Deficits in Motor Control

Primary vs secondary CNS lesions

Primary are directly due to injury, secondary develops indirectly as a result of the original injury

What are the FAST warning signals?

Face drooping, arm weakness, speech difficulty, time to call 911

UMN lesions initially - and -

Flaccid and hypotonic

Other motor cortex deficits

loss of motor strength (weakness), spasticity (hypertonicity), loss of selective muscle activation, abnormal synergies, coactivation

What are fractionated movements

Active selection of individual muscle groups

Spasticity-motor control graph of stroke rehab

I: flaccidity

II: synergies and some spasticity

III: marked spasticity

IV: out of synergy, less spasticity

V: selective control of movement

VI: isolated/coordinated movement

Cerebellar pathology?

Hypotonia, ataxia, action/intention tremor

• dyssynergia, dysdiadochokinesia, dysmetria, dysarthria, impaired occulomotor control, delayed reaction time, etc.

Another cerebellar issue is impaired - - in - -

Error correction, motor learning

Basal Ganglia (2)

Parkinson’s (hypokinetic): bradykinesia, akinesia, rigidity, resting tremor

Huntington’s (hyperkinetic): chorea, hemiballismus

• Dystonia (hypr)

Damage to S1 results in..

Altered proprioception, touch (PPC)

Damage to..

• Optic nerve

• Optic chiasm

• Optic tract

• V1 (s/i bank)

• Monocular blindness

• Bitemporal hemianopia

• Opposite VF in both eyes (L/R homonymous hemianopia)

• Oppositve VF, opposite S/I (1/4, L or R + Superior or Inferior Quadrantanopia)

Vestibular dysfunction

Gaze stabilization, posture/balance, vertigo or dizziness

Spatial neglect?

L side, damage to R (ignore it, not an eye issue)