process-specificity- ventral regions are preferentially activated when the task requires sequential organization & Storage (eg., as in forward digit span) while more dorsal regions are activated when the task additionally requires mental manipulation and reorganization (eg., as in letter number sequencing).

62
Q

Acetylcholine

A

Primary efferent neurotransmitter of the peripheral nervous system (limited role in CNS). Found mainly in: Pontomesencephalic region & Nuclear groups of the Basal Forebrain
-In the CNS Ach works on neurons subserving memory, attention and higher cortical processe

63
Q

Pontomesencephalic region Ach

A

neurons that project to intralaminar nuclei of the thalamus. Provide modulatory input then go to widespread areas of cortex. Incite cortical arousal throug indirect projections from thalamus to cortex.

64
Q

Basal forebrain Ach

A

project to widespread cortical regions. Medial Septal Nuclei & N of diagonal band of BF provide cholinergic input to the hippocampus

65
Q

Ach Receptors

A

2: Muscarinic and nicotinic
-Muscarinic- mediate the main cognitive effects on attention, learning and STM
-Nicotinic - triggger rapid neural & Neuromuscular transpission within the sympathetic & parasympathetic NS and at the neuromuscular junction.
Drugs wtih strong anticholinergic properties (e.g., antihistamintes,1st gen antipsychotics, tricyclics) may exert - influence on cognitive performance when administered to the edlery r thers with reduced cog or cerebral reserve

66
Q

Norepinephrine (Noradrenaline)

A

Locus Coeruleus & Lateral Tegmental are of pons & medulla
- innervate the entire cerebral cortex
- can be inhibitory or excitatory
-attentional shifting
-NE - “stress hormone” plays a role in modulating sleep wake cycles, attention, mood and may have a role in modlating pain
=role in depression, bipolar disorder, anxiety disorders such as OCD is well established
-ADHD drugs increase levels of NE and DA (except for strattera which only affects NE)

67
Q

Serotonin

A

Raphe Nuclei of the midbrain, pons and medula

  • rostral raphe projects to the entire forebrain including thalamus, cortex & basal ganglia.
  • projections play a role in anxiety, depression, OCD, aggressive behavior and certain eating disorders
  • Dorsal raphe–> cerebellum, medulla & spinal cord
  • regulate pain, breathing, temperature regulation & motor control
68
Q

Serotonin acting drugs

A
  • serotonin-specific reuptake inhibitors (eg zoloft, prozac)
  • SE and NE reup inhibitors (effexor)
  • above can be used with SE 2A antagonists (e.g., trazodone, mirtazapine) to augment tx for refractory depression.
69
Q

Dopamine

A

Substantia nigram pars compacta (SNpc) and VTA

  • Projection system has three parts
    1) mesostriatal system (SNpc–> striatum caudate +putamen); PD pathway disabling motor sx
    2) mesolimbic system (VTA–>medial temporal lobe, amygdala, cingualte, Nacc) reward functions and addictive behavior. overactivity assoc with +sx of SZ such as delusions and hallucinations (respond well to DA SE 2A antagonist drugs (e.g., clozaril, seroquel, rirsperdal)
    3) mesocortical system (VTA–> cortical regions of the frontal lobe) EF, WM, top down attention and initiation of motor activity. (-) sx f SZ, dysexec syndrome and bradykinesia
70
Q

Other Neurotransmitters

A

63 molecules that have proven or ptative action as NT in the brain: pituitary petides, circulating hormones, hypithalamic releasing hormones, amino acids, pioid petides and other clases.

71
Q

GABA

A

the one inhibitory NT, impt for memory, anxiety, arousal and neuromodulation. participate in short and long range inhibitory projections that innervate man yo of the same areas as other NT and provide counteracting inhibitory input.

  • Reticular nuclues of the thalamus- GABA neurons here may be critical for gating thalamo cortical interactions and for regulating sleep and arousal.
  • BF GABA neurons regulate attentional shifting and alterantion between response reinforcement contingenices
  • Antianxity drugs act to enhance GABA transmission
72
Q

Glutamate

A

most abundant excitatory NT in the brain, widely distributed and plays a key role in learning and memory

  • NMDA receptor is glutamatergic and implicated in LTP and synaptic plasticity/neurogenesis, new experience dependent memory encoding
  • too much glutamate leasd to cell death- art of stroke and AZ cascade
73
Q

NMDA receptor antagonists

A

TX neurodegenerative diseases by selectively inhibiting pathological aspects of glutamatergic activation while preserving the physiological activation of NMDA receptors thus restoring LTP

74
Q

Medication side effects

A

For example, many common medications used for treatment of hypertension, cardiac arrhythmia, glaucoma, and migraine have broad effects on β-adrenergic function that may or may not be part and parcel of their intended mechanism of action. Antihistamines may produce sedation and cognitive inefficiency through their effects on cholinergic and serotonergic systems. Benzodiazepines, when used to treat insomnia and other sleep disturbances, can affect daytime cognition, including memory and psychomotor speed by potentiating GABAA function.

75
Q

Akinetic Mutism

A

neurologic condition resulting from bilateral medial FL injuiry

  • pt does not move or speak but remains aware of ongoing events
  • can be seen in stroke syndromes, tumors of the olfactory groove and in final stage of certain neurodegenerative diseeases
76
Q

Basal Forebrain

A

group of structures located in the VM FL anterior to caudate and putamen. MAJOR SOURCE OF CHOLINERGIC INPUT

  • nucleus basalis
  • diagonal band of Broca
  • substantia innominata
  • medial septal nuclei
  • -> Damage here= memory loss with confabulation (conf associated with neighboring FL Damage)
77
Q

Two system theory of amnesia

A

The contemporary viewpoint that argues that the necessary and sufficient lesion producing human amnesia involves damage to two limbic circuits, one (medial) involving the hippocampus, and the other (lateral) involving the amygdala. According to this view, dense amnesia occurs only when both circuits are damaged, whereas less severe memory impairment may occur with partial damage. This theory provides an integrative account of how and why amnesia can be produced by lesions to the medial temporal lobe, diencephalon, and basal forebrain