Quiz 2 Flashcards
1
Q
2 main structures of the Diencephalon
A
- Thalamus
- Hypothalamus
2
Q
Thalamus
A
“CPU of the brain” – Transmits signals from all senses to cortex.
- He says all senses, aside from olfactory, which goes to limbic brain and olfactory first.
- Other than that, everything else goes to the thalamus.
• Sensory
• Motor
• Integrative
• Regulatory (from diffuse projecting nuclei)
3
Q
Lesions on the thalamus may cause?*
A
- Memory, cognitive, executive dysfunction
- Remember that damage to dorsomedial nucleus and mammillothalamic tract are damages in Korsakoff’s syndrome.
- anterograde amnesia
- retrograde amnesia, severe memory loss
- confabulation, that is, invented memories which are then taken as true due to gaps in memory sometimes associated with blackouts
- meager content in conversation
- lack of insight
- apathy - the patients lose interest in things quickly and generally appear indifferent to change.
4
Q
Hypothalamus
A
Primary function is homeostasis/regulation of:
- Water/electrolyte balance (ADH, thirst)
- Food intake (hunger, satiety)
- Temperature (sweating, shivering)
- Autonomic activity (blood pressure, rate/force of heart beat, respiratory rate/depth, digestive tract motility, etc.)
- Sleep-wake cycle/circadian rhythmicity
- General body metabolism
5
Q
The hypothalamus subserves what 3 systems?*
A
- Autonomic (through effects on brainstem, spinal cord centers)
- Endocrine (hormones, releasing factors affecting anterior pituitary)
- Limbic (primary output of limbic brain)
6
Q
Melatonin*
A
Synthesized in the pineal gland from serotonin via enzymes that are sensitive to diurnal fluctuations in light.
- In the absence of light synthesis of melatonin is enhanced.
- Modulates the sleep wake switch in the hypothalamus and lowers body temperature.
7
Q
Basal Ganglia
A
- Complex set of subcortical nuclei that modulate movement, perception, cognition, emotion
- In short, BG get information from cortex, modulate that information, and then modulate frontal cortex via thalamus.
- Such modulation results in either increased or decreased excitation of frontal cortex.
8
Q
Four parallel circuits (“loops”)
A
- Skeletomotor Loop - Sensory-motor control
- Oculomotor Loop - Control of orientation and gaze
- Prefrontal Cortex (Executive) Loop - Cognitive processes
- Limbic Loop - Emotional and visceral responses
9
Q
Damage to the basal ganglia can result in what kind of symptoms?
A
- Hypokinetic symptoms - Loss/decrease of motor/cognitive ability
- Hyperkinetic symptoms - Involuntary movements
10
Q
Parkinson’s Disease
A
- Hypokinentic dysfunction
- Motor sxs due to loss of dopaminergic neurons of substantia nigra that project to striatum of BG
- Results in decreased excitation from basal ganglia to thalamus with resulting hypokinetic sxs
11
Q
Akinesia (Dyskinesia)
A
- kinesis is Greek for movement
• Difficulty initiating activity
• Loss of postural reflexes (tends to fall backward)
• Shuffling gait, as if feet were stuck in place, w/ decreased arm swing and appearing stiff w/ little neck movement
• Sometimes followed by nearly normal gait but difficulty stopping or falling
• Masked face, blank stare (decreased blink)
• Writing may be small (micrographia), cramped, jerky.
12
Q
Bradykinesia
A
– Slowed movements
13
Q
Hypokinetic dysarthria
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(‘dys’ meaning abnormal or difficult; ‘arthr’ meaning articulating)
– Decreased intonation, low volume, variable speed of speech
14
Q
EPS (extrapyramidal symptoms)
A
-various movement disorders:
• Akathisia (restlessness)
• Muscular rigidity (bent over, “cogwheel rigidity”)
• Resting (pill-rolling) tremor
- Due to improper balance of neurotransmitters in BG
15
Q
Clinical picture of patient with Parkinson’s
A
- Sitting or standing with pill-rolling tremor
- Blank stare (decreased blink)
- Masked face
- Flexed (stooped) posture
- Paucity of movements
- Depression is common.
- Some experience apathy or psychotic sxs.
- Mood & cognitive sxs due to loss of neurons in locus coeruleus (NE), dorsal raphe nucleus (5-HT), nucleus basalis of Meynert (ACh), in addition to substantia nigra
- Depression in 40%-60%, but low suicide rate
- May have sensory sxs (e.g., pain).
- Mental deterioration, slowed cognition (bradyphrenia)
16
Q
Memory impairments resulting from Parkinsons
A
- Procedural memory – Ability to remember how to do procedures/tasks
- Working memory – Ability to remember information for 15-30 secs, which impairs pt’s ability to comprehend complex instructions or sentences
17
Q
Hyperkinetic Disturbances
A
- Disruption of chemical interactions within skeletomotor loop
- Results in increased excitation of thalamic neurons, which results in excessive stimulation of the cerebral cortex
18
Q
*Choreiform movements
A
Generalized irregular dance-like movements of limbs • Sydenham’s chorea • Chorea gravidarum • Huntington’s disease • Part of tardive dyskinesia
19
Q
*Sydenham’s chorea (St. Vitus’ dance)
A
- Most common cause of chorea
- Occurs primarily in females, typically after a bout of rheumatic fever
- Know this something about attacking antigen… there are jerky dance like movements.
20
Q
Athetoid movements
A
Continuous writhing of distal portions of extremity
• Huntington’s disease
• Sometimes in treated Parkinson’s disease
• Part of tardive dyskinesia
21
Q
Huntington’s chorea
A
- Inherited disease causing abnormality in BG, which leads to over-stimulation of frontal cortex, resulting in choreiform & athetoid movements
- Progressive, untreatable, autosomal dominant defect on short arm of chromosome 4
- Defective executive loop and cortical atrophy in temporal & frontal lobes causes cognitive deficits.
22
Q
Huntington’s & cognitive dysfunction
A
- Attention
- Slowed processing
- Defective retrieval primarily due to lack of organization
- Decreased verbal fluency and speech
- Visuospatial dysfunction
- Thinking, reasoning problems
- Executive dsysfunction
23
Q
Huntington’s & psychiatric symptoms
A
- Depression is the most common sx; high suicide rate
* May experience mania or hypomania, anxiety, emotional lability, irritability, aggressiveness, apathy late in disease
24
Q
Tardive dyskinesia
A
- a disorder resulting in involuntary, repetitive body movements. In this form of dyskinesia, the involuntary movements are tardive, meaning they have a slow or belated onset.
• Sxs may be temporary or permanent
• Caused by chronic Rx w/ antipsychotics, especially neuroleptics (typical antipsychotics)
25
Dystonia
- a neurological movement disorder, in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures
• Painful muscle spasms involving neck (spasmodic torticollis), back, eyes (oculogyric crisis), larynx (laryngospasm), hand (“writer’s cramp”), foot
26
Tourette’s syndrome (Gilles de la Tourette’s):
* Involuntary tics & involuntary movements
* Multiple motor tics accompanied by at least one vocal tic for a period of at least 1 year
* Excessive D2 activity in basal ganglia, especially right caudate
* May involve circuit including prefrontal cortex
27
Basal ganglia dysfunction (including loops including frontal cortex) may occur in:
* Attention-Deficit/Hyperactivity Disorder (ADHD) - Sxs of inattention, executive disinhibition, hyperactivity
* Schizophrenia
* OCD
* Depression
* Autistic spectrum disorder.
* Anergia (apathy) aka emotional flattening may occur w/ BG lesions.
* Lateralization may occur (e.g., aphasia & depression w/ left-sided lesions)
28
Limbic System*
• *KNOW THAT THE LIMBIC STRUCTURE IS THAT MEMORY AND EMOTIONS SYSTEMS ARE CONNECTED TOGETHER> AND THAT THAT IS CALLED THE LIMBIC SYSTEM
```
Comprised of:
• Amygdala
• Hippocampus
• Mammillary bodies (of hypothalamus)
• Anterior thalamus
• Cingulate cortex
• Fornix (connects hippocampus & mammillary bodies)
```
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Structures of limbic system
* Subcortical & cortical structures encircle brainstem, thalamus, basal ganglia
* Subcortical portion involved with subconscious, fast responses to stimuli with positive or negative values
* Cortical portion mediates conscious feelings
* Important for survival of species, including motivation, emotion, memory
* Sometimes the brain will respond before the conscious does. Like they may start sweating, increased heart rate, etc when they experience fear, but before they realize that its happening.
30
Amygdala
* Learning emotional significance of stimuli, particularly with biological significance
* Presence of food, water, salt, mates, rivals
* Prosody & facial expressions (particularly fear, anger, sadness)
* Responding to innate fears & learning new fears (conditioning)
* The most important structure in brain for fear
* Anxiety disorders associated w/ hyperactive amygdala
* KNOW THIS SLIDE REALLY WELL. The amygdala is the most important structure in the brain for fears. Anxiety, and other anxiety disorders, will often show overactive amygdala. Amygdala coordinates/starts the “fear response” or basically the freeze response. Amygdala is pretty permanent, and may only take one trial learning at times. Like with PTSD pts, sometimes you can get them to lay down other tracks over the earlier ones, but they will still be there.
31
Emotional responses coordinated by the amygdala
* Autonomic & endocrine responses via output to hypothalamus, brainstem
* Defensive behavior via output to brainstem
* Conscious awareness via output to prefrontal cortex, cingulate cortex
32
Hippocampal Formation
* Critical for declarative long-term memory
| * Damage occurs in Alzheimer’s disease
33
Nucleus Accumbens (NA)
* Major role in craving, pleasure, addiction
* Brain response to natural reinforcers & recreational drugs associated with elevated levels of extracellular dopamine in NA
34
Considered the reinforcement pathway and involved in addictions:
Mesolimbic pathway from the ventral tegmental area (VTA) to the nucleus accumbens
35
The most important structure involved in fear conditioning:
Amygdala
36
Has a critical role in associating stimuli and forming long-term, explicit memories:
Hippocampus
37
Cerebral Cortex (Neocortex)
* Unique to mammals
* Higher levels of functioning involving perception, motor output, thinking, planning, language; and aspects of attention, memory, emotion
* Connected to all other parts of brain; so it s the ultimate creator of our reality
38
Brodmann’s Areas
• Broadmann was a neuropscientist who studied the architecture of the brain and then labeled those areas with numbers, each number designating certain function.
39
Posterior Lobes
Parietal, Temporal, Occipital Lobes
• When thinking of posterior lobes/areas, think of SENSATION. Or sensory information. So they receive, encode, and store sensory information.
* Primary sensory areas – Processing of “raw” somatosensory, visual, auditory stimuli; but no processing here, just the recognition that there is a light), and auditory. Note primary is just the recognition or reception
* Secondary association areas – Integrating information within a modality; where the actual processesing information occurs
* Multimodal areas (tertiary association) – integration across functions or modalities
40
Somatosensory area (S-I)
* Also called “sensorimotor cortex” includes sensory strip posterior to central sulcus (Rolandic Fissure)
* S-I allows for conscious perception of touch, proprioception (joint/muscle position), temperature, pain, itch
* Arise from specialized receptors that project along specific pathways to specific cortical neurons, which ultimately must integrate information into a single percept
* Allows for such skills as stereognosis (the recognition of an object by touch)
41
*Various parts of body are topographically represented by specific neurons within S-I such that...
• Areas of greater sensitivity & two-point discrimination (greater resolution) are processed by more neurons, a principle common to all sensory modalities
* Its details vary according to experience.
* Examples: Compared to each other, a soccer player has relatively more sensory neurons devoted to feet, and a pianist has relatively more neurons devoted to fingers
42
Pain
* Not just sensation, it’s sensation that’s processed in the brain and PERCEIVED like that by the brain.
* The brain creates the perception of pain
* Pain can vary dramatically in intensity & quality depending on individual, previous experience, context
43
Nociception*
* Activity of neurons within certain pathways in response to noxious stimuli
* Meaning, something is activating neurons that sends that nociception (that something is happening to tissue that is causing a problem) to the brain, which constructs percept that something is bad for you or that you are hurting
44
Pain involves what components processed by different parts of brain via different pathways
1. Purely sensory/discriminatory perception of location & intensity of pain
• Processed in S-I & related secondary association cortex
2. The immediate emotional response to pain (unpleasantness) that is processed by anterior cingulate, insula
• Critical for adding emotional, motivational, memory components to the experience
3. Long-term implications of chronic pain arising from integration of sensory, affective, & cognitive components
• Processed by the prefrontal cortex
45
Nociceptive pain vs neuropathic pain
* Nociceptive pain - Pain caused by actual or potential tissue damage
* Neuropathic pain - Pain caused by damage to or dysfunction of nervous system (e.g., diabetic neuropathy, fibromyalgia, pain during depression)
- Damaged peripheral axons fire or cause adjacent axons to fire excessively
- Central sensitization
46
Central sensitization
• Neurons in CNS develop increased synaptic efficiency & fire inappropriately, causing pain to non-noxious stimuli, excessive pain to noxious stimuli, or spontaneous pain
* Can occur at specific segments of spinal cord
* Diabetic neuropathy, phantom limb pain
* Can occur in brain w/ or w/o peripheral pathology
* Fibromyalgia, depression, anxiety, irritable bowel syndrome (IBS), headaches
47
Neuropathic pain may occur in:
* Affective disorders, where mood or anxiety predominate
* Functional somatic syndromes (e.g., fibromyalgia), where pain predominates
* All of these tend to share cognitive dysfunction, non-restorative sleep, fatigue; Suggests that these disorders lie on a spectrum with common neuropathologies
48
Pain begets pain*
• CHRONIC PAIN MAY CAUSE FURTHER PAIN DAMAGE AND MAY INVOLVE EMOTION, COGNITION, SLEEP AND ENERGY.
- In a vicious cycle meaning that the depression makes the person more sensitive to pain, and that it then gets worse.
**With every instance of X (pain, or psychotic breaks, or xxx), if left untreated, lowers the threshold and will likely beget further pain. And it grows. And then you are more likely to get it again with each occurrence. This is explained by the central sensitization hypothesis.**
49
Moral of pain slides =
Treat pain and affective, cognitive, & vegetative symptoms as soon & as aggressively as possible to avoid sensitization & pathological vicious cycles.
• If severe chronic pain, use integrated multidisciplinary team.
50
The closer 2 points on the skin are from each other, the more difficult it becomes for the brain to differentiate one from another. To accomplish this, the somatosensory area uses:
- More neurons devoted to that skin area
51
The term “neuropathic pain” only refers to pain caused by damage to peripheral nerves (T/F)
False; b/c you can have fibro, depression, etc.
52
Visual Perception
An active, creative, constructive process that transforms transient light patterns on retina into stable, coherent percepts that are affected by prior experience and other brain modules.
• Accomplished by a “binding mechanism.”
• Such synthesis or binding does not appear to be accomplished in one place but rather all along and between the two pathways.
* Selective attention affects how this synthesis takes place in that certain features or spatial locations become “more important.”
* This attentional aspect of consciousness and the “binding problem” are considered to be among the most complex problems facing neuroscience.
53
Visual Perception in Occipital Lobe
• Primary visual cortex
| • Initial parts of association visual cortex
remaining parts are in parietal, temporal lobes
54
Visual Perception in Temporal Lobe
* Perception of objects, faces, color
| * Ventral stream from occipital to inferior/ventral temporal lobe processes object recognition (the “what” of vision)
55
Visual Perception in Parietal Lobe
* Perception of location, depth, stereopsis
* Dorsal stream from occipital to parietal lobe to guide movements (the “how” of vision)
• Parietal lobe is critical for selective (focused) attention
•
56
Selective attention
-The process by which a person can selectively pick out one message from a mixture of messages occurring simultaneously
* Focusing on “target” stimulus & avoiding distractors
* Bottom-up processes may bias attention by salient features of stimuli.
* Top-down processes from cortex helps to avoid distractions.
* It quiets noise so to speak and works as a spotlight, highlighting certain things.
57
*Agnosia
– “Lack of knowledge” due to perceptual deficit w/ intact sensation
• Gnosia- is greek for knowledge… a is lack of something. So there is intact sensation. Eye is fine optic nerve is fine, pathway is fine…its something more complex. And that’s where neuropsychologists come in.
58
*Apperceptive visual agnosia
– Lack of integration of normally perceived elements
• They can perceive the pieces, but they can’t integrate it and make sense of it.
59
Associative visual agnosia
– Normal perception w/o recognition due to defective memory or pathways to memory modules
• Can be quite specific
60
*Prosopagnosia
Inability to recognize familiar faces due to inability to disambiguate individual stimuli
• Usually not confined to faces
• Usually due to bilateral lesions in occipitotemporal cortex & white matter
• Usually can recognize facial expressions of emotion and “gross” features (e.g., gait, sex)
• They cant ambiguate between different stimuli….
• So they may be able to recognize the gate of the person or the voice of the person… but not the face. Ex is the man who mistook his wife’s face for a hat
61
If a tree falls in the woods with no one there, does it make sound?
• No. Sound is a product (a percept) of the brain.
62
Temporal Cortex
• Primary auditory cortex (Heschl’s gyrus, tucked within Sylvian fissure)
63
Pure word deafness
– Inability to comprehend spoken words, usually w/ left-hemisphere lesions
64
Auditory agnosia
– Inability to comprehend non-speech sounds, usually w/ right-hemisphere lesions
65
*Aphasia
- From ancient Greek aphatos meaning "speechlessness", derived from phat meaning "spoken"
- A disturbance of the comprehension and formulation of language
• It is difficulty with language, and it is ACQUIRED. You have a hard time comprehending the content of language, or what somebody is saying, or what the written word is. They can’t make sense. It may interrupt the syntax of what someone is saying (or the structure of how they are saying it) and the lexicon (or the meaning of words so words they’re using to create meaning). Also can disrupt phonemes (smaller parts to make up words). Like they can’t comprehend a word with two syllables (like understand the word “together”) or the boy was bit by the dog- who bit the boy? (they can’t answer this question?)’ people may be frequently misdiagnosed with schizophrenia b/c they can’t verbalize a response, when in fact, they are aphasic. They may be confused with being catatonic. Or if they are making word salad, they may be misdiagnosed there as schizophrenic as well.
66
Wernicke’s (receptive, sensory, fluent) aphasia
• Difficulty comprehending verbal content of language
67
3 major problems associated with Wernicke's aphasia
1) Impairment in categorization of sounds, or phonemic recognition
2) Impairment in speech, secondary to confusing phonetic characteristics
a. Motor systems are only as good as sensory systems that provide data on which motor systems rely.
3) Impairment in writing secondary to not knowing graphemes (pictorial representation of phonemes) that combine to form a word.
a. Patients also frequently experience apraxia (difficulty making movements), which extend beyond mere writing.
68
*Anomia
– Loss of naming ability, usually w/ left-hemisphere lesions
• Anomic aphasia – “pure” anomia, usually w/ left inferotemporal or anterior temporal lesions
• Different areas of temporal lobes are specialized for specific categories of nouns.
• Loss of retrieval of verbs w/ left premotor/prefrontal lesions
• *The main thing is to know the anomia term. Boston naming test is one of the best tests to look for anomia. So is it a visual perceptual issue or a naming issue. Anomia is one of the first issues to appear, and its one of the last things to repair or reappear after rehab.
69
*Receptive dysprosody
Difficulty comprehending emotion, intonation, inflection in language
• Usually from lesions in area homologous to Wernicke’s area in right hemisphere.
• Pt often experiences social, interpersonal difficulties due to failure to pick up subtle inflections and cues from others.
• Impaired recognition of facial expressions of emotion w/ right-hemisphere lesions (also w/ dysfunction of amygdala)
• Difficult comprehending the emotion, intonation, and inflection of language. Homologous is a way of saying the same basic area but in the opposite hemisphere.
• They are constantly misunderstanding what the other people are trying to express.
70
Music
* Primarily in right hemisphere, where prosody is processed
| * Prosody includes variations in loudness, pitch, timbre, & rhythm, the very properties by which musical sounds differ.
71
Temporal Lobe Deficits
* Explicit memory deficits, especially w/ lesions in hippocampal formation in medial area
* Left for verbal, right for nonverbal (e.g., faces, spatial information, melodies)
* Involved in forming, maintaining, & retrieving new and fairly recent memories
72
Sensory Integration
* Sensory integration of somatosensory, auditory, visual information
* Generates knowledge - Understanding of meaning & relationships among recognized sensory inputs
* Sends to frontal lobes for “final” integration with limbic input
* In short, higher level of abstraction starts here.
* Einstein had more grey matter here.
73
Acalculia
– Loss of math ability
74
Alexia
– Loss of reading ability
75
Dyslexia
• Usually refers to a developmental deficit
76
*Apraxia
-From the Greek root word praxis, for an act, work, or deed, preceded by a privative a, meaning without
– Loss of skilled or purposeful movement in absence of muscular weakness/paralysis, sensory loss, poor motivation, intellectual deterioration, poor comprehension, or other movement disorders such as tremor
• Especially an inability to make proper use of an object
77
Ideomotor apraxia
– Inability to perform or copy motor acts on command that can be done spontaneously
* Pt seems to have some idea of what to do but cannot execute it properly.
* Example: When requested to demonstrate how she would comb her hair, patient might stroke her face or hit her head with her hand.
78
Agraphia
– Loss of writing ability
79
That a movement disorder can occur with lesions in “sensory integration” area makes important point:
* Frontal lobe (responsible for formulating, elaborating, & executing motor acts) must have precise, highly integrated knowledge before acting
* Otherwise, “garbage in, garbage out.”
* *KNOW THIS people often confuse and make mistake on this.
80
*Constructional apraxia
• Difficulty drawing or constructing 2- or 3-dimensional figures or shapes from 1- or 2-dimensional units
81
*Anosagnosia
– Loss of awareness of deficits (physical & cognitive)
o THIS IS A TEST QUESTION. - likely something like “will have difficulty in getting them to participate in rehab” for the question.
82
Patients with Wernicke’s aphasia:
**B. Have difficulty comprehending language but may also speak w/ “word salad,” which makes little sense.**
83
Loss of awareness of one’s own deficits is called
• Anosagnosia
