Spinal Cord Injury Flashcards
Descending motor function:
Lateral corticospinal (pyramidal) tract
Joint sensation, position, vibration, discriminative touch
Posterior column
Pain and temperature
Lateral spinothalamic tract
Somatic motor
Anterior horn cells
Autonomic sympathetic
Intermediolateral cell column
Motor Signs of Spinal Cord Disorders
• Autonomic neuron signs
• Autonomic neuron signs
• Intermediolateral cell column (T1-L2)
• Sacral autonomic (PSY) neurons (S2-S4)
Intermediolateral cell column (T1-L2)
Horner’s syndrome:
IPSILATERAL
Intermediolateral cell column location
T1-L2
Horner’s syndrome:
• Miosis
• Ptosis
• Anhydrosis
• Enophthalmos
Sacral autonomic (PSY) neurons location
S2-S4
Sacral autonomic (PSY) neurons (S2-S4)
Urinary and bowel incontinence
• Loss of vibration sense
• Loss of position sense
• Loss of 2 point discrimination
• Loss of deep touch
• IPSILATERAL to affected side in dermatomes below or at the level of spinal cord lesion
TRACTS
SEGMENTS
• Posterior column
• Loss of pain sensation
• Loss of temperature sensation
• CONTRALATERAL to affected tract in dermatomes
beginning one or 2 segments below the level of the lesion
• Lateral spinothalamic tract
Pattern of lamination of the spinothalamic tract
• Sacral Sparing
• Lesion affecting the dorsal root will cause diminution or loss of all sensory modalities
• IPSILATERAL and in dermatomes supplied by the involved dorsal root
Dorsal root signs
Bilateral diminution or loss of pain and temperature sensations in dermatomes supplied by the involved spinal cord segments
Anterior white commissure signs
Hyperextension injuries, syringomyelia, intramedullary tumors
Central cord
Often cervical
Dissociated sensory deficits (loss of pain and temperature with preserved
proprioception affecting dermatomes at level of lesion)
As lesion enlarges, weakness, muscle wasting, absent DTRs in arms, and spastic paraparesis occur
Central cord
Anterior spinal artery territory ischemia (aortic dissection, aortic aneurysm surgery, atherosclerosis, vasculitis)
Anterior cord
Sudden loss of pain and temperature below level of lesion, paraparesis and urinary incontinence, but preserved proprioception
Anterior cord
Multiple sclerosis or demyelination, cervial spondylitic. myelopathy, spinal cord tumors, atlantoaxial subluxation, Friedreich ataxia, subacute combined degeneration
Posterior cord
Sensory ataxia (proprioceptive loss), paresthesia, weakness, extensor plantar responses, urinary incontinence, and hermitte phenomenon
Posterior cord
Trauma, multiple sclerosis or demyelination, cord compression
Lateral cord
(Brown-Séquard)
Weakness paresthesia, and proprioceptive loss ipsilateral to lesion Loss of pain and temperature contralateral to lesion
Lateral cord
(Brown-Séquard)
Trauma, cord compression
Complete cord
Loss of sensory, motor, and autonomic function below level of lesion
Complete cord
Amyotrophic lateral sclerosis, primary lateral sclerosis, progressive muscular atrophy, poliomyelitis, HTLV-1 infection, hereditary spastic paraparesis
Pure motor
Spastic paraparesis or tetraparesis with hyperactive DTRs (UMN)
Weakness (monoparesis, paraparesis, tetraparesis), atrophy, fasciculations
(LMN)
Pure motor
Intramedullary tumors, dermoid tumors, lipomas, metastatic
tumors
Conus
Rectal and urinary incontinence, loss of anal reflexes, impotence, saddle anesthesia (S3-5 dermatomes), little or no weakness
Conus
Intervertebral disk herniation, tumors, infections, arachnoiditis
Caudal equina
Areflexic and flaccid paraparesis with back pain that radiates down posterior aspect of both legs, sensory loss in distribution of involved roots, urinary and fecal incontinence
Cauda equina
Brown sequard syndrome
UMN at and below the level of the lesion
• Paralysis, spasticity, hyperreflexia, Babinski,
clonus
Ipsilat corticospinal tract sign
Brown sequard syndrome
• Decreased vibration, position, 2-point discrimination and deep touch at and below the level of the lesion
Ipsilat posterior column sign
Brown sequard syndrome
LMN in muscles supplied by affected cord segment
• Paralysis and atrophy, loss of myotatic reflexes, fibrillations, fasciculation, hypotonia
Ipsilat Ventral horn sign
Loss of pain and temperature beginning one or
2 segments below the level of lesion
Brown-sequard syndrome
Contralat spinothalamic tract signs
Brown sequard syndrome
Segmental loss of thermal sense in dermatomes one or two segments below the level of the hemisection due to the interruption of the spinothalamic fibers crossing in anterior commissure
Bilateral
• Degenerative disease of AHC and LCST
bilaterally
• UMN+LMN
• Progressive
• Involves brainstem motor nuclei
• Spared eye movement and sacral neurons for sphincter control
Anterior horn and Lateral Corticospinal Tract
Syndrome (Motor Neuron Disease or ALS)
• Lesion in central canal will
encroach on the anterior white commissure (crossing fibers of pain and temperature sensations
• Segmental and bilateral loss of pain and temperature in such dermatomes
Central Cord Syndrome (Syringomyelia)
Bilateral but selective degeneration of some of the posterior and lateral column tracts with loss of kinesthesia and discriminative touch,
UMN signs
• Vitamin B12 deficiency (pernicious anemia), Friedreich’s ataxia
Combined system degeneration syndrome
• Abrupt onset
• Flaccid LMN paralysis (spinal shock) occurs within minutes or hours below the level of the lesion and impaired bowel and bladder function
• Dissociated sensory loss characterized by loss of pain and temperature with preservation of posterior column function
• With time, UMN signs predominate
• Development of painful dysesthesia after 6-8 months
Anterior Spinal Artery Syndrome
Motor spinal shock
• Flaccid bilateral paralysis of all muscles innervated by segments of the spinal cord affected and myotomes below
• Sudden withdrawal of a predominantly facilitating or excitatory influence from supraspinal centers
• Shift into UMN in later stages
• Release of segmental reflexes below the level of the lesion from supraspinal inhibitory influences
Sensory spinal shock
All sensations are lost bilaterally at and below the lesion
• Hyperpathic zone at the border of the lesion and for one or 2 segments above it
Bladder function spinal shock
• Urinary retention for 8 days to 8 weeks
• Subsequently, a state of automatic bladder emptying occurs
• Sensory receptors in the bladder wall evoke reflex contraction of detrusor muscles
Bowel function spinal shock
• Paralysis and fecal retention
• Subsequently, intermittent automatic reflex defecation muscles
• Early sphincter dysfunction, urinary incontinence, loss of voluntary emptying of bladder, increased residual urine volume and absent sensation of urge to urinate
• Constipation, impaired sexual function
• Symmetric loss of S2-S4 sensations (saddle anesthesia)
• Loss of ankle jerk
Conus medullaris syndrome
Conus medillaris syndrome
• Symmetric loss of
S2-S4 sensations (saddle anesthesia)
Conus Medullaris Syndrome
Reflex
Loss of ankle jerk
• Early occurrence of radicular pain in dermatomes supplied by the affected roots
• LMN in muscles supplied by affected nerves
Cauda equina syndrome
Leading cause of disability especially among younger people, with high impact on years lived with disability
Traumatic spinal cord injury
Most common cause of traumatic spinal cord injury
MVA
Leading cause of disability especially among younger people, with high impact on years lived with disability
Laceration from missile injury, sharp bone fragments dislocation, or severe distraction, with or without transection
Distraction resulting in forcible stretching of the spinal column in the axial plane with shearing of the
spinal cord or its blood supply
Impact with persistent compression in burst fractures
Impact with only transient compression after hyperextension injuries
Traumatic spinal cord injury
MOI
Primary mechanism
• Initial mechanical injury due to local deformation and energy transformation
• Impact of bone and ligament against the SC
• Subsequent compression, stretching, crushing of the spinal cord
Traumatic spinal cord injury
MOI
Secondary mechanism
• Cascade of biochemical and cellular processes that are initiated by primary mechanisms
• Damage neural structures on cellular level
• Microvascular changes, excitatory amino acids, membrane destabilization, free radicals, inflammatory mediators and neuroglial apoptosis
4 group TSCI Pathobiology
Solid cord injury
Contusion/cavity
Laceration
Massive compression
grossly appears normal without evidence of softening, discoloration or cavity formation; damage can be seen on histologic examination
Solid cord injury
no breach or disruption in surface anatomy, no dural adhesions
Contusion/cavity
clear cut disruption of surface anatomy
Laceration
macerated or pulpified; with severe vertebral body fracture or dislocation
Massive compression
4 phases histopathology
- Immediate
- Acute
- Intermediate
- Late
• Actual mechanical disruption of tissues that occur at the time of injury
• Tears, compression, distortions
• Vasodilation, congestion (hyperemia) and petechial hemorrhages
• Some with no changes
• Pathology of SCI is also due to secondary mechanisms
Immediate phase (first 2 hours)
• Vascular changes, edema, hemorrhage, inflammation, neuronal and myelin changes
• Edema: vasogenic vs cytotoxic
• Pressure-induced ischemia, alter astroglial functions
• Seen from 3 hrs to 3 days after injury
• Vascular injury
• Occur primarily in gray matter following contusion injury
• Hemorrhages due to rupture of postcapillary venules or sulcal arterioles, either from mechanical disruption by trauma or from intravascular coagulation leading to venous stasis and distention
• Inflammatory
• Neutrophil influx peak at 2 days, disappear by 3 days
• Neuronal injury
• Necrosis and apoptosis
• Axonal swelling (retraction balls)
• Myelin breakdown - swelling of myelin sheaths and its fragmentation and phagocytosis by macrophages
• Oligodendrocyte death
Acute phase (hours to 1-2 days)
swelling of myelin sheaths and its fragmentation and phagocytosis by macrophages
Myelin breakdown
• Prominent glial responses with elimination of necrotic debris, beginning of astroglial scarring, resolution of edema, tissue revascularization and BBB restoration
Intermediate phase (days to weeks)
• Wallerian degeneration, astroglial and mesenchymal scar formation, development of cysts and syrinx and schwannosis
• SC replaced by fibrous connective tissue and collagen - act as barriers for axonal migration
• Cysts and syrinx - surrounded by astrogliotic wall and represent the final healing phase of necrosis; filled with ECF, residual macrophages, small bands of connective tissue and blood vessels; not clinical problem but do not provide a good substrate for regeneration
• Schwannosis - aberrant intra- and extramedullary proliferation of Schwann cells with associated axons; barrier to healing; aberrant axons can cause pain, spasticity and other chronic responses
Late phase (weeks to months/years)
act as barriers for axonal migration
SC replaced by fibrous connective tissue and collagen
surrounded by astrogliotic wall and represent the final healing phase of necrosis; filled with ECF, residual macrophages, small bands of connective tissue and blood vessels; not clinical problem but do not provide a good substrate for regeneration
Cysts and syrinx
aberrant intra- and extramedullary proliferation of Schwann cells with associated axons; barrier to healing; aberrant axons can cause pain, spasticity and other chronic responses
Schwannosis
-identify an unstable fracture
X-ray
• Lateral cervical radiograph -identify an unstable fracture
• Lateral, anteroposterior, odontoid view
• Up to 60% of fractures are missed on radiographs
• Conscious patient - dynamic flexion-extension radiographs to assess unstable ligamentous or osteoligamentous injuries
X-ray
Ct scan limitation
• Limitation: relative inability to detect changes in soft tissue including the spinal cord and ligaments
• Minimum neuroimaging required for symptomatic and unconscious patient
• Negative predictive value of 99-100%
X-ray + CT
• Best technique for imaging the spinal cord
• Indications:
• FND with normal x-rays
• Noncorrelation between neurologic deficit and x-ray findings
• Deterioration after treatment
• Failed attempts at closed reduction
MRI
Traumatic Spinal Cord Injury
Neurologic Assessment and Classification
ASIA (American Spinal Injury Association) Impairment Scale
Traumatic Spinal Cord Injury
Neurologic Assessment and Classification
Motor level
most caudal key muscle group that is grades 3/5 or greater, with segments cephalad to that level graded 5/5
Traumatic Spinal Cord Injury
Neurologic Assessment and Classification
Sensory level
most caudal dermatome to have normal light touch
AND pinprick sensations on BOTH sides
Traumatic Spinal Cord Injury
Neurologic Assessment and Classification
Neurologic level of injury
most caudal level at which BOTH motor and sensory modalities are intact
Brown-Sequard Syndrome
% of traumatic SCI
1-5
Brown-Sequard Syndrome
% Best prognosis for ambulation of the SCl syndromes
75-90%
Disproportionately more motor impairment of UE > LE
• Bladder dysfunction
• Varying degrees of sensory loss below the level of lesion
Central cord syndrome
Causes of central cord syndrome
• Most common in elderlies with preexisting cervical spondylosis with superimposed hyperextension injury of cervical spine
• Cord compression occurs between osteophyte-disk complexes anteriorly and in-folded ligamentum flavum posteriorly
• Falls
• MVA
Central cord syndrome
% most common sci syndrome
9
Central cord syndrome
Favorable prognosis for functional recovery
• Younger patients with good hand function
• Early motor recovery
• Absence of lower extremity impairment
• Affects the anterior 2/3 of spinal cord with preservation of the posterior columns
• Complete paralysis
• Loss of pain and temperature sensation below the lesion
• Preservation of touch and proprioception
Anterior cord syndrome
Anterior cord syndrome
% of traumatic SCI
3
Causes of anterior cord syndrome
Flexion injuries, direct damage from bony fragments or disc compression, or ASA occlusion
• Poor prognosis for functional improvement
Posterior cord syndrome %
1
Lesion of posterior column with loss of touch and proprioception below level of injury
• Preservation of pain and temperature
• Preservation of motor strength
Posterior cord syndrome
Posterior cord syndrome causes
• Hyperextension
• PSA occlusion
• Nontraumatic injuries (tumor or Vit B12 deficiency)
• Injury of the caudal spinal cord and associated sacral nerve roots within the spinal canal
• Conus: between L1-L2 vertebra
• Combination of UMN+LMN signs
Conus medullaris syndrome
Conus location
L1 - L2
Conus medullaris syndrome findings
• Saddle anesthesia
• Areflexic bladder and bowel
• Variable LE weakness and sensory loss
Skin is intact with non blanchable erythema
Stage I
Partial thickness skin loss involving the epidermis and dermis
Stage II
Full thickness skin loss extending to subcutaneous tissue but does not cross the fascia beneath it.
Slough or eschar may be visible; may be foul-smelling
Stage III
Full thickness skin loss extends through the fascia with considerable tissue loss; there may be muscle, bone, tendon or joint involvement
Stage IV
Depth unknown because slough or eschar obscures the extent of tissue damage
Unstageable
Occurs with prolonged pressure and shear forces at bone-muscle interface
Intact or non-intact skin w/ persistent, non-blanched, deep red, maroon or purple discoloration
Deep tissue injury
spreads to deeper tissue and bone, blood
Infection
severe fluid and protein loss
Wounds are catabolic
• Injuries above T6
• Loss of coordinated autonomic responses to physiologic stimuli
• Uninhibited or exaggerated SY response to noxious stimuli can lead to extreme HPN through vasoconstriction
• Stimuli: bladder dysfunction, bowel impaction, pressure sores, bone fractures or occult visceral disturbances
• Manifestations: hypertension, bradycardia, headache, sweating
• Severity of attacks correlate with severity of SCl
Autonomic dysreflexia
Autonomic dysreflexia manifestation
hypertension, bradycardia, headache, sweating
Orthostatic hypotension
• Gradual position changes
• Compression stockings
• Abdominal binders
• Medical therapy (a-adrenergic agonist midodrine, mineralocorticoid fludrocortisone
Autonomic dysreflexia
• Upper and midcervical spine (C3-5, output to phrenic nerve)
• Severity of respiratory failure and need for assisted ventilation is directly related to the level of severity of SCI
• Impaired cough strength and difficulty mobilizing lung secretions - increased risk for pneumonia
• Chest physiotherapy
• Vaccination
• DVT and pulmonary embolism
Pulmonary disease
• Neurogenic bladder
• Infections
• Vesicoureteral reflux
• Renal failure
• Calculi
• Impaired sensation of bladder fullness, motor control of bladder and sphincter function
• Clean intermittent catheterization
• Sexual dysfunction
Genitourinary complications
• Structured bowel regimen employing regular diet, 2-3L/day, 30g fiber
• Chemical and mechanical stimulation
Gastrointestinal dysfunction
Gastrointestinal dysfunction
• Structured bowel regimen employing regular diet,
2-3 L/day, 30 g fiber
deposition of bone within soft tissue around peripheral joints; pain and inflammation in affected joints
Heterotropic ossification
• Osteoporosis secondary to disuse - prone to fractures
• Heterotropic ossification - deposition of bone within soft tissue around peripheral joints; pain and inflammation in affected joints
• Tx: passive ROM, bisphosphonates, NSAIDs
Abnormal bone metabolism
Disruption of the descending inhibitory pathways, with increase in excitability of spinal reflexes and resting muscle tone
• Pain, decreased mobility, muscle spasms, contractures
Spasticity
Spasticity prevention
• Proper positioning, passive ROM exercises, appropriate splinting, oral mediations (baclofen, tizanidine, diazepam)
• Depression
• Suicidality
• Drug addiction
• Psychiatric complications
Inflammatory processes of the spinal cord, both infectious and noninfectious
Myelitis
involves white matter
Leukomyelitis
involves the gray matter; Polio virus
Poliomyelitis
involves cross sectional area of the cord
Transverse myelitis
additional involvement of the meninges
Meningomyelitis
Myelitis diagnostic studies
• Spine MRI with contrast
• CSF analysis
• Infectious agents
• Demyelination
Myelitis treatment
• Supportive
• Disease specific
Occur from direct spread (vertebral osteomyelitis, local surgical or anesthetic procedure) or hematogenous spread from distant infection
• Some with no source found
• Risk factor: IV drug use, immunosuppression
• Clinical findings:
• Back pain, fever
• Radicular pain followed by rapidly evolving motor and sensory deficits below level of lesion, sphincter disturbances
Spinal Epidural Abscess
Spine epidural abscess
Laboratory finding
• Peripheral leukocytosis
• Elevated ESR
• Blood cultures
• CSF analysis in unruptured abscess: increased WBC, increased protein, normal glucose
Spinal Epidural Abscess
Imaging
MRI
Spinal Epidural Abscess
Treatment
Drainage
• Stabilization of spine
• Systemic antibiotics
Development of fluid-filled gliosis-lined cavity within the spinal cord (intramedullary) =
Syrinx
• Cavity is irregular and disrupts the anterior horns of gray matter and gray matter ventral to central canal
Syringomyelia
Syringomyelia common loc
C2 and T9-11
• Can extend to brainstem =
Syringobulbia
Cape like distribution of decreased pain and temperature sensation in the back, arms and hands, in which occurs due to disruption of the crossing spinothalamic tracts
• Varying degrees of weakness in arms
(LMN type, involvement of cervical AHC) and legs (UMN, involvement of the lateral corticospinal tract)
• +/ - Horner’s syndrome - intermediolateral columns
• Preserved bowel and bladder function unless syrinx extend to sacral cord
Syringomyelia
Syringomyelia
Imaging
MRI
- direct communication between arteries and veins without interposition of pathologic network
Arteriovenous fistulas
vascular network interposed between feeding arteries and draining veins
Arteriovenous malformation -
• Radicular pain, sensory disturbance, leg weakness, bladder dysfunction
• Slowly progressive in most - due to compression
• 10% sudden onset - due to hemorrhage or infarction
• Weakness and numbness may increase after ambulation
• Pathognomonic bruit over the spinal cord in 25% for patients with intradural
AVM
• Often affects lower thoracic and conus medullaris
Spinal Cord Arteriovenous Shunts
Spinal Cord Arteriovenous Shunts
Imaging
Angiography
Spinal Cord Arteriovenous Shunts
• Treatment
• Complete closure of shunt
• Embolization
• Ligation of feeding vessel and excise the abnormality
• Rare
• 1-2% of vascular neurologic illnesses
• 5-8% of all acute myelopathies
• Sudden onset of symptoms
• Moderate-severe back pain at side of cord infarction (most often in thoracic region) followed by paraplegia within minutes
• Usually associated with paraparesis and loss of pain sensation below the level of infarction bilaterally with intact proprioception and vibration sense
• Loss of bladder control
• Causes: severe hypotension, aortic dissection, aortic surgery, cardioembolism, vasculitis, atherosclerosis
Spinal Cord Infarction
single;
anterior 2/3
Anterior spinal artery -
- dorsal 1/3; greater anastomosis
• Paired posterior spinal arteries
is discontinuous and require multiple feeders
Anterior spinal artery is
least amount of anastomosis; at highest risk
T4-T8
painless paraparesis or quadriparesis that may be sporadic or occur with postural changes but with no loss of consciousness or intracranial localizing features
Spinal TIAs
• Sudden onset paraplegia, loss of pain sensation, loss of bladder control, pain at infarction site
• Initial absence or hypoactivity of DTRs then becomes hyperreflexia
• Spinal TIAs - painless paraparesis or quadriparesis that may be sporadic or occur with postural changes but with no loss of consciousness or intracranial localizing features
• Occur in patients with foraminal stenosis during cervical or lumbar extension
Spinal Cord Infarction
Spinal Cord Infarction
Treatment
Direct to predisposing condition
• Aspirin
• Sudden onset of pain at the site of hemorrhage (most often the upper thoracic)
• Paresthesia and weakness occurring hours or days later below the level of spinal pain
• Urinary retention
Spinal Epidural and Subdural Hematomas
Spinal Epidural and Subdural Hematomas
Diagnostics
• CT - Spinal EDH - high density, oblong mass that sometimes impinges on the lateral aspect of the cord
• MRI
Spinal Epidural and Subdural Hematomas
Prognosis
Dependent on degree of neurologic deficit, timing of decompression (<12hrs)
Motor or sensory loss segmentally or below the level of lesion
• Loss of bladder or bowel control
• Back pain
• Progressive course
• Abnormal CT or MRI
Spinal cord tumors
Intramedullary
Ependymoma
Astrocytoma
Hemangioblastoma
Intradural, extramedullary
Meningioma Schwannoma
Neurofibroma
Extradural
Metastatic cancer
Primary bony lesions, including multiple myeloma
Spinal Cord Tumors
Most common metastatic tumors are found in
vertebral body and epidural space
• Source: lung, breast, prostate, Gl
Spinal Cord Tumors
• Diagnostics:
• Contrast enhanced MRI
• Biopsy and surgical excision
• Travel hematologically through arterial system or retrogradely through Batson venous plexus
• Leptomeningeal metastasis from extension from nearby bone or spread through CSF
Metastatic Cord Compression
Clinical features:
• Weakness, sensory loss, urogenital dysfunction
• PAIN
• Slowly progressive in compressive tumor growth vs acute in vertebral fracture due to tumor
• Red flags:
• Age >60
• Associated weight loss
• Worse at night
• Thoracic rather than lumbar pain
• tenderness
Metastatic Cord Compression
Metastatic Cord Compression
Imaging
Imaging of choice: MRI with contrast
• Visualization of cord, soft tissue involvement and edema
detect bony metastasis
CT scan
Metastatic Cord Compression
Outcome
poor
• Average life expectancy of 4-15 months
