Psyc2020 Quiz 2

nerve fibre and all the muscle fibres it innervates

The neuromuscular junction

Dorsolateral and ventromedial tracts

Control movement (normally independent movement) of limbs

Controls posture and whole body movement and the limbs involved in these activities

DIRECT: corticospinal tracts

INDIRECT: corticorubrospinal tracts

DIRECT: ventromedial corticospinal tracts

INDIRECT: cortico-brainstem-spinal tracts

80-90% of fibres decussate after the pyramids at the anterior white commissure to form the dorsolateral tract. Terminate in the CONTRALATERAL half of the spinal cord, sometimes directly on a motor neuron

Fibres stay IPSILATERAL through the pyramids, more diffuse, axons innervate interneurons in several segments of the spinal cord

Combines input from primary motor and sensory cortexes with feedback from somatosensory and vestibular systems.

Involved in gait, speech and balance, learning new motor sequences

Modulation of movement

Degeneration of the dopaminergic neurons of the substantia nigra pars compacta leads to a dopamine deficiency. Dopamine therfore cannot stimulate the D1 (excitatory) and D2 (inhibitory) receptors on the striatum which then go on to effect the direct and indirect pathway.

A positive symptom is a trait that is not normally present that is there because of the disease

Examples:
Tremor
Rigidity
Leaning (forwards or backwards)
Cogwheel rigidity
Postural hypotension

Negative symptoms are traits (normally present) that are absent due to the disease

Examples:
Hypokinesia (red. spontaneous movement)
Akinesia (slow initiation of movement)
Progressive slowing and freezing
Reduced range and scale of movement
Hypophonia (dull, weak voice)
Mask-like, unemotional expression

The chemical precursor to dopamine which is used as a treatment for Parkinson's etc because it can cross the blood brain barrier (unlike straight dopamine) and get converted to dopamine once past.

A neurodegenerative disease, manifested in adulthood. It is autosomal dominant (chromosome 4).

Degeneration of striatum (apparent enlargement of ventricles--> destruction of GAGAergic (and some cholinergic) neurons (no inhibiton)

Chorea (involuntary, irregular 'dancing' movements)
Athetosis (writhing, especially in hands)

Altered speech and writing
Bradyphrenia (slowed thought processes)
Bradykinesia (inability to adjust body's position)
Poor motor dexterity

A disorder characterised by intermittent motor or verbal tics with otherwise normal cognition and sensory activity.

Caused by imbalance of GABAergic activity in basal ganglia

Apraxia and contalateral neglect

Inability to use visual information to guide hands
- defecit is more severe in periphery of visual field
- errors in accuracy

Disorder of skilled movement eg inability to move parts of the body in a purposeful manner

Superior parietal lobe

Desired, predicted, estimated actual

Imagining or watching a movement activates the same part of the brain that is used to do that action --> we are sensitive to the actions of other people

Monkeys respond to goal-directed actions and sounds

'blind spot' where axons from the optic nerve exit the eye

Low sensitivity, high positional acquity, low convergence

Each cone gets a 1:1 wiring with the cortex (high positional acquity, low convergence) but requires a lot of light to be stimulated (low sensitivity)

A 1cm wide object at a distance of 57cm will subtend 1 degree of visual angle

Photoreceptors contain rhodopsin (G protein that is sensitive to light). Cell is normally depolarised and actively releases inhibitory neurotransmitter. When stimulated by light, the cell becomes hyperpolarised (less inhibition) which increases the bipolar neuron's firing.

Light receptors have an extensive network of lateral connections. These connections inhibit adjacent neurons whilst simultaneously firing and stimulating the visual cortex. When there is a boundary between strong and weak light, the photoreceptors in the strong light are inhibited less by the receptors in the weak light (so they fire more) and inhibit the weak light receptors more (so they fire less)

Medial fibres decussate at the optic chiasm, lateral fibres stay ipsilateral. This means that light from a particular area in space is processed by ONE visual cortex.

adjacent locations in the retina match adjacent locations in the cortex

Areas of the face (eyes, lips, nose) often fall on the fovea which is overrepresented in the cortex leading to a distortion of these areas

Top 4 layers: parvocellular

Bottom 2 layers: magnocellular

small cell bodies
small receptive fields

colour (cones)
stationary objects

large cell bodies

large receptive fields

achromatic (rods)
motion

simple cell receptive fields with widely separated subfields

simple cell receptive fields with narrowly separated subfields

fed by a number of simple cells, it will fire if it gets any input from any contributing cells.

layers 1-3 and 5-6 of V1

most are binocular

Simultaneous input from both eyes increases firing

Some cells favour one eye over the other - ocular dominance

complex cells underlie stereoscopic depth perception

Dorsal pathway - posterior parietal cortex

Ventral pathway - inferotemporal cortex

Damage to the visual cortex causes an area of loss in the visual field that may not be noticed

Even if a scotoma covers the area around the fovea, the fovea is not effected because it is processed in the deeper areas of the cortex - 'spared' from the damage

A patient has a damaged visual cortex and a large scotoma. No conscious perception of any visual stimuli within the scotoma. Patient can still judge orientation, intercept objects etc within the scotoma

Dorsal stream: visual spatial perception

Ventral stream: visual pattern recognition

Dorsal (magno): visually-guided behaviour (using visual info to guide motor actions

Ventral (parvo): conscious visual perception (colour, shape, orientation)

Patient cannot recognise faces. Result of damage to VENTRAL STREAM. Familiar faces elicit higher GSRs which suggests a motor response.

collect sound waves and funnel them into the ear, help localise sound by reflecting sounds of various frequencies into the ear

The tympanic window is much bigger than the oval window, a size disparity that amplifies sound 17 fold.

The ossicles' lever action amplifies sound 1.3 fold

All together = 22 FOLD AMPLIFICATION

Taking a cross section of the cochlea, there is a basilar membrane with specialised cells (with hair fibres on them), and a tectoral membrane resting on these hairs. The vibrations move the lymph fluid in the cochlea, which pushes these two membranes together, bending the hair cells. This causes chemical changes in the specialised cells beneath which elicits action potentials and a neural response. The auditory threshold of hair cell displacement is about 100 picometres.

To perceive sounds of about 100-5000Hz, neurons carrying the auditory signals work together, each firing in a slightly delayed rhythm (eg one neuron fires for the 3rd, 7th, 11th etc signal). The overall effect of this is a signal of a much higher frequency (eg 500hz) than a single neuron could produce.

The point of maximum displacement of the basilar membrane occurs very close to the start (to the stapes). As the vibrations travel down the membrane, the amplitude of displacement drops. Thus, areas of the membrane closer to the stapes code for higher frequency sounds whilst areas further away code for lower frequency sounds.

Cochlea --> cochlear nerve --> superior olivary nucleus --> inferior colliculus --> MGN --> auditory cortex

(heaps of interconnections between these structures and others eg for reflexes)

sound doesn't travel fast enough to prevent us from picking up on minute differences in the time that the sound arrives in one ear compared to the other

(coincidence wiring)

The head can cause an 'auditory shadow' which lowers the frequency of the wave as picked up by the ear on the other side of the head.
Low frequency sounds travel and bend around objects without being distorted as much as high frequency.

(superior olivary nuclei inhibiting the other)

The nerve from each cochlea has a number of synapses within the olive (medial superior - MSO). If there is a difference in timing of the ears the signals will arrive at these synapses at different rates. The MSO firing is maximised when two signals arrive at the same time. If sound has arrived earlier in the left ear, the two signals might meet at the synapse furthest from the left ear and closest to the right and the brain can decode this to localise the sound.

To do with interaural intensity differences. Both olivary nuclei are stimulated by their respective cochlea, and also inhibit one another. If a signal is more intense in one ear, the olivary nucleus on this side can fire more strongly and also inhibit the other nucleus more robustly. This is another method of sound localisation.

Both are in the superior temporal gyrus. The primary auditory cortex is more 'hidden' within the lateral sulcus and the secondary auditory cortex is more lateral (on the outside).

Columnar organisation: columns which respond to similar frequencies

Tonotopic organisation: areas of the cochlea correlate spatially to areas on the cortex (conserved all the way up the auditory pathway)

Results from damage to the tympanic membrane and ossicles. DOES NOT INVOLVE NERVOUS SYSTEM eg ossicles can fuse together

Auditory nerve fibres are not stimulated properly. PERMANENT. Caused by infection, trauma, loud sounds, drugs (eg streptomycin)

Caused by brain lesions in the temporal lobes
Loss of specific faculties eg language processing (left lobe) or discrimination of non-language sounds (right lobe)

Semicircular canals respond to ACCELERATION

Ampulae- large swelling filled with liquid
Capula - buoyant filament-like structure in the ampulae.

Fluid lags behind the semicircular canals when the head accelerates and when it catches up it pushes on the capula, stimulating hair cells. After constant velocity is reached the capula floats back to its neutral position.

Structures within the vestibular system covered with otoliths which respond to linear acceleration and gravity (constant)

Turning the head stimulates the ipsilateral lateral rectus and contralateral medial rectus which keeps the eyes in the same spot. The contalateral lateral rectus and ipsilateral medial rectus are also inhibited.

Eyes 'jumping' forward and then tracking back to maintain distant visual images when the head is rotating about an axis

'Bouncing vision'
Bilateral loss of the vestibulo-ocular reflex leaves the patient with the sensation that the world is 'bouncing' whenever their head moves. Information in the head about movements signalled by the vestibular organs is unavailable.

Exteroceptive (outside stimuli)

Interoceptive (internal stimuli)

Proprioceptive (body position knowledge)

Free nerve endings (temp, pain)

Pacinian corpuscles (quick adaptation to pressure)

Merkel's disks (slow adapting mechanoreceptors)

Ruffini endings (slow adapting mechanoreceptors)

Areas of the skin that correspond to a specific spinal cord segment (which dorsal root the afferent fibre from that area converges on)

Dorsal column medium lemniscus - information about touch and proprioception

Anterolateral - pain and temp

Spinothalamic: to ventral posterior thalamus

Spinoreticular: to reticular formation then thalamus

Spinotectal tract: to tectum

No major defecits in sensation, probably due to the numerous parallel pathways in the two systems

No specific representation- very diffuse throughout/ S1 and S2 respond to pain but they can be removed without loss of pain sensation. Removal of entire hemisphere has little effect also. Anterior cingulate gyrus is likely to be involved in the emotional response to pain

Periaqueductal grey has analgesic effects. Electrical stimulation reduces pain. PAG has receptors for opitate-based pain drugs, endorphins modulate PAG activity.

Communication is simply behaviour used by one member of a species to convey information to another (eg body language, gesture, eye contact).

Language is an element of communication that has symbols and rules for ways about assembling those symbols. Specifically human.

Loss of language processing ability after brain injury.

NOT
- impairment of intellectual function
- psychiatric disturbance
- primary motor or sensory defecit

- developmental disorder

- Broca's (M)
- Wernicke's (A)
- Transcortical sensory (A --x-- C)
- Transcortical motor (C --x-- M)
- Conduction (M --x-- A)

Disturbance in speech production. Damage to left inferior frontal cortex.

Loss of 'little words' between major messages

Disturbance in auditory comprehension. Damage to left posterior superior temporal gyrus.

Paraphasias, poor repetition, naming, disturbances of sounds, word structures

Failure to repeat. Damage to arcuate fasciculus (between Broca's and Wernicke's).

Phonemic paraphasias (errors in sound of language)

Disturbance of auditory comprehension. Unlike Wernicke's it has good repetition and semantic paraphasias.

Damage to tracts in tempero-parietal-occipital junction

Disturbance of initiating responses (selection defecit). Lesion of tracts superior/anterior to Broca's.

Normal comprehension and repetition just can't initiate speech

Does not view language in terms of production and coprehension. Emphasises language processing options- phonology, syntax, semantics

Phonetic: how phonemes are produced in different contexts (eg french vs english alphabet)

Phonemic: smallest unit of sound that can signal meaning

Broca's.
Content words are preserved but the others are lost (telegraphic speech).

Syntax problems: can understand individual words but not the meaning derived from their combination

methods for combining words to convey propositional meaning

words and their meaning

Posterior lesions (Wernicke's aphasia) tend to show more semantic disruptions.

Lesions can dissociate meaning and the lexical form of words leading to either
- intact meaning impaired naming
- intact naming impaired meaning

Broca's - CLASSIC = poor speech production

PSYCHOLINGUISTIC = syntactic problems

Wernicke's - CLASSIC = poor auditory comprehension
PSYCHOLINGUISTIC = semantic problems

Disruption in reading ability

surface- can't recognise 'shape' of words (direct route)

phonological - can't put the sounds of words together to make meaning (phonological route)

deep- surface and phonological combined

Agraphia - trouble spelling and or writing

Central - trouble visualising the 'shape' of the word (orthographical) or applying sound-to-spelling rules

Peripheral - distortions in writing or typing (motor)

Anterograde - can't form new memories after TBI

Retrograde - loss of old memorises prior to TBI

Explicit (declarative) and implicit (non-declarative)

Episodic (personal events) and semantic (facts)