cutaneous reflexes
flexion responses become habituated if stimuli is provided too often
patients with complete spinal transection display flexion reflexes indicating they must be spinal reflexes
thought to be the result of group II (B) afferents

cutaneous reflexes
stimulation of the sole results in flexion at the knee, ankle plantar flexion & toe flexion - ìplantar responseî which withdraws sole from the stimulus
after damage to pyramidal tract sole stroking results in ìBabinskiís signî - knee flexion, ankle and toes dorsiflex - notice this response is true flexion distinct from the plantar response

Role of cutaneous input during natural hand movements
Subjects had to lift object from table with a grip using thumb and index finger
Two applied forces
   - grip force between thumb & finger act
     perpendicular to table > grip > friction
   - load force - vertical force required to lift
     against gravity

Role of cutaneous input during natural hand movements
the ratio of grip to load force remains constant & slightly upon the slip ratio during the movement

for a given frictional surface the grip/load force is kept constant across objects of different weights

Role of cutaneous input during natural hand movements
change in surface qualities necessitates change in grip force thus changing grip/load ratio
grip & load force are modified based on cutaneous input

anaesthetizing the fingers prevents modifications

Role of cutaneous input during natural hand movements
recordings from single cutaneous fibers indicate that fibers fire more in the presence of more slippery surfaces & grip force can be modified within 100-200 ms
if slip occurs prior to actually lifting the object from the table (usually unperceived) cutaneous receptors will fire that modify the grip/load force ratio within 75 ms - much faster than voluntary response to slip

Role of cutaneous input during natural hand movements
no evidence that spindle discharge changes during these slips so they are thought to be of cutaneous origin
 

Role of cutaneous input during natural hand movements
although afferent discharge is phasic in response to changes in surface characteristics the change in grip force is maintained - i.e. the entire plan of action is modified in response to cutaneous input

Cutaneous input influences activity of many muscles - even elbow muscles

Human Spasticity
spasticity often seen after upper motoneuron lesion or in chronic stage of spinal transection
muscle tone evaluated in relaxed muscle by passive, slow limb movement
hypertonus means there is increased resistance to the movement

human spasticity
increased resistance results from inherent viscoelastic properties of the muscles & stretch reflex mediated contractions
in normal humans little stretch reflex in relaxed state
 - low gamma firing
 - low alpha MN excitability

human spasticity
3 differences in tendon jerk between normals & spastic patients
 -  1) threshold for reflex is < (light taps)
 -  2) size of response is >
 -  3) tendon jerks can be obtained in > number of muscles than normal

human spasticity
hypertonus is primarily the result of increased stretch reflexes (Fig 6.16, p. 197)
when tone is evaluated during muscle contraction there is little difference between normal & spastic muscle
this suggests that spasticity results from a failure to reduce the stretch reflex mechanisms during relaxation

human spasticity
Rothwell suggests that since spasticity is only present during relaxation then spasticity cannot be a factor in spastic patientís problems with voluntary movement.
it appears that excitability in the spinal pathway (e.g. presynaptic inhibition or MN excitability) is responsible for hyperactive stretch reflexes

human spasticity
appears to be no hypersensitivity of spindle
spasticity tends to impact the extensors of the leg & flexors of arm - these muscles tend to be ìanti-gravityî muscles
pattern of spasticity suggests that there may be a central control system of the ìanti-gravityî muscles

human spasticity
Clasp-knife phenomenon - best observed in knee extensor muscles - as knee is flexed by therapist tension builds then suddenly dissipates (Fig. 6.17, p. 201)
originally thought to be mediated by Ibs but probably mediated by group II and III non-spindle afferents
human spasticity
spastic patients have abnormalities in Ia reciprocal inhibition, Ib autogenic inhibition & Renshaw inhibition - no wonder hypertonus is present!

Spinal Cord Transection
acute transection is immediately followed by flaccid paralysis & areflexia (high reflex thresholds)
areflexia caused by removal of facilitatory descending inputs from supraspinal structures
first signs of recovery are reflex emptying of bladder and rectum & cutaneous reflexes in some muscles

spinal cord transection
flexion withdrawal reflexes are observed - may be accompanied by the mass reflex
tendon jerks eventually reappear & contractures may form in the lower limb due to enhanced flexor reflexes
dominant effect of transection is enhanced flexor reflex pathways (other than paralysis)

spinal cord transection
electrophysiological studies reveal modifications in the flexion reflexes (responses to nerve stimuli)
late component has lower threshold than normal
latency of late component is greater
late component is inhibited by a preceding flexor reflex stimulus to opposite leg

spinal cord transection
this finding suggest there are intact spinal pathways which can be used to promote some degree of interlimb coordination (CPG?)

Deafferentation
complex movements can be made in the absense of any sensory feedback & thereby any reflexes
although deafferented patients can make complex movements without vision the movements soon become uncoordinated (Figure 6.20 p. 209)
this indicates that effective motor commands can be generated in the absense of sensory input