Dan- Clinical Neuro Flashcards
Location of the parietal lobe
Behind frontal and before occipital. Has dorsal (where info, runs above) and ventral (what info goes below) pathways. Has attentional control network, info about space, feeds into frontal to make decisions. Stim processing responds to bottom up, from parietal to frontal. Has distinct areas and reviews info from v1
Functions of the parietal cortex
Space based attention, object based attention, reaching and grasping. Magnitude and processing (how many objects) and feature based attention (attend to parts of an object)
Hemispatial neglect
Disorder of space based attention. Case study LJ had confusion, flat affect, gaze to right, r dominance, stroke in r hemi. Key symptoms are damage to P lobe, ps don’t attent to left side but can if pointed out (not visual)
Testing hemispatial neglect
Asked p to draw middle of line, cross out every line, copy picture (will shift or miss half). Draw clock from memory (numbers on one side). No awareness but ppl W visual damage would know. Eye tracking, have shift even at rest, when searching, only right. When asked to describe buildings from memory, neglect L regardless of view
R vs l damage and neglect
Neglect more common in right compared to l as r dominant for visuo spatial attention/ get info from both hemis (ipsilateral and contra lateral) but left lesion don’t get neglect as right gets it from both (left only contra lateral info)
Neglect in other senses
Ps respond to sounds from affected hemis as if they occurred in the other side of space. Pavan I 2001 played sounds, ps showed worse audio location compared to control. Can also affect tough LJ couldn’t feel hand touch
Recovery
Can get better, the damage doesn’t but may be plasticity or ps learn strategies
Balints syndrome
Disorder of object based attention, bilateral damage to partiteal and occipital lobes. Need simultanagnosia, optic ataxia and ocular motor apraxia . Can each occur separately but these pjs don’t have balints syndrome
simultanagnosia
If 2+ objects presented, only see one at a time. If unseen jiggled, see it but not the first. Happens anywhere in visual field (not like neglect). Test: ask how many colours, if not connected say one, when connected say 2. See objects of diff heights, can tell when connected or small space between but not separate of W occluded (3rd object)
Optic ataxia
Goodale 94: RV had bilateral damage to dorsal stream, DF to ventral stream. When presented w shapes, RV could tell diff but DF couldn’t. RV grabbed inappropriately DF successful. Test by posting hand through pox, have orientation and position errors.
Occulomotor apraxia
Problem W planned eye moments, issues W saccade initiation, accuracy and smooth visual pursuit. May happen die to deficits in circuit between parietal and frontal eye fields.
Dyscalculia
Disorder of magnitude processing, developmental disorder but when caused by da,age called ascalculia. Issues understanding and manip numbers. 3-6% prevalence. Deficit in r inferior parietal lobule. Clocks, working back in time, l and r, dance steps, turning map
Numerical distance effect
Easier to if the larger of 2 numbers when there’s a greater distance. 8 kids and 8 controls did in mri. Controls showed greater activation in r intra parietal sulcus when working w close or far distances, affected didn’t show this price 2007
Theory of magnitude
Time space and number all need magnitude, share location in r intraparietal sulcus. Issues to do W issues in magnitude processing as similar cog functions likely to be processed in same area
History of depression treatment
Mainly SSRIS, created accidentally from tb treatments, mostly unchanged. Now deep brain stim for treatment resistant and TMS but invasive
Cognitive model of depression
Beck: attent to - stim, greater perception for -, ruminate about depressive ideas, recall depressive episodes more, - self schemas. Disner 2011: brain regions can be mapped onto bias thoughts
Biased attention
Amygdala used for emotion if and generation, in healthy it’s biased towards +. Problems in allocated attention could be reason. Attention in parietal cortex, pfc and VLPFC AND DLPFC, top down decision making, where to attend and disengaging. Siegle 2007: mri for unmediated depressed and normal, dep showed increased amygdala for - words and decreased DLPFC for all tasks so stronger and can’t disengage
Biased processing in depression
Reward processing affect in depression
Normallt supported by fronto striatal network, neural pathways that connect frontal lobe regions w basal ganglia/ striatum
NA is major input to striatum
Disruption basis for loss of pleasure
Emotion regulation
Heller 2009: ps shown good and bad pics, either just look, enhance or suppress response. Focuse on NA, dep couldn’t sustain reward pathway when enhancing, only for +, reported less + emotion. Reflects reduced pfc connectivity
Biased memory
Hard to tell memory vs encoding effect (what attend to ). Activity in amygdala does encoding and retrieval of emotional stim by mod regions for memory. Biased memory in dep linked to amygdala over activity, linked to activity in hippo, caudate putamen. Videbech and ravkilde 20p4: depressed have smaller hippo
Neurotrophic hyp of depression x theory of why smaller hippo
Post mortem data showed atrophy due to decreased BDNF in hippo. It encourages growth of new neurones and synapses. Impaired memory encoding e.g. of plasticity but not clear is cause or result of dep
Cortisol
E.g. of glucocorticoids, steroid that increased blood sugar, suppresses immune system and increases metabolism. Increases when stressed, low at night and spike when wake up (cortisol awakening response), raises memory when stressed. Depressed have higher levels
Monoamines (dopamine, serotonin and noradrenaline)
Dopamine for reward and motivation, supports consummately behaviours, released from VTA. Serotonin released from dorsal to forebrain. Nora: fight or flight, prepares body, linked to cortisol. Ssris have to overcome homeostatic feedback/take a month to work, side effects, can wash out over time, alongside other treatment
Ssri negatives
Star d 2006: everyone started level 1, no improvement get moved up. 1: ssri 14wks, 2: diff ssri and cbt, 3: diff ssri and lithium or thyroid, 4: ssri and serotonin norepinephrine reupatke inhibitor. 47% responded to level 1, 28% remission . 2: 25% remission so cbt same level, 3: 20%, 4:10%. Ppl dropped out more at each level, 70% showed remission (more in women,, wealthy, educated) meaning some didn’t respond at all
