Please enable JavaScript.
Coggle requires JavaScript to display documents.
Constraints - Coggle Diagram
Constraints
Individual
Sensory/Perceptual Impairments
Somatosensory
DCML lesion: loss of discriminative touch, light touch, kinesthesia
Spinothalamic/anterolateral lesion: loss of pain/temp/crude touch/kinesthesia
Somatosensory cortical lesion: loss of discriminative senses (proprioception, 2 pt discrimination, stereognosis, touch localization)
Visual
Depth perception deficit
Visual field cuts
Optic nerve lesion = loss of vision in one eye
Optic chiasm lesion = loss of vision bilateral lateral fields
Optic tract lesion = loss of vision contralateral and ipsi-medial fields
Visual acuity deficits
Oculomotor control deficits
MLF lesion = Internuclear Ophthalmoplegia
inability to adduct affected eye combined with nystagmus in unaffected eye
Common in MS patients
Eye malalignment
Tropia- constant eye malalignment
Can sometimes see without testing
ID with cover/uncover test
Phoria- inconsistent eye malalignment
Cannot see without testing
ID with cover/cross-cover test
Vestibular
altered posture/postural control
vertigo/dizziness
Nystagmus
uncontrollable repetitive eye movements, named by fast beat, caused by: alteration of input from PNS or CNS cannot downregulate input
Peripheral lesion
Follows Alexander’s Law
Alexander’s law: nystagmus will always beat in the direction of (relative) hyperstimulation; if lesion is on left, right is relative hyper stimulation so eyes will beat to the right
BBPV (benign paroxysmal positional vertigo)
Combination nystagmus (up/down/horizontal with torsional nystagmus)
Lesion on otolithic organ
Use canalith repositioning maneuver (CRM)
Central lesion
Does not follow Alexander’s Law
Direction changing or torsional or up/down beating
Impaired gaze stabilization
VCR (vestibulocollic reflex): helps keep neck stable so VOR can function well
VOR: helps us keep the world in focus when the head is moving
VSR (vestibulospinal reflex): maintains postural stability
Perceptual deficits
CVA/TBI
postural vertical (posture syndrome)
unilateral neglect (clock drawing test)
Left brain damage = apraxia (motor planning problem)
Saccule lesion = loss of visual vertical
Spatial relation disorders
Difficulty perceiving relationships between oneself & other objects, other objects & self, multiple objects, position in space (over, under, beside, behind, etc.), figure ground discrimination
Cognitive Impairments
Arousal/level of consciousness
Particularly important if CVA affected reticular formation
Attention/motivation
Critical to motor learning
Salience of neuroplasticity
Sustained attention requires focused attention
Focused attention requires arousal to be possible
Selective attention = ability to read with music in the background
Divided attention = multitasking
Orientation
understanding who and where they are and what's expected of them
Memory
Working memory
Conversion of short to long term memory
Recall of memories
Problem solving
If impaired, pt cannot manipulate/apply knowledge to new situations
Neuromuscular Impairments
Muscle weakness
Ortho muscle weakness can lead to neuroplasticity maladaptation
Paralysis/plegia: total or sever loss of muscle activity
Secondary caused by disuse following neurological impairment
Paresis: mild or partial loss of muscle activity
Primary caused by lesion in CNS/PNS
Abnormal muscle tone
Spasticity
velocity dependent increase in tonic stretch reflexes
Due to increased excitability of RST
Develops 1-6 weeks after neural damage
Loss of reciprocal inhibition
Test with fast passive movement
Test quads with pendulum test
Clonus
Baclofen often used to decrease spasticity
Affects CNS so it affects both agonist and antagonist
Can prevent motor learning
Botox can be used to decrease spasticity
More localized
hypertonia
muscle contracture due to additional chronic maladaptive plasticity brought about by increased spasticity
tone
Not velocity dependent
Assessed with Ashworth and modified Ashworth scales
0 = normal; 1 = end range resistance, catch and release; 1+ = tone increase through partial ROM; 2 = marked tone increase through majority ROM; 3 = considerable tone increase making passive movement difficult; 4 (modified scale only) = part(s) rigid in flexion or extension
Passively move joint at slow, constant speed
Hypertonicity = increased resistance to passive movement occurring later in recovery from CVA or TBI
Hypotonia = decreased resistance to passive movement occurring earlier in recovery from CVA or TBI
Common in patients with Down Syndrome or spinocerebellar lesions
Flaccidity = complete loss of tone (no resistance to movement) occurring in neural shock (as with a SCI), peripheral nerve injury, and acute phase of CVA or TBI
Brunnstrom scale
IDEAL progression of recovery from CVA
Moving from flaccidity (1) to spasticity (2) to increased spasticity with synergistic voluntary movement (3) to movement patterns out of synergy (4) to more complex movements with decreased spasticity (5) to disappearance of spasticity (6) to full recovery (7)
Rigidity
passive resistance to movement on both sides of the joint; not velocity dependent
Tardieu scale
Tests for tone AND spasticity by testing at 3 velocities
Normal tone
Reticulospinal tract (RST) and Vestibulospinal tract (VST) work together in normal nervous system. After CNS damage, dorsal RST and CST (both inhibitory) are damaged leading to medial RST and VST (both excitatory) becoming more active
Abnormal synergies
Mass movement and inability to isolate specific joint movements
UE flexion pattern (UMN lesion)
Elbow flexion, supination, shoulder AB/ER, scapular retraction/elevation, wrist/finger flexion
UE extension pattern (UMN lesion)
Shoulder AD/IR, pronation, elbow extension, scapular protraction, wrist/finger flexion
LE flexion pattern (UMN lesion)
Hip flexion/AB/ER, knee flexion, ankle DF/inv, toe DF
LE extension pattern (UMN lesion)
Hip extension/AD/IR, knee extension, ankle PF/inv, toe PF
Tested with active movement
“In synergy” = Brunnstrom 1-3
“Out of synergy” = Brunnstrom 4-6
Associated reactions
Can be bilateral
No standard test
Involuntary movements
Associated movements: unintentional movement of one limb during voluntary movement of another
from CVA or TBI
can be in either limb
Tremor: rhythmical, involuntary oscillatory movement of a body part
resting tremor (PD)
intention tremor (cerebellum lesion)
Choreiform movements: involuntary, abrupt, rapid, irregular, jerky movements
BG lesion: Huntington's Disease
Athetoid movements: slow, involuntary writhing and twisting
Athetoid CP
Dystonia: involuntary, sustained muscle contractions; twisting and repetitive movements and abnormal postures (maybe BG lesion?)
Coordination Problems
Lesions in: motor cortex, basal ganglia, cerebellum, proprioceptive system
Sequencing problem
Activation of muscles in wrong order
Activation of unneeded muscles
Co-activation of muscles
Timing Problem
Problems with initiating movement (increased reaction time)
Patients with CVA, TBI, PD
Slowed movement time
CVA, PD, CP, Cerebellar lesions
Problems terminating movement
Cerebellar lesions
Grading of activation problem
Dysmetria is inability to grade forces and problems judging range/distance
Hypermetria seen in pts w/cerebellar lesions
Hypometria seen in pts w/PD or other BG lesions
Test with finger-to-nose or heel-to-shin
Oromotor/dysarthria
Motor disorder of speech production (arthria/articulation)
Dysdiadochokinesia
Difficulty with rapidly alternating movements (pro/sup or toe taps)
Task Related
Demands of the task (what it takes to do task successfully)
Adaptive equipment
Ex. Adaptive skiing equipment; wheelchairs
Stability
May be easier for a person with PD
Transitions
Mobility
May be easier for a person with CB disorder
Manipulation
Concurrent tasks (divided attention)
Environmental
Challenges in the environment (what must be done to adapt to or navigate in the world)
Ramp to house
Surface
Visual
Closed (home)/Open (grocery store)
Predictable (no pets)/Variable (pets)
Stationary/In motion
Distractions
Noisy environments may be distracting for patients with TBI