Review Neuro Flashcards
when may the signs of uncal herniation be falsely localising?
if midbrain pushed against opposite side of tentorium
signs of uncal herniation, and explain related to anatomy
-ipsilateral dilated pupils, down and out: compression of ipsilateral oculomotor nerve which originates from midbrain
-contralateral leg weakness: compression of cerebral peduncle, motor fibres not crossed yet
-decreased consciousness: reticular formation in brainstem affected
when not to do LP and why
if ICP raised as could decrease CSF pressure, leading to coning by tonsillar herniation
signs of tonsillar herniation, relate to anatomy
-cardiac and respiratory dysfunction: brainstem affected
-decreased consciousness: reticular formation compressed
explain why bushings reflex leads to bradycardia
ischaemia at medulla activates SNS so BP rises and respiratory rate rises. baroreceptors react = bradycardia
explain why cushings reflex causes low respiratory rate
ischaemia at pons/medualla at respiratory centres
explain the pathophysiology of diffuse axonal injury
cortex is in 6 layers of grey matter, on top of white matter
WM can shear off grey due to different densities
trisects axons, disconnecting cortex+ WM
causes of central cord syndrome
syringomyelia
hyperextension/hyperflexion
features of central cord syndrome, relate to anatomy
-motor mostly, as ventral horns affected
-upper extremity many as usually at cervical level, affects medial CST (fibres destined for upper limbs)
-distal musculature mainly as lateral CST affected more than ventral
-bladder dysnfunction+urinary retention as hypothalamospinal tract descends in lateral funicular so lose descending modulation of micturition
explain 3 way propofol acts to cause general anaesthesia
- thalamus- less sensory info
- reticular formation- less cortical activation
- hippocampus- memory loss
- dorsal horn of SC- less pain transmission
structures in pain modulatory pathway
periaqueductal grey
substantia gelatinosa
dorsal horn
where can multiple sclerosis plaques form? give specific examples and the effects
anywhere in CNS
-CST: UMN signs
-DC: loss of modalities
-arcuate fasciculus: aphasia
why can MS cause optic neuritis?
optic nerve is white matter, demyelination damages white matter, leads to monocular blindness
why can MS cause diplopia?
impulses cant cross medial longitudinal fasciculus efficiently due to slowed conduction, so there’s a lag as one eye catches up
brown squared syndrome effects
-ipsilateral total segmental anaesthesia of dermatome at level (dorsal roots)
-ipsilateral LMN signs at dermatome (ventral roots)
-ipsilateral loss of DC modalities below
-contralateral loss of STT modalities below (maybe few segments lower due to lissauers tract)
-ipsilateral UMN below
? maybe ipsilateral horners - loss of input to spinal levels driving sympathetics to H+N