1. Functions
1.1. conduit of information to and from spinal cord
1.2. Initiates Spinal Reflexes
1.3. Controls body via spinal nerves
2. Anatomy
2.1. Boundaries
2.1.1. Foramen Magnum
2.1.2. Conus Medullaris
2.1.2.1. L1/L2
2.1.3. Cauda Equina
2.2. The mature SC is about 45 cm long and 1cm in diameter
2.3. Segmental organization
2.3.1. 31pair of Spinal nerves
2.4. Enlargements
2.4.1. Cervial
2.4.1.1. C5-T1
2.4.2. Lumbar
2.4.2.1. L1-S3
2.5. White Matter
2.5.1. myelinated axons
2.5.2. Funiculi
2.5.2.1. tracts
2.5.2.1.1. ventral/anterior
2.5.2.1.2. Lateral
2.5.2.1.3. Dorsal/Posterior
2.6. Gray Matter
2.6.1. Cell bodies
2.6.2. unmyelinated axons
2.6.3. interneurons
2.6.4. Ventral Horn (2)
2.6.4.1. LMNs
2.6.4.1.1. Medial Ventral Horn
2.6.4.1.2. Lateral Ventral Horn
2.6.5. Lateral Horn
2.6.5.1. Preganglionic autonomic neuron cell bodies
2.6.5.1.1. T1-L2
2.6.5.1.2. S2-S4
2.6.6. Dorsal horn (2)
2.6.6.1. Sensory
2.6.7. Columns
2.6.7.1. Rexed's Laminae
2.6.7.1.1. Dorsal Horn
2.6.7.1.2. Intermediate/Lateral Horn
2.6.7.1.3. Ventral Horn
2.7. Meninges
2.7.1. Dura
2.7.1.1. tough
2.7.1.2. extends into IV foramina
2.7.1.3. sensory nerve endings
2.7.1.4. Dural sac
2.7.1.4.1. to S2 level
2.7.1.5. Subdural space
2.7.1.5.1. potential space
2.7.1.5.2. serous fluid for lubrication and moistening
2.7.1.6. Epidural Space
2.7.1.6.1. fat
2.7.1.6.2. internal venous plexus
2.7.2. Arachnoid
2.7.2.1. subarachnoid space
2.7.3. Pia
2.7.3.1. denticulate ligaments
2.7.3.2. adhered to SC
2.7.3.3. filum terminale
2.7.3.3.1. coccygeal ligament
2.7.4. Clinical Implications
2.7.4.1. Lumbar Puncture
2.7.4.1.1. lumbar cistern
2.7.4.2. Spinal anesthesia
2.7.4.2.1. spinal nerve block
2.7.4.2.2. epidural nerve block
2.8. Blood Supply
2.8.1. Longitudinal arteries
2.8.1.1. Anterior Spinal artery
2.8.1.1.1. union of branches from vertebral artery
2.8.1.1.2. blockage
2.8.1.2. Posterior Spinal Ateries (2)
2.8.1.2.1. vertebral artery or
2.8.1.2.2. posterior inferior cerebellar arteries
2.8.1.2.3. blockage
2.8.2. Radicular arteries
2.8.3. Segmental Medullary arteries
2.8.3.1. vertebral and deep cervical supply the cervical region
2.8.3.2. posterior intercostal arteries supply thoracic
2.8.3.3. lumbar arteries=lumbar
2.8.3.3.1. Artery of Adamkiewicz
2.8.4. Watershed Area
2.8.4.1. T4-T8 area
2.9. structural Features
2.9.1. Cervical cord
2.9.1.1. oval
2.9.1.2. Dorsal columns
2.9.1.2.1. Gracilis
2.9.1.2.2. cuneatus
2.9.1.3. Ventral horn
2.9.1.3.1. larger
2.9.1.3.2. C3-C8
2.9.1.4. Highest ratio of white matter to gray
2.9.2. Thoracic
2.9.2.1. slim dorsal and ventral horns
2.9.2.2. Lateral horn present here
2.9.2.3. cord is smaller overall
2.9.2.4. cuneatus gone at about T6 level
2.9.3. Lumbosacral
2.9.3.1. round
2.9.3.2. Lateral horn at L1
2.9.3.3. Thicker dorsal and ventral horns
2.9.3.4. dec white to gray matter ratio
3. Tracts
3.1. Sensory
3.1.1. Dorsal Columns (medial Lemniscus)
3.1.1.1. discriminative touch and conscious proprioception
3.1.1.2. Gracilis
3.1.1.2.1. Lower Limb
3.1.1.2.2. medial
3.1.1.3. Cuneatus
3.1.1.3.1. Upper limb
3.1.1.3.2. lateral
3.1.2. anterolateral system
3.1.2.1. spinothalamic
3.1.2.1.1. discriminative pain and temperature
3.1.2.1.2. crude touch
3.1.2.2. slow pain pathways
3.1.2.3. somatotopy
3.1.2.3.1. opposite of dorsal columns so proximal is more medial
3.1.3. spinocerebellar
3.1.3.1. posterior
3.1.3.1.1. unconscious proprioception from lower limb
3.1.3.2. ventral
3.1.3.2.1. feedback from interneurons
3.2. Motor
3.2.1. Ventromedial
3.2.1.1. UMN
3.2.1.2. posture
3.2.1.3. balance
3.2.1.4. head and neck movments
3.2.2. Lateral coricospinal tract
3.2.2.1. voluntary movement
3.2.2.2. distal musculature
3.2.2.3. fine motor movments
4. Reflexes
4.1. Functions of spinal reflexes
4.1.1. Adjust for unexpected pertubations
4.1.2. allow for rapid protection from painful/damaging stimuli
4.1.2.1. withdrawal
4.1.3. organize patterns of coordination
4.2. Types
4.2.1. Superficial
4.2.1.1. skin and mucous membranes
4.2.1.2. corneal
4.2.1.3. cremasteric
4.2.2. Myotatic/Deep Tendon
4.2.2.1. Stretch
4.2.2.1.1. muscle spindle fibers
4.2.2.2. biceps, achilles
4.2.2.3. check nerve roots
4.2.2.4. feedback mechanism for keeping appropriate muscle tone
4.2.2.5. monosynaptic
4.2.2.5.1. alpha motor neurons to muscle group
4.2.2.6. Renshaw cells
4.2.3. reciprocal Inhibition
4.2.3.1. decreases activity of antagonists when an agonist muscle is active
4.2.3.2. occurs in response to myotatic reflex
4.2.4. Inverse Myotatic
4.2.4.1. increased tension
4.2.4.1.1. GTOs
4.2.4.1.2. antagonist contracts
4.2.5. Flexor reflex
4.2.5.1. Withdrawal
4.2.5.1.1. Pain fibers activated
4.2.5.2. Crossed extensor
4.2.5.2.1. contralateral limb
4.2.5.2.2. interneurons
4.2.6. Visceral
4.2.6.1. accomodation
4.2.6.2. carotid sinus
4.2.7. Pathological
4.2.7.1. Babinski
5. Spinal Control of Motor Coordination
5.1. Central Pattern generator
5.1.1. rhythmic output
5.1.2. simplify signals
5.1.3. interneurons in SC and BS
5.1.4. subject to Conscious control
5.1.5. example of how it works
5.2. Sensory influence
5.2.1. modulates activity of the CPG/SPG
5.2.2. how it works
6. Lesions
6.1. Semental Lesion
6.1.1. "patchy loss"
6.1.2. autonomic hard to detect
6.1.3. dermatomal sensory loss
6.1.4. myotomal motor loss
6.2. Vertical Tract Lesion
6.2.1. autonomic loss of
6.2.1.1. descending control of BP
6.2.1.2. pelvic viscera
6.2.1.3. thermoregulation
6.2.2. sensory abnormal or lost below level of lesion
6.2.3. Motor
6.2.3.1. muscle paresis/paralysis
6.2.3.2. UMN signs with LCST involvement
6.2.3.3. from level of lesion down
6.3. example of segmental vs vertical tract
6.4. Causes of Lesions
6.4.1. Trauma
6.4.1.1. crush
6.4.1.2. penetrating
6.4.2. Tumors
6.4.2.1. compression
6.4.3. Degenerative diseases
6.4.3.1. Spondylolysis
6.4.3.2. ALS
6.4.4. Demyelinating diseases
6.4.4.1. MS
6.4.5. Infections
6.4.5.1. Polio myelitis
6.4.6. Disorders of Blood Supply
6.4.6.1. Hemorrhage
6.4.6.2. infarcts
6.4.7. Developmental
6.4.7.1. Spinal Bifida
6.4.7.2. Cerebral Palsy
6.5. Deficits
6.5.1. Predictable
6.5.1.1. DCML
6.5.1.1.1. ipsilateral deficit
6.5.1.1.2. level and below
6.5.1.2. spinothalamic
6.5.1.2.1. contralateral deficit
6.5.1.2.2. 2 segments below
6.5.1.3. corticospinal
6.5.1.3.1. Motor deficit ipsilateral to damage
6.5.2. Spinal Shock
6.5.2.1. Initial LMN signs
6.5.2.1.1. flaccid paresis
6.5.2.1.2. hypo/areflexia
6.5.2.1.3. moderal dec in BP
6.5.2.1.4. absent sphincteric reflexes and tone
6.5.2.2. UMN Signs develop over weeks to months
6.5.2.2.1. Spasticity
6.5.2.2.2. hyperreflexia
6.5.2.2.3. Babinski
6.5.2.2.4. Some spincteric reflexes and erectile dysfunction may return but often without voluntary control
6.5.3. Chronic SC injury
6.5.3.1. neurological deficit stable
6.5.3.2. laste for years-decades
6.6. Syndromes
6.6.1. Definition
6.6.2. importance
6.6.3. Tranverse cord lesion
6.6.3.1. spastic paralysis
6.6.3.2. complete anesthesia
6.6.3.3. Urinary and fecal incontinence
6.6.3.4. Hyperreflexia
6.6.3.5. Breathing paralysis if lesion is above C5
6.6.3.6. anhidrosis, loss of vasomotor tone
6.6.3.7. causes
6.6.3.7.1. trauma
6.6.3.7.2. tumors
6.6.3.7.3. MS
6.6.3.7.4. transverse myelitis
6.6.4. Hemicord Lesion
6.6.4.1. Brown-Sequard syndrome
6.6.4.2. below level of lesion
6.6.4.2.1. ipsilateral
6.6.4.2.2. Contralateral
6.6.4.3. at level of lesion
6.6.4.3.1. ipsilateral
6.6.4.4. causes
6.6.4.4.1. penetrating injury
6.6.4.4.2. MS
6.6.4.4.3. tumors
6.6.5. Posterior Cord Syndrome
6.6.5.1. Bilateral loss
6.6.5.1.1. tactile discrimination
6.6.5.1.2. vibration
6.6.5.1.3. pressure
6.6.5.1.4. proprioception
6.6.5.2. causes
6.6.5.2.1. trauma
6.6.5.2.2. tumor
6.6.5.2.3. MS
6.6.5.2.4. neurosyphillis
6.6.6. Anterior Cord Syndrome
6.6.6.1. Motor
6.6.6.1.1. flaccid paralyis
6.6.6.1.2. areflexia
6.6.6.1.3. larger lesion
6.6.6.2. Pain and temp
6.6.6.2.1. B loss 1-2 segments below lesion
6.6.6.3. causes
6.6.6.3.1. trauma
6.6.6.3.2. MS
6.6.6.3.3. anterior spinal artery infarct
6.6.7. Central Cord syndrome
6.6.7.1. small lesions
6.6.7.1.1. Bilateral loss of pain and temp sensation in affected dermatomal areas
6.6.7.1.2. cervical lesions
6.6.7.1.3. causes
6.6.7.2. Large lesions
6.6.7.2.1. LMN effects
6.6.7.2.2. UMN signs
6.6.7.2.3. Dorsal Columns may be involved
6.6.7.2.4. Anterolateral tracts
6.6.7.2.5. causes
6.7. autonomic dysfunction with spinal cord injury
6.7.1. Know this table
6.7.2. worse the higher you go
6.8. Classification
6.8.1. Complete
6.8.2. incomplete
6.8.2.1. better prognosis
6.8.3. neurologic level
6.8.3.1. sensory and motor function
6.8.3.1.1. most caudal level
6.8.4. American Spinal Cord Injury Association form
6.9. Prognosis
6.9.1. Barriers of regeneration in CNS
6.9.1.1. inhibitory molecules
6.9.1.2. Glial scars
6.9.1.3. Dec Growth factors
6.9.1.4. Mature vs embryonic neurons
6.9.2. Secondary changes following SC injury
6.9.2.1. bleeding
6.9.2.2. edema
6.9.2.3. ischemia
6.9.2.4. Pain
6.9.2.5. inflammation
6.9.3. Research for Tx
6.9.3.1. therapeutic hypothermia
6.9.3.1.1. reduce secondary injury
6.9.3.1.2. promote growth
6.9.3.2. cell transplantation
6.9.3.3. growth factors
6.9.3.3.1. many neuroprotective and neuroregenerative compounds being studied
6.9.4. complications Second Year following SC injury
6.9.4.1. UTI
6.9.4.2. Spasticity
6.9.4.3. Chills and Fever
6.9.4.4. Decubiti
6.9.4.5. Autonomic Dysreflexia
6.9.4.6. Contractures
6.9.4.7. Heterotropic ossification
6.9.4.8. Pneumonia
6.9.5. Rehabilitation
6.9.5.1. Strenghtening
6.9.5.2. ROM
6.9.5.3. mobility/ ADL training
6.9.5.4. adaptive equipment
6.9.5.5. Environmental modifications
6.9.5.6. Body wt support gait training
6.9.5.6.1. incomplete spinal cord injury