Brunnstrom stages of recovery
Spasticity appears: Muscles begin to show basic movements, sometimes abnormally. For example, muscles may tighten involuntarily in response to a stimulus, such as a prod with a finger.
Stage 2
Decreased spasticity: Involuntary muscle movement starts to decline.
Stage 4
4+
A tap elicits a repeating reflex (clonus) which is always abnormal
- results from compression and damage to anterior part of spinal cord or ASA
- MOI is usually cervical flexion
- loss of motor, pain and temp below lesion
Anterior cord syndrome
- autoimmune disease resulting in neuromuscular junction pathology, associated w/ diabetes, RA, lupus
S&S include:
- extreme fatiguability and skeletal muscle weakness that can fluctuate within minutes or over an extended period
- ocular muscles usually affected first, can experience ptosis and diplopia
Myasthenia Gravis
Complex movement combinations: Increased complex voluntary movements.
Stage 5
Normal function returns: Full motor function returns
Stage 7
D1 Extension
Starting position: Flexion, adduction, external rotation
Ending position: Extension, abduction, internal rotation
- results from compression and damage to central portion of spinal cord
- MOI is usually cervical hyperextension
- UE damaged more than LE, more motor deficits than sensory
Central cord syndrome
- demyelination of sheaths that surround nerves in brain and spinal cord
- highest incidence in patients 20-35 years old
S&S include:
- visual problems, paresthesia, clumsiness, balance dysfunction, weakness, fatigue
- consists of periods of exacerbations and remissions
Multiple sclerosis
Flaccidity: The muscles on the affected side of the body are limp and unable to move.
Stage 1
3+
A very brisk response, which may or may not be normal
D1 Flexion
Starting position: Extension, abduction, internal rotation
Ending position: Flexion, adduction, external rotation
- usually caused by a stab wound which produces hemisection of spinal cord
- ipsilateral paralysis and loss of vibratory and proprioception
- loss of pain and temp on contralateral side
Brown-sequard's syndrome
- deterioration and irreversible damage within cerebral cortex and subcortical areas of brain
- risk increases w/ age and higher incidence in women
S&S include:
- difficulty w/ new learning, loss of orientation, word finding difficulties, depression, impaired self-care
- end-stage includes incontinence, functional dependence, inability to speak
Alzheimer's disease
Spasticity disappears: Coordination returns.
Stage 6
1+
A slight but definite response, which may or may not be normal
D2 Extension
Starting position: flexion, abduction, external rotation
Ending position: extension, adduction, internal rotation
- injury below L1
- peripheral nerve injury
- flaccidity, areflexia, impairment of bowel and bladder function
- full recovery not typical due to distance needed for axonal regeneration
Cauda Equina
- produces UMN and LMN impairments; loss of anterior horn cells and motor cranial nerve nuclei in lower brainstem produces weakness and muscle atrophy, demyelination of corticospinal and corticobulbar tracts produce UMN symptoms
- higher incidence in men 40-70 years old
S&S include:
- asymmetric muscle weakness, cramping, atrophy within hands, weakness spreads distal -> proximal
- spasticity, clonus, (+) babinski, fatigue, oral motor impairment and eventual respiratory paralysis
ALS
Increased spasticity: Involuntary movement increases due to improved neural connections between the brain and muscles.
Stage 3
2+
D2 flexion
Starting position: Extension, adduction, internal rotation
Ending position: Flexion, abduction, external rotation
- caused by compression of PSA
- loss of proprioception, two-point discrimination and stereognosis
- motor function preserved
Posterior cord syndrome
- demyelination of peripheral nerves' myelin sheaths resulting in axonal degeneration
- young adults and adults 50-80
- autoimmune response to respiratory infection; viral infections, Epstein-barr syndrome, cytomegalovirus
S&S include:
- motor, symmetrical weakness distal -> proximal, sensory impairment and possible respiratory paralysis
- peaks within 2-4 weeks, absence of DTR, inability to speak/swallow
GBS or acute polyneuropathy