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4 Lesions that will cause coma or loss of consciousness:

1. Upper brain stem
2. Midbrain and hypothalamus
3. Diencephalon
4. Bilateral lesions of cerebral cortex

Loss of consciousness in 1. _____ is brief in duration and sudden in onset;
More prolonged and profound loss of consciousness is described as 2. _____
3. Lesser grades of depressed consciousness characterized by variable degrees of impaired reactivity.

1. Syncope (fainting)
2. coma
3. Stupor or obtundation

5 Intracranial causes of coma:

1. head injuries
2. cerebrovascular accidents
3. CNS infections
4. Tumors
5. increased intracranial pressure

4 Extracranial causes of coma:

1. Vascular disorders (shock/hypotension caused by severe hemorrhage or myocardial infarction)
2. metabolic disorders (diabetic acidosis, hypoglycemia, uremia, hepatic coma, addisonian crisis, electrolyte imbalance)
3. intoxication (with alcohol, barbiturates, narcotics, bromides, analgesics, carbon monoxide, heavy metals)
4. miscellaneous disorders (hyperthermia, hypothermia, severe systemic infections)

Glasgow Coma Scale offers a practical bedside method of assessing level of consciousness based on 3:

eye opening and verbal and motor responses

1. Main center for bringing on sleep
2. through the release of
3. REM sleep occurs due to the release of?
4. from?

1. Midline raphe system of the pons
2. serotonin
3. NE
4. Locus ceruleus

Multiple types of sensory input including _____ can activate the reticular formation and produce a generalized increase in cerebral cortical activity or arousal.

somatosensory, auditory, visual, visceral

Activity within the _____ and _____ are both required for maintaining consciousness.

cerebral cortex and mesencephalic reticular activating system

4 Nuclear groups comprising the reticular formation include:

1. Median raphe
2. Paramedian reticular
3. Medial reticular
4. Lateral reticular

Median raphe nuclei:

The median raphe nuclear group includes the following midline nuclei: raphe obscurus and raphe pallidus in the medulla oblongata; raphe magnus in the caudal pons and rostral medulla; raphe pontis in the pons; and the dorsal raphe and superior central (Bekhterev) nuclei in the midbrain. The neurotransmitter of most raphe nuclei is serotonin.

Paramedian reticular nuclei:

The paramedian reticular nuclei are located lateral to the medial longitudinal fasciculus and the medial lemniscus. They include the paramedian reticular nucleus in the rostral medulla and caudal pons, and the reticulotegmental nucleus in the rostral pons and caudal midbrain.

Medial reticular nuclei:

The medial reticular nuclear group includes the nucleus reticularis gigantocellularis in the medulla oblongata, and the nucleus reticularis pontis caudalis and nucleus reticularis pontis oralis in the pons.

Lateral reticular nuclei:

The lateral reticular nuclear group includes the following nuclei: nucleus reticularis parvocellularis and nucleus reticularis lateralis in the medulla oblongata; the nucleus reticularis parvocellularis in the pons; parabrachial and pedunculopontine nuclei in the rostral pons and caudal midbrain; and the cuneiform and subcuneiform reticular nuclei in the midbrain.

The reticular nucleus of thalamus, located lateral to the _____, is a continuation of the brain stem reticular formation.

Internal capsule

3 Cholinergic system nuclei:

1. pedunculopontine reticular nucleus
2. lateral dorsal tegmental nucleus
3. nucleus basalis of Meynert

The _____, located in the basal forebrain, sends axons to almost the entire cerebral cortex. Degeneration of cholinergic neurons in this area is associated with memory decline in Alzheimer's disease.

nucleus basalis of Meynert

Four types of monoamine neurons have been identified within the brain stem reticular core:

1. dopaminergic
2. noradrenergic
3. adrenergic
4. serotonergic

3 dopaminergic pathways:

(1) mesostriatal (nigrostriatal), from the substantia nigra to the striatum (caudate and putamen). Interruption of this system is associated with Parkinson's disease.
(2) mesolimbic, from the ventral tegmental area to limbic nuclei. Overactivity of this system is associated with schizophrenic hallucinations.
(3) mesocortical, from the ventral tegmental area to the prefrontal cortex. Lesions in this system are associated with cognitive deficits in Parkinson's disease.

2 noradrenergic components:

1. locus ceruleus
2. lateral tegmental norepinephrine system

Adrenergic system

Adrenergic neurons are located in the same regions of the caudal medulla as the noradrenergic neurons. They project to the spinal cord, brain stem, thalamus, and hypothalamus. This system is small in comparison with the dopaminergic and nor-adrenergic systems and represents a minor component of the monoaminergic system.

Serotonergic system

Serotonergic neurons comprise nine cell groups designated B1 to B9.

The 1. _____ system neurons have a discrete topography and restricted area of terminal distribution, whereas the 2. _____ neuron systems have a more diffuse and wide-spread projection.

1. dopaminergic
2. noradrenergic, adrenergic, and serotonergic

Increase in life expectancy due to advances in: (3)

1. housing/sanitation
2. public health (antibiotics, vaccination, reduced infant mortality account for most of changes)
3. biomedical science (mostly decreased heart disease and stroke)

-Normal aging of the nervous system is non-uniform among individuals
-Aging of the nervous system involves both 2. _____ and _____
-Aging processes diminish efficiency of nervous system function and increase vulnerability, independently of neurodegenerative disease
-Significant components of nervous system aging can be reversed or delayed

1. non-uniform
2. Functional decline and adaptive responses

Normal aging: 4 Histologic changes:
-High degree of individual variation

1. SMALL, region-selective decrease in neuron number
2. Decrease in dendritic extent, spine density
- Increased in early senescence and reduced in later life
- Decreased in cerebellar Purkinje neurons
3. Modest decrease in synapses
4. Increases in Alzheimer's disease-associated pathological changes in small amounts

Normal aging-related cell loss was overestimated:
-Morrison & Hof and others suggest that previous data is contradicted when 1. _____ techniques are used (Beginning 1993-1994).
-Older methods did not allow estimation of volume of the structure containing the neurons being counted.
-Density estimates were thus confounded with age- or procedure-related changes in structural volume.
-Only estimates of 2. _____ within a structure can be used to evaluate neuronal loss.
-Implication is that all old data are suspect.

1. unbiased stereological (US)
2. total cell number

Neuronal loss in normal aging:
Where does cell loss take place?

1. Subiculum of Hippocampus
2. Nigrostriatal monoamine
3. Cerebellum (granule and purkinje cells)

Purkinje neuron vulnerability:
-Purkinje neuron density is associated with competency of 1. _____ and _____
-Also linked to 2. _____ learning (classical conditioning).
-3 Reasons for selective vulnerability:

1. balance and coordination
2. associative learning (classical conditioning)
3. High firing rate during waking and sleep
Continuous metabolic activity
High synaptic plasticity

*****Normal aging: 5 Gross changes:

1. 15% loss of mass
2. Cortical gyri decrease in size, sulci are wider
3. Enlargement of ventricles
4. Some arterial disease affecting large and small vessels is common
5. Not necessarily indicative of psychomotor or cognitive dysfunction

Normal aging: Dendritic extent:
Hippocampus:
-1. _____ and _____- dendritic length 2. _____ from middle (40-60) to old (68-79) followed by regression to middle age level in very old (86-95).
-CA2-3, CA1, Subiculum - complete stability across ages for normals.

1. Parahippocampal gyrus and dentate gyrus
2. increases

Normal aging: 7 Biochemical/Physiologic changes:

1. Reduced protein content
2. Increased DNA (due to gliosis)
3. Increased oxidative molecular damage - increased iron content (transitional metals)
4. Minimal decrease in lipid & water content
5. Reduced blood flow and oxygen consumption
6. Functional changes (e.g., ↓evoked potentials; ↓ long-term potentiation)
7. Loss of synapses

Normal aging: 5 Neurotransmitter changes:

1. Decreased Glut, NE, DA, ACh, 5-HT
2. Reduced biosynthesis
3. Impaired release
4. Little change in receptor number or sensitivity
5. Reduced sensitivity in postreceptor signal transduction pathways (ubiquitous, not selective)

Normal aging: Functional changes:
-High degree of individual difference
-Mild to moderate decline: (5)
-Deficits tend to be partially or fully alleviated by practice and reduction of time requirements.

1. Recent memory (rapid forgetting)
2. Executive function
3. Visuospatial function
4. Reaction time performance
5. Sensorimotor skills (e.g., driving)

Effects of aging on memory:
Primary memory (STM) (consider properties of performance, capacity, decay)?
-Age differences magnified by increasing attention requirements (i.e., dialing phone number versus verbal recall)
-Decay more rapid in old vs young ("rapid forgetting")
-"very impaired" in AD; not distinguishable from aging in early AD

Small decrease in digit span (10%)

Effects of aging on memory:
-If original learning is equated (increase time for older persons), deficits can be alleviated.
-Cued recall/recognition studies: PET imaging studies suggest that when performance of young and old are equated, old subjects have low activity in areas that are high in young, but show increases in other areas.
-Suggests _____ by engaging different memory systems. (e.g., right prefrontal cortex in young, both right and left in old)

Adaptive compensation

Effects of aging on Implicit and explicit memory:
**-"Priming" (cued recall) 1. _____ affected by age than free recall
-Serial position: primacy more affected than recency
-motor skill acquisition rate in some cases improved (but performance may be impaired because of psychomotor dysfunction) (e.g., older typists are slower and make more errors)
**-classical conditioning - slower learning, reduced magnitude of 2. _____

1. less
2. conditioned response (CR)

Effects of aging on memory:
Semantic memory:
-Confrontation naming (e.g., name these objects)
-Semantic fluency (name animals; name words starting in S)

1. Consistent age related deficit. Interpreted as reflection of "cognitive slowing" based on lack of age-related increase in "errors" and amelioration by conversion to a recognition task.
2. Contrast with clear deficits in AD

Effects of aging on other cognitive functions:
Language:
****-Vocabulary 1. _____
-Declines in 2:
-Word recognition 3. _____ in normal aging; impaired in AD.

1. intact or improved
2. spontaneous language production, sentence length
3. intact

Effects of aging on visuospatial function:

-Ability to perceive and manipulate visual information.
-Tests: reproduce figures or recognize similarity
- Form perception (object recognition): inferior temporal and occipital regions ("what" system)
- Spatial judgement (movement & spatial relationships) right occipitoparietal junction ("where" system).
- Moderate but robust decline with age; very predictive of overall cognitive decline
- Very impaired in AD (important clinical diagnostic)
-Clock-drawing test: (used as fast screening for AD)

Normal aging vs Alzheimer's Disease:
-AD involves progressive loss of memory and _____
-Often includes: Aphasia, apraxia, agnosia, visuospatial impairment, loss of executive function
-Early stages of AD difficult to differentiate from normal aging
-Only small percentage eventually show AD

at least one other cognitive domain (learning, reasoning, problem solving, abstract thinking)

Praxis

Something you are ordered to do

Dementia: definition
- Loss of intellectual functions (memory, learning, reasoning, problem solving, abstract thinking)
-Must be 1. _____ losses for diagnosis
-Involuntary functions 2. _____ (although lost in more advanced stages)
-Over 50 disorders known to cause dementia

1. multiple
2. intact

Dementia: Classifications
1. _____ Syndromes (hyperthyroidism, Cushings disease, nutritional deficiencies, AIDS dementia, etc.)
2. _____ Syndromes (Huntington's chorea, Parkinson's disease, Schilder's disease, Creutzfeldt-Jakob disease; brain tumors, brain trauma, meningeal infections
3. _____ (Alzheimer's disease, Vascular dementia)

1. Medical syndromes
2. Neurologic syndromes
3. Dementia

AD: 4 Functional deficits

1. Memory (especially new LTM) (declarative mem.) (i.e., H.M. - like memory deficit but not as selective)
2. Language (word finding, empty speech, circumloculation)
3. Visuospatial (figure reproduction, geographic disorientation)
4. Personality & affect (variable manifestation, depression, paranoia, etc.)

AD: Gross pathology
-Mostly nonspecific, similar to normal aging but more pronounced.
-Cortical atrophy (pronounced in early onset)
-gyral atrophy, widening of sulci
-all regions except 1. _____
-Limbic atrophy (pronounced in late onset)
-Ventriculomegaly
Gross features specific to AD are 2. _____

1. occipital lobes
2. atrophy of olfactory bulb & tracts; hippocampus

Which aphasias involved word finding difficulty?

Transcortical and Wernicke's aphasias

Visuospatial degeneration in AD affects what parts of the brain?

Visual association cortex:
occipitotemporal "what" cortex
occipitoparietal "where" cortex

Personality and affect changes in AD affect what part of brain?

Limbic system

AD: 5 Histologic changes

1. ****neuronal loss (not present in normal aging)
2. neurofibrillary tangles (NFT)
3. neuritic plaques (SP) w/ BetaAP (ABeta)
4. synaptic loss (due to axonal/dendritic loss)
5. cerebral amyloid angiopathy (CAA) accumulation of amyloid beta (ABeta) in small to mid-sized vessels of meningeal and superficial cortical vessels

Neuronal loss: Association Cortex
-Loss of corticocortical projection neurons in association areas of neocortex
-In neocortex, AD-associated neuronal loss involves 1. _____ and 2. _____
-Loss is relatively selective for 3. _____

1. inferior temporal cortex (ITC)
2. superior frontal cortex (SFC)
3. corticocortical projection

What kind of NT is lost in AD?

Glutamate

Histology of neocortical cell loss in AD:
-Midsize and small 1. _____ cells; _____neurons; associate with AD pathology and decrease in density
-Axons of 2. _____ corticocortical pyramidal cells most vulnerable:
3. 3 Affected layers?
-Global disruption of long neocortical connections.
-Diffuse cortical 4. _____ lost in all layers
-Primary cortices spared; Large layer V pyramidal cells forming brainstem and cord projections 5. _____

1. pyramidal cells; stellate neurons
2. glutamatergic
3. II (external granular layer)
III (external pyramidal layer)
V (internal pyramidal layer)
4. afferents (NE; ACh)
5. not vulnerable

Hippocampal/cortical circuitry in AD:
1. What is affected?
2. Early cell loss in EC and Subiculum _____ the hippocampus from input and output!

1. Entorhinal cortex, Hippocampus CA1, and Subiculum (all glutamatergic)
(compared with only the subiculum in normal aging)
2. isolate

Hippocampal/cortical circuitry loss in AD:
-Perforant pathway
- Originates in layer II of entorhinal cortex (EC) and terminates in dentate gyrus (DG) of hippocampus.
- Provides key interconnection between neocortex and hippocampus.
- Represents convergence of inputs from association cortex, funneling processed neocortical information into dentate gyrus. Has critical role in memory; synaptic plasticity.
- Input from: 1. _____, _____, and _____
-Hippocampus proper: most severe loss in 2. _____ and _____.
-3. Cell loss in 4:

1. visual, auditory, and taste association cortices
2. subiculum and CA1
3. olfactory bulb, cingulate gyrus, amygdala, and prelimbic cortex

First site of cell loss in AD is?

Entorhinal cortex, followed by cell loss in the hippocampus

3 Subcortical projection pathways (NT)

1. Dorsal bundle (noradrenergic)

Arousal/Wakefulness - Important for memory formation:
2. Basalo-cortical (cholinergic)
3. Septo-hippocampal (cholinergic)

Neuronal loss in aging and AD:
Only areas spared are:

1. Primary cortices
2. Nigrostriatal monoamine
3. Cerebellum

AD: Genesis of NFT
-NFT = paired helical filaments composed of 1. _____ protein
-2. _____ of tau from microtubles leads to destabilization (microtubule dysfunction, loss)
-3. _____ leads to aggregation
-Aggregations form 4. _____

1. hyperphosphorylated tau protein
2. Dissociation
3. Hyperphosphorylation
4. paired helical filaments (PHF)

Genesis of neuritic plaques:
-ABeta = abnormal cleavage of 1. _____, locus on chromosome 21
-APP normal membrane-spanning protein
-normal cleavage to soluble fragments (by Alpha-secretase) (1-40); non-amyloidogenic
-cleavage through membrane-spanning region yields ABeta (2. _____) = BAD
-fibril formation - Beta-pleated sheet

1. amyloid precursor protein (APP)
2. 42/43

AD: Biochemical/Physiologic changes (3)
Similar to normal aging but exacerbated

1. Reduced protein content
2. Increased oxidative molecular damage
3. Reduced blood flow and oxygen consumption

*****AD: Neurotransmitter changes
-4 NTs that show prominent early presynaptic loss
-2 NTs spared until late stages
-Reduced biosynthesis, release, etc. secondary to neuronal loss

1. ACh, NE, somatostatin, glutamate
2. GABA, DA

AD: Genetic factors (familial)
-25% of patients have relative with dementia or AD (sporadic)
-familial AD - multigenerational involvement, large pedigree (early and late onset forms)
-mutation on chromosome 21 affecting APP processing (early FAD)
-genes coding for presenilins (presenilin 1, chromosome 14; presenilin 2, chromosome 1)(Early FAD)

...

AD: Genetic factors (sporadic)
-Apolipoprotein 1. __ gene dose (chromosome 19)
-Many functions, cholesterol transport
-Highest concentrations in liver and brain (macrophages & astrocytes)
-Risk: alleles 2. _____ (increase of 20-90%)
-Possible mechanisms: different effects of alleles on 3. _____ of tau; amyloid fibril formation or protection from toxic effect of ABeta or free radicals.

1. E4
2. E4>E3>E2
3. hyperphosphorylation

AD: Pathogenic hypotheses
-beta amyloid (linked to genetic abnormality)
-tau protein (phosphorylation modulators)
-free radicals (linked to mitochondrial abnormality)
-accelerated aging
-infectious (prion)
-environmental toxicity

...

_____ - loss of ability to make decisions

Abulia

Syndrome?
Abulia- loss of ability to make decisions
Impaired ability to develop new strategies to deal with novel situation
Results in diminished work performance
Still has values, long-term goals and motivation related to work activities
Classic deficits on neuropsychological tests requiring sensory-linked planning
Trail-making test
Wisconsin Card Sort
Slower learning of set
Perseveration with old set when faced with shift in set

Dorsolateral syndrome

1. STM =
2. LTM =

1. Immediate memory = 7-digit recall
2. Remote and recent memory

Syndrome?
Unable to link plans for behavior to motivation and values; impulsive; change in personality
Performance on tests of dorsolateral prefrontal function are average or above
Illustrates orbitofrontal function: internal, limbic-linked (crazy emotions) planning

Orbitofrontal syndrome

Syndrome?
Akinesia
Motor impersistence

Dorsomedial Syndrome
*Illustrates dorsomedial prefrontal cortex function in initiating and sustaining of goal-directed behavior

Dorsomedial prefrontal cortex functions in _____ and _____ goal-directed behavior.

initiating and sustaining

1. Condition?
2. Site of lesion?
Improper execution of automatic behavioral routines (e.g., putting on several pairs of glasses; public urination)
Behavior driven by dorsolateral pfc is intact, but inadequately inhibited by orbitofrontal system

1. Utilization behavior
2. Orbitofrontal

With utilization behavior, behavior driven by dorsolateral prefrontal cortex is intact, but is inadequately inhibited by _____ system.

orbitofrontal

Apraxia

Inability to carry out an activity on command

Arousal (wakefulness/alertness):
1. _____ system in midbrain reticular formation (MRF) 2. 2 nuclei involved?
Lesion causes 3. _____
Stimulation promotes wakefulness; forward motion
MRF modulates cortical activity:
- Direct connections via 4. _____
- Indirectly via 5. _____
NR transmitter is 6. _____
Active during both 7. _____ and in _____

1. Indirect cholinergic (Ach)
2. Pedunculopontine nucleus (lateral group) and Laterodorsal tegmental nucleus
3. somnolence/lethargy
4. midline thalamic nuclei
5. thalamic reticular nucleus (NR) (enabling thalamic throughput)
6. GABA
7. wakefulness and in REM sleep

Arousal (wakefulness/alertness):
1. 3 Direct aminergic arousal systems (direct to cortex) (include associated NT)
2. 2 Non-aminergic arousal systems (NT)
3. Enabling circuit: (NT)

1. Tuberomamillary nucleus (histamine)
Locus ceruleus (norepinephrine)
Raphe nuclei (serotonin)
2. Nucleus basalis (acetylcholine)
Lateral hypothalamic neurons (orexins)
3. Lateral hypothalamic neurons (orexins)

NREM sleep (I-IV):
1. _____ of thalamocortical neurons
Slow wave activity driven by 2. _____
Low sk. muscle activity; slow eye movements
Reduced HR, BP & Resp. (parasympathetic predominance)
Lower core and brain temp; metabolic rate
Reduced cortisol, thyroid; increased GH, testosterone, prolactin, insulin, glucose

1. Hyperpolarization
2. Reticular thalamic nucleus (NR)

Awake - Stage I (claims not sleeping)
Unsynchronized
Drowsy (1. _____)
Stage 1: Synchronized (2. _____)
Stages 2:
Vertex wave/sleep spindle
Stages 3/4:
Slow rhythm (3. _____) (slow wave sleep)
REM
Waking-like EEG; eye movement; loss of muscle tone, ANS activity

1. Alpha
2. Theta
3. Delta

REM sleep:
Waking-like EEG
Hypotonia; especially neck
Increased BP & HR; irregular breathing
Rapid eye movements
1. _____ spikes
2. _____, _____, and _____ achieve high firing rates (active state)
Lower threshold for arousal than from IV
Subject most likely to remember dream when awakened from REM

1. Ponto-geniculo-occipital (PGO) spikes
2. Limbic system, hypothalamus, and brain stem

1. Direct arousal system is active during?
2. Indirect arousal system is active during?

1. ONLY during wakefulness
2. During BOTH wakefulness and REM sleep

Indirect pathway = _____ pathway

Ach pathway

Thin sheet of neurons that envelops thalamus and projects onto thalamic neurons

Reticular thalamic nucleus (NR)

Neurobiology of NREM sleep:
Interaction between sleep-inducing and arousal mechanisms
Onset driven by GABA cells in 1. _____
VLPO inhibits 2. _____ and _____ arousal systems
VLPO and direct (aminergic) arousal systems are mutually 3. _____
VLPO remains active during sleep
Delta waves spindling reflect intrinsic properties of 4. _____ neurons and _____
VLPO regulates onset and maintenance of 5. _____; abolished by lesioning

1. Ventrolateral preoptic nucleus (VLPO)
2. indirect (cholinergic) and direct (aminergic)
3. inhibitory
4. thalamocortical neurons and Reticular thalamic nucleus (NR)
5. Slow-wave sleep (SWS)

In waking up, the indirect arousal system is disinhibited indirectly due to inhibition of Ventral Lateral PreOptic (VLPO) area-mediated inhibition by the _____.

Direct (aminergic) system

Neurobiology of REM sleep:
Regulated by different populations of Ventral Lateral PreOptic (VLPO) neurons
The 1. _____ interacts with direct arousal system in onset and offset of NREM sleep -> _____
2. _____ interacts with subsets of arousal nuclei in initiation of REM: (4)
5. Remains inactive throughout sleep?
Activation of additional descending 5. _____ pathways mediating loss of muscle tone

1. cluster (core) subnucleus -> Tuberomamillary (histamine) nuclei
2. Extended subnucleus
3. Locus ceruleus, Raphe nuclei, Pedunculopontine nuclei, Laterodorsal tegmental nuclei
4. Tuberomamillary (histamine) nuclei
5. Glutamatergic

Circadian control of sleep cycle:
Intrinsic sleep cycle is 25 h
1. _____ entrain rhythms via direct retinal-suprachiasmatic pathway:
- Light
- food availability
- temperature
- social ques
2. _____ nucleus
- lesioning abolishes circadian cycles and REM cycle

1. Zeitgebers
2. Suprachiasmatic nucleus (SCN)

Narcolepsy:
Fall asleep at inappropriate times
1. _____ (weakness during emotional arousal)
Sleep paralysis and hypnopompic hallucinations
Components of REM occurring in wrong context:
- Loss of muscle tone during wakefulness (sleep paralysis or cataplexy)
- Vivid dreams during stage 1 (2. _____) or at the end of sleep (3. _____)
Associated with impaired function of 4. _____

1. Cataplexy
2. hypnogogic
3. hypnopompic
4. orexin

Attention:
Process of focusing on a single source of sensory input
Intentional: conscious, deliberate focusing (1. _____ cortex)
- Required for attention
Reactive: shift in attention due to potent or salient stimulus (bug bite) (2. _____ + area)
- Unconscious
Orienting response: 3. _____ + area and _____

1. Dorsolateral prefrontal cortex - required for attention
2. Parietal polymodal association cortex (area 7) - unconscious
3. Frontal eye fields (area 8) and superior colliculi

Condition?
-Initial severe impairment in intentional and reactive attention and orienting response (no stimulus will induce a left saccade)
-Left hemiakinesia (not hemiparesis because patient can move if arm is brought into right hemispace
-Left hemianopia (not due to damage to ascending visual pathways because normal vision occurs when left retinotopic visual fields are brought into the right hemispatial field
-Left hemibody sensory loss - able to detect stimuli in left hand when it is placed in right hemispace.

Hemispatial neglect - more common in right hemispheric stroke

Association cortex has a key role played by cortico-cortical pyramidal neurons in layers ____ and _____ of cortex

II and III

Location/movement "where" visual pathway (occipitoparietal) (dorsal stream) allows use of information from _____ attributes of objects

motion

Language:
-Localized in polymodal/supramodal cortex in 1. _____ region of 2. _____ hemisphere
-3. _____ is fundamental symbolic unit

1. Perisylvian
2. Left
3. Phoneme

Motor (speech output): 1. _____ area (____) and links to 2. _____ and _____ cortex

1. Broca's area (44, 45)
2. premotor and motor cortex

Sensory (language comprehension) : 1. _____ area (____) and links to 2. _____, _____, and _____ cortex

1. Wernicke's area (22)
2. auditory, visual, and somatosensory association cortex

_____ links Broca and Wernicke areas. All connections are bi-directional <-->

Arcuate fasciculus

Conduction aphasia:
1. Speech?
2. Phonemic paraphasias?
3. Comprehension?
4. Repetition?

1. Non-dysarthric speech, fluent
2. Phonemic paraphasias (phonemic substitutions)
3. Comprehension intact
4. Repetition impaired

Conduction aphasia:
-Traditional interpretation: impaired conduction of neural impulses from Wernicke's and Broca's areas via 1. _____, resulting in inaccurate translation of word representations into speech
-Current interpretation: entire 2. _____ represents hierarchical processor converting words into speech.
-Comprehension intact because Wernicke's area and associated sensory links are intact

1. arcuate fasciculus (part of superior longitudinal fasciculus)
2. perisylvian language cortex

Attempts to explain a single word by other means.

Circumlocution

Type of aphasia?
-Non-dysarthric speech, fluent
-Word-finding difficulty
-Semantic paraphasic errors (uses wrong words)
-Comprehension impaired
-Repetition unimpaired

Transcortical sensory aphasia

Type of aphasia?
1. Non-dysarthric speech, fluent
2. Phonemic paraphasias (phonemic substitutions)
3. Comprehension intact
4. Repetition impaired

Conduction aphasia

Transcortical sensory aphasia:
-Isolation of perisylvian cortex language processor from sensory association cortices supporting meaning
-Results in difficulty matching words to cortical sensory representations, so both _____ and _____ of speech is impaired
-Repetition is intact because the core phonologic processing circuitry is intact (Broca's and Wernicke's areas are spared)

generation and comprehension

Type of aphasia?
-Fluent, non-dysarthric speech
-Phonemic paraphasia, semantic paraphasic errors
-Impaired comprehension
-Impaired repetition

In effect, transcortical sensory aphasia + conduction aphasia

Wernicke's aphasia

Dysarthric speech:
1. What is it?
2. When is it exhibited?

1. labored, slurred speech with broken syllables
2. only during Broca's aphasia

Type of aphasia?
-Difficulty generating speech; labored, slurred (dysarthric)
-Comprehension intact
-Repetition impaired

Broca's aphasia

Cannot point to objects named or name objects

Apperceptive visual agnosia

Inability to carry out specific actions on command (e.g., use of tools)

Apraxia

Apraxia Anatomical components:
1. _____ cortex (recognizing the tool; representation in "what" system)
2. _____ cortex (naming the tool; representation in the language system)
3. _____ cortex (mind's eye image of tool movement in "where" system)
4. _____ cortex (mind's hand and arm representation of using the tool)

1. Ventral visual association cortex
2. Left perisylvian cortex
3. Dorsal visual association cortex
4. Premotor cortex

Condition?
-Body part-as-tool errors
-Unable to pantomime use of tool
-Can recognize correct use of tool

Ideomotor apraxia

Neuroanatomical basis of associative learning:
-Decortication fails to abolish 1. _____
-Lesions of cerebellum ipsilateral to trained eye abolish 2. _____ and prevent re-learning.
-Critical region is 3. _____ and _____ nuclei of cerebellum (deep cerebellar nuclei)
-4. _____ and _____ activity are not required for CR expression.

1. Conditioned response
2. Conditioned response
3. medial dentate and interpositus nuclei
4. Hippocampal and cortical activity

Associative Learning: Classical (Pavlovian) Conditioning:
-4 Targets:
-An initially neutral stimulus becomes a conditioned stimulus (CS), able to elicit a conditioned response (CR), through repeated temporal pairing with an unconditioned stimulus (US), that elicits an unconditioned response (UR).
- 3 Examples:

1. smooth muscle, cardiac muscle, glands, reflexive skeletal muscle
2. salivation, cardiac acceleration, eyeblink

Instrumental Learning (Operant learning):
-Target is a 1. _____ response, technically referred to as an "2. _____."
-Differs from associative (Pavlovian) learning in that voluntary behavior (R) is modified in form and frequency according to the stimuli (S) produced by the behavior itself.
-Associative = 3. ___; Instrumental = 4. ___.
Neural processes and their localization differ for S-S and S-R type learning.

1. voluntary skeletal muscle
2. Operant
3. S-S (stimulus-stimulus)
4. S-R (stimulus-response)

Instrumental Learning: Reinforcement:
-By definition, reinforcement describes a situation when the frequency of a response (voluntary behavior) is increased following the introduction or withdrawal of a particular stimulus.
-The stimulus modifying the response frequency can be considered a _____
-Primary reinforcing stimuli (e.g. food, water, sex) have direct biological relevance and intrinsic reward/incentive value

Reinforcer

Neuroanatomical basis of instrumental learning/reinforcement:
-At least 20 brain sites act as reinforcers when stimulated
-Medial forebrain bundle (anterior, posterior and lateral hypothalamus)
-Mesolimbic DA system activation critical: (3)

1. ventral tegmental area (VTA)
2. nucleus accumbens
3. prefrontal cortex

Neuroanatomical basis of instrumental learning/reinforcement:
-Lesion or pharmacological blockade of reinforcement pathway:
- abolishes self-stimulation
- "extinction" of reinforced behavior
- _____ (inability to experience hedonic effect of primary reinforcers)

Anhedonia

Short-term memory (STM):
-"Working memory" function ascribed to 1. _____
-Differs from STM in that information is available for cognitive manipulation
-Various STM registers involve other parts of cortex, e.g. :
- 2. Speech-associated STM (_____)
- 3. Visuospatial (2)

1. prefrontal cortex
2. premotor cortex
3. striate cortex; parietal cortex

Long-term memory (LTM):
-Days to years
-Requires structural/molecular basis for explanation
-3 Stages of formation: (location)

1. Encoding (medial temporal lobe - Hippocampus)
2. Storage (association cortex)
3. Retrieval - requires both medial temporal lobe and association cortex

Levels of memory processing:
-Sensory Register
-Short-term memory (1. _____)
=Long-term memory (2. _____)

-These divisions have meaning in terms of both information processing and their neurological bases

1. primary
2. secondary

Short-term memory:
-Seconds to minutes (usually)
- Time is not key
-Classically, limited to 1. _____ (words or patterns)
-Instantly accessible
-Can be maintained indefinitely by 2. _____
- Disrupted by 3. _____
-Digit span (neuropsych. test) (immediate in MLM)

1. 7 bits
2. rehearsal
3. interference

LTM and STM vs remote, recent and immediate memory:
-Long-term memory names a 1. _____ and refers to permanence; LTM is permanent but STM is not.
-Remote memory 2. _____ memory for events more remote in time (i.e., childhood, school, etc), versus recently acquired information that may or may not become permanent.
-With certain lesions that impair LTM but not STM, 3. _____ memory is relatively intact, whereas 4. _____ memory is impaired. - Lesion 5. _____
- Pass digit span test - Cannot repeat anything at the end of conversation
-Recent memory and STM are often misapplied. -Consider the difference between STM and recent memory carefully when making inferences and answering questions.

1. process
2. describes
3. remote
4. recent
5. Hippocampus

2 forms of long-term memory:

1. Explicit (declarative)
2. Implicit (non-declarative)

Explicit (declarative) LTM:

Facts/Events -> Medial temporal lobe (hippocampus)

Implicit (non-declarative) LTM:

1. Priming (S-S type conditioning) -> Neocortex
2. Procedural (Habits & skills) -> Striatum
3. Associative learning (classical & operant conditioning)
-> Emotional responses -> Amygdala
-> Skeletal musculature -> Cerebellum
4. Non-associative learning (habituation & sensitization) -> Reflex pathways

Declarative (explicit) LTM:
Memory for facts (1. _____)
Memory for events (2. _____)
3. _____ memory
Memory that is capable of being 4. _____ (in humans).
Type of memory disrupted by lesion of the 5. _____*
* Note that bilateral damage to the 6. _____ is required!

1. semantic
2. episodic
3. conscious
4. verbalized
5. medial temporal lobe
6. hippocampus

The 1. _____ is necessary for formation of LTM for 2. _____ information.
Non-hippocampal systems are involved in 3. _____ LTM and STM

1. hippocampus
2. declarative (explicit)
3. non-declarative

Neurobiological Mechanisms of LTM:
Active process with time-course.
Ability of electroconvulsive shock to produce retrograde amnesia is time-dependent.
90-95% inhibition of brain protein synthesis selectively disrupts 1. ___ but not 2. ___.

1. LTM
2. STM

Neurobiological mechanisms of LTM: Long-term potentiation (LTP):
LTP=Increase in strength of a synaptic response following electrical stimulation. May last indefinitely.
Alters biochemistry of 1. _____ receptors and initiates molecular cascade culminating in synthesis of new proteins and growth or pruning of synaptic connections.
Produced by brief high-frequency stimulation of neurons of the 2. _____, _____, and _____ collateral pathways of the 3. _____.

1. NMDA-type glutamate receptors
2. perforant, mossy fiber, and Schaffer
3. hippocampus

1. Main cortical inputs to hippocampus
2. Main output from hippocampus

1. Entorhinal cortex and perforant pathway
2. Subiculum

_____ is highly vulnerable to degeneration in Alzheimer's Disease

Entorhinal cortex

Hippocampal/cortical circuitry

Slide 29 - 2nd lecture

Neurotransmitter systems involved in memory:
Glutamatergic (1. ___)
2. 2 Cholinergic:
3. 2 Norepinephrine:
GABA

1. Long-term potential (LTP)
2. basalo-cortical and septo-hippocampal pathways
3. locus ceruleus, dorsal bundle

Bilateral lesion of hippocampus & Medial Temporal Lobe (MTL) causes:

1. Complete anterograde amnesia for explicit/declarative information
2. Impaired spatial memory (can't find way through house)

Memories are stored where?

Distributive representations

Corticobulbar tracts pass through _____ limb of internal capsule and middle part of crus cerebri (cerebral peduncles)

Posterior

Basal ganglia motor system:
1. Major site of INPUT is _____
2. Major site of OUTPUT is _____
3. GPi sends its inhibitory output to thalamic nuclei in fiber tracts (known as the ansa lenticularis, and lenticular fasciculus a.k.a. H2 fields of Forel) that run through or around the internal capsule
4. None of the Corpus Striatum projects directly to the spinal cord. However, the GP projects to the 3. _____, which then projects via the 4. _____ tract to the spinal cord where it modulates 5. _____ muscle tone.

1. Striatum
2. GPi
3. red nucleus
4. rubrospinal tract
5. flexor

Which cerebellar peduncle is responsible for output?

Superior cerebellar peduncle

With the exception of the _____, the midline portions of the cerebellum tend to project to midline deep cerebellular nuclei and the more lateral portions tend to project to their correspondingly more lateral deep cerebellular nuclei.

flocculus/nodulus

_____ cells are the only excitory cells in the cerebellular cortex.

Granule cells

Which nucleus projects from each portion of the cerebellum?
1. vermis
2. intermediate zone (medial part of hemispheres)
3. Lateral hemispheres

1. fastigial
2. globose and emboliform
3. dentate

Globose and emboliform nuclei are collectively refered to as?

interpositus

floccular/nodular lobe projects upon the _____ nuclei (in the medulla)

vestibular nuclei

Cerebellar Input/Afferents:
1. 4 via Inferior cerebellar peduncle
2. 1 via Middle cerebellar peduncle

1. Ipsilateral Dorsal Spinocerebellular Tract (proprioceptive inputs from body)
Ipsilateral Cuneocerebellar Tract
Contralateral Olivocerebellular (Brain stem) Tracts (proprioceptive input from whole body via the inferior olive)
Vestibulocerebellular (from vestibular nuclei)
2. Contralateral Pontocerebellular (from Pontine Nuclei, which receive input from many areas of cortex)

Cerebellar output/efferents:
1. Via superior cerebellar peduncle

1. Contralateral Dentatorubrothalamocortical tract (terminates in VL nucleus of thalamus (some indirectly via red nucleus), then relayed to cortex)

3 types of aminergic fibers to the cerebellum:

1. Climbing fibers
2. Mossy fibers
3. Aminergic fibers

Climbing fibers
a. originate in _____
b. synapse on _____
c. send collaterals to _____

1. Inferior olive
2. Purkinje cells
3. Deep nuclei

Mossy fibers
a. originate from a variety of tracts (3)
b. synapse on _____
c. send collaterals to _____

1. spinal cord, vestibular, and pontine nuclei
2. Granule cells
3. Deep nuclei

Aminergic fibers
a. _____ (noradrenergic)
b. _____ (serotonergic)

1. Locus ceruleus
2. Raphe nucleus

Both climbing and mossy fibers provide _____ input. The aminergic inputs modulate cerebellular activity.

Excitatory

For each, list Input synapses on to Cell Type and Cell Type Activity and Projects to:
1. Excitatory climbing fibers:
2. Excitatory mossy fibers:
3. Excitatory granule cell parallel fibers:
4. Excitatory granule cell parallel fibers & mossy fibers

1. Purkinje; Inhibit deep nuclei
2. Granule; Excite Purkinje cells
3. Basket/Stellate; Inhibit Purkinje
4. Golgi; Inhibit Granule

Basket, stellate and golgi cells are all _____

interneurons

1. _____ cells provide primary inhibitory (GABAergic) output of the cerebellular cortex by projecting to the 2. _____ deep nuclei (esp. dentate nucleus).

1. Purkinje cells
2. ipsilateral

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