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191 Cards in this Set
- Front
- Back
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Olfactory Nerve
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Cranial Nerve I
Sensory, smell Enter cribriform plate, go to olfactory bulbs, olfactory tracts Part of limbic system |
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Optic Nerve
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Cranial Nerve II
Transmits visual information from retina to brain |
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Oculomotor System Nerves (Cranial Nerves III, IV, & V)
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Oculomotor, Trochlear, Abducens
System that controls eye muscles |
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Oculomotor nerve
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Cranial Nerve III
all muscles of orbit, parasympathetic innervation for pupillary constriction |
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Trochlear Nerve
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Cranial Nerve IV
innervates superior oblique muscle, depresses eye and rotates inward. |
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What's special about the trochlear nerve?
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Only nerve that exits the brain stem posteriorly
Only nerve that decussates |
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Abducens
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Cranial Nerve V
contracts lateral rectus muscle, moves globe laterally |
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Trigeminal Nerve
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Cranial Nerve VI
Mixed (sensory and motor) Motor root and trigeminal ganglion (sensory) Branches of trigeminal ganglion: a. Eyes (opthalamic): innervates orbit, nose, forehead, scalp b. Maxillary: innervates skin over cheek, upper portion of oral cavity c. Mandibular: innervates skin over jaw, area above ear, lower part of oral cavity Motor component: chewing, mastication |
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Facial Nerve
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Cranial Nerve VII
mixed, primarily motor Motor root: muscles of face, ear, neck, eyelids, and facial expression. Sensory root: taste from anterior 2/3 of tongue |
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Damage to facial nerve
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Bell’s Palsy. caused by viral infections, flaccid paralysis on one side of the face, droopy. Ptosis: eyelids cannot open, droopy
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Vestibulocochlear Nerve
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Cranial Nerve VIII
sensory Vestibular ganglion, relay sensation of angular and linear acceleration Cochlear ganglion relay information concerning sound |
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Glossopharyngeal Nerve
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Cranial Nerve IX
mixed, taste, back of tongue, sensation from throat and upper respiratory tract |
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Vagus Nerve
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Cranial Nerve X
mixed, visceral information from thoracic and abdominal organs. |
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Spinal Accessory Nerve
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Cranial Nerve XI
purely motor. Extension of spinal cord, neck and upper shoulders, helps us move our head. |
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Hypoglossal Nerve
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Cranial Nerve VII
motor, allows you to move tongue |
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Brain stem nuclei (Cranial nerves)
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Nerves have nuclei in brain stem
Sensory nuclei are lateral, motor are medial. •Motor: nuclei are where nerves come out •Sensory: nuclei are where nerves come in |
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Differences between brain stem and spinal cord
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•Sensory tracts that run along the outside of spinal cord, in brain stem travel in the interior
•System of fibers from cerebral cortex doesn't exist in spinal cord Anterior portion of the brain stem is not a continuation of the spinal cord, fibers coming from cortex Posterior is where the motor information is coming down and it is a continuation of the spinal cord |
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Reticular Formation/Reticular Activating System
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At the center of the brain stem, particularly at upper levels (pons, midbrain).
Two primary functions: control of vital functions and arousal. Damaged = coma (means this system is influencing/activating thalamus and cortex) |
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Pacemaker cells
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Control breathing, heartbeat. Rhythmically fire. Hypothalamus tells faster or slower but rhythmic activity is natural, work even after CNS control gone
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Brain stem nuclei: Locus Ceruleus
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Produce norepinephrine
Thought that norepinephrine part of attention network |
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Brain stem nuclei: Raphe Nuclei
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Produce serotonin
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Brain stem nuclei: Mammillary bodies
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Produce histamine
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Brain stem nuclei: Ventral tegmental area
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Produce dopamine
Projects to nucleus accumbens to thalamus to cortex and directly to cortex |
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Acetylcholine & arousal
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Produced by nuclei in brain stem and in basal forebrain. Connected, project to thalamus. Basal forebrain projcets to entire cerebral cortex. When these neurons are active, whole cortex is active.
Neurons in basal forebrain involved in paying attention to outside world, focusing attention of cerebral cortex. |
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How do nuclei modulate attention (basic mechanisms of attention)
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Nuclei diffusely send out axons into cerebral cortex or through thalamus. Not a channel of information. Modulate activity of other areas, say fire more or fire less. The whole cerebral cortex is ready to respond or muted
Neurotransmitters of Reticular Activating System regulate cortical activity by altering firing of thalamic neurons. |
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Voluntary attention
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Higher order, but helped by arousal systems. Closely linked to saccades.
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Involuntary attention
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Something in environment automatically pay attention to it, i.e. loud noise
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Higher-order control of attention
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1. Vision main system that allows us to pay attention. Focus eyes on object of attention, look at directly, image on fovea, visual acuity, cones concentrated so you see exactly what object is. Saccades allow us to shift attention
2. Parietal cortex, where pathway, cells in parietal cortex active when we pay attention and when we intend to pay attention |
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Saccades
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Redirect center of sight in visual field. Areas of interest are fixated more frequently, background objects ignored.
•Shifting eyes: involve oculomotor system •Saccades generated in superior colliculus in brain stem, go to thalamus, then frontal eye fields (premotor) |
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Components of attention
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Sensory component of attention (see)
Motor component (react) Emotional component (cingulate cortex) |
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Neglect
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Deficit where we will not pay attention. Can manifest in many different ways.
•Person writing on page and ignores left side •Dressing, not paying attention to one side of body (motor) •Cannot process emotions on one side (emotional) •Not caring about one part of space vs. another (sensory) Representation of space in the brain in the where pathway (parietal cortex). Damaged = neglect |
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On which side do we usually see neglect? Why?
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Usually seen in left side. Right hemisphere damage.
Right side controls both left and right, redundant Left side controls right side only. If damaged, still some control from right hemisphere. |
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Systems needed for attention
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•Inferior parietal cortex: visual system, integration of sensory information
•Anterior cingulate: emotional aspect •Frontal eye fields: motor component, pursuit of eye movement, saccades |
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Saccadic Masking
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Image is not blurred during saccade.
The rapid movement of the eye over the scene produces a blurred, low-contrast image that is masked by the stable, high-contrast images before and after the saccade. |
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Neurotransmitters and sleep
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•Cholinergic & monoaminergic neurons linked to sleep-wake cycle, induce arousal by activating cortical neurons
•REM-OFF cells: fire in anticipation of and during waking state, decrease ahead of REM sleep (monoaminergic, histamatergic) •REM-ON cells: cholinergic, discharge in anticipation of and during REM sleep, thought to induce REM |
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What controls circadian rhythm and how?
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•Controlled by suprachiasmic nucleus, part of hypothalamus
•Secretes transcription factors, allow DNA to be produced into RNA, make proteins •Through endocrine system controls cycles |
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Ultradian rhythm
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rhythmic appearance of different stages of sleep
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Sleep stage 1
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Transition between sleeping and waking, some alpha waves
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Sleep stage 2/3
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high amplitude waves start appearing, spindles (movement of muscles)
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Sleep stage 4
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very high amplitude, low frequency waves (delta)
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EEG during sleep
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•EEG during wakefulness: beta waves
•EEG when close eyes, relaxing: alpha waves •Falling asleep: EEG gradually gets slower, amplitudes get larger. |
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REM
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Rapid eye movement. Wave resembles wakefulness the most, muscle tone lowest (inhibition of spinal motor neurons, motor neurons in brain stem that control eye movement not inhibited). When person woken up, report dreams.
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REM dreams
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Longer, primarily visual. Emotional. Nightmares. Bizarre, not directly related to everyday activities.
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Non-REM dreams
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shorter, less visual, less emotional, more conceptual, usually related to everyday life.
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Insomnia
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General cause not physiological, usually related to stress, emotional. Inability to sleep.
Treatments: Benzos. Increase release of GABA. Inhibitory. Shuts down cortex. |
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Apnea
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Stop breathing, wake up, cyclic depravation of oxygen, can cause cardiac problem. Two types.
-Obstructive sleep apnea: collapse of muscles in back of throat, back-pressure opens up throat -Central sleep apnea: mediated by CNS, much harder to treat. Happens more during REM sleep |
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Narcolepsy
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abnormal activation of sleep inducing system
-No voluntary component -Cataplexy: inability to move, loss of muscle tone -Sleep attacks: suddenly fall asleep -Hypnogogic hallucinations: dream-like episodes while awake -Excessive daytime sleepiness -Sleep paralysis: inability to talk or move while waking Treatment: stimulants/amphetamines for sleepiness and sleep attacks. Cataplexy treated with antidepressants, inhibit sleep. |
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Parasomnias
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Sleep walking
Sleep talking (Non-REM) Night terrors |
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Properties of primary sensory areas of cortex
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•Input from thalamic sensory relay nuclei
•Neurons small receptive fields, arranged in somatotopic map of sensory receptor surface •Injury to a part of the map causes a simple sensory loss combined to corresponding part of contralateral sensory receptor surface •Connections to other cortical areas limited, confined to nearby areas that process information in the same modality |
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Multimodal areas (where are they)
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•Prefrontal cortex
•Inferior parietal cortex •Inferior temporal gyrus, middle temporal gyrus |
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Dorsal Pathway
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Parietal cortex to frontal cortex
Integrates somatosensory, visual, auditory to know where things are in space, important for motor functioning, intimately connected with motor and premotor cortex |
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Ventral pathway
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Temporal cortex to frontal cortex
recognition system, know what objects are, facial recognition (inferior temporal gyrus,fusiform cortex) |
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Cognitive function of parietal cortex
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Sensory guidance of motor behavior and spatial awareness
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Superior parietal cortex lesions (list symptoms)
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•Asomatoagnosia
•Ideomotor apraxia •Optic ataxia Close to somatosensory area, motor functions Manipulation of space |
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Asomatoagnosia
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Foreign limb syndrome: cannot recognize own limb
Deficit in awareness of one's own body |
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Ideomotor Apraxia
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Cognitive difficulty performing movement, not paralysis, deficit responding to commands to move (i.e. tell someone to wave their hand, they cannot, cannot imitate, but they can spontaneously wave)
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Optic ataxia
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Sensory problem, cannot coordinate movements to try to grab something when it is visually guided, can do this in the dark. Reaching difficulty for objects not in center of vision.
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Inferior parietal cortex lesion (list symptoms)
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Neglect
Constructional Apraxia Close to visual area, spatial functions |
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Constructional Apraxia
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Problem with integration of components that make up a visual image
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Apraxia
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inability to perform something
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Ataxia
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inability to coordinate movement to accomplish something
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Other problems association with parietal lobe damage (list & define)
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Acalculia: inability to calculate
Agraphia: inability to write Alexia: inability to read |
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Cognitive function of temporal lobe
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Recognition of sensory stimuli and storage of semantic knowledge
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Lesion of temporal lobe (list symptoms)
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Agnosia: inability to recognize something
Prosopagnosia Object agnosia Semantic dementia |
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Prospoagnosia
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inability to recognize faces, lesion of inferior temporal gyrus (fusiform gyrus)
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Semantic dementia
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meanings are lost for objects and words, anterior temporal lobe
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Cognitive function of frontal lobe
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organizing behavior and working memory
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Dorsolateral prefrontal cortex (functions)
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Cognitive control of motor behavior
•Planning/Executing motor activity •Executive function •Working memory |
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Damage to dorsolateral prefrontal cortex
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Difficulty planning and executing, deficits on Wisconsin Card Sorting Task
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Cognitive functions of orbitofrontal cortex (functions)
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Social emotions, morals
Goal-directed behavior, decision-making, value of anticipated rewards. Emotional control of behavior |
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Damage to orbitofrontal cortex
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Sociopathy, disengagement, apathy
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Phineas Gage
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Lesion of left frontal lobe
apathetic, couldn't complete list tasks i.e. grocery shopping |
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Cognitive functions of limbic lobe
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Emotional aspects of cognition
Medial temporal lobe: memory, amygdala (fear conditioning), Entorhinal cortex, hippocampus (Storage and retrieval of declarative memory) |
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Supplementary and Premotor Cortex (functions)
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Context
Rules of movement Executing motor movements. Sends input into spinal cord. Coordination Active not just during movement, but before movement Delayed parts of learning processes (i.e. when organism must wait to respond, active during delay). Considering/integration emotional aspects |
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Subcortical areas involved in cognitive motor system
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Initiating movement: basal ganglia
Planning: cerebellum Provide feedback for the smooth execution of skilled movements, important for motor learning. Store memory for unconscious motor skills. |
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Parietal cortex and cognition in the premotor system
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Premotor cortex has reciprocal connections with association areas in posterior parietal cortex.
Need to know where things are. Potential for action |
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Potential for action
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Aspects of visual stimuli that are useful for action are analyzed in dorsal stream (Parietal cortex). Process properties of object that allow one to interact with it. Information sent to premotor neurons that encode potential motor acts. Select act based on meaning of object and individual’s intention. Suppress some actions and release others.
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Utilization Behavior Syndrome
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Instead of grabbing appropriate object, person grabs anything in environment, cannot suppress activity that is not useful.
Dysfunction of parietal/prefrontal cortex that are involved in potential for action |
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Mirror Neurons
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Involved in understanding/empathizing/imitating
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Language network
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Basal ganglia (caudate nucleus)
Broca’s area: inferior frontal Wernicke’s area: temporal/inferior parietal, left posterior and superior temporal cortex Posterior and inferior frontal cortex •Posterior: primary motor cortex •Ventral, anterior (base of motor cortex), represents tongue, larynx, pharynx, right in front of there is language area, tells tongue what to do and larynx and pharynx make sound Superior temporal gyrus, posterior aspects (temporoparietal junction) General aspects of temporal lobe itself |
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Two components of language function
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•Spoken, written words, grammar, meaning
•Prosody (intonation, emotional aspects, facial expressions, emphasizing) |
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Language and hemispheric dominance
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•Left: phonetic, grammar, words, sentence processing
•Right: prosody, emotional changes in pitch, helps convey speaker’s mood and intentions, interpret sentence meaning •Exception: some left-handed individuals have language on right |
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Prosody
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•Emotional component, tone of voice can impart emotional content (in right hemisphere)
•Semantic component, emphasizing meaning (left hemisphere) i.e. same word can have diff meaning depending on how you say it |
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Bilinguals
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•If you learn 2 languages as an adult, areas in left hemisphere that are next to each other active for each language
•In child: same exact areas active for both languages •Learning a native language produces a neural commitment to detection of the acoustic patterns of that language, interferes with later learning of a second language. Early in life, two or more languages can be easily learned because interference effects are minimal until neural patterns are well established |
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Language implementation areas
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Grammar, producing words, analyze incoming information through auditory system, comprehension
•Broca’s and Wernicke’s areas •basal ganglia, insular cortex |
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Mediational areas
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•Parietal, temporal, frontal association areas: support other aspects of language
•Not directly involved in production •Damage: can use language properly, but conceptual process lost, lose connection between language and thought (ideas/concepts) |
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Broca's Aphasia
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Problems:
•Speech production •Grammatical processing •Labored and slow speech •Articulation •Intonation •Repetition •Nouns are correct, but prepositions and conjunctions are poorly selected or missing altogether. Damage: •Broca’s area (inferior frontal gyrus) •Surrounding frontal fields •Underlying white matter •Insula •Basal ganglia •Anterior superior temporal gyrus |
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Wernicke's Aphasia
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Problems:
•Content of speech •Selecting words based on meaning •Comprehending sentences •Add/subtract sounds to words Speech is effortless, melodic, and produced at a normal rate. Damage: •Left posterior temporal lobe structures (auditory association cortex) |
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Conduction Aphasia
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Problems:
•Repeating •Assembling phonemes •Naming pictures and objects Preserved: •Comprehend simple sentences •Produce intelligible speech Damage: •Disrupting connection between Broca’s and Wernicke’s area. •Left STG •Inferior parietal lobe. •Can extend to left primary auditory cortex, insula, and underlying white matter. |
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Lesion of Caudate Nucleus
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Production aphasias (Broca's)
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Global Aphasia
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Problem:
•Comprehending language •Formulating sentences •Repeating •Speech reduced to a few words at best Preserved: •Nondeliberate speech i.e. routines such as counting or reciting days of the week, sing previously learned lyrics. Damage: •Widespread damage •Stroke in region supplied by middle cerebral artery |
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Transcortical Aphasia
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Damage to mediational areas
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Dorsolateral prefrontal cortex lesion (language)
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Problem:
•Motor problem, production lost Preserved: •Repeating (put concept in mind, can say it) |
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Cranial nerve damage (language)
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Problem:
•Paralysis of muscles, not same as aphasia can produce language but slurred |
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Working memory
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Short-term memory. Maintains current, transient representations of goal-relevant knowledge
Prefrontal cortex maintains a working memory |
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Verbal working memory (and areas involved)
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Rehearsal: Broca’s area
Phonological storage: posterior parietal cortex |
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Visuospatial working memory (and areas involved)
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retains mental images of visual objects and of the locations of objects in space
Frontal, premotor cortex |
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HM: what were his problems and what can we learn from them?
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Seizures. Removed medial aspects of temporal lobe. Hippocampus, amygdala, parahippocampal gyrus.
-Couldn’t form long-term memories, anterograde (after surgery). Know hippocampus involved in long-term storage -Long-term memory intact (childhood memories). Know memory not stored in hippocampus -Normal working memory (medial temporal lobe not necessary for WM) -Implicit memory intact (mirror drawing). Know Hippocampus not involved in storage of implicit memory |
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Explicit/Declarative Memory
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Two types:
•Episodic •Semantic Involves medial temporal lobe |
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Episodic Memory
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Time-dependent, biographical, memory of personal experiences.
Involves: dorsolateral prefrontal cortex, connections between hippocampus and DL prefrontal cortex important in storing episodic memory. Not site of memory storage, it is distributed, depends on aspect of memory you are recalling. |
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Semantic Memory
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facts
stored in distinct association cortices and retrieval depends on the prefrontal cortex |
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Implicit Memory
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Not conscious, don’t need to pay attention to it for it to happen, not hippocampal-dependent. Tightly connected to initial conditions under which it occurred.
Priming, skill learning, habit memory, conditioning. Involves: basal-ganglia, cerebellum, neocortex (premotor/motor cortex, parietal cortex) Classical conditioning: cerebellum crucial (association of stimulus of response), vermis (spinocerebellum) |
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Medial temporal lobe structures important for memory storage
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•Entorhinal: object memory
•Hippocampus: -Right: spatial memory -Left: verbal memory •Perirhinal cortex: object recognition •Parahippocampal cortex •Amygdala |
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Habituation (Aplysia experiment)
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Stimulus initially evokes a response, after continued exposure, system won’t respond anymore.
Caused by synaptic depression Touch gill of Aplysia, siphon empties. After repetition, habituation. |
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Synaptic depression
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Presynaptic neuron stimulated, undergoes changes that make it not release transmitter the same way it used to.
For Aplysia, sensory neuron releases less glutamate, less activation of motor system. Synaptic inhibition, number of synapses decreases. |
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Sensitization
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Synaptic activity enhanced. Number of synapses increases.
If one delivers a shock to Aplysia, it will release water (siphon reflex) but now even a much milder stimulus (touch) will result in exaggerated response. |
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Cellular basis of memory formation. What is necessary?
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Continued habituation/sensitization attains a certain degree of permanence and this permanence = storage. For long-term memories to be formed there has to be some type of structural change (which requires proteins).
Gene activation and protein production required for long-term memory formation. |
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Epigenetics
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Something in environment cause gene to be expressed in a permanent fashion. Cause protein to be made on a more permanent basis.
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Long Term Potentiation
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Equivalent of sensitization but more permanent
Need high frequency stimulation in presynaptic neuron, few repetitions. Enhanced response of postsynaptic neuron. |
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Long Term Depression
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Equivalent of habituation. Decrease in number of synaptic contacts between sensory and motor neurons.
Decrease response in postsynaptic neuron, need lower frequency stimulation but prolonged repetition |
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Aversive conditioning (cellular basis)
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Long-term potentiation in amygdala
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Habit formation (cellular basis)
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Long-term potentiation in basal ganglia/striatum
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Cellular basis of working memory
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Prefrontal cortical neurons respond in a sustained manner during working memory formation. Neurons normally cannot have sustained activity, which means when they are stimulated they respond with a short burst of activity. During WM same neurons show depolarization in a sustained manner, which means they continue to fire action potentials
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Neurotransmitters involved in working memory
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Reticular activating system: ACh that projects to prefrontal cortex makes cells more responsive (alerts system, allows activity tot take place). ACh helps here to sustain activity of these neurons during WM.
Enhancement of glutamatergic neurons or inhibition of GABAergic neurons |
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Explicit memories and hippocampus
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Amon’s horn
Stores memories through long-term potentiation & long-term depression |
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Glutamate and Long-term memory
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Either released directly (potentiation) or through secondary mechanisms (more calcium channels active, more NT released)
NMDA: glutamate receptor, antagonists = no long-term memory. Knock out genes that make receptors = no long-term memory |
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Spatial memory
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Resides in hippocampus. Learning about space, where things are supposed to be. Hippocampus has a representation of external world. Depends on glutamate, long-term potentiation.
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Schizophrenia: positive symptoms
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Things that are added, behavior people w/o disorder do not exhibit
•Hallucinations •Delusions |
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Schizophrenia: negative symptoms
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Something people w/o disorder have, but is suppressed in schizophrenia
•Flattened affect •Lack of motivation •Social withdrawal •Impoverished content of thought and speech |
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Schizophrenia: cognitive symptoms
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•Slow cognitive processing
•Memory problems (working memory) •Disorganization of executive functions •Cannot organize life (ADLs) •Disorganized symptoms •Also found in relatives •Not treatable by medications |
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Prodromal Symptoms
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Occur before onset
Negative symptoms |
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Twin/Adoption studies of schizophrenia
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Twin studies suggest genetic, but not 100% in identical twins so must be environmental factors
Adopted individuals: more like biological family, family may have schizoid symptoms First degree relatives highest risk, risk decreases as you get further away (i.e. second, third degree) |
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Genetic Mutations (two types)
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Mutations to single nucleotides, rare in schizophrenia
Duplications/translocations |
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Genetic mutations in schizophrenia
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Translocation b/w 1 and 11: DISC (dysfunction in schizophrenia gene), causes schizophrenia.
Studied family. Everyone who had mutations, had SOME kind of mental illness, but not necessarily schizophrenia Maybe basic building blocks of disorder are genetic, but interaction with environment plays a role in manifestation |
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MRI studies of schizophrenia: what is abnormality in structure?
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Thinning of the gray matter. NOT a white matter problem. Loss of volume.
Enlarged ventricles Gyri thinner, sulci wider |
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Schizophrenia: Where is loss of gray matter volume? What problems does this cause?
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•Prefrontal cortex: working memory, EF problems
•Temporal: superior temporal gyrus, auditory hallucinations •Hippocampus, amygdala: memory, emotion problems (integration of cognitive processing and emotional processing) •Temporal pole: paralimbic |
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Schizophrenia: What causes thinning of gray matter?
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Not neuronal loss, density of cells per unit area higher. Loss of synapses. Dendrites are not loss, but less dendritic spines (where synapses form).
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fMRI studies of schizophrenia
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Less activation in prefrontal cortex, particularly in more anterior sections
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What is problem with thalamus in schizophrenia?
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less cell bodies, mediodorsal nucleus (input from medial temporal lobe)
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Synaptic pruning: what is it and why is it important in schizophrenia?
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Everything developed in access, then pruned away, part of normal development, synapses lost but myelin and white matter grow.
Accelerated synaptic pruning in schizophrenia. Some types of dopaminergic receptors also reduced significantly. D1 receptor decreased in prefrontal cortex, correlates with loss of working memory in schizophrenic patients |
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Schizophrenia treatment: Antipsychotics
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Tranquilizers initially, get rid of positive symptoms
Side effects: Parkinsonian symptoms (rigidity). Tardive Dyskinesia (like Huntingtons’ uncontrollable movements, face/mouth, tongue). How do they work? Dopamine receptor antagonists. D2 primarily blocked. D1 lost in schizophrenia. Glutamatergic system: Antagonist of NMDA (ketamine): produce psychosis |
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How are mood disorders related to anxiety?
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•Stress
•Areas of brain involved have a lot in common |
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Secondary mood disorders
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caused by other disorders, medications (i.e. dementia)
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Symptoms of mood disorders
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•Primary related to mood: anguish (anxiety), apathy (lack of interest), negative feelings, anhedonia
•Secondary symptoms: sleep disturbance, appetite loss •Behavioral symptoms: psychomotor retardation/agitation, irritability •Cognitive: difficulty concentrating (attention), slow thinking, poor memory •Psychotic symptoms: only in severe cases, hallucinations most common |
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Mania
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Euphoria, racing thoughts, grandiose ideation, excessive energy
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Genetic factors in mood disorders
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•Similar evidence as for schizophrenia, but not as complete
•Bipolar stronger genetic component •Higher risk in relatives, multi-gene complex (probably) |
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Neuroimaging studies in mood disorders: what is the problem (general)?
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Not thinning of cortex, but activation is abnormal
Primarily problems with amygdala and cingulate cortex and their connections |
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Cingulate cortex in mood disorders
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•Subgenual: depression of activity in depressed patients correlates with outcome of antidepressants (less activity, more likely antidepressants work)
Connections: •Anterior cingulate cortex (genu, bending of corpus callosum), connected to amygdala, hippocampus, prefrontal cortex, connection with other paralimbic areas (orbitofrontal cortex, insula) |
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Amygdala in mood disorders
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Larger in depressed patients
Dorsolateral prefrontal: connection to amygdala through thalamus, shows abnormal activity |
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Hypothalamic-pituitary-adrenal axis (HPA axis)
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Hypothalamus controls whole endocrine system through pituitary gland
•Releases factors into pituitary so pituitary will release something •CRF: corticotropin releasing factor, in turn pituitary releases ACTH (adrenocorticotropin hormone) affects adrenal cortex to release glucocorticoids (stress hormones), increase sympathetic activity •Feedback: too much of a hormone, less produced and released |
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HPA axis in mood disorders
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•No negative feedback from glucocorticoids in depression
•Organism under chronic stress •Glucocorticoids have strong effects in medial temporal lobe How do we know? •Dexamethasone: injections should have negative effects, stop making CRF and ACTH •Can inject, if feedback working, response should decrease, but deficient in depressed patients |
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SSRIs
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inhibit the reuptake of serotonin, stays in synapse, enhance synaptic activity, more serotonin available at synapse, does not affect receptors
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MAOIs
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MAOs degrade monoamines, inhibit this degradation, more monoamines available. Effects on norepinephrine and serotonin are important.
•Bad side effects: peripheral effects, increase norepinephrine in periphery, increase blood pressure/sympathetic activity. Need dietary control |
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Tricyclics
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Inhibit serotonin and norepinephrine transporters, type of receptors, take across the membrane, drugs block, but also block other receptors that then cause side effects. Some cholinergic and histaminergic receptors. Drowsiness, dry mouth, urinary retention, extrapyramidal
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What neurotransmitters are involved in depression?
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Norepinephrine, serotonin
How do we know? Resperine: destroys stores of monoamines, depletes them, leads to depression in humans |
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Problem with monoamine theory of depression
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1. Medication doesn’t help everybody
2. Delay before clinical improvement seen, why isn’t one dose enough? Nothing known about delay, may not be direct effects. Controversial theory: antidepressants increase neurogenesis. |
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Electroconvulsive therapy
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effective in severe depression, side effect memory loss
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Treatments for mania
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Lithium: don’t know how it works. Liver toxicity.
Antiseizure medications |
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Anxiety Disorders
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•PTSD: Trauma causes. Hyperarousal, exaggerated startle response, nightmares, reliving traumatic episode
•Panic Disorder: panic attacks •Generalized anxiety disorder: continuous anxiety, no attacks •OCD: obsessions (unwanted thoughts), compulsions (reducing thoughts through behaviors), anxious if you don’t do compulsive acts •Social anxiety •Phobias |
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Neuroanatomy of anxiety disorders
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•Amygdala overactive
•OCD: striatum. Comorbid with Tourette’s syndrome (tics), chorea, both involve basal ganglia, so suggests basal ganglia involved in OCD |
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Treatments for anxiety disorders
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•CBT
•Benzodiazepines: enhance GABAergic transmission, inhibitory, enhance chloride through channel in receptor complex (hyperpolarizes cell, can’t fire as easily) enlarge channel so more chloride can pass through. Addictive (problem). Side effects: sedation, can degrade cognitive function, dependence •Antidepressants |
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Symptoms of Autism
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•Social impairment in interactions
•Stereotypic behaviors, restricted interests •Impaired verbal and nonverbal communication (receptive, expressive) |
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Asperger's Syndrome
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high verbal ability and no delay in language acquisition
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Genetic contributions to Autism
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X-linked, gene deleting, relates to synaptic structure (formation)
Sporadic mutations (environmental causes) |
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Anatomical correlates of social impairment in ASD
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•Orbitofrontal cortex
•Fusiform gyrus (facial recognition, engaging faces) •Inferior temporal gyrus •Amygdala: emotional content in faces •TPJ, STS: gaze, joint attention, Theory of Mind |
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Anatomical correlates of stereotypic behaviors/restricted interests in ASD
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•Anterior cingulate cortex
•Frontal and parietal regions |
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Anatomical correlates of language delays in ASD
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•Superior temporal gyrus/sulcus
•Wernicke’s (inferior parietal, superior temporal) •Broca’s •Striatum (direct involvement in speech production), cerebellum (motor planning for speech) •No consistent changes in ASD in these areas |
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Other structural abnormalities in ASD
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Cerebellum: lower number of Purkinje cells, send output (don’t know what this means)
Ectopia: during development, cells are produced in a particular area of brain and then migrate. When this goes awry, end up with collection of cells that are out of place (ectopias). |
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Theory of Mind: what is it and what structures are involved?
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ability to infer other people’s mental states, deficient in autism
•Medial prefrontal cortex: monitors one’s own though •Temporoparietal region: eye gaze, biological motion (superior temporal areas) •Amygdala: evaluation of social and nonsocial information for indications of danger in the environment Inferior temporal region: perception of faces |
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Rett Syndrome
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•Initially develop normally, and then after 2 years lose speech, lose ability to use hands. Repetitive hand movements, loss of motor control, intellectual retardation.
•X-linked, gene interferes with transcription (RNA to protein) |
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Why is Rett Syndrome seen only in girls?
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Necessary gene so when you don’t have gene can’t survive, males who have it will die and females have other gene to supply some transcriptions.
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Fragile X
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•X-linked
•Mental retardation, some overlapping symptomology with autism. Poor eye contact, dislike of being touched, repetitive behaviors. •Trinucleotide repeats (gene repetition of 3 nucleotides right next to each other) |
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Down Syndrome and relationship to Alzheimer's
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•Trisomy of chromosome 21, three instead of two
•When they live long enough, develop Alzheimer’s in 40’s •Gene that produces amyloid protein is on chromosome 21 •Region on chromosome 21 encodes ion pumps, calcium channel and glutamate channel related to mental retardation, abnormal neural transmission |
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Age related changes in the motor system
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•50-70% of cells die
•Parkinsonian signs part of normal aging •Posture, loss of postural reflexes, slow movement, frailty (neuronal changes in spinal cord) |
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Cognitive abilities that decline with age
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•Visuospatial
•Memory (working, long-term) •Attention •EF •Doesn’t interfere with ADLs |
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Cognitive abilities that don't decline with age
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•Vocabulary
•Information •Comprehension |
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Physiological functions disturbed in aging
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•Vision, sensory
•Sleep disturbance •Sex drive (hypothalamus doesn’t function well) •Appetite up and down |
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Structural brain changes during aging
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•Loss of brain weight
•Enlargement of ventricles •Frontal gyri thinner •White matter problems: loss of myelin, esp. in prefrontal and temporal cortex •Minimal neuronal loss (except in spinal cord) •Gray matter (loss of synapses) may be a good thing, correlate with wisdom, possible that this pruning is normal •Loss of plasticity (has to do with loss of synapses) |
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Three trajectories
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•Trajectory to dementia: normal, then drop and continue dropping, progressive cognitive decline
•Normal, decline consistent with age •No decline, small portion of population, perform superior to peers. Two interpretations: 1. Protective factors 2. Start at a higher level, but still declining (cognitive reserve) |
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Aging influenced by environment and genetic factors
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•Nutrition, activity
•Caloric restriction: eat less food a day, extend life, impossible in humans •Insulin signaling, involved in many systems including brain -Insulin growth factor (IGF1) when this receptor disrupted, animal lives longer •Growth hormone disrupted with aging, interrupting growth hormone during aging can result in increased lifespan •In most species, lifespan is influenced by body size |
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Alzheimer's: Clinical features
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•Defects in declarative memory
•Gradually memory is lost along with cognitive abilities such as problem solving, language, calculation, and visuospatial perception |
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Three structural changes in Alzheimer's
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Atrophy
Amyloid plaques Neurofibrillary tangles |
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Atrophy in Alzheimer's
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•Frontal regions shrink
•Lose tissue around ventricles (become larger) •Less brain matter •Gyri thin, sulci wide •Neuronal loss •Small medial temporal lobe (memory formation), hippocampus almost gone (happens early on) |
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Amyloid Plaques
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•Formed outside cells, likely damage neurons
•Do not correlate with cognitive abnormalities •Comes from protein on chromosome 21, amyloid precursor protein (APP) •Misfolding of proteins, aggregate and stick to each other •Amyloid Beta peptide forms aggregates •Soluble abnormal proteins: first form small aggregates that are soluble, can get stuck anywhere, in synapse, not allow dendrites to function, think these may be the cause and not large aggregates that we can see |
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Neurofibrillary Tangles
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•Correlate with clinical symptoms
•Occur first in parahippocampal gyrus, temporal pole (important for memory formation), long-term memory problems. •Tau protein: Helps microtubules form, microtubule associated protein, located in axons, helps the tracks form •Have tangle inside cell, tau not going down where it’s supposed to be •Abnormally phosphorylated, makes it aggregate inside cells •Cells die, tangle is all that remains, tombstone |
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What NT system affected first in Alzheimer's disease?
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ACh. Basal forebrain cholinergic system. Send axons all over cerebral cortex, involved in consolidation of memory, attention (focused).
Acetylcholine esterase (enzyme that degrades Ach), drugs approved by FDA that inhibit this enzyme, make sure more ACh is available at synapse. Short-lived cognitive and behavioral improvement |
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Inherited component of Dementia
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Chromosome 21, amyloids, APP, causative
Risk gene: Apolipoprotein E (APOE), many different variants, 2 different types in each person. APOE 4 gene allele, risk for Alzheimer’s jumps. RISK not causative. |
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Sporadic component of Dementia
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Head trauma, toxins, low level of education, diabetes, heart disease
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Parkinson's Disease
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Symptoms: dyskinesia, akinesia, rigidity, less movement, resting tremor
Areas affected: Substantia nigra pars compacta, dopamine Aggregated protein inclusions: Lewy bodies made up of alpha synuclein |
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Huntington’s Disease
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Symptoms: Chorea, uncontrollable movements
Areas affected: Striatum, neurons die, GABA Aggregated protein inclusions: Huntingtin, thought these aggregates are good |
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Amyotrophic Lateral Sclerosis
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Symptoms: flaccid paralysis, hyporeflexia, muscle atrophy
Areas affected: anterior horn of spinal cord, motor neurons die, muscles don’t get input so paralyzed, ACh Aggregated protein inclusions: phosphorylated neurofilament, tar DNA binding protein-43 (TDP-43) |
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Alzheimer's
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Symptoms: Memory loss progressing to complete loss of all cognitive functions
Areas affected: medial temporal lobe, parahippocampal gyrus and hippocampus then spreads, glutamate, acetylcholine early on (basal forebrain) Aggregated protein inclusions: amyloid, tau |
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Parkinson's Dementia
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Similar to Alzheimer’s, behavioral problems (i.e. visual hallucinations)
Areas affected: general atrophy of brain regions Parkinson’s comes first, them dementia |
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Frontal Lobe Dementia
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Symptoms: Disinihibition (orbitofrontal problems), apathy (personality change, no engagement in outside world), loss of judgment
Areas affected: prefrontal cortex and anterior temporal cortex Aggregated protein inclusions: Tau and TDP-43 |
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Lewey Body Dementia
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Symptoms: fluctuating cognition (attention, executive function), late development of Parkinsonian signs
Areas affected: general atrophy of brain regions, cortical cholinergic loss, striatal dopaminergic loss Aggregated protein inclusions: Lewy bodies, frontal cortex and other areas of cortex Dementia comes first, then Parkinsonian symptoms |
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Lewy Body Dementia vs. Parkinson's Dementia
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Matter of when things start, very related.
Lewy body dementia: Lewy bodies first appear in cerebral cortex, then get into motor system in basal ganglia. Parkinson’s: basal ganglia affected and then gradually gets to cortex. |
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Vascular Dementia
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Symptoms: depends on where vascular problem is, caused by strokes, multi-infarct or one stroke. Different from other dementias because not continuous degeneration, one event causes problems, stepwise, another event causes further degeneration
Area affected depends on vascular event Aggregated protein inclusions: none |
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Conceptual language areas
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distributed throughout association areas, conceptual knowledge
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Pattern separation
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ability to distinguish between two closely related images, episodes, or spatial configurations. Depends on projection from entorhinal cortex to dentate gyrus
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Pattern Completion
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partial cues to retrieve previously stored memories by filling in an incomplete pattern based on preexisting knowledge. Connections between Amon’s horn pyramidal cells.
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Neurotransmitter-receptor based theory of schizophrenia
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Drugs that reduce positive symptoms do so by blocking D2 receptors and some drugs that block D2 receptors reduce psychotic symptoms and other drugs that increase dopamine at synapses can produce psychotic symptoms
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