Week 8 Flashcards

Question

Posterior Parietal Cortex

Answer 1

``` • Outputs to secondary motor areas, FEF, and dlPFC • Subregions associated with eye, hand, or arm movements • Damage – apraxia and contralateral neglect ```

Answer 2

• Disorder of voluntary movement - not a simple motor deficit • Difficulty making movements on request, but can make the same movement under natural conditions when not thinking about it • Eg – can hammer a nail but cant demonstrate hammering when asked • Bilateral symptoms but damage usually unilateral – left PPC • Conscious planning of complex coordinated action

Answer 3

• Disturbance of ability to respond to stimuli on side opposite lesion • Usually right lesions and neglect left space • Patients fail to appreciate that they have a problem • Egocentric left – left of body – head tilt doesn’t change (tilt) field of neglect • Also neglect left side of body

Answer 4

• Intrinsic spatial coding: knowing what own body parts are doing • Intrinsic coding essential when body part is obscured from vision during planning and/or execution • PJ: 50yo F; head injury at 43yo, loss of consciousness • Jerking of the right arm at 48years, focal seizures, presented for assessment • No visual neglect or extinction, no other visual deficits • Perceives her right arm and leg to drift and fade unless she is able to see them • In bed, loss of knowledge in limb position • In public transport, other passengers tripping over her leg, which had drifted into the aisle • MR: cyst encroaching on the cortex and subcortical white matter of left superior parietal lobe

Answer 5

``` • Input from PPC • Outputs to M1, secondary motor, FEF • Evaluate external stimuli and decide to act – goals based • Decisions to initiate voluntary movement ```

Answer 6

• Complex heterogenous collection of interconnected nuclei • Modulatory function – loops receiving cortical input then back to cortex via thalamus (other non-motor functions) • Caudate and putamen (striatum), globus pallidus, subthalamic nucleus, substantia nigra • Inputs from cortex (sensory, motor, association) to striatum; output from GP and SN to motor and frontal cortex via thalamus • Critical role in selection and initiation of action • Complex, heterogenous interconnected nuclei • Connections excitatory or inhibitory • Initiate selected movement

Answer 7

Turn up increases output of target Turn down decreases output of target

Answer 8

Turn up decreases output of target Turn down increases output of target

Answer 9

``` Direct – enhances thalamic output Indirect – inhibits thalamic output But – indirect slightly delayed so brief enhancement then balance ```

Answer 10

``` Direct – enhances thalamic output Indirect – inhibits thalamic output SN input – turns up DIRECT and turns down INDIRECT To Enhances overall process ```

Answer 11

* This circuit model is speculative – details way more complicated * Other inputs, outputs, connections, and complexities not mentioned * Output (discharge rates) not the only important factor * Neuronal firing patterns likely important * Synchrony of higher level activity likely important * Coordinated activity of multiple interconnected nuclei – fine balance * Basics of function from disorders

Answer 12

Disorders of motor control: • Parkinson’s Disease – loss of modulatory dopaminergic neurons in the substantia nigra • Huntington’s Disease – loss of inhibitory GABAergic neurons in the striatum Note – these disorders have broader effects than just motor and involve neurodegeneration in multiple regions

Answer 13

• Loss of dopaminergic neurons in the substantia nigra • Increase indirect and decrease direct – decrease thalamic output • Latest – changes in neuronal firing patterns and synchrony rather than reduced discharge rate • Primarily affect indirect pathway • Ultimately - decreased cortical activity • Cardinal features – akinesia (slowed initiation), bradykinesia (slowed movement), muscle rigidity, tremor Direct – enhances thalamic output Indirect – inhibits thalamic output Enhancement of direct versus indirect reduced To Decreased thalamic output no SN • Reduction in spontaneous movement (hypokinesia) • Slow initiation of movement (akinesia); Slow gait, often with freezing and small steps, poor arm swing • Progressive slowing or freezing during a movement and reduced range and scale of movement • Postural instability = many falls • Dull, weak voice without inflections (hypophonia) and slow speech • Mask-like, unemotional expression

Answer 14

``` • Dopamine agonist: L-Dopa (precursor) • Increase dopamine generally • Efficacy drops with usage • Numerous side effects • Chronic high frequency deep brain stimulation (DBS) • Implanted device to stimulate STN (usually) • High frequency disrupts activity • Not sure how/why it works • Reduce inhibition of thalamus? • Replace irregular BG output to cortex with a regular, better tolerated pattern? • Disrupt abnormal frequencies? ```

Answer 15

• Genetic neurodegenerative disease – manifests in adulthood (35-55); life expectancy 10-25 years post onset • Autosomal dominant with complete lifetime penetrance, chromosome 4 – excessive build up of Huntingtin protein • Destruction of GABAergic neurons in striatum (caudate and putamen) – primarily affecting indirect pathway • Progressive striatal atrophy: medial caudate first (small spiny neurones), then putamen, then tail of caudate • Reduced (indirect) basal ganglia output Direct – enhances thalamic output Indirect – inhibits thalamic output Thalamic inhibition reduced Increased thalamic To excitation of motor cortex no SN to GPe • First signs affective: depression, anxiety, irritability, impulsivity, aggression • Then restlessness, clumsiness, forgetfulness, personality changes • Characteristic - athetosis (writhing movement) and chorea (jerky movement) • Poor motor dexterity, unsteadiness, reduced speed • Altered speech and writing, saccadic changes • They involve multiple joints and thus resemble voluntary action • They are briefly suppressible, and decrease during sleep • They increase with stress and with voluntary movements like walking

Answer 16

• Modulatory – fine-tuning and learning (other non-motor functions) • Inputs from cortex (M1 and secondary motor), descending motor signals from brain stem nuclei, somatosensory and vestibular feedback • Compare signals with feedback to correct ongoing movement that deviates from intended • Project to brainstem nuclei directly and cortex (M1 and secondary) via thalamus • Role in motor learning especially when sequence timing critical • Diffuse damage – lose precise control of direction, force, velocity and amplitude of movement; lose ability to adapt movement to changing conditions, disturbances in balance, gait, speech, eye movement • Cells in cerebellum that project to spinal cord especially sensitive to effects of alcohol – unsteady gait, disturbance of balance

Answer 17

• Loss of sensory co-ordination of distal limbs disrupting fine coordination – finger to nose test • Lack of muscle control or coordination of voluntary movements, such as walking or picking up objects. • Speech impacts • Alcohol abuse, certain medications, stroke, tumour, cerebral palsy, brain degeneration and multiple sclerosis

Answer 18

• Described voluntary behaviour as wilful – intentionally initiated following a decision to act (including rejection of the alternative of doing nothing) • Subjective experience – ownership of action, agency, conscious control – ‘I’ did something on purpose • But …. • Often act unconsciously or with minimal conscious control • Split brain patients – dissociation of action and awareness • Confabulation – plausible (but incorrect) reasoning about decisions to act with feeling of agency • People are subject to other illusions of ownership • People are subject to other illusions of control A bilateral slowly increasing negativity (EEG of SMA) (termed the ‘readiness potential’) was shown to precede voluntary action by Kornhuber and Deeke (1965) • Libet – have subjects perform a simple motor at random act while looking at a fast moving ‘clock’ – note the position of the clock when first aware of the intention to act • Onset of the readiness potential hundreds of ms before awareness of intention to act • “the brain evidently 'decides’ to initiate or, at the least, prepare to initiate the act at a time before there is any reportable subjective awareness that such a decision has taken place” • Soon et al (2008) – similar approach but using fMRI • Look at a letter stream – freely press one of two buttons – recall letter when motor decision was consciously made • Intentions mostly formed 1000ms before press • 2 brain regions encoded left vs right decision early – frontopolar cortex and parietal • Over 10 seconds before the decision to act (7 seconds on fMRI signal) • Timing of decision predicted in preSMA and SMA • 5 seconds before the decision to act • Dissociation between outcome of motor decision and timing