neuro prac exam qs Flashcards
what are the main neurological pathways?
sensory pathways:
-DCML pathway - fine touch, vibration, proprioception
-spinothalamic tract - pain and temp & crude touch
-spinocerebellar tracts - info from muscle and joints to the cerebellum which helps to co-ordinate mvt
motor pathways:
-corticospinal tract (lateral and anterior)- primary pathway for voluntary movement - transmits info from motor cortex down spinal cord to the muscles
-corticobulbar tract- controls muscles of the face
where do sensations travel eg pain?
-nociceptors will detect stimuli and send signals up to spinal cord
-signal decussates in spinal cord and travels up the contralateral side
-ascends up to the thalamus via the spinothalamic tract
-then travels to the somatosensory cortex for interpretation
where do sensations travel eg fine touch?
-sensations will travel from the sensory receptor up the spinal cord and into the brain
-eg DCML - fine touch - sensory receptors in skin will send signals through dorsal column of spinal cord and then go up to the medulla and then to the thalamus and then to the somatosensory cortex where the sensation is interpreted
what is the CNS?
the central nervous system- ie the brain and spinal cord
- brain processes and interprets sensory information, thinking, decision making emotions and controlling voluntary and involuntary actions
-spinal cord -transmits signals between the brain and the rest of the body
what are the rules of sensory testing?
-if a patient is tired during exam or at the end of exam - dont test sensation
-demonstrate first what you are going to do - touch side that’s normal first
-brief instructions
-patients eyes closed
-EXAMINE NORMAL SIDE FIRST (non stroke limb)
-ALWAYS TEST DISTAL TO PROXIMAL
-if patient is confused, distracted, dysphasic or inattentive - might not be possible
what areas of the brain are being tested during sensory testing?
-the somatosensory cortex in the parietal lobe - receives info from sensory receptors eg touch, proprioception, vibration etc
-the thalamus acts as a relay station for signals before they travel to the somatosensory cortex
how do you document sensory findings?
- could say sensation is intact
-sensation is reduced
-say where it is reduced
-which pathway eg light touch, sharp and blunt etc?
what are the implications of abnormal sensation in the neurological patient?
-sensory deficitts can disrupt proprioception and increase the risk of falls
-patients may have difficulty with co-ordinated movement - challenges with walking, transferring etc
-increased risk of injury eg pressure injuries like bed sores could develop if patient has impaired sensation
-can lead to altered gait patterns
-reduced tactile sensation in hands etc can make ADLs difficult
what is tone?
the resistance offered by muscles to continuous passive stretch
OR
defined as the resistance that is encountered when a joint of a relaxed person is moved passively
what are examples of non - neural and neural factors that contribute to tone?
non neural factors
- passive stiffness of a joint
-compliance of muscles, ligaments and joints
-age, limb temperature etc
neural factors
-age and emotional state
-activation of the contractile apparatus of the muscle
-active tension set up by the stretch reflex
describe all the types of abnormal tone
- high tone = hypertonia and low = hypotonia
-spasticity is velocity dependent increase increase in resistance to passive stretch of muscle (HIGH)
-rigidity- increased resistance to slow passive mvt that is constant throughout the range of mvt (HIGH)
-flaccidity is a decrease in resistance to passive movement
what is spasticity?
a velocity dependent increase in resistance in response to the passive stretch of a muscle with exaggerated tendon reflexes
what can cause spasticity?
-abnormal enhancement of spinal stretch reflexes
-may be due to inverted muscle spindle sensitivity
-loss of inhibition of stretch reflex
-loss of cortical inhibition
-imbalance in descending pathways
what are the implications of abnormal tone (high or low) in the neuro patient?
-high tone - both spasticity and rigidity can limit joint ROM - making mobility difficult
-low tone can lead to increased joint instability and risk of subluxation
-both high and low tone can cause poor posture
-spasticity can cause pain and contractures
what can affect spasticity?
-stress - increases it
-pain - increase
-fatigue - increase
-infection- increase
-positioning
-pressure sore
what is the role of the physiotherapist in managing tone?
-aim to normalise tone
-improve ROM
-decrease pain
-improve function
management :
-positoning - sitting
-passive movement - slow
-ice
-splinting
-weightbearing
what is the medical management of abnormal tone?
spasticity:
-baclofen - a GABA derivative that can decrease spasticity
-diazepam (valium) - GABA effect
-botox - toxin injected directly into affected muscle - blocks Act
-zanaflex - short acting muscle relaxer
describe the modified ash worth scale
it is a scale used to rate the level of spasticity in a patient when you are doing a tone assessment
- scale runs from 0-4
-0= no increase in tone
-1= slight increase in tone- catch and release or minimal at end of range mvt
-1+ -slight increase in tone - catch followed by minimal resistance through the remainder of the ROM
-2 - more marked increase in tone through most of ROM
-3 considerable increase in tone
4- affected part is rigid in flexion or extension (ie complete rigidity)
what abnormal postures do you see when a patient has spasticity? note both UL and LL
UL
-adducted shoulder
-flexed wrist
-flexed elbow
-thumb in palm
LL
-equinovarus
-stiff knee
-flexed knee
-adducted thighs
describe the decerebrate posture
the decerebrate posture results from damage to the upper brain stem
-the arms are adducted and extended with the wrists pronated and the fingers flexed
- the legs are stiffly extended with plantar flexion of the feet